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Localisation of Spinal Cord Lesions

Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN University of California, Davis, CA, USA

The ability to complete and interpret results of a neurological examination, compile a list of differential diagnoses, and understand the available diagnostic procedures and current treatment recommendations, is essential in the management of spinal cord disorders of animals. This lecture outlines a diagnostic approach to diseases of the spinal cord. Motor, sensory, reflex, and sphincter abnormalities may be used to determine the location of a lesion within one of four major longitudinal divisions of the spinal cord. The divisions are cervical (C1 to C5 spinal cord segments), cervical enlargement (C6 to T2), thoracolumbar (T3 to L3), and lumbar enlargement (L4 to Cd5). It is essential to remember that these divisions refer to spinal cord segments, not vertebrae, and that spinal cord segments do not correspond exactly with vertebrae of the same number. Some variations may be encountered due to slight differences between animals in segments that form cervical and lumbar enlargements. A disorder of each of the four regions of the spinal cord results in a combination of neurological signs that is specific for the region involved. Recognition of these clinical signs allows accurate localization of a spinal cord lesion. The presence of neurological deficits indicative of involvement of more than one region of the spinal cord is highly suggestive of multifocal or disseminated spinal cord disease. The functional differences between upper motor neurons (UMNs) and LMNs may be used to localize lesions to one of the functional regions of the spinal cord. Cell bodies of spinal cord LMNs are located in the spinal cord gray matter. Their axons leave the spinal cord via the ventral nerve roots to become part of a peripheral nerve, and to terminate in a muscle. The LMNs of the thoracic limb have their cell bodies in C6 to T2 spinal cord segments that form the cervical enlargement, while LMNs of the pelvic limb arise from the L4 through Sl spinal cord segments of the lumbar enlargement. Anal and urethral sphincter LMNs originate from S1 through S3 spinal cord segments. Signs of LMN dysfunction, which in diseases affecting the spinal cord reflect damage to the spinal cord segment(s) from which LMNs originate, are decreased or absent voluntary motor activity, decreased or absent muscle tone, normal, decreased or absent segmental spinal reflexes, and rapid, severe atrophy of an affected muscle due to denervation. Upper motor neurons arise from cell bodies located in the brain. Their axons form descending pathways of the spinal cord and terminate on interneurons that in turn synapse with LMNs. Lesions affecting UMNs result in UMN signs. These UMN signs result from an increase in the excitatory state of LMNs. Upper motor neuron signs include depression or loss of voluntary motor activity, normal or exaggerated segmental spinal reflexes, appearance of abnormal spinal reflexes (e.g., crossed extensor reflex), increased muscle tone, and muscle atrophy due to disuse. Unilateral signs resulting from spinal cord disease are unusual; however, signs frequently are asymmetric. In the majority of cases, a lesion resulting in asymmetric signs is located on the side of greater motor and sensory deficit.

Fatal respiratory paralysis resulting from interruption of descending respiratory motor pathways or damage to motor neurons of the phrenic nerve (C5 to C7 spinal cord segments) occurs in a complete transverse myelopathy. Lesions that are less than complete may not affect respiration, and in such cases other signs may be detectable. Ataxia and paresis of all four limbs usually are seen. Tetraplegia rarely is seen, as lesions of sufficient severity to cause tetraplegia also produce respiratory paralysis. Hemiparesis occasionally may be present in association with a cervical lesion. Lesions of the cervical spinal cord may result in paraparesis with minimal neurologic deficits in thoracic limbs. The reasons for this are poorly understood.

Spinal reflexes and muscle tone are intact in all limbs, and may be normal or exaggerated. Muscle atrophy generally is not present. However, disuse atrophy may develop in cases that have a chronic course. Anal reflexes are intact and anal tone usually is normal. Bladder dysfunction may occur due to detrusor muscle areflexia, with normal or increased urinary sphincter tone, and loss of voluntary control of micturition. Reflex dyssynergia may also be seen. Although voluntary control of defecation may be lost, reflex defecation occurs when feces are present in the rectum. Horner's syndrome (ptosis, miosis, and enophthalmos) rarely may be present in an animal with a severe destructive cervical lesion. Proprioceptive positioning and other postural reactions usually are depressed or absent in all limbs. Complete loss of proprioceptive positioning may occur without detectable loss of pain perception. Cervical hyperesthesia ("spasms," apparent pain on palpation, cervical rigidity, and abnormal neck posture) may be seen in some animals with cervical myelopathy. It should be noted that apparent cervical pain may also be seen in association with lesions affecting the brain stem and cerebrum. Occasionally an animal may hold a thoracic limb in a partially flexed position, a posture that may be consistent with Cl to C5 nerve root or spinal nerve entrapment ("root signature"), although this posture is seen more commonly with a disorder affecting the cervical enlargement. Disorders that affect the cervical region of the spinal cord must be differentiated from brain lesions that result in tetraparesis. This may be accomplished by doing a complete neurologic examination; however, occasionally this distinction may be difficult. In most circumstances a cervical lesion does not result in neurologic deficits attributable to involvement of the medulla oblongata; however, there are several notable exceptions to this rule. Positional strabismus, resulting from loss of the vertebral joint proprioceptive input to the attitudinal reflexes, may be seen in association with a cranial cervical lesion (Cl to C3 spinal cord segments). A cranial cervical lesion may also cause facial hypesthesia as a result of involvement of the spinal nucleus and tract of the trigeminal nerve. Cranial cervical trauma often results in clinical signs referable to injury to the caudal brain stem (head tilt, pharyngeal paresis, facial paresis) or cerebellum. The Schiff-Sherrington sign (syndrome or phenomenon) consists of hypertonicity of thoracic limb muscles and hyperextension of the neck, and is seen in association with spinal cord lesions caudal to the cervical enlargement. It is essential to differentiate this sign from thoracic limb hypertonicity resulting from a cervical lesion.

Ataxia and paresis of all four limbs usually are present. Occasionally paresis of thoracic limbs and paralysis of pelvic limbs may be seen. Spinal reflexes and muscle tone may be normal or decreased in thoracic limbs, and normal or exaggerated in pelvic limbs. The nature of thoracic limb reflex alterations depends on the exact craniocaudal location of a lesion within this region. Muscle atrophy often is severe in thoracic limbs. Panniculus reflex may be depressed or absent unilaterally or bilaterally due to interruption of the LMNs involved in this reflex (C8 and Tl spinal cord segments). If bladder dysfunction occurs, it is similar to that observed with a lesion in the cervical region, with loss of voluntary control of urination. Anal reflexes and anal tone most often are normal although voluntary control of defecation may be absent. Unilateral Horner's syndrome is commonly observed with a spinal cord lesion of the cervical enlargement, particularly a lesion involving Tl to T3 spinal cord segments or nerve roots. Proprioceptive positioning and other postural reactions usually are depressed in all four limbs. Alterations in these functions may be more pronounced in the pelvic limbs than in thoracic limbs. Occasionally, proprioceptive positioning is absent only in a thoracic and pelvic limb on the same side. Severe depression or loss of pain perception rarely is seen in association with a lesion of the cervical enlargement, except in intrinsic myelopathies (e.g., ischaemic myelopathy). There may be hyperesthesia at the level of a lesion of the cervical enlargement, thoracic limb lameness, or apparent neck pain.

The majority of spinal cord lesions of dogs or cats occur in this region. Typically thoracic limb gait is normal, and paresis and ataxia, or paralysis, are seen in pelvic limbs. Thoracic limb spinal reflexes are normal. Pelvic limb spinal reflexes and muscle tone are normal to exaggerated, depending on the severity of the lesion. Muscle atrophy is not seen in thoracic limbs. Pelvic limb muscle atrophy, if present, is the result of disuse and is seen in animals with a severe, chronic lesion. Anal reflexes and anal tone usually are normal or exaggerated. Voluntary control of defecation may be lost. Reflex defecation occurs when the rectum is filled with feces; however, it may not be at an appropriate time or place. Degree of bladder dysfunction varies depending on the severity of a spinal cord lesion. There may be loss of voluntary control of urination, detrusor muscle areflexia with normal or increased urinary sphincter tone, or reflex dyssynergia in which initiation of voiding occurs and is stopped by involuntary contraction of the urethral sphincter. The bladder can be manually expressed in some animals, but not in others due to increased tone of the urinary bladder sphincter. This is often referred to as a "UMN bladder". Although "overflow" incontinence may occur with lesions of the spinal cord in this region secondary to overfilling of the bladder, detrusor muscle tone and urinary sphincter tone are present, distinguishing this type of incontinence from that due to lesions of the lumbar enlargement and cauda equina ("LMN bladder"). Proprioceptive positioning and other postural reactions are normal in the thoracic limbs, and depressed or absent in the pelvic limbs. Pain perception is normal in the thoracic limbs and may be normal, depressed, or absent in the pelvic limbs. Panniculus reflex may be reduced or absent caudal to a lesion. In the lumbar region the panniculus reflex may be present in lesions caudal to L3 due to the pattern of cutaneous innervation of lumbar spinal nerves. There may be an area of hyperesthesia at the level of a lesion. The Schiff-Sherrington sign may be seen with a lesion in this region. Usually it is an indication of an acute and severe spinal cord lesion, although such a lesion may be reversible.

Involvement of this region by a pathologic process results in varying degrees of pelvic limb paresis and ataxia, or paralysis, and is often accompanied by dysfunction of bladder and by paresis or paralysis of anal sphincter and tail. Thoracic limb function is normal. Pelvic limb reflexes and muscle tone are reduced or absent. Muscle atrophy often is present in pelvic limbs. Conscious proprioception and other postural reactions may be reduced or absent in pelvic limbs. Anal tone and anal reflexes are reduced or absent. The rectum and colon may become distended with feces, and fecal incontinence, with continual leakage of feces, is often seen. Constipation may result from the inability to void feces. Paresis or paralysis of the urethral sphincters and detrusor muscle result in overfilling of the bladder and "overflow" incontinence. Affected animals have a large residual volume of urine in the bladder, and the bladder is easily expressed manually ("LMN bladder"). The Schiff-Sherrington sign occasionally may be seen with an acute lesion affecting this region of the spinal cord. The term cauda equina is used to describe the lumbar, sacral, and caudal nerve roots and spinal nerves as they extend caudally from the caudal tip (conus medullaris) of the spinal cord within the vertebral canal. Lesions that affect cauda equina result in clinical signs that are indistinguishable from lesions that affect the spinal cord segments from which the nerves of the cauda equina arise (L6 to Cd5).

Table 1. Diseases affecting the cervical region (spinal cord segments C1-C5) (common causes are included in italics).
Hereditary/congenital Atlantoaxial subluxation Congenital vertebral anomalies

Syringomyelia/hydromyelia Myelodysplasia Spina bifida Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disc disease (Type I/II) Cervical spondylomyelopathy Spondylosis deformans Synovial cyst Inflammatory/infectious Diskospondylitis Corticosteroid responsive meningitis-arteritis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/rickettsial/protothecal myelitis Protozoal myelitis Spinal nematodiasis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischaemic myelopathy Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Nutritional Hypervitaminosis A in cats Idiopathic Spinal intra-arachnoid cysts Osteochondromatosis Calcinosis circumscripta

Table 2. Diseases affecting the cervical enlargement (spinal cord segments C6-T2) (common causes are included in italics).
Hereditary/congenital Congenital vertebral anomalies Spina bifida Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Degenerative Intervertebral disc disease Type I/II Cervical spondylomyelopathy

Diseases affecting the thoracolumbar region (spinal cord segments T3-L3) (common causes are included in italics). Hereditary/congenital Congenital vertebral anomalies Spina bifida Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disk disease Type I/II Degenerative myelopathy Spondylosis deformans Synovial cyst Diffuse idiopathic skeletal hyperostosis Inflammatory/infectious Diskospondylitis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/Rickettsial/protothecal myelitis Protozoal myelitis Spinal nematodiasis .Spondylosis deformans Synovial cyst Inflammatory/infectious Diskospondylitis Distemper myelitis FIP meningitis/myelitis Protozoal myelitis Granulomatous meningoencephalomyelitis Spinal nematodiasis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischaemic myelopathy Progressive hemorrhagic megalomaniac Vascular malformations & benign vascular tumors Nutritional Hypervitaminosis A in cats Idiopathic Spinal intra-arachnoid cysts Osteochondromatosis Table 3.

Diseases affecting the lumbar enlargement (spinal cord segments L4-CD5 and cauda equina) (common causes are included in italics). Hereditary/congenital Spina bifida Sacrocaudal dysgenesis Congenital vertebral anomalies Myelodysplasia Syringomyelia/hydromyelia Pilonidal sinus/epidermoid cyst/dermoid cyst Spinal stenosis Degenerative Intervertebral disk disease Type I/II Lumbosacral vertebral canal stenosis Spondylosis deformans Diffuse idiopathic skeletal hyperostosis Synovial cyst Inflammatory/infectious Diskospondylitis Protozoal myelitis Distemper myelitis FIP meningitis/myelitis Bacterial/fungal/Rickettsial/protothecal myelitis Spinal nematodiasis Granulomatous meningoencephalomyelitis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischemic myelopathy .Granulomatous meningoencephalomyelitis Neoplastic Neoplasia Traumatic Spinal cord trauma Vascular Ischemic myelopathy Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Idiopathic Osteochondromatosis Spinal intra-arachnoid cyst Calcinosis circumscripta Table 4.

DECVN University of California Davis. BVSc. CA. LeCouteur. PhD.Progressive hemorrhagic myelomalacia Hemorrhage Vascular malformations & benign vascular tumors Idiopathic Osteochondromatosis Spinal intra-arachnoid cyst SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Richard A. DACVIM (Neurology). USA .

Fujisawa. Using the information associated with clinical signs. A C1–5 lesion might cause UMN signs to both the thoracic limbs and pelvic limbs but is not always apparent. Kanagawa. the patients with C6–T2 spinal cord lesion might show similar gait abnormalities with decreased or absent postural reactions on neurological examination. PhD Nihon University. The fundamental method to localise the spinal cord lesion including intervertebral disc disease is to localise the lesion into one of following spinal cord segments: cervical (C1–5). To perform proper treatment. especially surgical intervention. thoracolumbar (T3–L3) and lumbosacral (L4–S3).Intervertebral Disc Disease: Old and New Tips to Localise the Lesion WSAVA/FECAVA/BSAVA World Congress 2012 Daisuke Ito. Thoracolumbar Spinal Cord (T3–L3) Clinically the patients with this lesion typically show symmetric/asymmetric paraparesis or paraplegia. Lumbosacral Spinal Cord (L4–S3) Lesions in this spinal cord segment cause signs of LMN dysfunction in pelvic limbs and/or bladder function with symmetric/asymmetric paraparesis or paraplegia. tetraparesis or tetraplegia. postural reactions and LMN (lower motor neuron) and UMN (upper motor neuron) signs of the four limbs obtained by neurological examination. the examiner can localise the lesion. In neurological examination. A C6–T2 lesion typically causes LMN signs to the thoracic limbs (if the lesion involves the grey matter or nerve roots) and UMN signs to the pelvic limbs. some cases only show neck pain without proprioceptive or gait deficits. Spinal Cord Dysfunction and Neurological Signs Cervical Spinal Cord (C1–5) A lesion in this spinal cord segment can cause hemiparesis. Patients with lesions in this area may show decreased or absent postural reactions in four limbs. hemiplegia. and symptomatic disease can arise at any site where there is an intervertebral disc. DVM. Japan 23011742 Intervertebral disc disease is one of the most common disorders in dogs (but rare in cats). Cervicothoracic Spinal Cord (C6–T2) Similar to C1–5 lesion. the thoracic limbs have normal postural reactions and spinal reflexes. The absolute difference of neurological disorders between cervical and cervicothoracic lesions is the reflexes in the four limbs. cervicothoracic (C6–T2). However. localising the lesion is important. and the pelvic limbs have decreased or absent postural reaction with UMN signs of spinal reflex. L4–6 lesions cause signs of LMN dysfunction in the pelvic limbs with decreased to absent patellar reflex and intact . Clinical signs are typically ipsilateral to the lesion. but there are specific predilection sites.

Therefore an advanced imaging modality that can describe intervertebral disc protrusion/extrusion and compression of the spinal cord. In addition. such as myelography. intervertebral foraminal size and intervertebral disc space. the pudendal nerve (decrease to absent perineal reflex) and the pelvic nerve (LMN bladder dysfunction). it is important that the spine should be straight and the radiographic beam centred directly over the suspected area to avoid misinterpretation of vertebral alignment. Figure 1. computed tomography (CT) scanning and magnetic resonance imaging (MRI) must be performed for accurate localisation. the presence of these findings does not always provide accurate lesion and definitive diagnosis. Survey spinal radiograph (lateral view). because the neurons of the femoral nerve are in this area. Spinal Radiography Survey radiographs of vertebrae are often performed at the suspected area of the lesion during the diagnostic evaluation. Therefore spinal radiographs often cannot reveal any abnormal findings of soft tissue spinal compressive disease such as Hansen type I disc extrusion.withdrawal reflex. . The survey radiographic findings to suggest intervertebral disc extrusion are: Wedging or collapse of the intervertebral disc space Decrease in the articular facet joint space dimensions Thinning or alteration in the intervertebral foramen (shaped like horse's head) Radio-opaque disc material apparently within the spinal canal (Figure 1) To evaluate these findings on spinal radiographs. L7–S3 lesions cause signs of LMN dysfunction in the area which innervates the sciatic nerve (decreased to absent withdrawal reflex and gastrocnemius reflex). However. the limitation is that the spinal cord and non-mineralised intervertebral disc material cannot be seen on these radiographs.

but is sometimes found dorsally. Myelography provides a white parallel outline of the spinal cord through an injection of radio-opaque contrast medium into the subarachnoid space (Figure 2). It is difficult to localise the lesion when the spinal cord swelling occurs. myelography has been most commonly used to diagnose and localise the lesion of intervertebral disc disease. The disadvantages of myelography are: Invasiveness because the spinal needle enters the spinal cord in close proximity to the filum terminale and the spinal cord (for lumbar myelography) to inject contrast medium into ventral arachnoid space.Mineralised intervertebral disc material is apparently seen within the spinal canal (arrow) with collapse of intervertebral disc space (arrowhead). This technique can be used to detect intervertebral disc material compressing the spinal cord by observing the absence of the contrast medium in the sub-arachnoid space. Herniated disc material is usually seen ventral or lateral to the spinal cord. . Myelography During the past two decades.

Therefore CT myelography. it is difficult to distinguish herniated disc material and haemorrhage because both lesions show hyperdensity on CT images. might be needed for further evaluation. . The degenerated disc material is seen with a hyperdensity (white). bottom). However it is very difficult to assess the spinal cord itself because it is poorly distinguished from other soft tissue within the vertebral canal. Reconstructed CT images (sagittal view. Figure 3. The advantage of CT is that images can be reconstructed on computer and several views including sagittal. Myelography (healthy dog). transverse and horizontal images can be made to evaluate the lesion site (Figure 3). In addition. transverse view. CT with a subarachnoid injection of the contrast medium.Figure 2. Computed Tomography CT is also useful to detect herniated/protruded intervertebral disc material in the spinal canal. top.

Sagittal planes are important for understanding anatomical structures of the affected region of the intervertebral disc and the spinal cord. ventral or dorsal) and extent of extruded disc material by evaluating multiple planes. MRI allows concise localisation of extruded or protruded disc material including the affected area (right or left. T2weighted and contrasted T1-weighted images. and transverse images are important to know the exact location of any compressive material surrounding the spinal cord in a cross-sectional plane (Figure 4). Hence these two different views . Magnetic Resonance Imaging (MRI) Because of its efficient ability to reveal the localisation of intervertebral disc disease and the condition of the spinal cord.A hyperdense lesion can be seen on both the sagittal (arrow) and transverse (arrowhead) views. The MR images are usually collected at least in sagittal and transverse T1-weighted. MRI is rapidly becoming the gold standard imaging modality.

MR myelography can describe the lesion by detecting disappearance of CSF line (Figure 5. . left). The nerve root image can show accurate localisation of herniated disc material in association with nerve root (Figure 5. we would recommend other types of image using FE3D sequence (TR 45.8 ms) to reveal the nerve roots called a 'nerve root image'. TE 6. and MR myelography using fast spin echo single shot (TR 6000 ms. However. above and transverse T2weighted image. Additional views such as dorsal (coronal) images might be helpful to understand the location of the lesion and anatomical variations.are important to recognise the location of the lesion especially if surgical intervention is to occur. TE 1000 ms) to describe the line of cerebrospinal fluid (CSF) in preference to taking simple dorsal images. arrowhead). arrow). Figure 4. MR images (midsagittal T2-weighted image.9 ms.

An extruded intervertebral disc material compresses the spinal cord (arrow and arrowhead respectively). Figure 5. . MR nerve root image (left) and MR myelography (right).

Kanagawa. DVM. Japan .Herniated disc material is compressing the spinal cord (white arrow) and the nerve root adjacent to the disc material is apparent (black arrow). Disappearance of CSF line can be seen on MR myelography (arrowhead). Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Daisuke Ito. PhD Nihon University Fujisawa.

and the animal may appear normal at rest. circling) and mental status (e.. MVM. MRCVS Senior Lecturer in Veterinary Neurology. In part this is to exclude the possibility of non-neurological disease.g. Institute of Comparative Medicine. The hands-off examination allows evaluation of: posture (e. UK 18273874 Before embarking on the neurological examination it is essential to always first obtain a good history and perform a detailed clinical examination. BVSc. . Certain abnormalities may suggest that the problem actually lies within the brain (or cranial nerves) and not the spine. Some abnormalities (for example a high stepping gait) are only apparent when the animal walks. wide-based stance). Penderis. depressed). but in forebrain disease the major clinical sign is often altered behaviour.. Faculty of Veterinary Medicine.The Neurological Examination British Small Animal Veterinary Congress 2007 J.g. PhD. for example circling or a head tilt. alert.g. DECVN. Problems that may mimic a neurological lesion include metabolic problems (e. University of Glasgow Glasgow. Localise the lesion Determine the severity of the lesion Establish possible causes Establish a prognosis How Do We Perform the Actual Neurological Examination? We first start with the hands-off examination. gait (e..g. CertVR. head tilt. where we assess the animal as it walks around and interacts with its surroundings (usually the consulting room) Then start with the hands-on localisation (involving pinpointing the lesion to a smaller and smaller area) We also assess for signs of intracranial or cranial nerve disease Hands-Off Examination It is essential to watch the animal walk and interact with the surroundings. ataxia.. hepatic encephalopathy) and bilateral orthopaedic problems. What are we trying to achieve by performing a neurological examination: Establish if there is a neurological lesion.

... proprioception and evaluating for weakness: Evaluating the animal walking has already partly assessed proprioception and weakness Paw position response--tests conscious proprioception Hopping--allows you to assess for weakness in each individual limb Based on which limbs are affected some information about the localisation should be apparent: All four limbs affected: lesion is likely to be from the brain to the cervical enlargement (cranial to T3 spinal cord segment) or a polyneuropathy/polymyositis . the sacral segments)? Accurate localisation to specific spinal cord segments (e.e.Hands-On Localisation The idea of the hands-on localisation is to pinpoint stepwise the lesion to a progressively smaller area.g. upper motor neuron or lower motor neuron)? Are the tail..e.e. by focal pain or panniculus reflex) Determine the severity of the lesion Determine Which Limbs are Affected Not all spinal cord pathways are equally susceptible to injury and therefore when deciding whether a limb is affected we use that function that is lost first. Summary of the basic steps of the hands-on examination: Determine which limbs are affected Does the lesion affect the reflex arcs to the limbs (i. i. bladder and anus affected (i.

Spinal reflexes which are routinely assessed include the extensor carpi radialis (may be hard to elicit in cats and small dogs). the sacral and caudal segments)? Assess the anal reflex.If the pelvic limbs are affected and the thoracic limbs are normal. Factors evaluated Resting muscle tone Limb flexion and extension Spinal reflexes Muscle atrophy UMN lesion Normal Slight resistance Normal to exaggerated Little and late (disuse) LMN lesion Normal to decreased Decreased resistance Normal. flaccid bladder. If bladder function is impaired then it is important to ascertain whether there is increased sphincter tone (with urinary retention and overflow) or decreased sphincter tone (with a half full. Bladder and Anus Affected (i. or a pelvic limb peripheral nerve or muscle lesion If just one thoracic limb is affected the lesion is likely to be on that side in peripheral supply to that limb Does the Lesion Affect the Reflex Arcs (upper motor neuron or lower motor neuron)? If the reflex arcs to the limbs are involved then one or more of the abnormalities in Figure 1 may be present. Upper motor neuron or lower motor neuron lesions. Figure 1.e. .. patellar reflex and withdrawal reflex (pedal or flexor reflex). decreased or absent Early and severe (neurogenic) Are the Tail. this indicates a spinal cord lesion behind the cervical enlargement (caudal to T3). which is very easy to express). bladder function and tail function.

Figure 2. Localisation of lesions. .Based on the examination so far the lesion should localise to (unless multifocal or extensive) one of the areas illustrated in Figure 2. Accurate Localisation to Specific Spinal Cord Segments If the lesion is focal then it may be further pinpointed by evaluation for: Focal pain LMN lesion: assess which muscle groups are affected Panniculus reflex: allows accurate localisation in the T3-L3 region of the spinal cord and assesses the brachial plexus (outflow of the panniculus reflex) Determining the Severity of the Lesion Due to varying susceptibility of different spinal pathways injuries can usually be graded. The critical prognostic feature is the presence or absence of conscious pain in the affected limbs.

g.. uncharacteristic behaviour) Circling: in the majority of cases this is towards the lesion. This includes decreased facial sensory awareness.. i. loss of obedience training.Grade 0 Normal 1 Pain: not severe enough to result in any neurological dysfunction 2 Paresis with or without pain 3 Plegia: total loss of voluntary movement in the affected limbs (and/or tail) 4 Plegia with loss of voluntary urinary function 5 Plegia with loss of voluntary urinary function and loss of deep pain Syndrome Approach to Intracranial and Cranial Nerve Lesions If the lesion could involve the brain then a simple method of localising intracranial and cranial nerve (CN) lesions is to try and group them in one of three 'syndromes' or regions of the brain. conscious proprioceptive deficits and the so-called 'hemi-neglect' or 'hemi-inattention' syndrome Blindness opposite to the lesion (central blindness. hypoglycaemia or hepatic encephalopathy. with intact pupillary light reflexes) Decreased levels of consciousness. loss of house training.g. e.. Multifocal lesions may affect more than one region. Clinical Signs of Cerebellar Disease . but can be away from the lesion Head turn (the head is not tilted: the ears are still horizontal): usually towards the lesion Conscious sensory deficits opposite to the lesion. typically to the level of a stupor An important differential diagnosis of diffuse and symmetrical cerebral lesions is the presence of a metabolic or toxic cause. The syndromes include: The forebrain and/or the associated cranial nerves I and II The cerebellum The brainstem and/or the associated cranial nerves III to XII Clinical Signs of Forebrain Lesions Seizures Altered behaviour (e.e. The neurological deficits are described and an attempt is made to fit the neurological abnormalities into one of the three syndromes.

Clinical Signs of Brainstem Disease The brainstem. IV trochlear nerve and VI abducent nerve Most important function: motor to the extraocular muscles and pupil constrictor . The observed clinical spectrum varies from depression to stupor to coma The important cranial nerves in clinical practice associated with the brainstem: III oculomotor nerve. Damage to the brainstem will usually result in damage to numerous adjacent brainstem structures. Interference with the vital brainstem functions will usually result in rapid death due to failure of respiratory function Alteration in mentation. body and head and in the unconscious maintenance of balance. usually with an exaggerated limb movement (hypermetria) but in some instances decreased limb movements (hypometria) Truncal ataxia and even a truncal sway Head tremor Muscle hypertonia Bilateral menace response deficits in the presence of intact vision and facial nerve function Unilateral cerebellar lesions will usually result in deficits on the same side as the lesion. Diffuse cerebellar lesions will therefore result in a loss of this moderating influence and interfere with the unconscious maintenance of balance. but rarely the sympathetic pathways) Brainstem nuclei of cranial nerves III to XII Brainstem nuclei controlling (amongst others) motor function and the vital functions (respiration and cardiac function). range or force of movement). is an extremely important region of the brain.The cerebellum has an important function in controlling and moderating movements of the limbs. with clinical signs of: Symmetrical ataxia with no loss of strength Dysmetric gait (altered rate. as the continuation of the spinal cord tracts and the site of numerous tightly packed cranial nerve nuclei. These include: Ascending afferent pathways (primarily the proprioceptive tracts) Descending efferent pathways (primarily the motor tracts.

UK . PhD. deviation of the face to the unaffected side and/or dry eye and nose in combination VIII vestibulocochlear nerve Function: hearing and balance Lesion: ipsilateral deafness and ipsilateral vestibular dysfunction XI hypoglossal nerve Function: motor to the tongue muscles Lesion: bilateral lesion--tongue paralysis. Unilateral masticatory muscle atrophy (unilateral motor lesion). Author Information (click the author's name to view other papers and abstracts submitted by this author) Jacques Penderis. inability to blink.Lesion: dilated pupil and/or abnormal eye position or paralysis of the extraocular muscles V trigeminal nerve Function: motor to the masticatory muscles and sensation to the face and eyeball Lesion: dropped jaw (bilateral motor lesion). although in some cases the tongue can deviated towards the unaffected side. DECVN. Loss of sensation to face. cornea or nasal mucosa (sensory lesion). Unilateral lesion--unilateral tongue atrophy and protrusion of tongue to affected side. VII facial nerve Most important function: motor to the muscles of facial expression Lesion: look for drooping lip or ear with drooling saliva from affected side of mouth. MVM. MRCVS Institute of Comparative Medicine. Faculty of Veterinary Medicine University of Glasgow Glasgow. CertVR. BVSc.

g. DACVIM (Neurology). awareness and motor function) are normal. Awareness and arousal (consciousness) are dependent on the function of the ascending reticular activating system (ARAS). or cerebellar signs. so we talk about animals having a region-specific localisation . ascending sensory systems (tactile. brainstem disease. Or. given a set of clinical signs (normal and abnormal).. brainstem (midbrain. pons and medulla oblongata). Massey University. In veterinary medicine. proprioception and nociception). The NeuroMap and accompanying table are designed to help you localise neurological lesions.g. motor function (posture and gait). you can read from the NeuroMap which neural functions could be disrupted and conversely. cranial nerve function. Thomson. from which is constructed a ready reference table (Table 2) that can be used in conjunction with the BrainMap for localizing lesions. including: behaviour and arousal. encephalitis). Palmerston North.the forebrain. then you can list the possible causes and make a diagnostic plan. New Zealand 24418236 This talk follows on from the previous talk. The NeuroMap is based on mapping the main neural functions on a diagram of the nervous system.. The NeuroMap depicts the location of the main neural functions tested in the neurological examination. Thus. 2. decreased arousal can occur with focal lesions in the brainstem (e.g. this is the first and most fundamental step in managing a neurological case. which neural functions will be normal.. Each region is associated with characteristic neurological signs. you can work out from the NeuroMap where the lesion is likely to be located. and the cerebellum. Functions Assessed During the Neurological Examination 1. BVSc (Hons).e. New Zealand Veterinary Association. Once you've localised the lesion. there are three main regions of the brain . Functional Brain Divisions Functionally. If a lesion is in a particular area. In this session. tumour) or diffuse lesions of the cerebrum (e..g. This is located in the brainstem and has diffuse projections throughout the forebrain. . it can only be expressed if other neural functions (e. we'll discuss further the components evaluated in a neurological examination and add them to a BrainMap (see Figure 1). it is useful to talk about five different arousal levels. Behaviour is primarily associated with the forebrain (limbic system). forebrain disease.Localising Neurologic Lesions Using the NeuroMap: Brain World Small Animal Veterinary Association World Congress Proceedings. DECVN. and spinal reflexes. However. so please refer to those notes prior to reading this. 2013 Christine E. PhD VetLearn.

thus. lesions in that region can cause vestibular signs (nystagmus. e. Loss of subconscious proprioceptive input to the cerebellum results in ataxia (incoordinated movement). Upper motor neurons (UMN or 'central MN') arise from both motor centres and influence brainstem and spinal cord lower motor neurons (LMN or peripheral MN). 3. Dysfunction of agonist-antagonist contraction causes tremor. thereby ensuring that movement occurs with the correct rate. cerebellar dysfunction can cause hypermetria and spasticity. requires a noxious stimulus to arouse it Unconscious. A specific region of the cerebellum processes vestibular input.. Input from the limbs and body is via spinal nerves and the spinal cord travelling to the ipsilateral cerebellum (subconscious proprioception) or the contralateral forebrain (conscious proprioception). This is called metria. Overall. Arousal level Normal Obtunded Stuporous Comatose Description Bright. Head proprioception arises from the vestibular apparatus in the inner ear. Proprioception is awareness of body position (see previous session notes).g. travels to the brainstem and then cerebellum (SCP) or forebrain (CP). as that is the site of attachment of CNN III and IV. no brainstem reflex function Note: 'Depressed' is a psychological term and is inappropriate. 4. innervating extraocular muscles. As specific cranial nerves are associated with different areas of the brain. cat playing with a feather. the output from the cerebellum is inhibitory.g. Therefore. cranial nerve signs can be quite localising. range. and force of movement.. while forebrain lesions usually have minimal effect on gait but will affect learned movements. The cerebellum functions to coordinate the activity of extensor and flexor muscles to achieve the correct tone in opposing muscles for sustaining posture and smoothing movement. The cerebellum uses SCP input to influence the output from the UMN centres. cannot be roused by even a noxious stimulus Brain dead No cerebrocortical electrical activity. e. brainstem lesions can severely perturb gait (paresis). strabismus may suggest a rostral brainstem lesion. therefore. animals with spinal cord lesions have intact cranial nerve function. tends to fall asleep if left undisturbed. alert and responsive Dull. head tilt). but can be aroused by non-noxious stimuli Somnolent. Motor function in quadrupeds is controlled by motor centres in the brainstem (for semiautomatic activities such as locomotion) and from the motor cortex in the contralateral cerebrum for voluntary motor activity (learned. 5. . skilled). Cranial nerves are primarily associated with the brain.Table 1.

the left forebrain is likely to be involved. and knuckles (CP deficit) on the right side. cerebellum. or spinal cord. coordination. you will be able to see which neurological functions will be compromised and which will still function normally. but not cranial nerve reflexes. both the signs of dysfunction and signs of normal function have helped you localise the lesion. then this also supports a lesion in the forebrain and not the brainstem.6. identify the pathways associated with each deficit and see where they coincide .g. so the lesion is probably quite large. Conversely. too.. Vision is also associated with the forebrain (primarily contralateral). which is associated with specific aetiologies (e.that is likely to be the location of the lesion. and general locomotion. Identify the CP pathway on the NeuroMap: the lesion could be in the spinal cord or forebrain (contralateral). blind in the right eye. then the animal may have multifocal disease.. Thus. spinal cord reflexes. Obtundation can occur with diffuse lesions of the forebrain. Reflexes involving both spinal and cranial nerve reflexes are tested during the neurological examination. For example. thus. may be compromised with spinal cord lesions. . and spinal reflexes are intact. Conversely. If you cannot account for all signs with a single lesion. inflammation or tumour). Those reflexes involving cranial nerves may be compromised with brain lesions. If the function of other cranial nerves (III–XII). but not spinal cord lesions. with a coin) representing a lesion.g. The NeuroMap Figure 1 depicts the location of the main neural functions tested in the neurological examination. If you cover a region of the brain on the NeuroMap (e. if you have a case with specific neurological deficits. consider an animal that is obtunded.

sensory cortex No Yes Yes No Yes Brainstem Yes Yes. major site of planning motor UMN nuclei in Yes. important for Yes. Summary of neural signs that can occur with lesions in different parts of the brain Function Conscious proprioception Subconscious Proprioception Nociception Motor systems Forebrain Yes. for motor Yes coordination. Table 2. but UMN tracts .Figure 1. caudal brainstem Cerebellum No Yes Spinal cord Yes Yes Yes. The NeuroMap of the brain Roman numerals refer to cranial nerves.

emotion and memory Arousal Yes Limbic system Yes.function and voluntary movement Motor cortex (UMN). limbs and tail No No No Yes (the ascending reticular activating system (ARAS) CN III–XII No No Cranial nerves CN VIII head and eyeball positionb Intact Noa Spinal reflexes Intact Intact Could be reduced/lost a = Part of CN XI (accessory nerve) arises from the cervical spinal cord. b = Important links between the cerebellum and vestibular system mean that some vestibular signs may occur with lesions in certain parts of the cerebellum. functions in voluntary motor activity. BVSc (Hons). Behaviour. Figure and tables reprinted with permission from: Thomson C. important in posture and locomotion. New Zealand Veterinary Association Massey University Palmerston North. DECVN. DACVIM (Neurol). Thomson. New Zealand . ISBN 9780702034824. but it is hard to see signs of its dysfunction with lesions in this area of spinal cord. 2012. Thomson C. Hahn C. Hahn C. PhD VetLearn. body. Elsevier Health Sciences. No LMNs. ISBN 9780702034824. Note: Seizures will only occur with forebrain disease. Veterinary Neuroanatomy: A Clinical Approach. Cranial nerves have LMNs innervating head and neck muscles no UMNs (no weakness) LMNs innervating neck. 2012. Veterinary Neuroanatomy: A Clinical Approach. Elsevier Health Sciences. the ARAS projects to widespread areas of forebrain CN I. but has a minor role in gait. References 1. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. II quadrupeds.

Damage to any one of those components will cause reduction/loss of the reflex.The Brain and Cranial Nerves ACVIM 2012 Christine E. Remembering the NeuroRAT (Session 35. Thomson. cranial nerve function. A key feature about the NeuroMap is that you don't need a degree in neuroanatomical-ese (terminology) to get a basic understanding of what could be happening in the nervous system of your patient. in which the five main neural functions tested in the neurological examination are mapped onto a diagram of the brain. DACVIM(Neurology). See Session 35 re 'central' and 'peripheral' MNs. proprioception and nociception). motor function (posture and gait). In this session we'll draw a NeuroMap (see Figure 1) to help with localizing brain lesions and from that construct a ready reference table (Table 2) that can be used in conjunction with the BrainMap. and spinal the origin. particularly if it is not something you do frequently. DECVN. It is accompanied by a ready reference table. . Using the neurological examination to identify both the neural functions that are normal and those that are abnormal (dysfunctional). The NeuroMap is based on mapping out the location of the main functions of the nervous system. New Zealand 23241061 This session follows on from Session 35. it can be seen from the NeuroMap what neural functions may be disrupted with a lesion in a certain area and conversely. Figure 2 & Table 1) to help differentiate between lesions affecting upper (central) motor neurons (UMNs) and lower (peripheral) motor neurons (LMNs). 4. ascending sensory systems (tactile. what neural functions will be normal. See Figure 1. Using the battery and light bulb analogy to remember that signs of dysfunction can be due to a lesion located anywhere along the neural pathway . a central connection in the CNS (brain or spinal cord. The NeuroMap is a simple.The Neuromap: A Simple Guide to Localizing Neurological Lesions . Spinal sensitivity (hyperpathia) can further localise the lesion in spinal cord cases. for reflexes involving the cranial and spinal nerves. PhD Palmerston North. respectively) and a LMN that connects back to the muscle via a neuromuscular junction. These functions are behaviour and arousal. middle of the pathway or at the pathway termination. 5. 3.Spinal Cord and Peripheral Nervous System.input from a sensory receptor in the periphery. visual aid that can help with localizing lesions in the nervous system. Thus. Session 35. The NeuroMap. A reflex has three parts to it . 2. BVSc(Hons). Localising the neurological lesions can be challenging. It uses the same key concepts discussed in Session 35 as follows: 1. The NeuroMap: A Simple Guide to Localizing Neurological Lesions .

or brainstem disease or cerebellar signs). brainstem (midbrain.g. Note: the commonly used term 'depressed' is a psychological term and is inappropriate: 1. decreased consciousness can be due to focal lesions involving the brainstem or diffuse lesions of the cerebrum. Normal . Subconscious proprioception projects to the ipsilateral cerebellum.Functional brain divisions: Functionally. no brainstem reflex function Proprioception from the limbs and body travels cranially along the spinal cord. UMNs influence lower (peripheral) motor neurons that exit the CNS in cranial and spinal nerves. Neurological Functions Assessed During the Neurological Examination Behaviour is primarily associated with the forebrain (limbic system). whereas conscious proprioception projects to the contralateral forebrain (somatosensory cortex) (see session 35 notes). respectively. the brain can be divided into three main regions: the forebrain. forebrain disease. Comatose . requires a noxious stimulus to arouse it 4. The motor cortex of the forebrain functions primarily to direct voluntary. but its expression is dependent on other neural functions being normal. five different levels of arousal can be described.bright. Because clinical signs of brain disease are characteristic for each region. then we talk about animals having a region-specific localization (e. In quadrupeds. Awareness and arousal are associated with the ascending reticular activating system (ARAS) of the brain stem and its diffuse projections into the cerebrum. cannot be roused by even a noxious stimulus 5. but can be aroused by non-noxious stimuli 3. pons and medulla oblongata) and the cerebellum. limbs and tail. alert and responsive 2. The tracts passing into the spinal cord are called pyramidal UMNs as they pass through the structures in the caudal brainstem called the 'pyramids'. Obtunded . The motor cortex influences LMNs in the brainstem that give rise to cranial nerves. so subtle changes in arousal might be missed. In veterinary cerebrocortical electrical activity. tends to fall asleep if left undisturbed. Brain dead . One of the best ways to determine arousal levels is by observation. Stuporous . body. Brainstem UMN centres give rise to extrapyramidal UMNs (tracts do not pass through the pyramids) influencing . learned movements in the head.somnolent. Clinically. Motor function: Upper (central) motor neurons in quadrupeds originate in the forebrain (motor cortex) and brainstem motor nuclei. the brainstem UMN centres are important for posture and locomotion and semi-automatic activities such as chewing and swallowing. and LMNs that exit the spinal cord as spinal nerves. from brainstem and spinal cord. Proprioception for the head is from the vestibular apparatus in the inner ear. What is the animal's awareness like when it is left quietly in the environment? As soon as you start handling the animal it will be stimulated..dull.

LMNs in cranial and spinal nerves. hypermetria and tremor. V. ataxia (incoordinated gait). it has to know where the body parts are located in space. range and force of movement ('metria'). brainstem lesions can severely perturb gait (paresis). Thus. Thus.. IX and X. Head function Olfaction Vision Innervation Ia IIa Clinical testing Dysfunction Observation. The cerebellum's job is to coordinate motor function to achieve posture. VIII. body and head (subconscious proprioception). while forebrain lesions usually have minimal effect of gait. Testing the function of cranial nerves is outlined in Table 1. as the wiring of their reflex arc is intact. has reduced facial sensation and cannot swallow) probably has brainstem disease affecting cranial nerves VII.IIa & IIIe (parasympathetic) Blindness. Specific cranial nerves are associated with each region of the brain. Conversely in an animal with purely brain disease. the spinal reflexes should be intact. Table 1. mentation. dilated pupil Note: mydriasis can also be due to primary ophthalmic disease or CN III dysfunction Anisocoria. It also coordinates the contraction/relaxation of agonist/antagonist muscles acting around the joint. cannot blink and has a droopy ear. Cranial nerves: Noting cranial nerve dysfunction can be quite localising. IIIe Pupillary light reflex parasympathetic. To coordinate motor function. odourant such Dysosmia as food Maze test Menace response . Cranial nerve reflexes may be compromised if the cranial nerve. An animal that has multiple cranial nerve signs (e. Spinal reflexes should be intact (present) in animals with brain lesions. As the cerebellum has a calming down (inhibitory) effect on motor function.g..IIa & VIIe Pupillary light reflex . Mydriasis ( CN II (input) or CN III parasympathetic output) Miosis ( sympathetic Pupil size IIa. but clinically they are not associated with spinal cord function. Therefore. cranially directed proprioceptive tracts and UMN centres). cerebellar disease can result in altered posture. e Pharmacological testing sympathetic. cerebellar dysfunction can result in excess motor function. Testing the function of cranial nerves. characteristically this causes spasticity. Reflexes: Both spinal and cranial nerve reflexes are tested. e . an animal with spinal cord disease should have intact cranial nerve function (identifying normal function is just as important as identifying those neural functions that are abnormal in lesion localisation). and the correct rate. Such a brainstem lesion will probably have compromised other functions in the brainstem (e. or the region of the CNS associated with the reflex has been damaged.g. so it must constantly receive proprioceptive information from the limbs. has a head tilt.

mandibular) Mastication Ve . external nares. IVe. (Note cerebellar lesions and primary ophthalmic lesions can also affect pupil size) Eyeball position VIIIa IIIe.. ears Symmetry of position of lip commissures when head is held up vertically.dynamic (vestibular) Facial hypoalgesia . IV or VI).ipsilateral with brainstem disease . ventral eyelid .g. . rolling Spontaneous nystagmus. dorsal eyelid. IVe.static (LMN affecting cranial nerves III.mandibular Muscle atrophy Dropped jaw if bilateral Facial expression VIIe Facial symmetry Facial paresis/paralysis Palpebral reflex Va & VIIe Auriculo-palbebral reflexes Va & VIIe Movement of muzzle. circling.maxillary br) Auriculo-palbebral reflex Va & VIIe (stimulate just in front of the external ear canal) Jaw tone Assess the bulk of the masticatory muscles e. VIe Visual tracking of moving objects Eyeball position in different head positions Vestibulo-ocular reflex VIIIa & IIIe. Vie Tactile stimulation Va different regions of the face . VI) Vestibulo-ocular reflex (VIIIa & IIIe. VIe) Gait and movement Head tilt.all three branches (ophthalmic.contralateral with forebrain disease Facial sensation Va . mandible Palpebral reflex . eyelids. temporalis and masseter muscles Strabismus . IVe.innervation). abnormal vestibule-ocular reflex Strabismus Deranged body posture and ataxia Vestibular function VIIIa . Head position Eyeball position (also involves III.muzzle and ventral eyelid.Va & VIIe (dorsal eyelid ophthalmic br. maxillary. IV.

you can identify on the NeuroMap where the wiring for one of the functions is.thus the lesion must be in the left forebrain. you will be able to see which neurological functions will be compromised and which will still function normally. both the signs of dysfunction and signs of normal function have helped you localise the lesion. The right side of the body is affected.. vision (forebrain).g. knuckling on right forepaw and hind paw. As cranial nerves (III–XII) are functioning normally. blindness in the right eye. That all fits. reasonable gait (UMN from the brainstem) then the lesion is not in the brainstem or the cerebellum. representing a lesion in it. and obtundation. What other functions are passing through this region? Sensory input from both the pelvic and thoracic limbs and arousal are associated with the forebrain. a & e Tongue XIIe Observation . Dysphagia Xe) Salivation Swallowing Phonation Respiration Dysphonia Respiratory stridor laryngeal obstruction. and the animal has intact subconscious proprioception. e. e. paresis/paralysis unilateral or bilateral X & XI.Pharyngeal function Laryngeal function IX & X. Thus. If you cover a region of the brain on the NeuroMap. e = efferent (output) The NeuroMap (Figure 1) depicts where the main neural functions tested in the neurological examination are located.LMN signs. Both vision and conscious proprioception are received in the contralateral forebrain . relatively normal gait. Conversely if you have an animal with particular signs.g. a & e Gag reflex (IXa.. Xa & IXe. Aspiration Atrophy. . usage Withdrawal from tactile stimulus a = afferent (input).

Function Proprioception a) Conscious b) Subconscious Nociception Yes. Roman numerals refer to cranial nerves. important in posture and locomotion. The NeuroMap of the brain. limbs and tail Forebrain Brainstem Cerebellum Spinal cord Motor systems Yes. major site of UMN nuclei in quadrupeds. important for planning motor function and voluntary movement Motor cortex (UMN).Figure 1. Cranial nerves No Yes No Yes. for motor coordination. caudal brainstem Yes Yes. somatosensory cortex No Yes Yes Yes. body. but no UMNs (no weakness) Yes Yes Yes Yes UMN tracts LMNs innervating neck. Table 2. functions in voluntary motor . Summary of neural signs that can occur with lesions in different parts of the brain.

No LMNs. the ARAS projects to widespread areas of forebrain have LMNs innervating head and neck muscles No No No Yes (the No ascending reticular activating system (ARAS) CN III–XII CN VIII head and eyeball positionb Intact No Cranial nerves CN I. II Noa Spinal reflexes Intact Intact Could be reduced/lost a=Part of CN XI (accessory nerve) arises from the cervical spinal cord. Elsevier Health Sciences. Behaviour. Note: seizures will only occur with forebrain disease. DACVIM Massey University Palmerston North. ISBN 9780702034824. New Zealand . AL. but it is hard to see signs of its dysfunction with lesions in this area of spinal cord.activity. Thomson. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. emotion and memory Arousal Yes Limbic system Yes. but has a minor role in gait. b=important links between the cerebellum and vestibular system means that some vestibular signs may occur with lesions in certain parts of the cerebellum References Figures and tables reprinted with permission from Veterinary Neuroanatomy: A Clinical Approach by Christine Thomson and Caroline Hahn. May 2012.

Even without specialist facilities for definitive diagnosis. can easily mimic some common neurological presentations such as gait abnormality. Furthermore. A detailed clinical examination should therefore be performed before embarking on the neurological examination. Are You Dealing With a Nervous System Lesion? A number of non-neurological conditions may mimic a nervous system lesion. MRCVS. Disease severity helps to determine prognosis of the differential diagnoses. The third question is answered by compiling the information on the patient signalment and history of the problem with the anatomical diagnosis to determine the differential diagnosis. DVM. Garosi. infectious or neoplastic diseases of the nervous system may also affect other body systems. to name a few. Diagnostic tests are then carried out to investigate the differential diagnosis. What Are the Goals of the Neurological Examination? The aims of the neurological evaluation are to answer the following questions: Do the clinical signs observed refer to a nervous system lesion? What is the location of this lesion within the nervous system? What are the main types of disease process that can explain the clinical signs? How severe is the problem? The first two questions are answered by performing a general physical and neurological examination and aim to determine the anatomical diagnosis (location and distribution of the lesion within the nervous system). Manor Farm Business Park. UK 19885013 Introduction The lack of initial thoughts as to where exactly the problem might be within the nervous system and what kind of disease processes may be there is the most common cause of failure in the diagnosis of neurological condition in dogs or cats. a great deal of information can be gained from the neurological examination with some basic knowledge and a logical stepwise approach. DECVN.The Neurological Exam British Small Animal Veterinary Congress 2010 Laurent S. RCVS & European Specialist in Veterinary Neurology Davies Veterinary Specialists. cardiorespiratory diseases or metabolic disturbances. Higham Gobion. Orthopaedic problems. neuromuscular weakness or collapse. The choice and interpretation of these tests must rely on a clear knowledge of the anatomical diagnosis and the expected disease processes. some inflammatory. Why Should You Attempt to Localise the Problem Within the Nervous System? .

affecting multiple parts of the nervous system) or diffuse (i. brainstem. Finally. What Are the Principles of Lesion Localisation? Before rushing into the specifics of the neurological examination. muscle. the differential diagnosis is entirely dependent on the anatomical diagnosis. if present. the clinician should be able to determine whether or not the animal is neurologically sound. L4-L6 spinal cord segments. attention should be focused on what questions you want answered: Is there any neurological abnormality detected? Which part(s) of the nervous system may be involved to explain these abnormalities? Is the lesion localisation focal. multifocal or diffuse? The first question does not require any detailed knowledge of neuroanatomy or neuroanatomical pathways. If there is failure to localise the lesion. running a limited number of investigations aimed at narrowing down the differential list to a specific part of the nervous system can only be good as it should result in less cost for the owners and less time taken to reach a diagnosis. Neurological abnormalities detected on examination should be listed and added to the list of abnormal findings collected from the history. T3-L3 spinal cord segments. By simple observation and testing a number of reflexes and responses. multifocal (i.e. The location is the anatomical diagnosis.The purpose of the neurological examination is to determine the neurological abnormalities and. peripheral nerve. Attempts should then be made to explain all the abnormal findings by a single lesion within one of the following regions of the nervous system: focal forebrain. affecting globally and symmetrically one or more parts of the nervous system). C1-C5 spinal cord segments. C6-T2 spinal cord segments. the location of the lesion or lesions responsible for causing these abnormalities.. Furthermore. neuromuscular junction. based on that. From a diagnostic point of view. Such information can then be used to narrow down the differential list even further (see section on how to establish a differential diagnosis list). a number of disease processes may only be diagnosed by exclusion of other causes mimicking a similar clinical history and presentation. for the clinician. localising the lesion also involves determining whether the problem is focal. Narrowing down to which part(s) of the nervous system may be affected can undeniably present a number of advantages. detect any functional deficit. Lesions within these regions of the nervous system result in predictable and specific neurological signs. Aside from determining which part of the nervous system is affected. L7-S3 spinal cord segments. Each of these abnormal findings should then be correlated to a specific region or to specific pathways within the peripheral and/or central nervous system. cerebellum. Note that in localising a lesion. This process of exclusion implies evaluating the correct part of the nervous system to confidently rule out these mimics. Normal findings are as important as the abnormal ones in localising the lesion. the interpretation of any diagnostic test results can be a very challenging task for the clinician in the face of negative findings (as seen with some vascular or degenerative diseases of the central nervous system) or findings that do not match the clinical history. The neurological examination aims to test the integrity of these various components of the nervous system and. it is not necessary ..e.

neuromuscular junction and muscles. They only evaluate the spinal segment(s) within the intumescences corresponding to the stimulated nerve. the pupils' reaction to light. ventroflexion of the neck (associated with neuromuscular disorder or severe cervical spinal cord grey matter lesion) and spinal curvature (kyphosis or lordosis). A normal gait requires intact function of the brainstem. The aim of performing such diagnostic tests should only be to confirm or exclude the differentials in the list and not replace . Determination of a differential diagnosis list is essential in choosing and interpreting any diagnostic test however sophisticated they may be. paretic (weak) or lame (from either neuromuscular disease or an orthopaedic disorder) and which limb(s) are involved. visual or tactile placing response. Spinal reflex evaluation should be considered as a continuation of the evaluation of the gait and postural reactions and not as a sole entity. jaw and tongue function and command of the muscles of facial expression. Lesions at the level of these intumescences result in loss of segmental spinal reflexes as well as reduced muscle tone and size. head turn (associated with ipsilateral forebrain lesion). as well as the animal's ability to generate movement in the part tested.that all the clinical signs referable to one location or syndrome be present. Posture evaluation helps to appreciate the general symmetry of the animal and its balance while standing. How to Establish a Differential Diagnosis List The differential diagnosis list is entirely dependent on the location of the lesion within the nervous system. Spinal reflex evaluation helps to narrow down further the lesion localisation by testing the integrity of the C6-T2 and L4-S3 intumescences as well as respective segmental sensory and motor nerves that form the peripheral nerves and the muscles innervated. The reactions commonly tested are the paw replacement (or 'knuckling' response). swallowing. the lesion localisation is considered as multifocal or diffuse. Cranial nerve examination helps to evaluate functions such as balance. especially the limbs. They do NOT require consciousness. awareness of its environment and attitude to being handled. hopping. Hands-On Examination The primary aim of postural reaction testing is to detect subtle deficits that were not obvious on gait evaluation. vision. It can also reveal abnormal postures such as head tilt (associated with vestibular disorder). If a single lesion cannot explain all the listed abnormal findings. How to Practically Localise the Problem Within the Nervous System The neurological examination can be divided into two main parts. Evaluation of the gait should be done with the aim of determining whether the patient is ataxic (uncoordinated). Hands-Off Examination The first step in the neurological examination should focus on evaluating the animal's state of consciousness. These reactions test the animal's awareness of the precise position and movements of parts of its body. cerebellum. spinal cord and sensory and motor peripheral nerves. Spinal reflexes are segmental.

presence of asymmetry. MRCVS. consideration should only be given to diagnostic tests that help to narrow down the list further and to those that can be afforded by the client.. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Laurent S. DECVN. onset and progression as well as distribution within the nervous system. Garosi.the clinical evaluation. What To Do Next? With a clear understanding of the region of nervous system involved and the differential list reduced to no more than three or four disease processes. UK . The differential diagnosis list can be developed taking into account signalment. historical data (mode of onset and evolution of the condition. Hertfordshire. RCVS & European Specialist in Veterinary Neurology Davies Veterinary Specialists Higham Gobion..) and neurological findings (location and distribution of the disease within the nervous system). DVM. These tests should ideally be run from the least invasive (and least expensive) to the more invasive test. Disease processes that can affect the nervous system are classically categorised according to the mnemonic VITAMIN D: Vascular Inflammatory/Infectious Traumatic/Toxic Anomalous Metabolic Idiopathic Neoplastic/Nutritional Degenerative Each of these disease processes has a typical signalment.

You can read from the NeuroMap what neural functions may be disrupted with a lesion in a certain area and conversely. The NeuroMap is a simple visual aid that has been designed as a ready reference guide to assist you in localising lesions. if a neural function is not associated with that region. then it could damage pathways in that region and cause signs of dysfunction. the light won't work. However. an animal has a proprioceptive deficit and is standing on top of its paw (knuckling). Localising neurological lesions can be challenging. 2) it doesn't matter where a lesion is sited along the neural pathway (origin. the clinician can see where each of the neural functions being tested is located in the nervous system. Whenever possible. If a lesion is in a particular region. If there is a problem with any component. Thomson.Spinal Cord and Peripheral Nervous System ACVIM 2012 Christine E. Based on the results of the tests. If not. cranial nerve function. the peripheral nerve or spinal cord pathway or brainstem (middle). then it will not be affected. proprioception and nociception) motor function. A key feature about the NeuroMap is that you don't need a degree in neuroanatomical-ese (terminology) to get a basic understanding of what could be happening in the nervous system of your patient. Using the NeuroMap. and spinal reflexes. then the animal is considered to have a multifocal lesion. It is accompanied by a ready reference table. Once the lesion is localised. either because neural pathways begin or end there. Identifying the . Spinal sensitivity (hyperpathia) may further localise a spinal cord lesion. Two key concepts underlie lesion localization: 1) you need to note both the neural systems that are functioning normally. or the sensory cortex of the forebrain (termination). New Zealand 23241060 The aim of the neurological examination is to determine whether neurological dysfunction is present and. which makes certain diseases more likely. PhD Palmerston North. BVSc(Hons). or are passing through it.The NeuroMap: A Simple Guide to Localizing Neurological Lesions . particularly if it is not something you do frequently. where the lesion causing the dysfunction is located in the nervous system. The NeuroMap is based on mapping out the location of the main functions of the nervous system. if so. the clinical signs of dysfunction will be similar. DECVN. The lesion could be in the sensory receptor (origin). This is analogous to a battery (origin). which parts of the nervous system are functioning normally and which parts are functioning abnormally. For example. we try to see if the signs can all be accounted for by a single lesion. what neural functions will be normal. DACVIM(Neurology). The neurological examination involves evaluating five neural functions: behaviour and arousal. as well as those that are dysfunctional (Figure 1). wire (middle) and light bulb (termination). middle or termination). Can a single lesion account for all the observed signs .both the normal and abnormal? A number of functions are associated with most regions of the nervous system. the possible causes can be listed and an appropriate diagnostic and subsequent treatment plan can be implemented. the clinician determines whether the animal has neurological deficits and if so. ascending sensory systems (tactile.

LMN = lower motor neuron . Figure 1. In this instance. Therefore that which is NORMAL (C). Normal AND abnormal function in the nervous system helps to localise a lesion.g. . UMN disease damages UMNs (motor neurons in the brain or spinal cord).this indicates a conscious proprioception deficit (see later text) and can be represented by pathway B in Figure 1. is just as important to identify as that which is ABNORMAL for localising the lesion. Consider the animal knuckling on its hindpaws .neural pathways that are functioning normally indicates to the examiner that the lesion is probably not located in the region that those systems occupy. limbs) and autonomic LMNs supply smooth muscle (e. Upper and lower motor neurons: UMN = upper motor neuron . but we know that A is also compromised and C is functioning normally.. Thus the lesion must be at X and not Y. but the cutaneous trunci reflex (pathway C) is intact. the axon is largely in the periphery. the urinary bladder).you could also think of it as a 'central motor neuron' as the neuron is confined to the central nervous system (CNS = brain and spinal cord).g. The lesion could be anywhere along that pathway. along the spinal cord to the brainstem where it crosses sides and travels rostrally to the sensory cortex of the forebrain. LMNs supply striated muscle ( could also think of it as a 'peripheral motor neuron' as although the neuronal cell body is found in the CNS. X represents the lumbosacral spinal cord. The proprioceptive pathway (B) begins in the foot and travels up specific nerves to the spinal cord. The animal also has loss of the withdrawal reflex in that limb (pathway A).. while LMN disease damages LMNs (motor neurons that are mainly in the peripheral spinal and cranial nerves.

thoracolumbar disease. UMN disease (damage to the UMNs) LMN disease (damage to the LMNs) Decreased to absent Sign Reflexes Normal to increased Atrophy Disuse: Mild. brachial plexus giving rise to the radial nerve). A = Atrophy (of muscles). The NeuroRAT ..g. For the dog.g. specific muscles Tone Normal to increased Decreased to absent A spinal cord segment is a region of spinal cord to which is attached a pair of dorsal (sensory) nerve roots and a pair of ventral (motor) nerve roots. R = Reflexes. Functional regions of the spinal cord are based around where the limb innervation attaches. The dorsal and ventral roots fuse to form a spinal nerve. C3 spinal nerve). then we talk about animals having a region-specific localisation e.think of the Neuro RAT. The table lists the changes that may be present caudal to the lesion. thoracolumbar (T3–L3: trunk). this creates the regions: cervical (C1–5: neck). To help remember how to differentiate between lesions affecting upper (central) motor neurons and lower (peripheral) motor neurons ..reflexes. atrophy and tone. . spinal nerves attach bilaterally to each spinal cord segment. generalised Neurogenic: severe. T = Tone. Because clinical signs of spinal cord disease are characteristic for each region.Figure 2 and Table 1. lumbosacral intumescence (L4–S3: pelvic limbs and viscera) and caudal segments (Cd1–5: tail).g. cervical intumescence (C6–T2: thoracic limbs). or spinal nerves may fuse in a plexus to form specific named nerves (e. they may remain discrete (e.. These segmental spinal nerves form much of the peripheral nervous system (PNS) of the body and limbs.

Subconscious proprioception is particularly important for posture and locomotion. This information is projected to the cerebellum which then uses it to modulate motor function associated with postural and locomotory muscles. Damage to any one of those components will cause reduction/loss of the reflex. As the upper (central) motor neuron has been compromised. A C1–C5 lesion will result in UMN signs to both the pelvic and thoracic limbs. It originates in receptors in muscles and tendons. viscera such as the fullness of the urinary bladder). Thus in this example. where the limb innervation originates. Loss of inhibitory UMNs can result in excess LMN activity and reflex function. respectively. the pelvic limbs will have intact reflexes. the LMN to the thoracic limbs will also be compromised. then the reflex arc and its LMN and the neuromuscular junction will be intact.g. UMN versus LMN disease: If an animal has a lesion at one of the intumescences (cervical or lumbosacral). If an animal has a lesion cranial to the intumescence (e. Increased muscle tone and reflexes: UMNs can facilitate or inhibit LMNs. thermal and noxious stimuli) and the internal environment (e. Thus. loss of inhibitory UMN may result in increased extensor tonus (spasticity). the muscle will still be innervated. Loss of facilitatory UMNs can result in paresis (decreased movement). Note: an animal will have UMN signs to the pelvic limbs if the lesion is located anywhere in the spinal cord cranial to L4. If the lesion was in the cervical intumescence.this information is projected to the contralateral forebrain for conscious awareness. Sensory function and proprioception: Also remember that it is not just motor neurons that will be compromised by a lesion in the spinal cord. respectively) and a lower (peripheral) motor neuron that connects back to the muscle via a neuromuscular junction. in the case of thoracolumbar disease. Thus UMN signs are not nearly as localising as LMN signs.. . thoracolumbar or cervical lesion). These signs are quite localising and the clinician can tell which specific nerves. Atrophy of specific muscles within that limb and reduced muscle Tone.. This includes sensory information about body position (proprioception). about the external environment (tactile. Continence can also be affected (see below). for reflexes involving the cranial and spinal nerves.the information that is projected to the ipsilateral cerebellum. the UMN supplying the pelvic limbs have been compromised. and as the muscles still have their LMN innervation. they will have tone and any muscle atrophy will be mild due to disuse. but LMN signs to the thoracic limbs. the animal is described as having UMN signs to the pelvic limbs. then it is likely to compromise the lower (peripheral) motor neurons innervating that limb resulting in LMN signs: reduced Reflexes. both at rest and during movement. or which specific spinal cord segments. have been compromised. The perineal and the cutaneous trunci reflexes are also used to evaluate sacral and thoracolumbar spinal cord function. but the sensory innervation will also be affected from the body caudal to the lesion. The main reflexes used to assess limb innervation are the patellar and withdrawal reflexes in the pelvic limbs and the withdrawal reflex in the thoracic limbs. it's the sort of information that is used to keep the limbs located under the body's centre of gravity. the animal will have UMN signs to the pelvic limbs. a central connection in the CNS (brain or spinal cord.Reflexes: A reflex has three anatomical parts to it: input from a sensory receptor in the periphery. There are two kinds of proprioception: 1) subconscious proprioception .g. 2) conscious proprioception . As the LMNs supplying extensor (antigravity) muscles dominate those supplying flexor muscles.

the anal sphincter may be dilated and the animal will be faecally incontinent. the reflex arc for the withdrawal reflex will still be present in the pelvic limbs. but it will not be able to consciously perceive the noxious stimulus.] Note: As both conscious and subconscious proprioceptive tracts travel up the spinal cord.g. Innervation of the urinary bladder and anal sphincter: Sensory input from the bladder wall. Thus. the parts of the body caudal to the lesion are often ataxic or the limbs have a stumbling gait. and the animal may stand on the top of its paw(s).. urinary sphincter and perineum travels to the sacral spinal cord (S1–3). uncommonly one elimination system only may be affected. or cross its feet when ambulating. It will probably have ataxia (incoordination of gait). lesions affecting the sacral spinal cord will result in LMN signs with reduced detrusor muscle tone and perineal reflex. If the lesion is cranial to the sacral spinal cord.Subconscious proprioception will be compromised in an animal with cerebellar disease (affecting pathway termination). when a noxious stimulus is applied to the hind foot. floppy. the kitten patting at a feather). but the cranially directed nociceptive tracts will be interrupted. and because of poor tone in the striated sphincter. [Copies of subconscious proprioceptive information is sent to the forebrain too (kinaesthesia) so the animal can be consciously aware of posture and locomotion. from the paw) will not be received. Thus. . Nociception involves the transmission of noxious (tissue-damaging) stimuli by spinal nerves to the spinal cord where it stimulates local reflex function (e. This implies severe spinal cord damage. The LMNs innervating the bladder wall and the sphincters result in muscle tone and are necessary for reflex function. so it may stand base-wide or base-narrow. the bladder will be full. Similarly. withdrawal reflex) or is projected to the forebrain for conscious perception. then the LMNs supplying the bladder wall and the striated muscle of the urinary and anal sphincters will be intact. Cranially directed pathways convey information about the fullness of the bladder and rectum to the brain for conscious perception. In an animal with a transected thoracolumbar spinal cord. The sacral spinal cord (S1–3) is the origin of LMNs supplying the bladder wall smooth muscle (parasympathetic innervation . to lose conscious perception of a noxious stimulus requires that the spinal cord has been extensively damaged. Sympathetic LMNs arise from the cranial lumbar spinal cord and stimulate contraction of smooth muscle at the neck of the bladder and relaxation of bladder wall muscle for urine storage. Conscious proprioception is important for awareness of movement. An animal that has forebrain disease will still have good posture and locomotion (subconscious proprioception is intact).. The bladder will be large. It may not know where its limbs are with respect to its centre of gravity. It travels to the forebrain in many pathways distributed across the transverse area of the spinal cord.g. it will be easy to express and the animal will probably be dribbling urine. Spinal cord disease often affects both urinary and faecal continence. and poor tone in the anal sphincter.this stimulates detrusor muscle contraction during voiding) and the striated muscle of the urinary and anal sphincters (contraction maintains continence). turgid and difficult to express. Thus. spinal cord lesions often affect both types of proprioception. Tactile input is a key component of this. the animal may stand on top of its foot ('knuckling'). Thus.. the latter sign occurs because of loss of UMN inhibition to the LMNs innervating the urinary sphincter. the animal will still pull its foot away. particularly movement that is voluntary and learned (e. Thus. but the information from tactile receptors (e.g.

that is possible with a lesion in the C6–T2 region. What other functions are passing through this region? Yes. Figure 3. knuckling on all four limbs. you can identify on the NeuroMap where the wiring is for one of those functions [e. Thus. loss of thoracic limb reflexes). Conversely. Summary of effect of lesions in different areas of the spinal cord.g. UMN to the pelvic limbs and sensory input from both the pelvic and thoracic limbs.yes. Loss of Presence of Presence of LMN proprioception and UMN signs to limbs. tetraparesis. (C6–T2)].Using the NeuroMap: If you cover a region of the spinal cord in the NeuroMap (representing a lesion in it). if you have an animal with particular signs (e. The NeuroMap for the spinal cord and spinal nerves. the thoracic reflexes. Cutaneous Faecal incontinencec affected trunci and perineal reflexes intact .. both the signs of dysfunction and signs of normal function have helped you localise the lesion. Table 2. Loss sensory input signs of other reflexes TL and PL both affected Location of lesion Cervical C1–5 Loss of urinary and faecal continence TL and PL No LMN signs in TL UMN bladdera both and PL..g. you will be able to see which neurological functions will be compromised and which will still function normally. The pelvic limb reflexes are intact implying that their LMN are intact . That all fits. but with intact pelvic limb reflexes.

distended. a = UMN bladder .flaccid. New Zealand . perineal reflex intact LMN signs to pelvic viscera. May 2012. easy to express. Elsevier Health Sciences. depends on lesion severity. Thomson. Note: whether or not all signs are present.Cervical intumescence C6–T2 Thoracolumbar T3–L3 TL and PL both affected PL only TL. perineal reflex intact LMN signs in PL UMN bladder Cutaneous trunci Faecal incontinence reflex intact. Perineal reflex intact No LMN signs in TL UMN bladder or PL Faecal incontinence Cutaneous trunci reflex lost caudal to lesion. but may not be aware that it is defaecating. PL = pelvic limb. faecal incontinence Normal continence PL only affected (TL normal) PL only (TL normal) Cranial lumbosacral L4–S1 Caudal lumbosacral S1–S3 Caudal nerves Cd1–5 PL only affected (TL normal) No UMN signs to limbs No UMN signs to limbs No UMN signs to limbs TL normal. full. b = LMN bladder . dribbling urine. c = animal will deposit faeces with good emptying of colon. difficult to express.turgid. DACVIM Massey University Palmerston North. d = may see some proprioceptive deficits or paresis with an S1–S3 lesion as S1 and S2 make variable contributions to the sciatic nerves. Loss of perineal reflex LMN signs to tail LMN bladderb LMN anal sphincter (dilated anus). PL probably normald Decreased tail sensation TL = thoracic limb. ISBN 9780702034824. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. References Figures and tables reprinted with permission from Veterinary Neuroanatomy: A Clinical Approach by Christine Thomson and Caroline Hahn. loss of cutaneous UMN bladder trunci reflex if lesion Faecal incontinencec in C8–T2. AL.

The vestibular nuclei are also connected to the neurons in the spinal cord via descending pathways which adjust tone in the muscles of the neck. Fujisawa. including the cochlea. CN VIII has bipolar neurons. Neuroanatomically and functionally. Kanagawa. This coordination of eye and head movement is called the . Peripheral Component The membranous labyrinth and the vestibular portion of the vestibulocochlear nerve are the peripheral vestibular components in the inner ear. and position of the eyes in relation to head position or movement. Central Component The central part of the vestibular system includes structures within the brainstem and cerebellum. The vestibulocochlear nerve comprises sensory neurons of the 8th cranial nerve (CN VIII). The vestibular nuclei are connected to the nuclei of the oculomotor (CN III).Peripheral or Central Vestibular Disease: Yes. The function of the utricle and saccule is to detect gravity and linear acceleration and that of the semicircular canals is to detect head rotation. and to neurons in the rostral portion of the cerebellum. and the utricle. The first step to diagnose cases with vestibular system abnormalities is localisation of the lesion: determining whether the lesion is in the peripheral or central vestibular system is critically important for making differential diagnosis and predicting prognosis. which manages auditory function. orientation and balance of the head and trunk. trochlear (CN IV) and abducens (CN VI) nerves and aid in control of eye movements. which manage vestibular function. It Matters WSAVA/FECAVA/BSAVA World Congress 2012 Daisuke Ito. those functioning in the vestibular system are located in the vestibular ganglion and those functioning in the auditory system are located in the spiral ganglion. saccule and semicircular canals. The membranous labyrinth is a series of fluidfilled chambers and tubes. These ganglia are located within the bony labyrinth of the petrous temporal bone close to the facial nerve (CN VII) and sympathetic innervation to the face. Coordination of Eye Movements In the healthy animal. In addition this system coordinates activity with portions of the cerebellum. PhD Nihon University. head rotation induces a compensatory eye movement in the opposite direction to the initial head movement. the vestibular system can be divided into peripheral and central components. The vestibular portion of CN VIII connects to the vestibular nuclei sited in the medulla oblongata of the brainstem. DVM. trunk and limbs to oppose gravity to maintain posture. Japan 23011746 Functional Neuroanatomy of the Vestibular System The vestibular system is a special proprioception system responsible for the proper maintenance of posture.

nystagmus. IV and VI to control the extraocular muscles. although the direction of nystagmus sometimes changes in . Following the fast phase. As a result. head tilt is towards the side of the lesion. if the head of the animal is turned to the left. otitis media interna) causes left head tilt. the animal may show fast eye movement towards the right. If the head is further turned continuously after initiating the slow phase. Physiological nystagmus describes the normal vestibulo-ocular reflex. however. Several variations of direction including horizontal. pathological nystagmus occurs in animals with vestibular disease and can be classified into spontaneous nystagmus and positional nystagmus. left inner ear disease (i. if the animal had left vestibular disease. movement of the endolymph in the left horizontal semicircular canal increases the activity of the hair cells. and this is called nystagmus to the right side. because of the loss of antigravity muscle tone on both sides the affected animal may not be able to hold the neck in a normal position. vertical and/or rotational nystagmus can be observed. For example. Information then enters the appropriate motor nuclei of the CN III. Clinical Signs of Vestibular Disease Damage to either the peripheral or central vestibular system leads to various vestibular dysfunctions including head tilt. the slow phase is resumed. For example. and stimulated from information acquired in the semicircular canals. The fast phase is directed opposite to the side of lesion. In cases with peripheral vestibular lesion. Therefore the examiner should try to induce positional nystagmus by positioning animals in lateral and dorsal recumbency. strabismus. In contrast. Therefore spontaneous vertical nystagmus suggests that the lesion is in the central nervous system. vision). such as upside down.vestibulo-ocular (or oculo-cephalic) reflex. Nystagmus A series of slow and fast phase of the rhythmical eye movement is called nystagmus. this slow phase is interrupted by corrective fast movement of the eyes in the same direction of head turning (the 'fast phase' of the vestibulo-ocular reflex). Head Tilt Head tilt is a condition of loss of antigravity muscle tone on one side of the neck. Bilateral vestibular lesions usually do not cause a head tilt. Spontaneous nystagmus is the nystagmus which occurs when the head is in a normal stationary position. Nystagmus of central vestibular origin may be vertical. in contrast the endolymph activity in the right horizontal semicircular canal is decreased. A unilateral central vestibular lesion can cause a head tilt to either side. A series of slow and fast phases is called nystagmus. For example. but sometimes it can be induced by altering the head position. horizontal or rotational. usually due to unilateral vestibular dysfunction. It is impossible to localise the lesion by assessment of positional nystagmus. The direction of spontaneous nystagmus in animals with acute unilateral peripheral vestibular lesion is horizontal or rotational nystagmus. These responses result in movements of the eyes toward the right and are termed the slow phase of the vestibulo-ocular reflex. The direction of nystagmus is defined as the direction of fast phase. Nystagmus of peripheral origin often disappears a few days after its appearance because of compensation by other balance systems (cerebellum. Positional nystagmus can be seen when the head is placed in unusual positions..e. ataxia and gait disturbance. the head tilts towards the loss of muscle tone.

it may be difficult to localise the vestibular lesion because most of the clinical signs can be seen in association with lesions affecting either the peripheral or central components. rotational or vertical. Clinical signs Head tilt Nystagmus Peripheral lesion Towards the side of the lesion Horizontal or rotational. Ventral or ventolateral strabismus can be seen in animals with vestibular disease when the head is raised and the neck is extended (positional strabismus). same side of lesion Rarely seen Yes (possible). or spontaneously. the fast phase is directed opposite to the side of lesion Yes Yes Facial nerve paresis to same side as lesion Possible to same side No Central lesion To either side Horizontal. Ataxia and Gait Disturbance Either peripheral or central vestibular dysfunction can be the cause of ataxia and gait disturbance. Usually strabismus is seen on the same side as the lesion. Clinical Localisation of Peripheral Versus Central Vestibular Disease From the clinical signs mentioned above. X or XII might be affected. Neurological signs of peripheral vs central vestibular dysfunction. Usually bilateral vestibular diseases do not show spontaneous and positional nystagmus. Figure 1. VII. the fast phase to either side.direction in animals with a central lesion. VI. An accurate history and physical and neurological examination are essential to success. IX. usually same side as Ataxia and gait disturbance Strabismus Cranial nerve deficits Horner's syndrome Postural . The most important key to determine the lesion location is to identify other clinical signs as compatible with only components of the peripheral vestibular system or that could only be explained by a central lesion (see Figure 1). may change the direction with head position Yes Yes Cranial nerves V. Strabismus Strabismus is an abnormal position of the eyes. Vomiting and Salivation Some animals show vomiting and salivation secondary to vestibular diseases.

other cranial deficits.reaction deficits Mental status Signs of cerebellum deficits Normal No lesion Depressed. inflammatory. Peripheral Vestibular Diseases Otitis media-interna. In addition. there are CN VII and sympathetic innervations. and to perform an accurate neurological examination. Inflammatory polyps derive from the lining of the tympanic cavity or auditory tube and are commonly seen in cats aged 1–5 years old. Central Vestibular Diseases Any diseases. One specific clinical sign of central vestibular disease in association with vestibular function is vertical nystagmus. Central Vestibular Lesion The single strongest sign of central vestibular disease is the presence of conscious proprioceptive deficits. Idiopathic vestibular syndrome. Therefore key clinical signs in animals with peripheral vestibular diseases may be facial nerve paresis and/or Horner's syndrome (ptosis. Proprioception and other cranial nerves should be normal. enophthalmos. behavioural changes and seizure. including neoplastic. There is no age tendency in cats. Nasopharyngeal polyps. cerebellum deficits including intentional tremor and dysmetria (hypermetria). stuporous or comatose Possible. Diagnosis of idiopathic vestibular syndrome is by exclusion of other diseases. such as abnormal mental status including depression. which involve the brainstem or cerebellum have the potential to cause vestibular dysfunction. and is also well recognised in cats. central vestibular lesions may cause neurological signs and cranial nerve deficits other than deficits of CN VII and CN VIII. miosis and protrusion of the third eyelid) ipsilaterally to the clinical signs of vestibular dysfunction. The examiner must be cautious not to mistake ataxia for proprioceptive deficits. Animals do not show proprioceptive deficits due to peripheral vestibular dysfunction. Bacteria themselves may cause dysfunction and toxin produced by the bacteria may affect to the inner ear. . stupor or coma. but dogs tend to be older (~12 years old). dysmetria or intentional tremor Peripheral Vestibular Lesion Near the peripheral vestibular system. toxin ingestion and miscellaneous. The second most common cause of peripheral vestibular disease in dogs. Otitis is the most common cause of peripheral vestibular disease in the dog and also common in cats. Therefore sometimes the disease is known as idiopathic geriatric vestibular disease.

DVM.Differential diagnosis should be made according to other clinical signs. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Daisuke Ito. Japan . Kanagawa. PhD Nihon University Fujisawa. including age and speed of onset of the clinical signs.

or rolling toward or away from the side of the lesion Conscious proprioceptive deficits. It is the most consistent sign of unilateral vestibular dysfunction. Platt Department of Small Animal Medicine & Surgery. Clinical signs due to disease of the peripheral vestibular system: Head tilt. College of Veterinary Medicine. USA 18668729 Introduction The onset of a head tilt is a cardinal sign of vestibular disease. Therefore. Unfortunately. University of Georgia. which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. falling. the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal. Athens. a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation.The Emergency Head Tilt (V195) Western Veterinary Conference 2009 Simon R. it is essential to approach these cases aiming to primarily further localise the neurological lesion. falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis. nor does it indicate a specific aetiology. circling. The vestibular system has two functional components. central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. circling. Generally. rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare Diagnostic Plan for Patient with Vestibular Dysfunction . GA. miosis and enophthalmos) with middle and inner ear lesions Clinical signs due to disease of the central vestibular system: Head tilt.

travel history. or magnetic resonance (MR) imaging. Spontaneous nystagmus resulting of central origin can be purely vertical. imaging of the tympanic bullae with radiography. The fast phase is directed away from the side of the lesion. Pathological nystagmus can be spontaneous or positional. previous ear disease. This can be only by diagnosed by ruling out the other causes. but this is not specific for this aetiology.Obtain a comprehensive history of the onset of the disease. In most cases. the other signs of vestibular disease include pathologic nystagmus. horizontal or rotational. serum chemistry. A brainstem auditory evoked response (BAER) test may be of value in examining the auditory portion of cranial nerve VIII (vestibulo-cochlear nerve) as well as potentially assisting in localising the disease to the peripheral or central components. In the absence of a systemic health concern. Horner's syndrome (usually indicative of peripheral disease). Information regarding previous systemic disease. The differentials for peripheral and central vestibular disease are discussed below. for example upside down. This will be followed by improved gait over a 7-day . There are less specific neurological signs that may be associated with vestibular dysfunction that include. and cats do not have facial paresis or Horner's syndrome. Positional nystagmus refers to nystagmus that is present only when the head is placed in an unusual position. cranial nerve deficits (multiple cranial nerve dysfunction usually indicates central disease. there is resolution of the vestibular abnormality. A unilateral acute peripheral lesion often causes spontaneous nystagmus with horizontal and rotational components. it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. The next steps may be determined by the lesion localisation. I would recommend immediate withdrawal of the medication. If toxicity is suspected due to antibiotic administration (metronidazole and aminoglycosides). however. previous medication administration (both topical and systemic). If the patient is closely monitored over this time course. In addition to the head tilt. positional strabismus and ataxia characterized by a base-wide stance and swaying of the trunk and head. A minimum data-base should be performed on all cats which should include haematology. computed tomography (CT). Spontaneous nystagmus is nystagmus that occurs when the head is not moving and is in the normal position. Postural reactions are normal in this disease. Diagnosis of central disease is based upon CT or MR imaging of the brain and analysis of cerebrospinal fluid (CSF). There are several very important components of the examination that can assist with the lesion localisation. Ancillary tests for patients with peripheral disease include otoscopic examination. the possibility of toxin exposure and head trauma is important. urinalysis and thoracic radiographs. The onset of the vestibular disease may be so acute that is accompanied by vomiting. and thyroid function testing. Perform a complete neurological examination. a practical approach can be taken with peripheral vestibular disease cats. Causes of Peripheral Vestibular Disease Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog and cat. but facial nerve paresis can occur with central or peripheral disease). head tremor (indicating cerebellar disease) and an altered level of consciousness (indicative of central disease). marked resolution of the nystagmus can be seen. conscious proprioception deficits (indicative of brainstem disease).

If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered. coli and Pseudomonas spp. Antibiotic therapy should be continued for 6-8 weeks. Otitis media-interna. Corticosteroids are usually not required and are avoided if osteomyelitis is present. or nasopharynx. Tear production should be monitored to detect sicca associated with facial nerve (CN 7) involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. In animals with recurring otitis. eustachian tube. In acute cases oral prednisone 0. Neoplasia. which arise from the lining of the tympanic cavity. E. Up-to 50% of cases of peripheral vestibular disease are due to otitis media-interna. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful.5% acetic acid solution and caustic ear cleaning substances are avoided if possible. There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. the clinical signs and infection recur and can be more difficult to treat. ceruminous gland adenocarcinoma and lymphoma. The bacteria commonly responsible for this disease are Staphylococcus spp. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means. Ototoxicity. The head tilt may never completely resolve. The infection can directly damage the inner ear with spread to the labyrinth.. In cases of concurrent otitis externa and media with a ruptured tympanic membrane.. underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. the external and middle ears are gently flushed with saline or a 2. but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth.25 mg/kg once daily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued.period and improvement of the head tilt over a 2-month period. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. Polyps are pedunculated masses. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals. The deafness caused by such drugs is often permanent . Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. Nasopharyngeal polyps. Streptococcus spp. Neoplasia of the structures of the ear includes squamous cell carcinoma. If the culture results are negative but bacterial otitis interna is suspected. then oral enrofloxacin 5 mg/kg every 12 hours for dogs or cats or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered. Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases. Aminoglycosides are contraindicated in otitis interna/media.

Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem. deficits are permanent. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. however. English Cocker. If the abnormality is bilateral. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome. Doberman. The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper. altered mental status. With bilateral disease. falling. Recurrence can occur. In severe cases. .g. nystagmus. Metronidazole toxicity. Whilst all the above infections can cause vestibular disease. The most common topical drug implicated in this scenario is chlorhexidine. Burmese. The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle. these animals may not have a head tilt or nystagmus. Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt. The onset is acute and usually occurs when animals receive high doses for a long duration (e.whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. and abnormal head movements. after being on high doses for 7 to 12 days). ataxia. and opisthotonus may be present. Numerous breeds have been associated with congenital vestibular disease (German shepherd. Beagle. Neoplasia. They may also be deaf. and vomiting. Many learn to compensate by 2-4 months of age but some will remain permanently affected. seizures. they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities.. bacteria and Cryptococcus. Dosages greater than 30mg/kg/day can result in vestibular disease. rolling. Trauma. feline infectious peritonitis (FIP). respectively. Tonkinese). Head trauma may cause the onset of vestibular disease. and a side-to-side movement of the head in the horizontal plane. they will frequently have a symmetrical ataxia. strabismus. Clinical signs may include generalized ataxia. Congenital disease. Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. Siamese. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs. Toxoplasma. nystagmus. a wide-based stance. Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs. Causes of Central Vestibular Disease Inflammatory disease. neurological as well as systemic. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease. there is usually no abnormal nystagmus and normal nystagmus cannot be elicited. which may be peripheral or central depending upon the severity of the trauma. Occasionally. anorexia. circling.

Drobatz KJ. Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. the other form of CVD.227(4):570-574.17(3):304-310. et al. DECVN University of Georgia. et al. et al. 2. 2006. Results of magnetic resonance imaging in dogs with vestibular disorders: 85 cases (1996-1999). its causes may be due to sepsis. Clinical signs. MRCVS. Evans J. neoplasia. Dennis R. Dickinson PJ. and outcome after surgical and medical treatment of otogenic intracranial infection in 11 cats and 4 dogs. Troxel MT. J Am Vet Med Assoc 2001. Kortz GD. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. United States . Signs of neurologic dysfunction in dogs with central versus peripheral vestibular disease. Sturges BK. Ischemia may be embolic or thrombotic and is the most common form of CVD.20(3):648-656. Garosi LS. Recovery from this disorder can be complete but can depend on the underlying disorder. hypertension or may commonly be idiopathic.Cerebrovascular disease. In some areas of the country this can result from aberrant parasite migration through the nervous system. is bleeding into the parenchyma of the brain that may extend into the ventricles. BVM&S. J Vet Intern Med. J Vet Intern Med 2003. Levesque D. GA. Knowles K. J Am Vet Med Assoc. magnetic resonance imaging features. endocrine disease.218(3):385-391 3. Non-traumatic hemorrhage. College of Veterinary Medicine Dept. of Small Animal Medicine & Surgery Athens. Diazepam as a treatment for metronidazole toxicosis in dogs: a retrospective study of 21 cases. 2005. DACVIM (Neurology). References 1. Vite CH. 4. Penderis J. Platt.

Obtain a comprehensive history of the onset of the disease. which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. GA. the other signs of vestibular disease include pathologic nystagmus. central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. There are several very important components of the examination that can assist with lesion localisation. Spontaneous nystagmus resulting of central origin can be purely vertical. circling. There are less specific neurological signs that may be associated with vestibular dysfunction that include: conscious proprioception deficits (indicative of brainstem disease). University of Georgia Athens. hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal. cranial nerve deficits (multiple cranial nerve dysfunction usually indicates central disease. USA 18293641 The onset of a head tilt is a cardinal sign of vestibular disease. falling. previous ear disease. rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare DIAGNOSTIC PLAN FOR PATIENT WITH VESTIBULAR DYSFUNCTION 1. Spontaneous nystagmus is nystagmus that occurs when the head is not moving and is in the normal position. the possibility of toxin exposure and head trauma is important. Horner's syndrome (usually indicative of peripheral disease). DACVIM (Neurology). circling. miosis and enophthalmos) with middle and inner ear lesions Clinical Signs Due to Disease of the Central Vestibular System Head tilt. previous medication administration (both topical and systemic). BVM&S. Therefore. positional strabismus and ataxia characterized by a base-wide stance and swaying of the trunk and head. 2008 Simon Platt. travel history. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. but facial nerve paresis can occur with central or peripheral disease). a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation. horizontal or rotational. Positional nystagmus refers to nystagmus that is present only when the head is placed in an unusual position. Information regarding previous systemic disease. Perform a complete neurological examination. for example upside down. College of Veterinary Medicine. DECVN. or rolling toward or away from the side of the lesion Conscious proprioceptive deficits. falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis. DIFFERENTIATION OF VESTIBULAR LESIONS Clinical Signs Due to Disease of the Peripheral Vestibular System Head tilt. MRCVS Department of Small Animal Medicine & Surgery. Unfortunately. It is the most consistent sign of unilateral vestibular dysfunction. A unilateral acute peripheral lesion often causes spontaneous nystagmus with horizontal and rotational components. it is essential to approach these cases aiming to primarily further localise the neurological lesion. Pathological nystagmus can be spontaneous or positional.Vestibular Disease in Dogs and Cats WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. and an altered . The vestibular system has two functional components. The fast phase is directed away from the side of the lesion. Generally. the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. head tremor (indicating cerebellar disease). nor does it indicate a specific aetiology. 2. In addition to the head tilt.

however. imaging of the tympanic bullae with radiography. or magnetic resonance (MR) imaging. If the patient is closely monitored over this time course. it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. the clinical signs and infection recur and can be more difficult to treat. but this is not specific for this aetiology. Otitis Media-Interna Up-to 50% of cases of peripheral vestibular disease are due to otitis media-interna. A brainstem auditory evoked response (BAER) test may be of value in examining the auditory portion of cranial nerve VIII (vestibulo-cochlear nerve) as well as potentially assisting in localising the disease to the peripheral or central components. underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. the external and middle ears are gently flushed with saline or a 2. and cats do not have facial paresis or Horner's syndrome. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. The head tilt may never completely resolve. A minimum database should be performed on all cats which should include haematology. serum chemistry. but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth. 4. then oral enrofloxacin 5 mg/kg every 12 hours for dogs or cats or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered..level of consciousness (indicative of central disease). oral prednisone 0. Antibiotic therapy should be continued for 6-8 weeks. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means. The infection can directly damage the inner ear with spread to the labyrinth. Aminoglycosides are contraindicated in otitis interna/media. computed tomography (CT).5% acetic acid solution and caustic ear cleaning substances are avoided if possible.25 mg/kg oncedaily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered. coli and Pseudomonas spp. In the absence of a systemic health concern. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided. In animals with recurring otitis. In acute cases. If the culture results are negative but bacterial otitis interna is suspected. CAUSES OF PERIPHERAL VESTIBULAR DISEASE Idiopathic Vestibular Syndrome Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog and cat. The onset of the vestibular disease may be so acute that is accompanied by vomiting. I would recommend immediate withdrawal of the medication. Corticosteroids are usually not required and are avoided if osteomyelitis is present. This will be followed by improved gait over a 7-day period and improvement of the head tilt over a 2-month period. marked resolution of the nystagmus can be seen. there is resolution of the vestibular abnormality. a practical approach can be taken with peripheral vestibular disease cats. In cases of concurrent otitis externa and media with a ruptured tympanic membrane. Tear production should be monitored to detect sicca associated with facial nerve (CN 7) involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. In most cases. and thyroid function testing. E. The bacteria commonly responsible for this disease are Staphylococcus spp. Diagnosis of central disease is based upon CT or MR imaging of the brain and analysis of cerebrospinal fluid (CSF). Streptococcus spp. The differentials for peripheral and central vestibular disease are discussed below. Ancillary tests for patients with peripheral disease include: otoscopic examination. 3. If toxicity is suspected due to antibiotic administration (metronidazole and aminoglycosides).. The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued. This can be only by diagnosed by ruling out the other causes. urinalysis and thoracic radiographs. The next steps may be determined by the lesion localisation. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals . Postural reactions are normal in this disease.

and abnormal head movements. nystagmus. however. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. neurological as well as systemic. Numerous breeds have been associated with congenital vestibular disease (German shepherd. Recurrence can occur.Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases. CAUSES OF CENTRAL VESTIBULAR DISEASE Inflammatory Disease The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper. or nasopharynx. Neoplasia The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle.. Many learn to compensate by 2-4 months of age but some will remain permanently affected. Congenital Disease Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. bacteria and Cryptococcus. Siamese. Nasopharyngeal Polyps Polyps are pedunculated masses which arise from the lining of the tympanic cavity. The most common topical drug implicated in this scenario is chlorhexidine. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease. Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. which may be peripheral or central depending upon the severity of the trauma. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome. Neoplasia Neoplasia of the structures of the ear includes squamous cell carcinoma. Tonkinese). they will frequently have a symmetrical ataxia. strabismus. Ototoxicity There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. With bilateral disease. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs. they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities. Doberman. these animals may not have a head tilt or nystagmus. Burmese. The deafness caused by such drugs is often permanent whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. The onset is acute and usually occurs when animals receive high doses for a long duration (e. Toxoplasma. ataxia. eustachian tube. They may also be deaf. after being on high doses for 7 to 12 . beagle. Whilst all the above infections can cause vestibular disease.g. English cocker. circling. rolling. Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt. a wide-based stance and a side-to-side movement of the head in the horizontal plane. there is usually no abnormal nystagmus and normal nystagmus cannot be elicited. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful. falling. ceruminous gland adenocarcinoma and lymphoma. Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem. Trauma Head trauma may cause the onset of vestibular disease. Metronidazole Toxicity Dosages greater than 30 mg/kg/day can result in vestibular disease. If the abnormality is bilateral. feline infectious peritonitis (FIP).

deficits are permanent. Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs. DACVIM (Neurology). nystagmus. Clinical signs may include generalized ataxia. BVM&S. Ischemia may be embolic or thrombotic and is the most common form of CVD. respectively. and vomiting. neoplasia. its causes may be due to sepsis. altered mental status. In some areas of the country this can result from aberrant parasite (Cuterebra) migration through the nervous system. College of Veterinary Medicine University of Georgia Athens. U . Recovery from this disorder can be complete but can depend on the underlying disorder SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon Platt. the other form of CVD. Georgia. and opisthotonus may be present. MRCVS Department of Small Animal Medicine & Surgery. seizures. Cerebrovascular Disease Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. DECVN. In severe cases.days). is bleeding into the parenchyma of the brain that may extend into the ventricles. Occasionally. endocrine disease. hypertension or may commonly be idiopathic. anorexia. Non-traumatic hemorrhage. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery.

profound metabolic abnormalities or cardiovascular disease may be unable or unwilling to walk. neurophysiology. Animals with severe orthopedic disease. The examination should allow the determination of: 1. and the use of a systematic and logical approach to examination. The presence of neurological disease Not all animals that appear to have neurological disease do so. to a diagnosis. . a detailed knowledge of all the specific tracts and structures within the brain is not necessary to do basic localization of intracranial disease! Understanding the major areas of the brain. Contrary to what most neurophobic clinicians believe. or may have changes in behavior that may mimic neurological disease. In some cases animals with neurological disease (e. Based on this differential list a logical diagnostic plan can be formed leading. BASIC ANATOMY Neurological examination: A complete neurological examination should be done on all animals suspected of having neurological disease. and the recognition of clinical signs resulting from loss of function of specific areas of the nervous system. determining the location of a lesion and whether it is solitary or multifocal/diffuse enables the clinician to form a differential list of the most likely diseases.Localization of Brain Lesions VETERINARY NEUROLOGY SYMPOSIUM 2005 Dr. how they interact and what their major functions are at a fairly simplistic level is all that is required. idiopathic epilepsy) may have a normal neurological examination. (eg localization of multifocal disease would be more typical of infectious or inflammatory disease rather than primary brain neoplasia) 2. Peter Dickinson. WHY IS LOCALISATION SO IMPORTANT? 1. PhD. allows the clinician to localise diseases to specific parts of the brain. Localisation allows accurate choice and "targeting" of appropriate diagnostics (eg CT may be more appropriate when imaging the bony structures of the middle ear in peripheral vestibular disease versus MR imaging of the brainstem for central disease) 3. History is especially important in this regard. BVSc. hopefully.g. Diplomate ACVIM (Neurology) 18285591 Clinical neurology is based on a sound understanding of neuroanatomy. The nervous system is logically arranged. Together with history and signalment. The significance of lesions defined by diagnostic tests (eg MRI) is determined in part by the correlation of their location with the clinical localisation.

aggression etc suggests brain disease. Abnormalities of the vestibular system (CN VIII) are a common cause of abnormal posture particularly head tilt.Incoordination of voluntary movement Dysmetria . hemi. For example a dog with brain disease and obtundation may not bother to look around when a new person enters the room (inappropriate). Decreased mentation may be associated with diffuse cerebral disease or brain stem disease due to disruption of the reticular activation system. hemi. observe the animal in the examination room. brainstem. trunk and limbs with respect to gravity. however a dog with significant cervical pain due to a herniated disc may also not look around either. para. para. especially in cats. tetra/quadri) Paralysis/plegia . Rigid extension of the thoracic limbs may be seen with severe (T3-L3) spinal cord lesions. Gait: Paresis . Responds only to abnormal stimuli (e. painful stimuli). spinal cord and neuromuscular system) as well as resulting from nonneurological disease such as orthopaedic. tilting to one side. No response to any stimuli. It is important to distinguish between animals that truly have decreased levels of mentation and animals that are "quiet" due to generalised systemic disease or pain. .Brain? Spinal cord? or Neuromuscular? And subsequently to more specific areas. tetra/quadri) Ataxia . Severe damage to the brainstem may result in a decerebrate posture with opisthotonus (extension of the neck and limbs). cardiovascular and metabolic disease.Inappropriate force or range of movement (hyper/hypo) Abnormalities of gait may be the result of disease in many areas of the nervous system (cerebrum. and how they help in neurolocalisation. In some cases this can be difficult and may require repeat examinations. The severity of the problem NEUROLOGICAL EXAMINATION: SUMMARY Below is a summary of the components of a neurological examination.Absence of voluntary movement (mono.2. stiff neck carriage or hunched postures. However postural abnormalities are not restricted to intracranial disease. Look for abnormal positions of the head. Posture: Again. Extension of the thoracic limbs may also be seen with cerebellar disease (decerebellate). leaning. For each section there will be a discussion of the sorts of abnormalities that may be found with intracranial disease. which is appropriate in this circumstance.Decreased voluntary movement (mono. or outside.g. head pressing. (Schiff-Sherrington sign) Neuromuscular weakness may also result in postural signs such as cervical ventroflexion. 3. whether they are specific localisers of intracranial disease. Spend time just watching the animal in the examination room. usually affecting the forebrain. Animals with bilateral vestibular disease will often have a wide based stance although this may also be seen with neuromuscular weakness. The localisation of the problem(s) grossly. Mentation/behaviour: ***** Altered mentation /behaviour is almost always associated with intracranial disease. cerebellum. Decreasing level of mentation Normal Obtunded Stuporous Comatose Normal response to stimuli Decreased response to normal stimuli. Does the animal respond appropriately to its environment and external stimuli? Inappropriate or compulsive behaviour such as pacing. Animals with spinal cord disease may also have abnormal postures particularly if they have spinal pain resulting in low.

Tight circles are usually caused by vestibular disease whereas wider circling is often the result of forebrain disease. Constriction of the pupil (parasympathetic) Signs: Loss of eye movement. but poor localisers! Contralateral CP deficits may be the only signs seen with cortical brain lesions. Ataxia Ataxia (uncoordinated movement) may be seen with cerebellar. and finally to the sensory motor cortex. Postural reactions: Tests aimed at assessing an animals ability to maintain an appropriate posture include tests of conscious proprioception (CP) such as the paw position test and reflex stepping. (Trochlear) limited clinical use Location: MIDBRAIN Functions: Extraocular eye muscle (dorsal oblique) . and as part of the assessment of motor strength. wheel barrowing and hemiwalking. muscle spindle and golgi tendon ) and body. Some of the major functions and more common clinical findings are listed below. Motor pathways cross over at the level of the midbrain so that lesions cranial to this point cause contralateral deficits. Cranial nerve examination: Abnormalities of cranial nerves are one of the most important indicators of intracranial disease. they are extremely useful for localising lesions. loss of pupillary light response (PLR) IV. A lesion anywhere in this pathway can cause A CP deficit. loss of motor pathways. I. A basic understanding of anatomy and function is all that is required. sensory information must pass from the toe. as well as appropriate motor responses. (Olfactory) limited clinical use. The important things to remember are: Dogs and cats essentially walk on their brainstems (red nucleus in the mid brain is V important) therefore cortical lesions rarely cause profound paresis but brainstem lesions or spinal cord lesions do. hopping. Once the abnormal foot position is recognised. Because the cranial nerve cell bodies (nuclei) and peripheral nerves are located in specific areas of the brain. up the spinal cord and brainstem to the thalamus. (Oculomotor) Location: MIDBRAIN.Neurological causes may result from loss of sensory perception of limb /body position. Circling usually occurs towards the side of the lesion. Circling **** Circling is nearly always a reflection of intracranial disease. the motor cortex and the basal nuclei (which are located along the length of the brainstem). There may also be overshooting of head movements and tremors. lesions caudal cause ipsilateral deficits. All of these tests require the integration of both sensory information from the limbs (touch. (Optic) see below III. Postural reactions are therefore very sensitive indicators of neurological disease. since motor deficits are often minimal. For a normal CP in the pelvic limb. the motor response must travel all the way back down again to the limb to correct the abnormality. II. Paresis The dog and cat have 2 major areas of motor neurones in the brain. pressure. Functions: Extraocular eye muscles (most). vestibular or spinal cord disease Dysmetria Lesions involving the cerebellum (sometimes spinal cord pathways to the cerebellum) can result in gaits where there are movements that are too long (goose stepping)(hypermetria) or too short (hypometria). or loss of cerebellar "regulation" of movement.

loss of palpebral reflex and menace response. Central nuclei medulla (rostral) + cerebellum Functions: Maintenance of balance/posture. (Vestibulocochlear) Location: Peripheral receptors in temporal bone. The facial nerve and sympathetic nerves to the eye pass through the middle ear and may be involved in otitis media/interna and vestibular disease. Pupil size is determined by parasympathetic (CNIII) and sympathetic input. Masticatory muscles Signs: Loss of palpebral reflex. head tilt/leaning/circling. . (Facial) Location: Medulla (rostral) Functions: Muscles of facial expression. lacrimation. Loss of facial sensation. Vision/PLR Assuming that animals have normal ophthalmological examinations. Atrophy of temporal/masseter muscles (enophthalmos due to atrophy of pterygoid muscle) VI. loss of vision and PLR is often associated with intracranial disease. dry eye VIII. laryngeal paralysis. (Abducens) limited clinical use Location: Medulla (rostral) Functions: Extraocular eye muscles (lateral rectus. salivation (parasympathetic) Signs: Facial droop. strabismus. deafness IX/X/XI. this can be used to further localise lesions. (Hypoglossal) uncommonly involved clinically Location: Medulla (caudal) Function: Tongue muscles (intrinsic) Signs: Deviation/atrophy of tongue. arise from the brain stem very close together in the region of the cerebellar pontine angle and are often affected at the same time. Lesions resulting in loss of PLR and vision usually affect the common pathway ie optic nerve/chiasm/ optic tract. lip droop.VII. hearing Signs: Ataxia. Loss of vision may be determined by loss of the menace response and watching an animal in its environment (negotiating obstacles). retractor bulbi) VII. dysphagia Some important anatomy Cranial nerves V. (parasympathetic to heart viscera) Signs: Dysphagia. Parasympathetic input is most important for resting pupil size and results in pupil constriction. since the sympathetic pathway is more complex and passes from the brainstem to the thoracic spinal cord (nerve roots T1-T3) then back up the neck via the cervical sympathetic trunk and the middle ear before reaching the eye! Because part of the visual pathway is necessary to stimulate the PLR.mydriasis (dilation) Loss of sympathetic innervation . (Trigeminal) Location: PONS (motor) PONS-C1 (sensory) Functions: Facial sensation.miosis (constriction) /ptosis/enophthalmos (Horner's syndrome) Mydriatic pupils usually localise to intracranial disease due to loss of either the stimulus to cause pupil constriction (optic nerve/chiasm/optic tract) or loss of CN III (midbrain). megaloesophagus XII. vomiting. Miotic pupils (Horner's syndrome) more commonly reflects disease outside the brain. decreased gag.VIII.V. Loss of parasympathetic innervation . nystagmus. (Glossopharyngeal/Vagus/Accessory) Location: Medulla (caudal) Functions: Pharyngeal/laryngeal muscles.

Signs may be subtle and involve changes in behaviour.CONCLUSIONS: Signs resulting from intracranial disease are not always specific for disease affecting the brain. but can also be found with extracranial disease such as masticatory muscle myositis. Less severe. paraspinal. Although cervical spinal pain is usually associated with cervical disease. DSAM. Profound and rapid (1-2 weeks) atrophy is seen with lower motor neuron lesions. resulting in cortical dysfunction (eg hypoglycaemia secondary to an insulinoma) Lesions affecting the brainstem/cerebellum will often result in significant clinical signs because there are a lot of important structures in a fairly limited space. Localised masticatory muscle atrophy may be associated with trigeminal nerve deficits. particularly interactions with the owner. Always listen to the owner regarding such changes. Station Farm. Six Mile Bottom. PhD. However by knowing which ones are specific for intracranial disease.Lesions resulting in loss of vision alone must be distant from these common pathways and usually involve damage to the visual cortex in the occipital lobe(s) at the caudal aspect of the brain (or the projections to the cortex) Spinal reflexes: Most important for localising spinal cord disease. BVSc. and limb muscles should be palpated to assess muscle atrophy. RCVS-Recognised Specialist in Small Animal Medicine (Internal Medicine) Dick White Referrals. and by combining findings from multiple abnormalities we can usually determine whether the neurological abnormalities are due to intracranial disease and if so where specifically the abnormalities are located. Diplomate ACVIM (Neurology) Understanding Vestibular Disease British Small Animal Veterinary Congress 2010 Jon Wray. Suffolk. SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Peter Dickinson. MRCVS. BVSc. UK 19885011 . it may also be seen with intracranial disease such as large space occupying masses or infectious/inflammatory disease. It is important however to remember that the underlying cause may be within the cortex itself (eg tumour) or extracranial. It is not uncommon however to have quite large lesions affecting the cerebrum with minimal or no obvious clinical signs. gradual disuse atrophy may be seen following UMN lesions. Other findings: Seizures arise from the cerebral cortex and are a specific indicator of cerebral dysfunction. NEUROLOGICAL EXAMINATION . CertVC. Reflexes may be increased in nature with lesions Muscle/spinal palpation Muscles of mastication (temporalis/masseter).

Head tilt.Relevant Anatomy The role of the vestibular apparatus is to assist balance by integration of sensory detection of position. vertical or rotary. environmental. Nystagmus occurring when the head is in a static position is termed 'spontaneous nystagmus' whereas nystagmus only induced by altering head position (for example by positioning the animal in dorsal recumbency) is termed 'positional nystagmus'. vaccination/worming. Nystagmus is an oscillatory movement of the eyes and jerk nystagmus refers to this oscillation being slow in one direction and more rapid in the other (as opposed to pendular nystagmus seen in Siamese. trunk and head. In addition to the above finding. Initial Assessment A thorough history should precede clinical examination and should include dietary. A general physical examination is mandatory even though the examiner may be immediately suspicious of disease localised to the vestibular system. variable changes in proprioceptive positioning and additional cranial nerve deficit. IV and VI. The key component of the initial assessment is a carefully performed neuroophthalmic examination with the aim of . Loss of balance associated with vestibular disease frequently causes nausea in acute cases and vomition may be marked in some dogs. falling or circling towards the side of the head tilt. and to the spinal cord) and projections to the flocculonodular lobe of the cerebellum Axons connecting the two areas Traditionally and logically it is useful to categorise vestibular disease as affecting either the peripheral or central neuroanatomical segment of the vestibular apparatus Clinical Signs of Vestibular Disease The cardinal clinical signs of vestibular disease are of head tilt and jerk nystagmus. should be differentiated from head aversion and it should be borne in mind that disorders causing aural or dental pain may also be associated with apparent head tilt. previous medical and therapeutic assessment. nystagmus may be horizontal. gravity. The direction of nystagmus is named after the direction in which the fast phase occurs. In vestibular disease. family and in-contact animal. acceleration and rotation with position of the eyes. these last are useful in differentiating lesion localisation. animals with vestibular disease may display an ataxic. or rotation of the head along its central axis so that one ear is held lower than the other. which are principally concerned with eye movement. The vestibular apparatus comprises: A 'peripheral portion' consisting of sensory receptors to detect gravity and linear acceleration (within the saccule and utricle) and rotational movement (within the semicircular canals) housed within the membranous labyrinth of the inner ear in the petrous temporal bone A 'central portion' comprising the vestibular nuclei of the medulla oblongata in the brainstem (from which pathways project to the nuclei of cranial nerves III. rolling gait with wide-based stance. Birman and Himalayan cats due to a congenital disorder of the visual pathway).

Occasionally animals may be encountered with bilaterally symmetrical vestibular disease. Clues to help differentiate central from peripheral vestibular disease are listed in Figure 1.Cranial nerve VII only XII Horner's syndrome Differential Diagnoses Possible but uncommon Possible . rotary or horizontal. particularly of cranial nerves V-XII. for example. on the same side) proprioceptive loss implies central vestibular disease.e. Rotary or horizontal May alter with head position Possible. In most circumstances the fast phase occurs away from the side of the lesion. and to determine whether there is evidence of peripheral or central involvement. The facial nerve (CN VII) due to the position of its nucleus within the rostral medulla and course via the petrous temporal bone may be concurrently affected in both peripheral and central vestibular disease causing loss of tone in muscles of facial expression and absent blink/menace.. enophthalmos. assessment for conscious proprioceptive deficits. Whilst the neuroophthalmic examination should be complete in every way. Paradoxical vestibular disease may occur with central lesions of the cerebellum or caudal cerebellar peduncle. Clues to Differentiate Central from Peripheral Vestibular Disease. the presence of horizontal or rotary nystagmus may be seen with either peripheral or central vestibular disease. These patients are characterised by severe ataxia accompanied by a low laterally 'swinging' head carriage. but proprioceptive deficits occur ipsilateral to it. strongly suggest brainstem involvement in the disease process and implicate central vestibular disease. causing Horner's syndrome (miosis. Figure 1. Similarly the sympathetic innervations of the eye and face may be affected by lesions within first-order neurons as they course through the brainstem but also (and more commonly) within the third-order neuron which courses adjacent to the tympanic bulla. and careful identification of other cranial nerve abnormalities. Although ataxia may be severe with either. In this situation the head tilt and circling occur away from the side of the lesion.identifying whether the animal with vestibular disease has changes which are focally affecting the vestibular apparatus (or whether. third eyelid protrusion). the key components are a very thorough assessment for evidence of aural disease. Other cranial nerve deficits. Nystagmus has a fast (corrective) phase and a slower (pathological) phase. Whilst vertical nystagmus and positional nystagmus are seen only with central vestibular lesions. ipsilateral to lesion No Possible No Other cranial nerve deficits May affect cranial nerves V. Central vestibular disease Nystagmus Proprioceptive loss Altered level of consciousness Peripheral vestibular disease Vertical. ipsilateral (i. multifocal disease may be present).

Radiography. otitis media-interna and sometimes in association with hypothyroidism. neoplastic D--Degenerative Further Investigation Further investigation is best guided by the clinical history and lesion localisation based on neuroophthalmic examination. may be very valuable. traumatic Metronidazole toxicity Trauma Central vestibular disease Ischaemic or haemorrhagic vascular disease Idiopathic peripheral vestibular disease Ototoxicity caused by a range of topical products Trauma Congenital peripheral vestibular disease Hypothyroidism Meningoencephalitis: --Infectious --Non-infectious (unknown aetiology) Thiamine deficiency Tumours of the brainstem/ cerebellopontine angle Neurodegenerative disorders and storage diseases Otitis media-interna Labyrinthitis Polyps Tumours of the middle/inner ear Peripheral vestibular disease A--Anomalous. Samples of fluid from the tympanic bulla may be collected via myringotomy for cytology and culture. 'Vitamin-D' mnemonic V--Vascular I--Idiopathic T--Toxic. No investigation may need to be undertaken. though superimposition of bony structures renders radiography inferior to more advanced (and expensive) techniques such as computed tomography (CT) and magnetic resonance imaging . Peripheral vestibular disease is most commonly seen with topical ototoxic agents. in which discontinuation of the agent will usually result in recovery. Figure 2. for instance if the clinical history or patient records indicate the strong possibility of peripheral disease caused by topical ototoxicity or where central disease is caused by metronidazole toxicity. provided that images are taken with meticulous attention to positioning. A rational approach once toxic causes have been excluded is for a thorough evaluation of the external ear canal and tympanic membrane (usually best performed under general anaesthesia and is significantly enhanced by magnifying equipment such as video-otoscopy) and evaluation of the tympanic bulla and bony labyrinth by diagnostic imaging. Differential Diagnoses of Central and Peripheral Vestibular Disease. idiopathic vestibular disease. anatomical Chiari-like malformation M--Metabolic I--Inflammatory N--Nutritional.Principal differential diagnoses of peripheral and central vestibular disease are listed in Figure 2.

Suffolk. CertVC. RCVS-Recognised Specialist in SA Medicine (Internal Medicine) Dick White Referrals Station Farm Six Mile Bottom. Some rarer nutritional and metabolic causes of central vestibular disease are best delineated by magnetic resonance sequences. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Jon Wray. protein content and for evidence of infectious organisms by cytology and polymerase chain reaction (PCR) analysis. The pharynx should also be evaluated for polyps. UK . DSAM. in which case collection may risk brain herniation. Assessment of thyroid function should be performed but results may be difficult to interpret. MRCVS. BVSc. If neurodiagnostic imaging is performed consideration should be given as to who is to perform and interpret such images as well as the simple availability of equipment. Neurodiagnostic imaging by MRI or CT is invaluable provided that such images are collected with meticulous positioning and thorough understanding of neuroradiology. it is best performed after neurodiagnostic imaging as this may detect evidence of raised intracranial pressure. CSF is assessed for cytology.(MRI). Central vestibular disease is usually investigated by assessment of structural abnormalities of the brainstem and cerebellum by neurodiagnostic imaging. which may not be appreciated by individuals without expertise in this area. and assessment of cerebrospinal fluid (CSF) usually via cisternal puncture.

head tilt. nystagmus--it looks like the animal is off balance) and spinal or less commonly peripheral nerve disease (due to decreased proprioceptive information arriving from the limbs--this is more subtle). most importantly in spinal disease. flaccid paresis/paralysis with reduced muscle tone and reflexes and muscle atrophy is expected. Gait Ataxia simply means uncoordinated gait. MRCVS Faculty of Veterinary Science. This information along with the history (most importantly the speed of onset. DVM. body posture and. assessing the animal's mentation. Ataxia can be due to cerebellar lesions (often associated with hypermetria. In contrast. in the pelvic limbs (paraparesis/plegia). One can often see excessive wearing of the nails and hear scuffing of the feet during movement. Paresis is weakness of the gait. modulating its activity. intentional tremors--drunken gait). The LMN is the efferent neuron that connects the central nervous system with the effector organ (muscle or gland). progression of the signs and presence or absence of pain) and signalment allows for establishment of a shortlist of possible differential diagnoses and guides the diagnostic investigation. Both paresis and paralysis (-plegia) can be used to describe the deficits in only one limb (monoparesis/plegia). an UMN lesion results in spastic paresis/paralysis with normal to increased muscle tone and reflexes due to loss of its inhibitory effect over the LMN. Liverpool 18568130 The neurological examination aims to determine whether the underlying cause of the patient's clinical signs is indeed due to a lesion in the nervous system and. With a lesion affecting the LMN. . where that lesion localizes to and how severe it is. Neurological Examination of the Spine The aims of the hands-on examination are to determine which limbs are affected and to classify the lesion as affecting the upper motor neuron (UMN) or lower motor neuron (LMN). in all four limbs (tetraparesis/ plegia) or on one side of the body (hemiparesis/ plegia). wide-based stance. The cell body is in the spinal cord grey matter or within the nucleus of a cranial nerve and its axon becomes the peripheral nerve. The UMN is the efferent neuron that originates in the brain and synapses (indirectly through an interneuron) with a LMN. The University of Liverpool. reduced voluntary movement. Paresis can be classed as ambulatory or non-ambulatory (when the animal still has voluntary motor function but cannot ambulate unaided).Where is the Lesion? Localizing Spinal Lesions British Small Animal Veterinary Congress 2009 Rita Gonçalves. the gait. vestibular disease (commonly with leaning and falling to the side of lesion. Paralysis is complete loss of voluntary movement. DECVN. if so. and initial examination starts with simple observation of the patient. A thorough history should be collected.

Pressure is applied to the spinous and transverse processes of the vertebrae in all spinal segments. the information needs to be recognized by the sensory nerve. Usually they remain intact in muscular disease and junctionopathies (like myasthenia gravis) Muscle bulk and tone--both are reduced in LMN lesions and normal to increased with UMN disease Spinal reflexes--the easiest and most reliable are the patellar reflex in the pelvic limbs and the withdrawals in both the pelvic and the thoracic limbs. These tests confirm the presence of a neurological disorder and can detect subtle dysfunction. manifested by vocalization and/or turning the head and trying to bite. C6-T2. Assessment includes: Paw position. in which case the limb will be retracted but no signs of conscious awareness of the pain will be evident. whilst normal or increased reflexes localize the lesion to the UMN Cutaneous trunci reflex (panniculus)--helps narrow down lesion localization in the thoracolumbar region. Lesions at these segments of the spinal cord result in LMN signs in the corresponding limbs (Figure 1). which then course through the brachial plexus and innervate the cutaneous trunci muscle. It is important to differentiate a pain response from a local withdrawal reflex (which should be present if both the peripheral nerve and spinal cord segment of the stimulated peripheral nerve are intact). Pain sensation is tested by applying heavy pressure with haemostats to the bones of the digits (don't forget to test different digits) or to the long bones of the limbs Spinal palpation--looking for areas of hyperaesthesia or deformities. this reflex is present from T2 to about L4-L5 and a cut-off in this region suggests a spinal cord lesion just cranial to the cut-off level. Don't forget to examine the tail and anus (perineal reflex). helping identify which limbs are affected. the spinal cord can be divided into four areas: C1-C5. travel up the entire spinal cord cranial to that area and be interpreted by the brain. in which case it will be completely absent on the side of the lesion and normal on the contralateral side Pain sensation--the spinal pathways that carry pain sensation are located deep in the spinal cord so only a severe lesion will impair pain perception (making this an important prognostic factor). hopping and placing responses--test the awareness of the position and movement of the limbs. ascends the spinal cord to the level of C8-T1 where bilateral synapse occurs with the motor neurons of the lateral thoracic nerve. Reduced reflexes in a limb identify a LMN lesion in that limb. After pinching the skin. resulting in bilateral contraction of these muscles. Loss of the cutaneous trunci reflex can also be due to a brachial plexus lesion. the sensory information enters the spinal cord approximately two vertebral spaces cranially. For conscious perception of pain.Functionally. T3-L3 and L4-S3. Normally. The LMNs for the thoracic limbs are located in the cervical intumescence (C6-T2) and the LMNs for the pelvic limbs are in the lumbosacral intumescence (L4-S3). Manipulation of the neck in all directions is also very helpful in identifying cervical pain .

minor contusive injury). Grades Grade 1 Grade 2 Grade 3 Grade 4 Clinical signs No deficits. Wheeler.. and normal conscious proprioception and paralysis of the pelvic limbs) can be seen with acute severe thoracolumbar lesions but does not have prognostic significance Figure 1. support the animal's weight and check whether there is any voluntary movement present (better prognosis if there is) Deep pain perception--this is the most important prognostic factor. The reported success rates vary widely and Figure 2 is a amalgamation of several study results that can be used as a guideline. it is of great importance to determine when it was lost (if deep pain perception is absent for longer than 24-48 hours then there is a poor prognosis for recovery) Prognosis The prognosis mostly depends on the underlying aetiology of the neurological deficits (e. just pain Paresis. spinal neoplasia vs. Lesion location and signs in limbs.g. Guide to prognosis of spinal injuries. Lesion location C1-C5 C6-T2 T3-L3 L4-S3 Polyneuropathies Severity of Disease Motor function--if the animal is non-ambulatory. Figure 2. It is important to know the prognosis for recovery with either surgical or conservative treatment for the different degrees of severity of the signs so appropriate clinical decisions can be made. which maintain voluntary movement. If absent. One of the most common conditions seen causing spinal disease is degenerative intervertebral disc disease.Other clues: cranial nerve examination may reveal Horner's syndrome if the lesion is in the cervical spinal cord. ambulatory Paralysis Prognosis with Prognosis with conservative treatment surgical treatment 100% 84% 81% 97% 95% 93% 95% Thoracic limbs UMN LMN Normal Normal LMN Pelvic limbs UMN UMN UMN LMN LMN Paresis. Shiff-Sherrington posture (hyperextension of thoracic limbs. Adapted from Sharp. SJ (2005). non-ambulatory 84% . NJH.

2005.Grade 5 Recurrence References No pain sensation 7% ~35% 60% Ascending myelomalacia in 5-10% dogs ~10-20% 1. UK . 2005. Gloucester: BSAVA Publications. Olby. In: Small animal spinal disorders: diagnosis and surgery (second edition). The neurological examination. BSAVA manual of canine and feline neurology (third edition). N. Wheeler SJ. Garosi L. 2003. Philadelphia: Elsevier Mosby. MRCVS Faculty of Veterinary Science The University of Liverpool Liverpool. SR. diagnosis and treatment. Olby. BSAVA manual of canine and feline neurology (third edition). In: Platt. Garosi L. 24-34. SR. Ithaca. Gloucester: BSAVA Publications. eds. DECVN. New York: International Veterinary Information Service. 2005. 3. N. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Rita Gonçalves. 4. In: Platt. Lesion localisation and differential diagnosis. eds. Clinical neurology in small animals: localization. 1-23. Sharp NJH. 2. Thoracolumbar disc disease. DVM. Braund KG.

This will guide the veterinary surgeon and technician for appropriate neurodiagnostic testing and also with patient management. Columbia. bowel and bladder function and ability of the patient to perceive pain. voluntary motor control from the . neurological and orthopaedic examination. It is important to question the owner about their pet's living environment with respect to flooring. College of Veterinary Medicine. For example. The veterinary practitioner and technician work with the pet owner to tailor the appropriate care that enables the animal to return to activity. Coates. integrity of spinal reflexes. University of Missouri.Nursing and Management of Dogs with Weak Pelvic Limbs British Small Animal Veterinary Congress 2011 Joan R. MS. For example. DVM. BS. it will be more of a challenge for a dog that has concurrent intervertebral disc herniation and severe hip osteoarthritis to regain ambulatory status. remain intact and are capable of reflex motor activity. Neurological Assessment Neurological assessment is key to documenting lesion localisation. which may play a role as to which treatments and exercises are realistic. however. The neurological examination will closely assess ambulatory status and motor function. During the evaluation process. pain management. bladder assessment and supportive care. ability to navigate indoor versus outdoor access and about the temperament of their pet. The pelvic limb LMNs. Patient Evaluation Nursing and management of a dog with neurological-related weakness in the pelvic limbs begins with obtaining a comprehensive history and patient examination. DACVIM (Neurology) Clydesdale Hall. located in segments L4–S2. Patient examination requires a physical. Animals with only pelvic limb paresis have neurological disease caudal to the second thoracic spinal cord segment. Department of Veterinary Medicine. A thorough patient history will evaluate the owner's expectations for outcome and abilities to care for their pet at home. aged and large-breed dogs have concurrent medical or orthopaedic conditions. USA 21494057 Introduction Management of the weak (paretic) or recumbent dog is contingent upon a team approach that begins with patient evaluation. Increased access to dedicated facilities specific for animal rehabilitation and physical rehabilitation has become an important component in the care of animals with neurological disease. Lesions in the region of T3–L3 produce general proprioceptive (GP) ataxia (loss of coordination) and UMN paraparesis. severity of lesion and prognosis. an assessment will be made to determine whether the owner is capable of following through with rehabilitation exercises and at-home patient care or prefers in-patient or out-patient therapy for their pet. an animal with LMN signs will be predisposed to decubitus ulceration from loss of muscle mass over bony prominences. Neuroanatomical localisation will provide an assessment of whether the weakness is upper motor neuron (UMN) or lower motor neuron (LMN) (see Figure 1). MO. Often.

Abnormalities related to femoral. Voluntary visceral functions such as micturition may be lost when UMN or sensory pathways in the spinal cord are damaged. The patellar reflex is normal and pain perception is perceived from the medial aspect of the first digit and the thigh. Similarly. Lesions involving spinal cord segments of L4–S2 injure the motor neurons that form the lumbosacral plexus. spinal cord lesions in the region of T3– L3 segments result in: Paresis GP ataxia Decreased or absent postural reactions Normal reflexes or hyperreflexia Impaired micturition Variable degrees of sensory loss caudal to the lesion Lesions in the area of L4–S2 or those that involve the cauda equina (the L7 and S1–S2 spinal nerve roots and spinal nerves) produce pelvic limb paresis of the LMN type. which transmit position sense signals from receptors in the pelvic limbs to the brain. sciatic. Figure 1. Pain perception (nociception) is lost only if the lesion is bilateral and severe. Ataxia results from damage to the spinal cord's general proprioceptive pathways. the animal is able to support weight on the pelvic limbs but will have a plantigrade posture or stance. Muscle atrophy from disuse will develop with time. Because the femoral nerve is spared. The spinal reflexes are normal or exaggerated. pudendal and pelvic nerves are encountered in these patients. Neurological examination findings for UMN and LMN signs. pelvic and caudal nerves. Pelvic limb reflexes are depressed or absent and the muscles may be hypotonic. pudendal.brain is lost because the motor pathways in the spinal cord are damaged. Abnormalities of visceral function result from an injury to the motor and sensory neurons that innervate the bladder and the anus. Neurogenic muscle atrophy develops. In summary. The clinical signs are related to motor and sensory dysfunction of the involved nerves. Upper motor Lower motor neuron neuron signs (T3–L3) signs (L4–S2) Muscle tone Increased (spasticity) Decreased (flaccidity) . Anaesthesia caudal to the lesion results from disruption of pain pathways from the pelvic limbs to the brain. extensor hypertonus or spasticity also may develop. Exaggerated reflexes result when UMN inhibitory influence on the LMNs is lost. Sensory dysfunction results from an injury to the sensory neurons and nerve fibres located in this region of the spinal cord. Lesions involving the caudal segments of the spinal cord and the cauda equina damage nerve fibres that form the sciatic.

Efficacy. When assessing pain perception a noxious stimulus should be applied to the digits using a haemostat while taking care not to damage the skin. Goals are to reduce pain and improve function as much as possible. Considerations should also be given for short-term and long-term therapeutic regimens. Effectiveness of pharmacological opiates may vary with route of administration: parenteral. However. .disuse Rapid and severe neurogenic Present Decreased to absent Present Normal to exaggerated Presence of pain perception is the most important prognostic indicator.g. Tolerance to opiate effects may develop during repeated and chronic administration. Dogs with intervertebral disc extrusions that have surgical decompression within 24 hours from time of injury have a 60% chance of recovery to ambulatory function. acute versus chronic) assist with development of a pain management protocol. Opioid analgesics are classified into various groups based on their pharmacological activity. turning towards and trying to escape from the stimulus or other behavioural responses that indicate cortical perception. cost and safety need consideration with any type of pharmacological therapy. Direct delivery of opioids to the spinal cord (epidural anaesthesia) is used to produce effective anaesthesia for surgical procedures. a dog that recovers pain perception within 2 weeks after surgery has a better chance of recovering ambulatory function. In veterinary medicine. tolerability. Moreover. rectal.Muscle atrophy Weakness (paresis) Spinal reflexes Pain Perception Slow . epidural. Side effects may include altered consciousness. and relieve anxiety and distress. this may include clinical interventions and pharmacological and rehabilitative approaches singly or in combination. oral and transdermal (fentanyl patch) drug delivery.. Each limb is assessed individually along with the tail. Recognition of different pain types (e. Opioid analgesics modify pain perception and behavioural reactions. a dog with a spinal fracture and complete loss of pain perception has a poor to hopeless prognosis. Routes of administration may factor into effective pain control. loss of pain perception as a result of spinal cord injury indicates severe spinal cord injury and a guarded prognosis. inflammatory versus neuropathic. Opioids are more effective for postsurgical and traumatic pain and considered less effective for neuropathic pain. The patient is observed for vocalisation. Opioids that are pure agonists may provide more effective pain control than agonist-antagonist opioids. Withdrawal of the limb by itself during the stimulus does not indicate deep pain perception. In general. including dysphoria and respiratory depression. Type and dosage of opioid selection varies upon severity of pain. potency and clinical use. Pain Management An effective treatment plan for pain management provides acceptable analgesia with few side effects.

strict cage rest is important to prevent excessive activity in animals with spinal disease. it should be assumed that animals with spinal cord disease are unable to voluntarily urinate or complete the micturition process. Concurrently. Secondary overflow incontinence occurs when bladder pressure exceeds urethral pressure. Bladder Function Until proven otherwise. an alternative NSAID or adjunctive use of a different class of analgesic needs consideration. A lesion in this area will abolish the detrusor reflex. Only a short-term antiinflammatory regimen of prednisone is recommended. UMN bladder dysfunction occurs with lesions between the pons of the brain stem and L7 spinal cord segment. Specific disease processes vary widely in optimal corticosteroid usage. . The bladder becomes large and firm and the urethral sphincter tone is increased. Moreover. The most common cause of voiding problems in the neurosurgical patient is urinary retention secondary to the underlying neurological disease. LMN bladder dysfunction occurs with a lesion within the sacral spinal cord and nerve roots. A prospective study determined that the prevalence of UTIs in dogs with thoracolumbar and lumbar intervertebral disc disease (IVDD) was 30% with a higher incidence in dogs that were female and those that had a lower intraoperative body temperature. bladder overdistention and damage to the kidneys. If one NSAID does not appear to remedy the pain. This may actually make bladder expression difficult. It is important to obtain a confirmatory diagnosis before glucocorticoid usage. The internal sphincter is innervated by the hypogastric nerve and remains intact. With an UMN bladder both the motor and sensory pathways of the detrusor reflex are affected. chronic use of corticosteroids without monitoring can lead to deleterious side effects. Initial rapid improvements without a differential diagnosis can be misleading. Dogs with neurogenic-related urine retention and intermittent and/or indwelling urinary catheters have potential risks for UTI. A 'washout' period (48–72 hours) should be allowed before administering a different NSAID. dexamethasone or prednisone have been administered at anti-inflammatory doses to control inflammatory response and pain and to reduce spinal cord oedema. The bladder is difficult to express manually. The detrusor muscle becomes flaccid (detrusor atony) as a result of over-distension secondary to absent detrusor contraction and external sphincter tone is lost. Trauma is the most common cause for this type of dysfunction. For compressive spinal cord disease. and the pelvic plexus.The plethora of different non-steroidal anti-inflammatory drugs (NSAIDs) available for use in dogs and cats provides the practitioner with a choice for the most appropriate NSAID which will best complement pain management while minimising patient side effects. Risks associated with urine retention include developing urinary tract infection (UTI). Inflammatory pain also can be alleviated through anti-inflammatory actions of glucocorticoids. Animals with LMN bladder dysfunction also will lose their perineal reflex and sensation. NSAIDs appear to have synergistic effects with opioids and may allow for lower dosage of both. Response to specific NSAIDs may vary with each individual patient and the type of pain. Concurrent use of more than one NSAID or of an NSAID with glucocorticoids should be avoided.

Intermittent urinary bladder catheterisation often is indicated and has a lower risk of inducing a urinary tract infection over indwelling closed-system urinary catheterisation techniques.5–25 mg /dog orally q8h (start at low dose) 0. minimising the duration is important. dyspnoea Gastrointestinal Cisapride Increase acetylcholine release Supportive Care Supportive care to improve psychological and physical well-being is especially important in the recumbent patient.25–0. Urinalysis and urine culture should be periodically performed to monitor for UTI. tachycardia Hypotension. indwelling).5 mg/kg orally q12–24h 0. Drug Mechanism of action Dosage Side effect Decrease urethral sphincter tone Prazosin Phenoxybenzamine Diazepam Alpha-adrenergic agonist Alpha-adrenergic agonist Centrally acting skeletal muscle relaxant 1 mg/15 kg orally q12–24h 0. Bedding should be supportive enough to evenly distribute the patient's weight .5 mg/kg orally q8h Gastrointestinal. If an indwelling system is selected. tachycardia Sedation. Pharmacological therapies for urine retention include drugs that improve bladder contraction and relax the urethral sphincters (Figure 2). excitation Increase detrusor muscle contraction Bethanecol Cholinergic 2.Bladder atony from overdistension can result from non-neurogenic or neurogenic causes. Figure 2. Drug therapies to assist with urinary bladder emptying in dogs. Basic principles need to be followed to prevent bladder overdistension in animals with urinary retention. Urinary bladder expression can be difficult in dogs with UMN disease or obesity and is considered a painful procedure in dogs that have recently had spinal surgery. Manual bladder expression is indicated if the bladder is easily expressed. Residual urine after expression is a potential source of infection and can lead to overflow incontinence and detrusor atony. Overdistention also can result from pelvic fractures and recumbency. itself. but residual urine should be periodically monitored by ultrasonography or urinary bladder catheterisation. Urinary bladder emptying can be done by manual expression that can be facilitated using pharmacological therapies or by use of catheters (intermittent. bradycardia. Nonneurogenic bladder atony is secondary to urinary obstruction and disruption of the tight junctions of the detrusor myofibres.5–2 mg/kg orally q6–8h Hypotension.

Superficial and deep heat therapy can further reduce muscle spasm and improve circulation. during these exercises to allow adequate rest periods of 2 minutes between the walking periods. thus reducing damage to muscles during exercise. Physical Rehabilitation Physical rehabilitation is integral in management of neurological diseases and enhancement of neuroregenerative processes. An ice pack covered with a towel to protect the skin is applied for 10–20 minutes three times daily. Elements to implement early in the recovery process include standing exercises. Massage is used in the beginning to relax the patient and loosen the muscles. the limb will need assistance in flexing. Physical rehabilitation during recovery from neurological disorders is important not only for strengthening and increasing flexibility but also for pain reduction and improvement in quality of life. a gait pattern can be established. Hydrotherapy also can play a role in increasing circulation of the limb vasculature and prevention of decubitus ulcers. Water buoyancy helps in rehabilitation of weak muscles and painful joints by minimising the amount of weightbearing on joints while generating the gait cycle. which assists with preservation of muscle strength. While non-ambulatory outside of the treadmill. The goal is to have the limbs in a normal position while bearing only a portion of the body weight. As the patient begins to ambulate. With the paraplegic or paraparetic patient in the underwater or land treadmill. though. In these cases. During passive ROM. Absorbent materials (lamb's wool. The patient will need to be turned on a frequent basis (every 4 hours). Cleanliness and dryness are critical to prevent faecal and urine scalding. which serve to enhance ROM.especially over bony prominences to prevent decubitus ulcers. Having the pet owner and technicians intimately involved with the postoperative care is important in the patient's overall wellbeing and quality of life. diaper pads) need to cover supportive materials (air. joints of limbs are extended and flexed through normal ROM 5–10 minutes several times a day. hydrotherapy and basic supportive care. muscle strength. the animal may first begin to show motor function while in the underwater treadmill. Underwater treadmill therapy is most effective as the animal is beginning to regain the ability to ambulate. Toe pinch exercises that use the flexor reflex will activate muscle contraction as well as providing resistance with the limb in extension. therapeutic exercising includes standing and more dynamic ambulation activities. range of motion (ROM). Animals with LMN weakness may only show muscle fasciculation or contraction rather than complete limb flexion. Neuromuscular electrical stimulation is applied to selected muscle groups that undergo disuse atrophy. Disuse and immobilisation can cause loss of muscle mass and debilitating joint contracture. balance and overall daily . foam mattresses). pain and swelling is applied for the first 48–72 hours or until the incision is no longer warm to touch. Cryotherapy of the surgical incision to reduce inflammation. Rehabilitation in immediate postoperative and recumbent patients begins with massage and passive ROM. It is important. Active ROM includes swimming and standing exercises.

Other modalities of physical therapy and supplemental therapies that complement mobility therapies include thermal. walking on mattresses. 2. Halling KB. 5. Millis DL. 2004. Veterinary Clinics of North America: Small Animal Practice 2005. St. Rehabilitation for the neurologic patient. Stevenson M. Leg weights are used when one leg is weaker. massage. Twedt DC. USA . 35: 1389–1409. Coates . Steiss JE. Static and mechanical forms of stretching techniques are performed in conjunction with ROM exercises to prevent fibrosis and contracture of joints and muscles. rehabilitation protocols are individually tailored to meet patient's needs during the recovery process. ultrasonography. Repetitions of 10 of 2–3 sets at one to three times a day are guided by whether the patient fatigues. In disorders such as degenerative myelopathy. Physical agent modalities. Olby NJ. acupuncture and weight loss. eds. As the strength improves with neurological recovery. College of Veterinary Medicine University of Missouri Columbia. et al. Veterinary Clinics of North America: Small Animal Practice 2005. Stiffler KS. 3. DVM. Sling-assisted walking. Olby N. 35: 1317–1333. 4. Gait training exercises encourage more ambulation to affected limbs. it will be important to avoid fatigue and further muscle injury. 2008. open water swimming. Prevalence and characterization of urinary tract infections in dogs with surgically treated type I thoracolumbar intervertebral disc extrusion. Muscle or joint contracture is difficult to overcome but therapeutic ultrasound may reverse or lessen tendon. eds. Levine D. electrical stimulation. sit to stand and weaving. Quedgeley: British Small Animal Veterinary Association. cavaletti rails and physioroll or ball balancing are all useful for developing strength and coordination. DACVIM(Neurology) Department of Veterinary Medicine. exercises will then include stair or hill climbing. 35: 330–336. Sherman J. References 1. Physical therapy and rehabilitation of neurologic patients. Olby NJ. In: Platt SR. BS. MS. pulling weights. Joan R. Louis: Saunders Elsevier. This process can be initiated with assistive walking devices and during hydrotherapy. 394–407. Proprioceptive neuromuscular training using a mattress or balance boards improves the awareness and use of limbs at rest and in motion. Veterinary Surgery 2006.function. 1131– 1135. MO . et al. Kirk's Current Veterinary Therapy XIV. In: Bonagura JD. In summary. joint and ligament contractures. BSAVA Manual of Canine and Feline Neurology. Nursing and rehabilitation of the neurological patient.

Paresis can be mild. Ataxia with limb paresis (weakness) may be due to peripheral nerve. The Cranial Nerve Examination . back. neck and thoracic limbs. Gait--a normal gait requires proper function of all sensory and motor peripheral nerves and tracts through the spinal cord and brainstem and the cerebellum. With severe paresis the animal is unable to stand but still has some voluntary movement. spinal cord or brainstem lesions. GA. The owner's opinion of any behavior changes is important to note. The Hands-on Evaluation A. Platt Department of Small Animal Medicine & Surgery. rage. A demented animal is awake but dull and inappropriate. The Hands-Off Evaluation Mentation--can be observed while collecting the initial history. Head incoordination and tremors may be observed when animals lift their heads or attempt to drink and eat and indicate a lesion of the cerebellum. Paralysis is the total loss of all voluntary movement--indicates brainstem or spine disease.Video Tour of the Neurological Examination (V196) Western Veterinary Conference 2009 Simon R. USA 18668730 The neurological examination is performed to determine if a neurological problem is present. stupor and coma. University of Georgia. moderate and severe. Circling or pacing may be observed and indicate a lesion of the cerebrum or diencephalon. The cerebrum is less important in animals and lesions there may cause only temporary alterations in gait. where it is located in the nervous system and how severe it might be. spinal cord. delirium. pelvic limbs. The neurological examination starting from the front to back of the animal may be divided into the evaluation of the head. College of Veterinary Medicine. Paresis is not seen with cerebellar lesions. Lesions of the cerebrum and diencephalon (thalamus) produce dementia. Athens. Ataxia is an uncoordinated gait and may be due to sensory peripheral nerve (rare). Lesions of the midbrain can produce stupor and coma. gait. A depressed animal is quiet but appropriate. anus and tail. brainstem or cerebellar lesions. Animals usually circle toward the side of the lesion. Posture--a head tilt (the ear on one side closer to the ground) is associated with a unilateral lesion of the CN VIII.

The palpebral reflex is elicited by touching the medial and lateral canthi of the eyes and observed as the eyelids closing. The menace response evaluates CN II and the Facial nerves (CN VII) and their connections through the brainstem. Pupil size is observed in normal room light. Trochlear nerves (CN IV)--tested by eyeball position and eyeball movement. . the diencephalon and occipital lobes of the cerebrum--tested by observing the animal walk around an unfamiliar environment to see if they bump into objects. general visual capabilities. Ventrolateral strabismus occurs with lesions of CN III. The pupillary light reflex evaluates CN II and the Oculomotor nerves (CN III)--tested by shining a light into the pupil and observing pupillary constriction in the eye tested (the direct response) and the opposite eye (the indirect response). or throwing cotton balls. and eyeball movement. which is evaluated with the palpebral reflex and the aural and buccal reflexes. Pupils may be small with lesions of the sympathetic innervation to the pupil. and a medial strabismus is seen with lesions of CN VI. Vision is the function of CN II. which ascends up the neck from the vagosympathetic trunk and produces a Horner's syndrome. eyeball position. Temporal and Masseter muscle atrophy is observed by palpation and is associated with lesions of CN V and primary muscle diseases of the head musculature. the pupillary light reflex and pupil size. Trigeminal nerves (CN V)--tested by evaluation of temporal and masseter muscle size and tone as well as facial sensation. a contralateral dorsolateral strabismus is seen with lesions of CN IV. Optic nerves (CN II)--evaluated using the menace response. Loss of jaw tone is usually associated with bilateral lesions of CN V and restricted range of motion is often due to primary muscle diseases of the head musculature. Jaw tone and motion is observed by manipulation opening and closing the mouth. brain and cerebellum--tested by advancing the hand or fingers toward the eye and observing the animal blink the eyelids or retract the globe. Oculomotor nerves (CN III)--tested by the pupillary light response. evaluates CN V and CN VII. Pupils may be large with lesions of CN II or CN III or midbrain.Olfactory nerves (CN I)--tested by blindfolding the animal and offering food to observe if they can find the food with their sense of smell. Eyeball position--a true strabismus occurs when the eyeball is deviated into an abnormal position when the head is in the normal position.

The aural and buccal reflexes are elicited by touching or pinching the ear or lip respectively and observing movement of these; evaluates CN V and CN VII. Abducent nerves (CN VI)--tested by evaluation of eyeball position and eyeball movement (lateral and retraction). Facial nerves (CN VII)--tested by evaluation of facial symmetry, palpebral, aural and buccal reflexes and by Schirmer tear tests. Vestibular nerves (CN VIII)--tested by evaluation of head posture (tilt with disease), spontaneous and physiological nystagmus, positional strabismus, gait (dysequilibrium with disease) and hearing ability. Positional strabismus is an abnormal eyeball position when the head is placed in abnormal positions but not at resting posture. This is different than true strabismus as eyeballs are not paralyzed in abnormal positions. As the head is moved both eyeballs move to the same degree. Positional strabismus most commonly occurs with a lesion of CN VIII or the vestibular regions of the cerebellum. The eyeball on the affected side drops more than the eyeball on the normal side as the nose is elevated. Physiological nystagmus is observed when the head is moved and the eyes move slowly (slow phase) away from the direction of head movement then rapidly snap back (fast phase) toward that side. These eye movements are repeated several times when the head is moved side to side or up and down and require the integrity of the CNs III, IV, VI and VIII. Pathological nystagmus may occur without head movement with lesions of the CN VIII, the rostral medulla oblongata or cerebellum. Nystagmus has a fast and slow phase. Nystagmus may be horizontal, vertical or rotary. The nystagmus is named by the direction of the fast phase. Hearing is grossly tested by observing a response to a noise such as whistling. Glossopharyngeal nerves (CN IX), Vagus nerves (CN X) and Spinal Accessory nerves (CN XI)--these nerves are often evaluated together by evaluation of the animal's swallowing ability, upper respiratory tract and esophageal function. Swallowing is observed by applying pressure to the hyoid bones or stimulating the pharynx with a finger. Stridor or increased respiratory noise through the larynx may be due to unilateral or bilateral laryngeal paresis or paralysis and may be heard with the bare ear or a stethoscope. Dysphonia may be observed or noted in the history. Regurgitation may be observed or noted in the history and may be due to megaesophagus most commonly secondary to esophageal muscle disease and less commonly from lesions of CN X.

Hypoglossus nerves (CN XII)--evaluated by examination of tongue size and function. B. Postural Reaction Examinations Not all necessary but can be very helpful in 1) confirming a neurological deficit and 2) determination of asymmetry. Wheel-barrowing can detect deficits not appreciated during the gait evaluation. In tetraparetic animals, this test may be performed to determine if the thoracic limbs are more involved than the pelvic limbs. Hopping is evaluated by lifting the opposite thoracic or pelvic limb and both pelvic limbs or thoracic limbs and pushing the animal forward and laterally to observe their ability to walk or hop on each thoracic or pelvic limb independently. Equal responses should be seen on both sides. Conscious proprioception when performed correctly can be a very important tool to detect subtle dysfunction. The animal is supported slightly, the paw is then turned so standing is on the dorsal surface. The animal should return the paw to the correct position within a few seconds. The animal should not be leaning against the examiner nor should the examiner be supporting the animal's weight. C. The Reflex Examination Spinal cord reflexes pass through specific peripheral nerves and spinal cord segments, so if a spinal reflex is depressed or absent the lesion is localized to that specific site. These tests will determine if the lesion is lower motor neuron (LMN) or upper motor neuron (UMN). Factors evaluated UMN Lesion Resting muscle tone Spinal reflexes Normal Normal to exaggerated LMN Lesion Normal to decreased Usually normal to decreased (or even absent), but may be increased (pseudo-hyperreflexia) Early and severe muscle atrophy (neurogenic)

Muscle atrophy

Little and late muscle atrophy (chronic stages: disuse atrophy)

Thoracic limb spinal reflexes: The Biceps tendon reflex (C6-8 spinal cord segments) The Triceps tendon reflex (C7-T2 spinal cord segments) The Extensor carpi radialis muscle reflex (C7-T2 spinal cord segments)

The Flexor withdrawal reflex also referred to as toe pinch reflex (C7-T2 spinal cord segments) Pelvic limb spinal reflexes: The Patellar reflex (L4-5 spinal cord) Gastrocnemius muscle reflex (L6-S2 spinal cord) The Cranial tibial muscle reflex (L6-S2 spinal cord) The Flexor withdrawal reflex (L6-T2 spinal) The Crossed extensor reflex occurs if the opposite limb extends when the flexor reflex of the other limb is elicited. The presence of an obvious crossed extensor reflex usually indicates a lesion above spinal cord segment L4. The Anal reflex (S1-3 spinal cord segments). The perineal area on each side is pinched with hemostatic forceps and the anus muscle will contract. If a reduced reflex is suspected, a gloved finger should be inserted into the anus and strong anal muscle contraction should be felt if normal. The Tail reflex (S1-Cd5 spinal cord). As the perineal area is stimulated with forceps or a finger the tail will contract toward the anus. Panniculus reflex. Allows accurate localisation in the T3 to L3 UMN region of the spinal cord, and assesses the C8 to T1 region of the brachial plexus (outflow of the panniculus reflex). In the occasional normal animal the panniculus is either unreliable or totally absent. D. Pain Evaluation Focal pain--palpate down the spine feeling for focal pain, muscle spasm and heat. If the dog does not react to light palpation then moderate pressure is applied. Flex the neck from side-toside, dorsally and ventrally. Extend and flex the lumbosacral junction while trying not to flex other joints. The presence of pain implies pathology of the meninges, nerve roots, vertebral joints, spinal muscles or discs. Pathology of the spinal cord itself is not painful unless it involves the meninges as well. Deep pain--is tested by applying pressure to one of the digits with hemostatic forceps and observing a behavioral response. Withdrawal of the toes is only the flexor reflex. If no deep pain is observed on one digit, all digits should be tested. A complete loss of deep pain signifies a severe spinal cord lesion and a grave prognosis. Based on the above tests the lesion should be localised to one of the following areas (unless multifocal or extensive):

1. Forebrain (cerebrum / diencephalon) 2. Cranial nerves (peripheral or central {brainstem}) 3. C1 to C5: UMN to all limbs 4. C6 to T2: LMN to thoracic limbs and to UMN pelvic limbs 5. T3 to L3:Thoracic limbs are normal and UMN to pelvic limbs 6. L4 to S1:Thoracic limbs are normal and LMN to pelvic limbs 7. S1 to S3All limbs normal, but LMN to bladder, perineum and/or tail 8. Polyneuropathy/polymyopathy: LMN to all four limbs

References 1. Glass EN, Kent M. The clinical examination for neuromuscular disease. Vet Clin North Am Small Anim Pract 2002;32(1):1-29 2. Thomas WB. Initial assessment of patients with neurologic dysfunction. Vet Clin North Am Small Anim Pract 2000;30(1):1-24 Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN University of Georgia, College of Veterinary Medicine Dept. of Small Animal Medicine & Surgery Athens, GA, United States

short choppy strides that gradually get shorter until collapse.g. They can be focal or generalized. In dogs. lesion localization can be difficult. neuromuscular junction (NMJ) and muscle. Muscle pain can be difficult to localise since it is often diffuse and the owner may report that the animal vocalizes when handled or seems generally painful. Chandler. Pain can also be a characteristic of muscle disease. weight loss. a voice change (e. collapse. How can the clinician determine that these systems are dysfunctional? Historical Findings in Neuromuscular Disease Generalized Neuromuscular Disease Owners may report signs of generalized weakness (paresis). and neck ventroflexion. high pitched bark) in recurrent laryngeal nerve dysfunction. Focal Neuromuscular Disease Common focal cranial nerve signs include a lip droop in facial nerve paralysis. inability to get into the car. Focal muscle atrophy is also possible. UK 182807 Introduction Neuromuscular diseases in dogs and cats are a diagnostic challenge. PhD. A C1-5 or C6-T2 spinal cord lesion such as disc herniation. The key to success with investigating these conditions is to start with a thorough history and detailed physical and neurological examination.Diagnostic Approach to Canine and Feline Neuromuscular Disease ACVIM 2006 Kate E. Neuromuscular conditions include diseases of the peripheral nervous system (PNS). DECVN. However. As with all neurological problems. Physical and Neurological Findings in Neuromuscular Disease Generalized Neuromuscular Disease When faced with the tetraparetic animal. owners may notice a reduced level of activity. flaccid paralysis. Brachial plexus lesions could lead to atrophy of specific muscle groups in the thoracic limb. BVetMed. or lameness or paresis affecting isolated limbs in isolated peripheral nerve lesions. or a junctionopathy such as myasthenia gravis may cause motor deficits in all four limbs (Olby.. generalized muscle loss (which might be reported as weight loss). which owners sometimes report as an abnormal head shape. particularly if it is inflammatory in nature. polyneuropathy. neuroanatomical localization of the lesion by performing a full neurological examination is absolutely vital in order to correctly identify the patient with a neuromuscular disorder. In cats. there a number of key clinical findings that can differentiate between neuromuscular disease and other . MRCVS London. the most common clues include: exercise intolerance. go upstairs or jump. for example masticatory muscle myositis may lead to bilateral masticatory muscle atrophy. 2004).

a list of differential diagnoses needs to be determined. Focal Neuromuscular Disease Signs of focal cranial nerve deficits may be detected on cranial nerve examination. short-strided. Lower motor neuron paresis is characterized by reduced spinal reflexes (again. The most useful spinal reflexes are the patellar reflex and withdrawal reflexes. and absence of atrophy. Patients with polyneuropathy tend to have a more flaccid paralysis. However. Once a neuroanatomical localisation has been achieved. 2002. 2003).. a brachial plexus tumour (malignant peripheral nerve sheath tumour) may cause focal atrophy of specific muscle groups in the thoracic limb.. spinal reflexes are usually normal. decreased salivation and bradycardia (Harkin et al. biceps. A thorough list of differentials for neuromuscular diseases has been provided by Braund (2003). choppy gait with an absence of proprioceptive ataxia. as well as having upper motor neuron signs depending on the site of the lesion. However spinal cord lesions that cause paresis are also associated with ataxia and have significant conscious proprioceptive deficits. the patellar and withdrawals are the easiest to interpret). Autonomic neuropathies additionally may exhibit signs of anisocoria or dilated pupils. Generalized muscle disease tends to cause a stiff. Examples of Common Differential Diagnoses of Peripheral Nervous System Disease Degenerative . The concept of upper motor neuron and lower motor neuron disease is extremely helpful in this situation. generalized muscle disease such as polymyositis usually leaves the spinal reflexes intact unless there has been profound muscle atrophy or fibrosis. Some of the most common cranial neuropathies are facial nerve paralysis and trigeminal nerve paralysis. gastrocnemius and extensor carpi radialis reflexes are unpredictable in normal dogs and are particularly difficult to elicit in cats. Other examples of focal neuromuscular signs are specific atrophy of muscle groups. Cave et al. for example. a disorder of the neuromuscular junction. Upper motor neuron paresis is characterized by normal to exaggerated spinal reflexes.causes of tetraparesis. It is also important to remember that spinal reflex deficits occur commonly in polyneuropathies however in myasthenia gravis. Animals with myasthenia gravis tend to have a short strided gait which gets progressively gets worse during attempted exercise and then improves after rest. decreased tear secretion . A C1-C5 spinal cord lesion will cause upper motor neuron weakness in all four limbs whereas a generalized neuromuscular disease such as a polyneuropathy will lead to lower motor neuron signs in all four limbs. Gait Dogs and cats with both upper motor neuron weakness and neuromuscular deficits may both have a weak (paretic) gait. normal to increased tone in the musculature. abnormal sensation (paraesthesia) and conscious proprioceptive deficits may also be seen. reduced muscle tone and neurogenic atrophy. decreased pain response (hypalgesia) or sensation (hypaesthesia). Similarly. Triceps. since the proprioceptive pathways are not affected. in neuropathies with a sensory component.

Several breed associated neuropathies have been reported e. e. diabetic neuropathy Neoplastic Paraneoplastic neuropathy.. hyperadrenocorticism..g. organophosphates Vascular Ischaemic neuromyopathy Examples of Common Differential Diagnoses of Muscular Disease Degenerative Labrador Retriever hereditary myopathy. Rottweiler distal sensimotor polyneuropathy Anomalous Storage diseases.g.. fucosidosis Metabolic Hypothyroidism.g. e. peripheral nerve tumours Inflammatory Polyradiculoneuritis Idiopathic Facial nerve paralysis Traumatic Brachial plexus avulsion Toxic Toxic neuropathies. glycogenosis Metabolic . vincristine. chronic hypoglycaemic neuropathy.. e.g. congenital muscular dystrophy Anomalous Storage disorders.

Magnetic resonance imaging is indicated in some situations. physical and neurological examination has determined the presence of neuromuscular dysfunction. electrolyte disorders or multisystemic disease.g. Haematology and biochemistry are important to determine signs of metabolic. Toxoplasma gondii.g. A diagnostic plan then needs to be instigated depending on the differential diagnosis list.g.. or if there is also central nervous system involvement e.Hyperadrenocortical (Cushing's) myopathy. Acetylcholine receptor antibody testing may be indicated. polyradiculoneuritis. Neospora caninum. Radiographs and ultrasound may need to be used to detect any signs of neoplasia or multisystemic disease. history. Serology may need to be performed for suspected infectious agents e. clinical findings and localisation. monensin Vascular Ischaemic neuromyopathy Diagnostic Work-Up Once history. a differential diagnosis list will be selected depending on signalment. e... malignant hyperthermia Neoplastic Paraneoplastic myositis. hypokalemic myopathy. skeletal muscle tumors Inflammatory Polymyositis. Creatine kinase needs to be carefully noted. e..g. Clinical electrophysiological techniques including electromyography and nerve conduction studies will be extremely useful to further localise the extent of any neuromuscular disease and to confirm sites of abnormality prior to other diagnostic tests. Toxoplasma gondii Idiopathic Facial nerve paralysis Traumatic Fibrotic myopathy Toxic Toxic myopathy. protozoal disease. Neospora caninum. ACTH stimulation and low dose dexamethasone tests may need to be performed to look for underlying endocrinopathy. Endocrine tests such as TSH and T4. as this may increase markedly if there is significant muscle involvement.g. protozoal disease. hypothyroid myopathy.. These methods are . for example if a brachial plexus tumour is suspected. Cerebrospinal fluid analysis may detect abnormalities if nerve roots are inflamed e.

BVetMed. Ed. By SR Platt and NJ Olby.ivis. Olby NJ. In: BSAVA Manual of Canine and Feline Neurology 3rd Edition.. Braund K. DECVN. It may be possible to differentiate between peripheral nerve. NMJ. there are still many neuromuscular diseases in dogs and cats that are not fully understood and treatments are limited in some situations. Cave TA et al. Braund's Clinical Neurology in Small Animals: Localization. Chapter 14. PhD. Lastly. in order to provide the most appropriate treatment and to give an accurate prognosis for the owner. Ed. The most commonly biopsied nerves include the peroneal and tibial branches of the sciatic nerve because both are commonly involved in polyneuropathies and are easy to surgically approach. Diagnosis and Treatment 2003 online at www.220(5):633. physical and neurological examination are the most important steps in investigating a neuromuscular condition. Correct and precise neuroanatomical localisation will greatly assist in drawing up a list of differential diagnoses. Unfortunately. Poncelet L. and muscular disease. The nerves and muscles to be biopsied should be selected on the basis of clinical signs and electrophysiological testing. However. Nerve and muscle histopathology should be performed by a specialist neuromuscular laboratory in order to obtain the most information from the sampled tissue.. Vet Rec. Chapter 4. J Am Vet Med Assoc.153(13):387.discussed in detail by Poncelet (2004). Harkin KR et al. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Kate Chandler. MRCVS The Queen Mother Hospital for Animals The Royal Veterinary College Hatfield. This will then be helpful in selecting the most appropriate diagnostic tests. It is therefore worthwhile pursuing a full diagnostic work-up to achieve a definitive diagnosis. 2002. By SR Platt and NJ Olby. Summary History. nerve and muscle biopsy are indicated depending on the results of electrophysiological testing and other clinical findings. Great Britain . References 1. In: BSAVA Manual of Canine and Feline Neurology 3rd Edition. 4. 3. many specific neuromuscular conditions can be treated such as the endocrinopathies and inflammatory conditions. 2.

and nociception) 3. you can determine where the lesion is likely to be cited. 2013 Christine E. Motor function 4. If a lesion is in a particular area. Cranial nerve function 5. these are: cervical (C1–5: neck). Can a single lesion account for all the observed signs (normal and abnormal)? If not. that suggests the lesion is not in the region of the nervous system housing that neural system.Localising Neurologic Lesions Using the NeuroMap: Spinal Cord World Small Animal Veterinary Association World Congress Proceedings. thoracolumbar (T3–L3: trunk). BVSc (Hons). In the dog. conversely. By noting from these test results which systems are functioning normally and which are abnormal. However. DACVIM (Neurology). then by referring to the NeuroMap (and accompanying table). then you can list the possible causes and make a diagnostic plan. Functional Regions of the Spinal Cord These are based around where the innervation to the limbs connects. New Zealand Veterinary Association. Thomson. lumbosacral intumescence (L4–S3: pelvic . indicating specific aetiologies. Clinical signs of dysfunction indicate that a lesion is disrupting that neural system. but that can be challenging. proprioception. Spinal reflexes Spinal sensitivity/pain may help to further localise a spinal cord lesion. Palmerston North. once you've localised the lesion. particularly if it is not something you do frequently. Key point: Identifying both the neural functions that are disrupted and those functions that are still normal are essential in lesion localisation. The Neurological Examination The following neural functions are assessed in the neurological examination: 1. As diseases are often location-specific. then the animal may have a multifocal lesion. The NeuroMap is derived from mapping the main neural functions on a diagram of the nervous system. if a neural system is functioning normally. they comprise specific spinal cord segments. Massey University. New Zealand 24418237 The first step in neurology cases is to localise the lesion. you can read from the NeuroMap which neural functions could be disrupted and. which neural functions will be normal. DECVN. PhD VetLearn. Ascending sensory systems (tactile. Behaviour and arousal (awareness) 2. cervical intumescence (C6– T2: thoracic limbs). The NeuroMap and associated table are simple aids that have been distilled from years of clinical practice and can assist you in localising lesions.

. but the bulk of the cell (the axon) is in the periphery.limbs and pelvic viscera). UMN versus LMN Disease When a lesion affects an intumescence (cervical or lumbosacral). Differentiating between UMN and LMN lesions Sign UMN disease LMN disease Decreased to absent Neurogenic: severe.' Reflexes A reflex comprises three parts: sensory input from a peripheral receptor. they may even be increased due to loss of inhibitory UMN influence. resulting in LMN signs such as reduced/lost Reflexes. Upper and Lower Motor Neurons A UMN is confined to the central nervous system (CNS = brain and spinal cord). it can damage cell bodies of the lower (peripheral) motor neuron cell bodies supplying the limbs. Conversely. thus it might help to think of it as a 'peripheral motor neuron. thoracolumbar disease. and reduced muscle Tone. but when UMNs are damaged. when the lesion is cranial to the intumescence. and caudal segments (Cd1–5: tail). Table 1. Damage to any one of those components will result in a reduction or loss of the reflex. Atrophy of specific muscles innervated by those LMNs. The Neuro RAT (Reflexes. Damage to LMNs results in reduced/lost reflexes. thus it might help to think of it as a 'central motor neuron.g. Atrophy. animals are considered to have a regionspecific localisation: e. and output via a lower (peripheral) motor neuron that connects to the muscle via a neuromuscular junction. As the clinical signs of spinal cord disease are characteristic for each of these regions. the animal is described as having UMN signs to the limbs as the upper (central) motor neuron has been compromised. generalised Tone Normal to increased Figure 1. then the LMNs to that limb will be intact (good tone and intact reflex arcs). reflexes will still be present. specific muscles Decreased to absent Reflexes Normal to increased Atrophy Disuse: Mild. a central connection in the brain or spinal cord for reflexes involving the cranial and spinal nerves. respectively. Tone) .' An LMN has its cell body in the CNS.

will result in loss of nociception. as both types of information travel up the spinal cord. But if the lesion is in the intumescence. Innervation of the Urinary Bladder and Anal Sphincter . withdrawal reflex).The Neuro RAT is a useful mnemonic to help differentiate between the signs of UMN disease and LMN disease. SCP is used to keep the limbs located under the body's centre of gravity and is particularly important for setting posture both at rest and during locomotion. animals with spinal cord disease usually have both conscious and subconscious proprioceptive deficits.the cerebellum. e. thus only severe spinal cord lesions. thermal and noxious stimuli) and the internal environment (e.g. Note: Normal proprioceptive reactions require both sensory and motor functions to be intact.. compromising the width of the cord.. the dog lifting paw to 'shake hands. Proprioception is awareness of body position. There they can stimulate local reflex function (e. viscera such as the distension of the urinary bladder or rectum). This can cause reduced/lost proprioception. An animal with deficits in CP may stand on top of its foot ('knuckling'). bilaterally. Sensory Function and Proprioception Spinal cord lesions can also compromise sensory function caudal to the lesion.g. If such a lesion is cranial to an intumescence. Thus. resulting in an ataxic (incoordinated) gait. Subconscious proprioception projects to a subconscious area of the brain .' Tactile input is a key component of CP.g. There are many nociceptive pathways travelling to the brain. The nociceptive information is also projected to the forebrain for conscious perception.. and sensory input from the external (tactile. or cross its feet when ambulating. an animal with deficits in subconscious proprioception may stand basewide or base-narrow. Input from muscle and joint receptors is important in SCP. both the withdrawal reflex and conscious perception will be lost. but there will be no conscious perception of the stimulus. Nociception Noxious (tissue-damaging) stimuli travel via spinal nerves into the spinal cord. However. Conscious proprioception (CP) is projected to the sensory cortex of the contralateral forebrain and is used by the animal for voluntary or skilled motor function. then the withdrawal reflex to that limb will still be intact.

Sensory input synapses in the sacral spinal cord triggering reflex activity (e. implying that their LMN are intact . Using the NeuroMap If you cover a region of the NeuroMap with your finger or a coin (representing a lesion in it) you will be able to see which neurological functions will be compromised and which will still function normally. Conversely.thus. turgid. there is reduced or lost muscle tone (bladder wall and sphincters) and reflexes. That all fits. the perineal reflex will also be intact.g. Conversely. The pelvic limb reflexes are intact. conveying information about the distension of the bladder and rectum for conscious perception. . Such an animal will have a bladder that is large. Loss of LMN supplying the anal sphincter may lead to a dilated sphincter and faecal incontinence. if you have an animal with particular signs. But as the thoracic reflexes are intact. flaccid. the bladder will be full. Identify on the NeuroMap where the wiring is for one of those functions. perineal reflex) and also projects cranially to the brain. and the bladder wall and striated urinary and anal sphincters will still have tone . Thus. the perineal reflex will also be compromised. For example. Where would a lesion have to be to compromise the proprioceptive tracts for all four limbs? C1–5 or C6–T2. they stimulate contraction of smooth muscle at the neck of the bladder and relaxation of bladder wall muscle for urine storage. you can use the NeuroMap to help localise the lesion. That makes it likely that it is a C1–5 lesion. LMN innervation will be intact. Sympathetic fibres originate from the cranial lumbar spinal cord. and easy to express. with proprioceptive deficits in all four limbs and intact reflexes in all limbs. with UMN lesions cranial to the sacral spinal cord. it may dribble urine. and difficult to express. both the signs of dysfunction and signs of normal function have helped you localise the lesion. that is possible with a lesion in the C1–5 region. consider an animal that is tetraparetic.yes. rectum..The innervation of the urinary bladder. Would that cause the tetraparesis? Yes. then the lesion can't be at C6–T2. When LMNs originating in the sacral cord are damaged. It receives sensory input from pelvic viscera and perineum and gives rise to parasympathetic LMNs supplying the bladder wall (for detrusor muscle tone and its contraction in urination) and somatic LMNs supplying the striated urinary and anal sphincters (urine and faecal retention). anal sphincter and perineum is associated mainly with the sacral spinal cord (S1–3).

trunk. The NeuroMap for the spinal cord and spinal nerves Table 2. Summary of effects of lesions in different areas of the spinal cord Presence of LMN Loss of Presence of signs to limbs sensory input UMN signs Loss of other reflexes TL. PL. Perineal reflex intact Cervical intumescence C6–T2 Thoracolumbar T3–L3 Trunk (caudal PL only No LMN signs in TL UMN bladder to lesion).Figure 2. (TL normal) or PL Faecal incontinence tail Cutaneous trunci reflex lost caudal to lesion. trunk. PL probably . perineal reflex intact LMN signs to pelvic viscera. Faecal incontinencec Cutaneous trunci and perineal reflexes intact TL. TL and PL tail both affected TL. PL. LMN bladderb LMN anal sphincter Cranial lumbosacral L4–S1 Caudal lumbosacral Tail. perineal reflex intact PL. tail No UMN signs to limbs No UMN signs to LMN signs in PL UMN bladder Cutaneous trunci reflex Faecal incontinence intact. loss of cutaneous UMN bladder trunci reflex if lesion in Faecal incontinencec C8–T2. PL only tail Location of lesion Cervical C1–5 Loss of urinary and faecal continence No LMN signs in TL UMN bladdera and PL. PL.

Thomson. faecal incontinence Normal continence TL = thoracic limb. full. difficult to express b = LMN bladder . Note: Whether or not all signs are present depends on lesion severity. PL = pelvic limb a = UMN bladder . PhD VetLearn.turgid. DECVN. Veterinary Neuroanatomy: A Clinical Approach. Thomson C. BVSc (Hons). New Zealand Veterinary Association Massey University Palmerston North. Elsevier Health Sciences. dribbling urine c = Animal will deposit faeces with good emptying of colon. ISBN 9780702034824. DACVIM (Neurol). References 1. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. distended. New Zealand .S1–S3 Caudal nerves Cd1–5 normald Tail limbs No UMN signs Loss of perineal reflex LMN signs to tail (dilated anus).flaccid. 2012. easy to express. but may not be aware that it is defaecating. Hahn C.

motor 3. cranial nerves 5. Christine Thomson. mentation and behaviour 4. Successful localisation is half the battle in the diagnosis of a clinical neurology case. MRCVS. spinal reflexes . Once you have established where you think the lesion is located then the diagnostic procedures and case management follow logically.Brain Cases: Understanding the Signs Part 1 & 2. 1. DACVIM (Neurol). BVSc (Hons). 1) THE GENERAL NEUROLOGICAL EXAMINATION In the general neurological examination of any animal. Dip ECVN Glasgow. Scotland. PhD. These seminars are aimed at helping you to understand the reasons why 'brain cases' present as they do. Lists of likely diseases are found in any good general or specialist neurology text book. Ability to perform a standard neurological examination 2. most neurological lesions can be localised and with that knowledge a list of likely diseases can be drawn up and diagnostic strategies determined. Where's The Problem?-Localising Brain Lesions ACVIM 2003 Dr. UK 18272993 What is required to localise a brain lesion? 1. A brain map From these three items. NOTE: you do not need to know the names of all the pathways and anatomical structures involved! INTRODUCTION Localising the lesion is essential in clinical neurology as different neurological locations are susceptible to different diseases. the following functions are tested and evaluated. Ability to recognise both normal function as well as neurological dysfunction 3. pain. sensory-proprioception. tactile 2.

g. or to determine that it is in more than one of these areas-i. e. vestibulospinal-vestibular nucleus to the spinal cord.. orthopaedic 2. L4-S3. spinothalamic-spinal cord to thalamus. Sensory . caudal segments ii. myelencephalon/medulla oblongata 3. multifocal/diffuse disease. The names of the main tracts are provided in case you want to cross reference your information. pons. multifocal or diffuse NOTE: signs of peripheral and cranial nerve dysfunction can occur with either central (CNS) or peripheral (PNS) pathology. The lesion is based in the nervous system (NS) or another system e.g. Spinal cord-C1-5. 1. Brain-forebrain.. T3-L3. C6-T2.e. Neurological Function and Dysfunction in the Brain 1.. The aim is to localise the lesion to one of these areas.. the brain can be subdivided usefully into the following areas based on similarity of function of the neural structures within those areas. Cerebellum The 5 functions outlined in the general neurological examination are tested when examining for brain disease NOTE: Naming of neural tracts-prefix = origin of the tract and suffix = destination of the tract e. Main Anatomical Areas of the Brain For clinical testing. Forebrain-cerebral hemispheres and diencephalon (thalamus and associated structures) 2. Brain stem-midbrain. brain stem or cerebellum 3.g.Once this information has been obtained and evaluated then the examiner should be able to determine whether 1. If the lesion is neurological whether it is localised to the a. Whether it is focal. Central NS (CNS) i. Peripheral NS (PNS) including the neuromuscular components and cranial nerves (CN) I-XII b.

hopping Deficits . Conscious proprioception (CP) Conscious proprioception is the sensory information that the forebrain receives and uses in the planning and execution of motor activity that is more complex than basic posture and gait e. NEx. trot. it may be perceived at the conscious level (forebrain) or the unconscious level (cerebellum).. respectively.g. forebrain Unconscious proprioception (UCP) Unconscious proprioception is the sensory information that the cerebellum receives and uses to coordinate motor function to maintain appropriate posture during sitting. not base-wide or base-narrow.brainstem.hip sway. joint receptors).g.stumbling.peripheral receptors (muscle spindles. muscle tension and length. reflex stepping/sliding paper test.g. joint angle etc. then spinal cord (spinocerebellar tracts) to terminate in the ipsilateral cerebellum.sensory ataxia (incoordination of movement). project through peripheral nerves. hopping.postural observation during rest and motion-the animal's feet should be in an appropriate position under its body to bear weight e. The trunk and neck should be held in an appropriate position. joint and tendon receptors) project through peripheral nerves. Pathway . canter etc) Pathway . where it crosses to the opposite side. abnormal posture (at rest and during motion. tactile placing Deficits . This is conscious (CP) and unconscious proprioception (UCP). tendons and joints mainly goes to the cerebellum and conveys information about body posture. The input from the muscle. UCP is required for basic posture and gait. cat playing with a mouse.. The information to the sensory cortex of the forebrain is more concerned with the precise knowledge of where and how the limbs are positioned e. then spinal cord (fasciculus gracilis and cuneatus) through the brainstem. that the foot is weight bearing on its palmar/plantar surface... to terminate in contralateral cerebrum. dog catching a Frisbee.a) Proprioception is the sensation of body position. they should not go too wide or too narrow or get caught up on each other. may fall to the side) .peripheral receptors (touch. not too high/low and with sufficient lateral truncal tone to stop the animal falling to either side.primarily paw position/knuckling. The feet should track efficiently during movement. NEx. standing and basic ambulation (walk. NEx . In a nutshell. knuckling Brain areas involved .. Proprioceptive sensory information is conveyed on long neural tracts from receptors in the limbs and trunk to ipsilateral cerebellum and the contralateral cerebrum. CP is required for complex voluntary movement. pressure.

generalised arousal/alertness... tremor.brainstem (caudal). forebrain 2. NEx. hence disruption to this tract may result in the classical UMN signs of increased muscle tone and spinal reflexes.. vestibulospinal tract). thus forebrain disease has minimal effect on gait.brainstem disease -> weakness. hopping. whilst cerebellar disease -> incoordination of movement.hypo/anaesthesia Brain areas involved . rubrospinal and corticospinal tracts). Facilitatory function . pathways (upper motor neuron-UMN tracts) project through brainstem to CN nuclei and through the spinal cord to terminate on lower motor neurons (LMN).observation of stance and gait. but not weakness. weakness/paresis. peripheral nerves. extensor postural thrust Deficits. NEx .peripheral receptors. The information that arrives at the reticular formation is relayed diffusely to the cerebral hemisphere.superficial pain = pinprick.g.. Note: LMN are found in both the cranial nerves and the peripheral nerves. the main motor centres are located in the brainstem.. Flexors: UMN tracts facilitating flexors-primarily run in the lateral white matter of the spinal cord (e. hypermetria and vestibular signs. wheelbarrowing. (medial medullary reticulospinal) has a massive inhibitory influence on LMN.g.g. UMN signs more likely to occur with spinal cord lesions than brain lesions. this is what causes normal. deep pain = bone-crushing pain Deficit .brainstem.brainstem motor initiating centres. the motor cortex of the forebrain is of much greater importance. Forebrain disease may lead to clumsy fine motor skills e. Motor In quadrupeds.ataxia. Pathway . dog catching a Frisbee. It is also projected to the reticular formation (ARAS-see below) of the brain stem.Extensors: UMN tracts facilitating extensors-primarily run in the ventral white matter of the spinal cord (e.Brain areas involved . cerebellum b) Pain Pathway . Inhibitory function . cat batting at a ball. These UMN tracts may stimulate or inhibit LMN. spinal cord (spinothalamic tract) to the contralateral sensory cortex of the forebrain. The cerebellum coordinates motor activity by projecting to the motor centres of the brainstem. whereas in humans and primates. of the UMN tracts in particular. but not overt weakness . Brain areas involved . Cerebellar disease can cause ataxia.

Coma-the animal is unconscious and cannot be aroused by any form of stimulus.Behaviour is both instinctive and learned from experience thus requiring intact memory Behaviour and memory circuits are located in the forebrain and particularly involve the limbic system and hippocampus. This diffuse network of neurons is located throughout the brain stem. . bold animal becoming timid etc. Obtundation (somnolence)-the animal tends to sleep when left undisturbed.loss of house-training. but can be aroused by a nonnoxious stimulus e. The respiratory.forebrain. auditory areas) and to the ARAS. Signs of decreased mentation are obtundation. This information stimulates the ARAS.. Cranial nerves The twelve pairs of CN are numbered with Roman numerals and are sequentially ordered from rostral to caudal. cardiac and vomiting centres are also associated with the reticular formation. (death!).g. Incoming sensory information is projected to both precise brain areas (e.. sensory cortex.Awareness/consciousness is associated with ascending reticular activating system/formation (ARAS) function. Mentation and behaviour a) Mentation .g. stupor and coma. which in turn diffusely stimulates the entire cerebral cortex causing awareness and arousal.NOTE: ataxia is incoordination of gait and can be sensory and/or motor in origin NOTE: When evaluating motor function such as gait. failure of recognition of animate/inanimate objects Brain areas involved . Decreased consciousness can occur with focal lesions in the brain stem affecting the ARAS. but remember that intact brainstem motor function is required to perform the behaviour 4. you will be assessing proprioception as well as the motor function. NEx . Stupor-the animal sleeps/is unconscious. 3.owner's history and observation (owner and clinician) Deficits .. visual cortex. noise. response to non-noxious and noxious stimuli (as indicated) Brain areas involved . b) Behaviour . change in animal's character e.brainstem and forebrain. and can only be aroused by a noxious stimulus such as pain e. hard pinching of the toe. NEx-observation of animal's interaction with the environment. or it can occur with diffuse forebrain disease.g..g.

Localising a lesion in a long neural pathway . The CN are the peripheral nerves of the head region. For example-the palpebral reflex: touching the margins of the palpebral fissure.see table 3. II). brainstem (III-XII). middle. CN VII efferent portion of the reflex arc to the facial muscles. however. Tone . to produce the signs? All pathways and neural structures are closely surrounded by other neural structures. CN X and XI). Some of the CN are involved in reflexes.v.g. So. NEx. Similar signs of dysfunction can result regardless of where the pathway is interrupted by disease. Segmental spinal reflexes The spinal reflex pathways are restricted to the spinal cord.)..I and II-are associated with the forebrain III and IV-midbrain V-XII-pons and myelencephalon. it also requires an intact cerebellum for correct function.ART).see table 3 Brain areas involved . Brain disease could cause UMN signs due to damage to descending inhibitory motor pathways. this is less likely than with spinal cord lesions (q. Deficits .forebrain (I. Reflexes .. CN VIII-although it attaches to the brainstem. Some of them supply striated muscle and damage will result in signs of LMN disease (Atrophy (severe). Figure 1. which consequently have afferent. 2) INTERPRETING THE NEUROLOGICAL EXAMINATION General principle for localisation: Neural pathways can be affected anywhere along their length-origin/receptor. cerebellum (VIII) 5. termination. but they may also extend into the body (e. how do you know where a lesion is located along the length of a pathway. So you look to see whether nearby neural structures are also affected. stimulates reflex blinking-CN V afferent. central and efferent components similar to that of spinal segmental reflexes.

This pathway travels for a long distance. Conversely. pathways B and C are located nearby in different regions of A. but there are signs of dysfunction in pathway C. Identifying both normal and abnormal functioning of the nervous system is important in the neurological exam. Note that identifying both normal function (pathway B) and abnormal function (pathway C) have contributed to the neuro-anatomical diagnosis on pathway A. Therefore. brainstem and cerebellum Table 1.Example . Table summarising where each function is located in the brain and spinal cord (see also figures 3a and b) Function Motor Mentation Behaviour Forebrain Minimal Brain stem CP and UCP Major initiating centres None Cerebellum UCP Coordination. in cases presenting with a certain set of brain/CN signs you should be able to localise the lesion to one of these areas. For part of that distance. Pathway B is functioning normally. not initiation None None Spinal cord CP and UCP Motor tracts None None Proprioception CP Diffuse areas ARAS Major centres . Figure 2. it should be relatively easy to predict the signs that you would expect with disease located in each of the three main functional areas of the brain. Using these diagrams and table 1. The three main functional areas of the brain.signs of disease affecting pathway A are present in an animal. forebrain. it is likely that pathway A has been affected by a disease in the region in which it lies close to pathway C. 3) THE BRAIN MAP The following diagrams show the location of the neural structures associated with the functions previously discussed.

Location of proprioceptive pathways and areas associated with mentation in the brain Figure 3b. Location of motor areas. .CN I. UMN/LMN = upper/lower motor neuron. ARAS = ascending reticular activating system Note: CP crosses sides in the brain stem so that the left side of the body will be perceived in the right forebrain and vice versa. behaviour and cranial nerve attachments in the brain. UCP = unconscious proprioception. UCP terminates in the ipsilateral cerebellum so that the left side of the body projects to the left side of the cerebellum Figure 3a.II III.IV (midbrain) V-XII (VIII) None Spinal reflexes None ?UMN influence None UMN & LMN signs CP = conscious proprioception.

only occur with forebrain disease. then the aim is to list the most likely diseases that could be causing the problem. but Behaviour-OK damage to motor/mentation can preclude normal behaviour III-XII can be affected (see table 3) Normal Normal Can see vestibular signs Cranial nerves I. Clinical signs that are likely to occur with disease in different areas of the brain. but not weakness Mentation-OK Mentation Decreased mentation Decreased mentation with with diffuse forebrain focal brainstem disease disease Altered Behaviour No direct effect. takes into account the history and signalment of the animal as well as the results of the physical and neurological examinations and the localisation of the lesion. There are many. I try to list the top three likely diseases in order of priority. II-visual disturbances most likely Normal Spinal reflexes Note: Forebrain disease can also cause circling (usually to the side of the lesion) andseizures: Seizures or fits. Identifying which diseases are likely. many diseases and rather than learning them by rote. Causes of Diseases affecting the brain and cranial nerves-DAMNIT! After localising the lesion based on your neurological examination. . I use the mnemonic 'DAMNIT' to help remember the sorts of diseases that can affect the nervous system (NS).OK Minimal effect Brainstem disease CP deficits Cerebellar disease CP-OK UCP deficits-if caudal brain UCP deficits-ataxia.Based on the above diagrams mapping the main functional areas of the brain. stumbling. Table 2. Neurological exam Proprioception CP UCP Motor function Forebrain disease CP deficits Knuckling. a diagnostic plan is formulated. you can determine what functions could be compromised with pathology in each of the different brain areas. gait is reasonable UCP . stem lesion postural deficits Weakness-can be severe Incoordination spasticity and tremor. From that.

Diffuse lesion: (bilateral forebrain). ataxia and UCP deficits.g. multiple CN deficits (e.. decreased mentation (FB or BSt).D A Degenerative Anomalous (congenital). stumbling.. weakness. contralateral visual deficits. Angiomatous (we use this term 'cos we could not find a better word for vascular-based conditions!) M N I Metabolic including endocrine Neoplastic Nutritional Inflammatory/Infectious/Immune-mediated Idiopathic Iatrogenic T Toxin Trauma EXAMPLES OF CLASSICAL CASES Forebrain (FB) 1. contralateral CP deficits. brain stem or cerebellum. seizures (FB). visual deficits (FB) and vestibular (BSt or cerebellum) signs. E. tumour: aimless walking possibly circling.g. Note: Vestibular signs could be due to pathology in the inner ear. How would you differentiate the location of the pathology? . e.g. Focal lesion.g..seizures Brainstem lesion (Bst) CP deficits. +/. multiple CN signs (III-XII). gait is reasonable but some stumbling might be noted. possibly vestibular signs Multifocal disease E. decreased mentation to coma Cerebellar lesion UCP deficits. vestibular signs and facial paresis). +/seizures 2. spasticity. tremor. CP deficits on both sides. maybe a bit dull. decreased awareness to coma. BAR. animal may "forget" to use the contralateral limbs in voluntary movement.. Mentation.

Table 3. The cranial nerves, testing and signs of dysfunction; a = afferent, e = efferent Head function Olfaction Vision Innervation Ia IIa Clinical testing Observation, food Maze test Menace response-IIa & VIIe PLR-IIa & IIIe (parasympathetic) Pupil size IIa, IIIe PLR (parasympathetic) Pharmacological testing Sympathetic -e (Cerebellum) Eyeball position IIIe, IVe, VIe (also VIIIa) Visual tracking Eyeball position in different head positions Strabismus-constant position (LMN of CN III, IV, VI), changing position (UMN/central). Anisocoria, mydriasis, miosis +/- other signs of Horner's syndrome Dysfunction Dysosmia-difficult to prove clinically Blindness, dilated pupil (although this can be due to just CN III dysfunction)

Vestibulo-ocular reflex VIIIa & Loss of vestibulo-ocular reflex IIIe,IVe,VIe Facial sensation Va-all three branches Touch Palpebral reflex-Va & VIIe (medial and lateral canthus) Auriculo-palbebral reflex Va & VIIe (just in front of ear for V) Mastication Ve-mandibular Jaw tone Masticatory muscle bulk Facial expression VIIe Facial symmetry Palpebral reflex Va & VIIe Auriculo-palbebral reflex Va & VIIe Muzzle movement, Ear Muscle atrophy Dropped jaw-only if bilateral Facial paresis/paralysis Loss of blink and ear reflex twitching Facial hypalgesia Loss of blink and ear reflex twitching

movement Lip commisure symmetry Vestibular function VIIIa Head position, Eyeball position Head tilt, circling, rolling (also involves III, IV, VI) Vestibulo-ocular reflex (VOR) (VIIIa & IIIe, IVe, VIe) Gait and movement Pharyngeal IXe and Xe function Laryngeal function Xe and XIe Gag reflex (IXa & IXe,Xe), Swallowing Voice Respiration Tongue XIIe Spontaneous nystagmus, Strabismus Deranged body posture and ataxia Dysphagia, Salivation, Aspiration Dysphonia Respiratory stridor-laryngeal obstruction

Observation-LMN signs, usage Atrophy, paresis/paralysis-uni or bilateral Withdrawal

NOTE: the menace response is a learned RESPONSE not a hard-wired reflex. It is a response as it has to be learnt, it is absent in young animals-typically appearing in kittens and puppies between 8-16 weeks of age Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Christine E. Thomson, BVSc (Hons), MRCVS, PhD, DACVIM (Neurol), Dip ECVN SACS University of Glasgow Veterinary School Bearsden Rd. Glasgow, G61 1QH SCOTLAND

Cervical Vertebral Stenotic Myelopathy I & II (V462, V463) Western Veterinary Conference 2005 Stephen M. Reed, DVM, DACVIM The Ohio State University , Columbus, OH, USA279239 The recognition and diagnosis of disease involving the nervous system in the horse is often a multiple step process. The neurological examination helps to provide a neuroanatomic localization of the problem and helps to determine which diagnostic tests are indicated, such as radiography, myelography, electromyography and cerebrospinal fluid analysis. Many central nervous system (CNS) diseases can result in similar clinical signs, making the specific cause difficult to determine. A diagnosis rests on identifying the specific neurological functions, which are deranged, and associating them with the anatomical regions of the nervous system, which are damaged. It should include a careful and complete musculoskeletal examination. The neurologic examination of the horse should proceed from the head caudally, and should be consistent and systematic in order to reduce the likelihood of omitting parts. The neurologic examination begins with an observation of the animal at rest and should include its mental attitude, level of consciousness, head, neck, trunk and limb posture, as well as for signs of abnormal behavior. A closer examination of the head for cranial nerve deficits should be performed. Examination of the eyes includes the blink response, its ability to negotiate in a strange environment and an ophthalmologic exam. If a horse has a lesion in the eye or optic nerve, it will have ipsilateral blindness. A contralateral blindness would indicate a lesion in the optic tract or lateral geniculate nucleus. The pupil size is under control of the autonomic nervous system and is affected by the level of environmental light and the level of fear or excitement. To test the pupillary light response, a light should be directed in each eye and an observation of pupil constriction should be noted. Injury to the 3rd, 4th or 6th cranial nerves results in a deviation of the eye. The trigeminal nerve is a large nuclei, which contains both sensory and motor branches. Injury to this nerve results in a dropped jaw and loss of sensation to the face and nares. The seventh nerve supplies motor innervation to the ears, eyelids and nose. If the seventh nerve is injured, a droopiness of the ear or eyelid will result along with deviation of the face to the unaffected side. With injury to the vestibulocochlear nerve, the horse often has a head tilt toward the affected side and nystagmus with the fast phase away from the site of the lesion. Damage to the nerves which supply the muscles of the larynx and pharynx will result in difficulty with swallowing, breathing and vocalization. When signs of damage to these nerves are present, the examiner should carefully check for guttural pouch infection, a caudal brainstem lesion, or injury to the nerve somewhere along its course from the brainstem to the appropriate muscle. The head and neck should be manipulated to check for signs of pain and to determine the range of motion. Symmetry of the neck and forelimbs is then evaluated. This may involve palpation as well as observation. Normal animals stand with their legs about shoulder and hip width, with the weight equally distributed on all four legs. A base wide stance may be seen with spinal cord, cerebellar or vestibular disease. It often indicates a loss of proprioception or balance. If a horse has a "knuckled" or non-weight bearing limb, it may be a result of loss of proprioception or paralysis in that limb that may be due to a peripheral nerve, spinal cord or brainstem lesion. If the limb appears painful, close examination for musculoskeletal disease is indicated.

The gait, which is predominately controlled by the forebrain, brainstem, spinal cord, peripheral nerve and muscle function, should be examined thoroughly. Gait abnormalities include weakness, ataxia, dysmetria and spasticity. Weakness is often seen as dragging of the toes and stumbling when walking, or trembling and lack of support at rest. Signs of weakness may be seen with cerebral, brainstem and spinal cord lesions, as well as with peripheral nerve, neuromuscular junction, and muscle lesions. With a brainstem or spinal cord lesion, weakness is present in all limbs caudal to the lesion. Ataxia often denotes a proprioceptive deficit and is characterized by poor coordination of movements. The lesion causing an ataxic gait may be located in the cerebellum, vestibular system, spinal cord, brain stem or peripheral nerve. Ataxia includes abnormal foot placement, crossing of the limbs, circumduction of a limb when circling and stepping on other feet. Severely ataxic horses will often pace. Spasticity is best described as a "tin soldier" gait--the animal showing very little flexion of its joints when moving. Dysmetria is best described as an inability to regulate the rate and direction of motion. In contrast to a spastic gait that has a decreased range of joint movement, the motions in animals with dysmetria often appear exaggerated. Gait deficits are graded with zero as normal or no gait deficit and a 5 as a recumbent animal. A grade 1 deficit is very subtle, grades 2 and 3 are obvious on initiation of movement and a horse with grade 4 deficits may fall or nearly fall when moving. If no head, neck or forelimb neurologic deficit is identified, abnormalities in the trunk and hindlimbs must be explained by a lesion between T2 and S2. The final segment of the neurologic examination is the finding of the explanation for any deficits of the tail, anus and other structures innervated by the sacral and coccygeal spinal cord segments. This can be accomplished by determining whether the horse can lift or move its tail, has good anal tone and normal reflex. The pathogenesis of CVSM is unknown but appears to be multifactorial. Etiologic factors such as genetic predisposition, hormonal changes, nutrition, trauma, and exercise are the most investigated. Early on, a genetic predisposition to CVSM in horses was suspected based on the frequency of this problem in certain families of Thoroughbreds, however, lack of many close relationships in a group of 47 horses with CVSM gave rise to thoughts on other etiologic factors. Although some investigators have failed to demonstrate genetic determination of CVSM, others believe that genetic factors that determine the length of the neck, cervical vertebral biomechanics, and body size play a significant role in the development of CVSM. In the most recent investigation of the heritability of CVSM, the author suspects that a genetic predisposition, wherein horses inherit increased sensitivity to environmental factors affecting cartilage growth, is likely. On postmortem examination of 30 horses with CVSM, the authors demonstrated narrowing of the vertebral canal and noticed that commonly these horses had bony changes characteristic of degenerative joint disease, including osteoarthritis and malformation of the articular processes. In this study the importance of nutrition in the development of CVSM was suggested. Mayhew et al (1978) found that horses with CVSM, to a far greater extent than control horses, had decreased differentiation of cartilage and osteopetrosis sometimes associated with osteonecrosis and osteoclasia. These degenerative changes in the cervical vertebral articular processes and costochondral junctions of horses with CVSM were associated with osteochondrosis dissecans. He proposed CVSM to be a "performance" or "production" disease with a multifactorial etiology, comprised of genetic predisposition, overnutrition, and environmental and iatrogenic modifying factors. Similar to these findings were histopathology results of vertebrae involved in

and osteochondrosis of the articular processes may result in instability and malalignment of adjacent vertebrae. All of these may contribute to spinal cord compression. 1990). and hypertrophy of soft tissue structures. Stewart et al. controlled investigations have failed to confirm this relationship (Knight et al. excess protein. Mayhew et al. The accelerated rate of gain. In these horses the compression of the spinal cord can be attributed to the bony and soft tissue proliferation at the affected articular processes. Binkhorst 1976. however. however. 1991. however. This finding is supported by the improvement most of these horses show following medical and surgical treatment with subsequent radiographic evidence of reduction of the bony proliferation. in older horses (> 4 years) CVSM is generally associated with significant arthropathies of the caudal cervical articular processes. and excess . but controversy exists on this statement (Savage 1998) as well as on the role of numerous dietary factors in the development of these diseases. The genesis of the degenerative joint disease in older horses with CVSM is speculative. Nutritional factors that have been associated with the incidence of developmental orthopedic disease are a dietary imbalance in the calcium/phosphorus concentration. Multiple investigators have shown that horses with CVSM have an increased incidence and severity of degenerate joint changes in the axial skeleton (Dimock and Errington 1939. this group did have a high incidence (45%) of osteochondrotic lesions in both the axial and appendicular skeleton. and similar to Binkhorst's findings. Reed 1997). The effects of trauma and exercise in predisposed animals are hypothesised to contribute to the development of osteochondrosis and CVSM (Donawick et al. may indicate that the pathogenesis of both conditions is similar and may respond to the same preventive and therapeutic measures (Stewart et al. is essential in the pathogenesis of CVSM. but does not belong in the osteochondrosis syndrome. 1985). This is why Hurtig and Pool (1996) suggest CVSM is a manifestation of developmental orthopedic disease. but that the primary predisposing factor in the pathogenesis of CVSM is the insufficient diameter of the cervical vertebral canal at the site where spinal cord compression occurs. although offspring from horses with CVSM did not develop myelocompressive lesions themselves. 1989). Osteochondrotic lesions are the result of abnormal endochondral ossification. Binkhorst (1976). There has not been general agreement on the importance of degenerative joint disease of the cervical vertebrae in the pathogenesis of CVSM. Rooney (1969) has proposed that malformation of the articular processes is the predisposing lesion and.myelocompressive lesions. secondary osteoarthritis of the articular processes. not of growth. excess zinc. has been related to osteochondrosis and CVSM in horses. Stewart et al (1991) reported that the site of the most severe osteochondrotic lesions did not always correlate with the site of vertebral stenosis. The positive correlation between osteochondrosis and CVSM. indicating that the lesion was an osteochondrotic type defect (Stashak et al. This suggests that osteochondrosis of the articular processes is not the direct cause of CVSM. copper deficiency. thus. however. 1991) and Wagner et al (1985) demonstrated that. currently the role of external trauma is thought to be the most important (Mayhew 1999). 1978. found only 8% correlation between lesions of the articular processes and histologic changes in the spinal cord. In contrast to young horses in which the role of degenerative joint disease in the pathogenesis of CVSM appears controversial.

carbohydrate. The three most important nutritional factors appear to be excessive dietary digestible energy, excessive dietary phosphorus, and dietary copper deficiency (Savage 1998). Carbohydrate excess in the diet is thought to contribute to developmental orthopedic disease through an endocrine imbalance involving elevation of serum insulin concentrations and decreased serum thyroxine concentrations, resulting in a lack of cartilage maturation (Glade and Belling Jr. 1984; Glade and Luba 1987). Based on this hypothesis a "paced growth" program for the prevention and therapy of CVSM has been recommended in order to slow down body growth in height and weight (Donawick et al. 1989). Savage et al (1993a) demonstrated that high digestible energy diets, composed of both carbohydrates and corn oil components caused osteochondrotic lesions in foals, but that these are not solely due to an excessive average daily weight gain. It is suggested that feeding high digestible energy diets result in endocrinologic alterations that mediate local cartilaginous factors and selectively activate genes that cause a specific alteration in matrix phenotype (Savage 1998). A dietary calcium/phosphorus imbalance has been implicated in CVSM (Binkhorst 1976) and particularly excessive phosphorus (388% of the requirements) appears to be correlated with an increased incidence and severity of osteochondrotic lesions in foals (Savage et al. 1993b). Copper deficiency leads to defective lysyl oxidase, which is a copper-dependent enzyme required for proper maturation of connective tissues. A low copper diet (15 ppm) produced 3 times as many osteochondrotic lesions of the appendicular and 7 times as many osteochondrotic lesions of the axial skeleton, as compared to foals fed a high copper (55 ppm) diet (Knight et al. 1990), however, copper supplementation did not eliminate developmental orthopedic disease, supporting the presence of other etiologic factors. Similar results were obtained when foals fed 7 ppm of copper had a much higher incidence of macroscopic osteochondrosis than foals fed 30 ppm of copper (Hurtig et al. 1993). Zinc has an antagonistic effect to copper and it has been postulated that diets excessive of zinc could cause secondary copper deficiency (Knight et al. 1985), but this has not been proven in the horse. Conclusion CVSM is the most common non-infectious cause of spinal cord ataxia in the horse. Stenosis of the cervical vertebral canal and subsequent myelocompression is the cause of this neurologic disease. Although the etiology of CVSM is not fully understood, diagnostics and therapeutic options for affected horses have improved over the last years. The specificity and sensitivity of predicting CVSM from survey radiographs using the sagittal ratio method is high, however, myelography remains necessary for localisation of compressive lesions. Further research is required in the field of antemortem diagnostics, i.e., defining criteria to evaluate myelograms and evaluating the use of computed tomography. Ventral interbody fusion has been proven an effective surgical procedure, however, complete recovery does not occur in all horses, and risks associated with post-operative performance must be carefully considered by the owners. Stephen M. Reed, DVM, DACVIM The Ohio State University Columbus, O

Acute Neurological / Spinal Injury
Simon LeMin1, BVSc, MACVSc; Jason Mouatt2, BVSc, FACVSc 1 Animal Emergency Centre; 2Veterinary Specialist Service, Underwood, QLD, Australia18

Patients with acute collapse and spinal dysfunction can be challenging, emotional and urgent cases. Signs are often severe and sudden. Affected animals often present in distress, as do their owners. However, the majority of these acute spinal cases carry a good prognosis if adequate treatment is given in a timely manner. The initial assessment and management are often a key step in successful recovery. An understanding of the possible causes, options for treatment and likely outcomes will often greatly influence the treatment and the owners' willingness to treat their pets.

There are a wide range of potential causes of acute collapse in dogs and cats. This presentation will deal mostly with spinal causes, however it is important to have a systematic approach to collapsed patients to allow differentiation between neurological and other causes of collapse (e.g., toxic, musculoskeletal, metabolic, respiratory causes) As always, a thorough history and clinical examination are essential with all patients. The clinician should consider the possibility of other causes of acute collapse including: Metabolic--e.g., Addison's disease, DKA, hypoglycaemia Respiratory--laryngeal paralysis , brachycephalic airway disease Cardiac disease / syncope, acute haemorrhage Heat stress Toxins--Tick paralysis, Snake bite Generalised LMN disease--myasthenia gravis, polyradiculoneuropathy Orthopaedic disease--bilateral cruciate rupture, bilateral tibial crest avulsions Blood biochemistry and CBC are often indicated to assess for concurrent disease and electrolyte abnormalities. Neurological cases are usually differentiated on clinical and neurological examination well before xrays or further tests are done. The initial neurological assessment should include: Signalment--breed, age, sex History--Time of onset, Rate of progression, inciting factors, mental changes Distant examination / Posture--mono-, hemi- , para-, quadra paresis or paralysis, back arching, head position, etc Gait analysis--ataxia, hypermetria, short stepping, "lameness", circling, etc Close examination--Muscle wasting, toe scuffing, self trauma The neurological examination can essentially be broken into a few questions or steps: 1. Is this case neurological 2. Lesion localisation 3. Differential diagnosis list 4. Further diagnostic tests The major differentiating factor in patients with spinal disease (compared to other causes of collapse) will be the lack of conscious proprioception. This is most easily tested with knuckling tests of

each paw, but hopping, wheelbarrowing hemi-walking and placing responses are also tests of proprioception that can be used. It must be remembered that some very painful, ill or mentally depressed patients will not respond normally to tests for proprioception. Supporting the patient's weight when testing proprioception will provide a more reliable response in some of these patients. Presence of seizures or cranial nerve deficits will usually also suggest neurological brain) disease. Lesion localisation allows the clinician to develop a list of differential diagnoses and therefore provide a diagnostic and treatment plan, and some sort of prognosis. Presence of seizures or cranial nerve deficits suggests brain or multifocal disease. Spinal lesion localisation is achieved with: Spinal reflexes Hyperpathia / pain focus Superficial pain dermatomes (for some LMN lesions) Spinal reflexes allow localisation to a smaller segment of the spinal cord. It is essential to understand the interpretation of these reflexes. A reduced reflex suggests damage to the lower motor neuron motor arc. This can occur anywhere in the peripheral nerve or the spinal cord segment that the nerve comes from. (LMN changes = reduced or absent reflex). If the reflex is not reduced in a neurologically affected limb, then the reflex arc and associated spinal segment must be intact, meaning the spinal lesion is proximal to the spinal segment tested by that reflex. These Upper motor neuron spinal lesions (UMN) cause normal or increased reflexes. Forelimb tests include withdrawal (flexor reflex), Biceps, triceps and extensor carpi radialis reflexes. Withdrawal is very reliable however the other reflexes can be difficult to elicit and are often therefore unreliable. Hindlimb reflexes include withdrawal, patella reflex, cranial tibial, sciatic and gastrocnemius reflexes. Withdrawal (Sciatic nerve) and Patella reflex (Femoral nerve) are more reliable than the others and test the 2 major nerves in the hindlimb. Use of these reflexes usually allows localisation to one of 4 spinal segments--C1-5 (UMN to fore and hind); C6-T2 (LMN fore, UMN hind); T3-L3 (no deficits in fore, UMN hind); L4-S3 (no deficits in fore, LMN in hind) Panniculus reflex is a useful localising tool if there is a definite cut off. Panniculus is usually not present caudal to L4. Testing should begin caudally and work cranially 1 vertebrae at a time. A distinct cut-off point (i.e., present cranial, but absent caudal to a specific point) will usually indicate a spinal dysfunction 1-2 vertebrae cranially. Unilateral panniculus is pathognomonic for a high thoracic (T1-3) or brachial plexus injury. Complete absence of panniculus is non diagnostic. Normal panniculus does not rule out a spinal dysfunction. Presence of a pain focus is usually very helpful, both in localising the disease and developing a differential diagnosis list. Neck manipulation should be done slowly and carefully, particularly in compromised patients where there is the possibility of a traumatic injury or vertebral instability. The neck should be isolated into cranial and caudal parts and each section flexed laterally, dorsally and ventrally. A normal dog should be able to touch the tip of the nose to the iliac crest without pain. Deep palpation of the ventral wings of the vertebrae may also elicit pain. Thoracic, lumbar and sacral vertebrae should all be deeply palpated slowly and deliberately. The chest and abdomen should be supported with the other hand when palpating, as most dogs will drop down with unsupported thoracolumbar or lumbosacral pain. Painful neurological disease is consistent one of 5 things-- IVDD, neoplasia, trauma, meningitis or discospondylitis. Non painful spinal disease is more commonly associated with parenchymal disease such as vascular accidents, intramedullary neoplasia, and degenerative disease. Schiff Sherrington syndrome--this describes a severe extensor rigidity of the forelegs associated with a high to mid thoracic spinal dysfunction due to compromise of the border cells and ascending inhibitory tracts to the forelegs. This sign has often been described as a poor prognostic sign, however

this is not always the case and prognosis depends more on the cause and severity of signs rather than just the presence of Schiff Sherrington posture. Deep pain assessment is a critical prognostic aid with spinal dysfunction and collapse. Generally speaking, patients that have not lost motor function should still have deep pain. Deep pain tests the deepest white matter tracts of the spinal cord and compromise to these tracts usually represents severe cord trauma. Loss of deep pain does not necessarily indicate a hopeless prognosis, although it certainly makes the outlook more guarded. Rather it suggests aggressive, rapid therapy is indicated to provide the best chance of a good outcome. Deep pain DOES NOT equal withdrawal--remember withdrawal of a limb is a reflex and will occur even after spinal transection. Deep pain requires a conscious response from the patient (cry, turning around, biting etc).

The major differential diagnoses include:

1. Intervertebral disc disease(IVDD)
IVDD is the most common cause of acute collapse seen in veterinary medicine, and may be chronic to peracute in onset. Affected patients are mostly painful and usually have no history of recent severe trauma associated with onset. Occasionally acute traumatic disc extrusion can occur following a severe external force. In non chondrodystrophic dogs, this often causes cord concussion but minimal ongoing compression and surgery may not benefit. Chondrodystrophic dogs usually cause a marked continued compressive lesion of the cord. Myelography, CT or MRI is required to differentiate these two situations. IVDD usually occurs in either the cervical or thoracolumbar region with each having differing signs Cervical IVDD Predominantly a small breed / chondrodystrophic dog disease. Occurs usually in dogs over 2 years of age (mostly middle aged dogs). Most dogs show screaming pain with variable neurological compromise ranging from none, to severe hemi- or quadriparesis. C2-3 is the most common site and the incidence reduces at each more caudal space. Therefore most dogs with neurological signs will show conscious proprioceptive deficits in fore and hind legs, and in theory UMN reflexes in all legs (although this is sometimes inconsistent in the forelegs). Pain is evident on careful neck palpation, lateral flexion and dorsal and ventral neck flexion. Some dogs will show a "root signature" due to nerve root compression within the canal. Radiographs of the neck are often difficult to interpret but narrowed IV spaces of mineralisation in the canal may be suspicious. Myelography is required for definitive diagnosis. Clinical cervical disc disease is rare in cats. Thoracolumbar IVDD Predominantly chondrodystrophic dogs, with peak incidence between 3-6 years. Larger dogs have a lower incidence and usually occurs in middle aged to older dogs. Majority (75%) of IVDD cases are between T11-12 and L1-2. Occasionally affects mid to caudal lumbar vertebrae. Rarely affects cranial to T10. Often mild cases confused with abdominal pain (usually without GIT signs). Most affected dogs will have focal pain on spinal palpation. Many will have panniculus cutoff. Hind leg ataxia/paralysis usually with CP deficits and UMN reflexes (if lesion above L4). Forelegs should be "normal".

Deep pain presence is major prognostic sign. Clinical signs depend on the site affected--in many signs are progressive (as expected with a slow growing mass). Neoplasia Neoplasia may originate from the spinal cord. bone tumours (osteosarcoma. CSF analysis is often normal or shows subtle changes only. or exacerbation by acute disc protrusion.Cats--IVDD much less common. Most dogs are aged Dobermans or Doberman crosses. Most patients show evidence of chronic disease on radiographic and myelographic examination. but may be due to sudden cord concussion from the unstable thickened dorsal annulus.g. Over half show asymmetric signs initially. In dogs. 2. HL ataxia / paralysis). occasionally dogs with mild or no clinical disease can have acute collapse episodes. vascular compromise of a chronically compromised spinal cord.root signature. discospondylitis. Onset is usually instantaneous and severe. 4. but does occur. lymphosarcoma is most common. or as a secondary metastasis from elsewhere in the body. Maximal signs occur within 24 hours. Exact cause is still controversial but essentially involves infarction of a spinal segment following embolism of a piece of fibrocartilagenous tissue. This tissue is hypothesised to come from the nucleus pulposus. progressing to bilateral signs. They are usually quadraparetic. but other large breeds can be affected C6-7. May produce UMN or LMN signs depending on area of cord affected. CT scan or MRI. Trauma Fractures may be pathological (developmental e.. usually in middle aged to older cats with similar signs to dogs (pain. and often are reported to scream out at the time of collapse. Myelogram is normal or may suggest mild cord swelling. . Affected dogs may or may not have neck pain +/. MRI will show a transverse myelopathy with oedema (hyperintense T2 signal) at the affected site. however between 25 and 40% of cases will have an acute and severe onset (presumably due to vascular compromise or pathological fracture). Radiographs are normal. The exact cause for this is unknown. however tumours compressing meninges or nerve root are often painful. bone neoplasia. Diagnosis requires cervical myelography with traction views. "Wobbler" Syndrome Dogs with caudal cervical spondylomyelopathy / disc associated wobbler syndrome usually show a slow chronic weakness. with some forelimb extensor rigidity and UMN hindlimb reflexes. non chondrodystrophic breeds. 3. meninges. Definitive diagnosis and histopath usually requires surgical exploration. About 80% of cases occur between 3 and 6 yrs of age. tissues of the vertebral canal. However. Fibrocartilagenous embolism (FCE) Occurs mostly in large breed. chondrosarcoma. Affected dogs are NON PAINFUL after 10-60 minutes. nerve roots. Traumatic injuries usually have a history to suggest possible injury. 5. fibrosarcoma) and nerve sheath tumours are most common. Pain is variable--intramedullary tumours are not painful. In cats. atlantoaxial instability. etc) or traumatic. C5-6 and C4-5 most commonly. myelography. Affected dogs often have a history of high exertional exercise at onset. Diagnosis may require radiographs (bony destruction).

Occasionally see acute neurological condition--often associated with the bacterial waste products and toxins affecting cord function and not necessarily to the degree of cord compression. 2.e. cord hypoxia and further associated injury. 7. cardiovascular. Avoid medications that may severely drop blood pressure unless absolutely necessary. shoulders. Meningitis often shows generalised or multifocal spinal pain. Analgesia may allow a painful animal to relax and stay restricted more easily. radiographs) should be performed with the patient attached to the board / table until unstable vertebral injury can be ruled out. Discospondylitis Infection of 1 or more intervertebral discs. it may also show signs consistent with a focal spinal disease (especially GME). Maintain spinal cord perfusion--the normal spinal cord has an autoregulatory ability which ensures adequate vascularity during mild hypotension. Straps should be very firm and be placed across the head. displacement. Any patient transport or diagnostics (e. radiographs / myelogram). T13-L1 and L7-S1. head trauma etc) but if spinal dysfunction may be present it is important to recognise early. Brain Disease There are a wide range of inflammatory diseases than can be highly variable in their presentation. Diagnosis involves ruling out other causes of spinal pain (i. and spinal pain. etc suggesting a more generalised problem. Deal with other problems (haemorrhage. T5-6. PART 3. 6. Most common sites are C6-7. difficult to settle. respiratory. but can be anywhere. etc. In many cases patients may need chemical restraint. May also see acute vertebral instability secondary to bone lysis. Trauma patients may have multiple other injuries. . 2 radiographic views are essential for diagnosis-look for damaged vertebral bodies. Therefore IV fluids are strongly advised in the compromised spinal patient. Systemic Stabilisation It is important to thoroughly assess all patients. EMERGENCY MANAGEMENT OF THE ACUTE SPINAL PATIENT 1. intermittent pyrexia. midbody (caudal ribs) and pelvis. Usually bacterial (Staph intermedius most commonly) but may be fungal.Vertebral damage reflects severity of the lesion and the direction of force. Diagnosis on lateral spinal radiographs--lytic area around disc with surrounding sclerosis and possibly new bone production. Urine and blood cultures may allow growth and sensitivity of causative agent. Myelography rarely necessary. Most patients show weight loss.g.. Analgesia--many acute spinal conditions are extremely painful and can lead to patients being stressed. aggressive. narrowing or widening of vertebral spaces. Clinical / neurological examination provides a better assessment of severity of the cord compromise than the radiographic picture. Attempt neurological assessment prior to use of analgesics. CSF analysis and perhaps advanced imaging. therefore prolonged hypotension will lead to decreased blood flow to the cord. It is a basic tenet of emergency medicine to "treat the most life threatening condition first"--remember that a severed spinal cord in a veterinary patient is life threatening as in most cases it will lead to euthanasia. lethargy. A damaged cord however loses this ability. This is best done by taping or strapping the patient in lateral recumbency to a board or table prior to any radiographs or major manipulation. Meningitis. mental dullness.. Prevention of further damage Trauma--rigidly restrain patient--If there is a risk of unstable vertebral fracture/s the patient should be stopped from excessive movement and further vertebral displacement. However.

Where possible. Repeated neurological assessment--watch for changes in neurological grade. Low (antiinflammatory) doses of 0. This occurs mostly by blocking free radical peroxidation and destruction of the white matter tracts. Bladder management--Neurologically affected dogs often don't or can't urinate.. therefore mostly indicated if owners are prepared to consider surgical intervention. however oral prednisolone (0. do not use) 30mg/kg SLOW IV Follow with 15mg/kg at 2 and 6 hr later. diarrhoea. repositioning if the vertebral column is stable. Preferably collect prior to administration of any corticosteroids. Regular (every 4 hours) expression or placement of an indwelling urinary catheter and closed collection system should be started early in the management to avoid detrusor atony.2mg/kg may reduce some cord oedema. general anaesthesia should be used. Early Referral if surgery is indicated . Generally not indicated unless it will change the treatment. Medications--There is always dispute over medication use with acute spinal injury. CSF analysis--should be collected if meningitis is high on the differential list. do not allow increased exercise as further nuclear extrusion is common and may cause further cord compromise. The general guidelines are: Do not use unless within 8 hr of initial injury (if not sure. Further diagnostic Tests Myelogram--essential in assessment of potential IVDD and neoplasia cases. Regular turning. Initial Diagnostics Radiographs--important to rule out overt fractures. 4. Methyl prednisolone sodium succinate (MPSS--Solu-Medrol®)-this has been shown to improve clinical outcomes in people and some animal studies. as poorly positioned radiographs and tense animals often cover up lesions. Use of high doses is CONTRAINDICATED.Suspect IVDD cases should be strictly confined to reduce movement-strict cage rest should be enforced.5mg/kg) may provide a similar benefit in non surgical cases with less side effects.e.1-0. but disc space narrowing and vertebral foramen clouding/opacity may provide suspicion of IVDD. General management Regular assessment. Good padded bedding. neoplasia and (especially cervical) fracture cases. Intervertebral disc disease and vertebral canal neoplasia can rarely be definitively diagnosed on radiographs. urine scalding and urinary tract infection. sepsis. death). However the fact remains that few drugs have consistently shown statistical improvement in outcomes of spinal patients. vertebral luxation or subluxation. or 15mg/kg q6hr. 6.5-5mg/kg/kr for 23 hrs Do not exceed 24 hours use Higher doses (60-90mg/kg) are detrimental Use after 8 hrs may increase neural necrosis Dexamethasone--HAS NO PROVEN BENEFIT in acute spinal trauma. or 2. 3. Dexamethasone is very ulcerogenic and side effects often severely complicate spinal management (i. 5. Advanced imaging--CT / MRI--sometimes useful for assessment of IVDD. Take 2 views where possible. obvious neoplasia and discospondylitis. If early improvement is seen.

Medical management is indicated for IVDD on the initial occurrence that shows only pain or mild neurological signs. and some residual deficits may remain. TREATMENT OPTIONS AND OUTCOMES 1. Fitch et al (JAHAA 2000. those with marked neurological signs. Therefore patients require adequate nursing and time. Cervical IVDD--is usually treated with ventral slot surgery to allow removal of extruded nucleus from the spinal canal. Surgery is indicated in all patients with severe or recurrent pain not responsive to medical therapy. About 50% of grade 4 lesions will recover and a 7% recovery rate with grade 5 (loss of deep pain) lesions. However the large majority of suspected cases show some improvement within 5-10 days and the majority of those cases will go on to good function. Generally recovery takes from 1-6 weeks. although this can be slow and uncomfortable and recurrence is not uncommon. Thoracolumbar IVDD--Hemilaminectomy is the treatment of choice for grade 2 and worse cases. Length of deep pain loss was not quite as significant in this study. 3. a 25% recovery within 12-36 hours and <5% recovery after 48 hours. p 417) presented a 62% recovery rate in patients with no deep pain. They also suggested a poorer level of pre and postoperative neurological condition in those with more caudal cervical lesions. or those with progressive signs. Surgery provides minimal assistance and medication appears also to provide little change in the course of the disease. 2. FCE There is little specific treatment available for FCE cases. Patients with acute collapse have a superior outcome if treated with surgery at an early stage by an experienced surgeon. Loss of deep pain has been widely discussed and carries a poorer prognosis. They suggested the rate of loss of deep pain was more prognostic. 12/14 with neurological dysfunction and 6/7 plegic dogs had improved and by 12 months post-op all by one dog had completely recovered.5% improvement rate by the time of discharge from hospital. Overall recovery in large and small breed dogs appears to be about 85%. Seim and Prata (1982) reported on 54 patients undergoing ventral slot--within 48 hours all with neck pain. Scott and McKee (JSAP 1999. p68) suggested C2-3 and C3-4 lesions carried a significantly better prognosis than those more caudal. but not hopeless prognosis. A 4. Conservative management (strict rest) provides up to 90% recovery in grade 1-3 cases. Recovery depends on the severity of the spinal damage. There is no difference in the recovery rate in those with UMN or LMN changes. Conservative management generally requires longer recovery times. Gill et al (JAAHA 1996) reported on 30 dogs undergoing dorsal laminectomy for IVDD with 69% normal 2 weeks after surgery and al dogs clinically normal at long term follow-up. Wobbler syndrome . Smith el al (AVP 1997.9% occurrence of post-operative respiratory difficulty has been described with cervical surgery requiring ventilation post-op.p 58) reported a 29. however loss of deep pain with LMN signs is generally a poor sign. however dorsal laminectomy. hemilaminectomy and ventral fenestration are all described. Gambardella et al (Vet Surg 1980) found a 56% rate of recovery rate if surgery done within 12 hours of deep pain loss. Those with deep pain carry a poorer. IVDD Treatment essentially can be surgical or medical. 10/13 ventilated patients survived and 9/10 recovered neurologically. and that those with peracute loss of deep pain had a far poorer prognosis than those with gradual loss. In contrast.PART 4. In patients with deep pain present success (return to normal or near normal pain free function) is 90% or above.8% resolution rate and 49.

Trauma Conservative management is indicated in patients with mild clinical signs and stable vertebrae and clinical signs. most patients recover well and some will have prolonged good recovery. Survival with Osteosarcoma was 31 and 300d. severe vertebral instability or deteriorating neurological status or uncontrollable pain warrant surgery. Severe neurological status. Acute deterioration however often does not correlate to obvious spinal compression and therefore surgery may not be beneficial and may actually further destabilise the area. Median survival with Meningioma was over 1400 days. p245) described 20 vertebral body tumours with various treatmentsPrognosis is generally poor--MST was 135d and OYS was 10%. but clinical signs should improve rapidly after beginning treatment. Patients with severe vertebral instability or acute deterioration may warrant myelography to assess cord compression. although some will recover in the short term with conservative management. Neoplasia The prognosis with neoplastic lesions is generally very guarded. There are a number of surgical options for both cervical and thoracolumbar stabilisation. A range of surgeries to decompress or stabilise the affected vertebrae have been described and a recent report suggested that there is no obvious statistical difference between published results of various techniques. Cervical surgery has been reported to have a 36% perioperative death rate. Multimodal therapy including radiation appears to offer an improved outcome perhaps. About an 80% success rate is seen with surgery. 6. . This involves 3-6 weeks of splinting and rest. Treatment often takes 3-6 months. Levy et al (JAAHA 1997. Thoracic and lumbar lesions can be supported by a dorsal back splint taped from the shoulders to the pelvis (+ cage rest). survival with lipoma was 2520d. 5. Discospondylitis Most patients respond well to appropriate antibiotic therapy. The placement of implants in an infected site is not ideal and if possible should be avoided. rest. Cervical lesions often respond well to good padded neck support with 89% recovery reported in one study.p307) described outcomes in 37 dogs. Survival with Myxoma / myxosarcoma was 570 and 1080d. NSAIDs and time. Fungal discospondylitis carries a very guarded prognosis. Median survival with nerve sheath tumours was 180d. and possibly surgery to stabilise the vertebral bodies. Loss of deep pain at the time of the injury carries a poor prognosis generally. 4. Adequate stabilisation provides a guarded to good prognosis in patients with deep pain. however it appears their recovery is slower and more difficult than that of ambulatory patients. Surgery may also be required to achieve an adequate biopsy and culture of the affected site in non responsive cases. There is debate as to whether acutely collapsed patients truly carry a poorer prognosis. Intramedullary tumours provide a hopeless prognosis.Treatment for acute collapsed wobbler patients generally requires surgery. Tumour type often can not be determined until surgical biopsy. However a significant number of patients still improve. In German Shepherd dogs this is usually a systemic disease. The message is that with surgery. Dernell et al (JAAHA 2000.

2005 Luisa De Risio. Axonal regrowth occurs spontaneously (1 mm/day) along the connective tissue scaffold. Faculty of Veterinary Medicine. pelvic. Neurapraxia--refers to a transient interruption in nerve function (impulse conduction) due to ischemia and/or mild paranodal demyelination. Degenerative changes also occur in the axons proximal to the injury site but usually involve only one to three nodes of Ranvier. Wallerian degeneration occurs. Axonotmesis may result from severe stretching or crush injury of the nerve.e. MACVSc Animal Emergency Centre Underwood. QLD. hypo/areflexia. crushing. complete and occurs within one to two weeks once the compression and edema resolve. however it might be difficult or even impossible to differentiate severe axonotmesis from neurotmesis on the basis of clinical assessment. Small non-myelinated fibres supplying . motor and nociceptive dysfunction (i. FACVSc Veterinary Specialist Services Underwood. Peripheral nerve injuries have been classified based on the degree of functional and structural integrity of the nerve trunk:(4.Simon LeMin. University of Parma Italy 18284787 Traumatic peripheral nerve and nerve root injuries are common in companion animals and may be caused by motor vehicle accidents. significant neurological dysfunction and neurogenic muscle atrophy are expected. 18. sacrocaudal). The degree of proprioceptive. Recovery is usually spontaneous. Schwann cells. In general. 3. proximal femoral). no deep pain perception). The slightly smaller myelinated fibres controlling motor function are the next most susceptible. fracture/luxations (sacroiliac. may help distinguishing between neurapraxia and axonotmesis or neurotmesis. Scar tissue tends to interfere with sprouting axons and may result in neuroma formation. proprioceptive deficits. Large myelinated fibres. QLD. As in axonotmesis the distal segment undergoes Wallerian degeneration. bite wounds.. 19) 1. but the proximal axons will not regrow to their end-organ since there is no guiding scaffold (Schwann cell basal lamina and the endoneurium have been disrupted). their basal lamina and the endoneurium remain intact. 17) Clinical signs associated with peripheral nerve injury include: pain. but the time until return to function depends on the extent of injury and the distance from the denervated end-organs. stretching. DMV. It is associated with complete proprioceptive. Consequently. gunshot wounds. Australia Peripheral Nerve Injury WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. lower motor neuron type motor dysfunction (paresis/plegia. neurogenic muscle atrophy). BVSc. surgical intervention is necessary to assist regenerating axons to reach and reinnervate their appropriate end-organs. Neurogenic muscle atrophy is unlikely to occur. Our ability to estimate clinically the severity of a nerve injury is mostly based on the relationship between the diameter of a nerve fibre and its susceptibility to compression. supportive connective tissue). Neurotmesis--is the most severe type of injury and is characterised by complete severance of the nerve trunk (axons. but the Schwann cells. Australia Jason Mouatt. The nerve injury may result from compression. There is no structural damage to the axons and their supportive connective tissue. nociception is usually preserved. 16. 2. Neurapraxia is the mildest form of nerve injury and it is commonly caused by blunt trauma or compression. BVSc. Axonotmesis--few to several axons and surrounding myelin are disrupted (structural damage).(3. (supplying mainly proprioceptive function) are the most sensitive to injury. 8. Local demyelination may take 4 to 6 weeks to resolve. The neurological examination. Neurogenic muscle atrophy is severe. surgical "misadventures"). DECVN Animal Health Department. laceration or complete transection. motor and nociceptive deficit is proportional to the number of axons that are damaged. The degree of proprioceptive and motor dysfunction can be variable. muscle hypotonia. and hypo/anaesthesia. Distally to the point of injury the axons and their myelin sheaths degenerate and undergo phagocytosis. fractures (humeral. especially if repeated overtime. and iatrogenic lesions (misplaced intramuscular injections.

abdominal ultrasound and a coagulation profile. Electrodiagnostic tests are useful in assessing nerve integrity. 8. Survey radiographs are indicated when the nerve injury is likely to be associated with fractures (i. the presence of motor unit activity in the biceps brachii muscle of a dog or a cat with brachial plexus injury implies that some functional axons must have survived through the musculocutaneous nerve. F-wave studies allow assessment of ventral nerve root function and may be useful in cases of proximal motor nerve injuries such as brachial plexus avulsion. sacrocaudal) or with intramedullary pinning. For example. the absence of compound muscle action potentials does not indicate the severity or permanency of the nerve damage because transient conduction block due to edema may also prevent conduction down a nerve. A recent study in human medicine has shown that ultrasound can be a useful diagnostic aid in the determination of the precise localisation of the injured site along the involved peripheral nerve. followed by motor function and finally by nociception. In certain cases it might be indicated to perform also thoracic radiographs. proprioceptive function will be impaired at first. Therefore.(6. Sensory function can be assessed by means of sensory nerve conduction velocity (SNCV) study and cord dorsum potential (CDP). 13.(9) These information are extremely helpful to decide whether and exactly where segmental nerve resection and reanastomosis should be performed. By eliciting a withdrawal reflex (stimulating an area that the animal can definitely feel) and simultaneously recording EMG activity from a flexor muscle.. 7. 17) However.(10) We have successfully used ultrasound to visualise sciatic nerve entrapment following penetrating wound in the caudal thigh of dogs previously attacked by a boar. The presence of deep pain sensation in the dermatome of a certain nerve implies a much better prognosis than its absence. 13) It is important to remember that with brachial plexus nerve root avulsion there may be inconsistency in the pattern of sensory versus motor deficits as the ventral nerve roots appear more susceptible to damage than the dorsal nerve roots.(3. Immediately after a brachial plexus or a peripheral nerve injury electromyography (EMG) can be used in the awaken animal to determine if some axons are still functional in the injured nerve and therefore if the muscle is still innervated by that nerve. humeral.(14) If EMG studies are repeated over time they may help monitoring disease progression. the absence of the CDP with a normal SNCV indicates a complete nerve root injury above the dorsal root ganglion. distribution of nerve injury and in monitoring reinnervation. functionality. motor unit action potentials will be recorded if any muscle function remains.nociception are the most resistant to compression.(17) A thorough knowledge of the dermatomes and autonomous zones of the principal nerves of the limbs is essential to perform an accurate assessment of sensory function.(6) Intraoperative nerve action potential are used in human medicine in order to identify functional regeneration of an injured nerve and accurately trace the length of regenerating axons and the length of nonviable nerve. Ultrasound may be helpful in assessing nerve anatomy and further characterise traumatic nerve lesions in companion animals.(6) Five to 10 days after peripheral motor nerve injury (that is the time required for the degeneration of the distal axonal segment). serum biochemistry profile and urinalysis to assess general health condition prior to anaesthesia for electrodiagnostics and/ or diagnostic imaging. (1. with increasing compression of a nerve. the type of injury and the diagnosis of neuroma.e. 17) The diagnostic investigation for patients with peripheral nerve injury will include: A minimum data base consisting of complete blood count.(5) Computerized tomographic (CT)--myelography is indicated in the diagnosis of brachial plexus nerve root avulsion since it allows visualization of meningeal diverticula and abnormalities of . femoral. 7. denervated muscle fibres exhibit spontaneous depolarizations that can be recorded by EMG (in the anaesthetized animal) in the form of fibrillation potentials and positive sharp waves. pelvic. severity of damage. The presence of giant motor unit potentials on EMG indicates reinnervation. For example. in a dog with sensory dysfunction following brachial plexus injury. Clinical signs associated with dysfunction of most commonly affected spinal peripheral nerves have been thoroughly described. Motor nerve conduction velocity (MNCV) and the recorded amplitudes of muscle evoked action potentials provide an accurate evaluation of the severity of the damage to the LMN.

Physical therapy should be started in the early stages following nerve injury in order to maintain range of motion and minimise muscle atrophy. it has been demonstrated that conventional MRI can detect signal changes in injured nerves and in denervated muscles. In human medicine. The surgical techniques (epineural. in human medicine. neurolysis). Excessive scar formation at the suture line will markedly decrease the progression of regenerating axons. immediate nerve repair is recommended. by a piece of glass or a knife). Therefore medical management (analgesics. It is interesting to note that these guidelines are quite similar to the ones used in human medicine even though patient cooperation during clinical and electrodiagnostic assessment is much higher than in veterinary medicine and more sophisticated facilities are usually available. and if indicated also diagnostic imaging) are advised. An essential part of neurorrhaphy is accurate anatomical alignment of the nerve fascicles.the spinalnerve roots. If the nerve has been severed sharply (e. 12) When these techniques have failed or are not indicated and delayed nerve repair is not an option. In a recentprospective study of 40 human patients suffering severebrachial plexus injuries. severe and irreversible. axonometric or neurotmetic. excessively long femoral intramedullary pin. This latter complication results from abnormal sensation in an affected area due to pathological changes in the peripheral and/or central nervous system and may be difficult to control pharmacologically. CT-myelography was found tobe 85% accurate in predicting the intraoperative findings.(15. Special microsurgical instrumentation and magnification (ocular loupes or operating microscope) are required to perform a meticulous neurorrhaphy. Hence.(11) In addition. these include: muscle atrophy and joint contracture (that can be prevented/ addressed with physiotherapy). electrodiagnostics.(2. perineural. and the wound is not contaminated. anti-inflammatories and analgesics are indicated to relieve inflammation and pain. Unfortunately. intramedullary pin removal/shortening. the use of custom designed phase array coils has led to the development of MR neurography (MRN). anti-inflammatories) and frequent re-evaluation (neurological examination. Muscle-tendon transfer alone or in association with carpal/tarsal arthrodesis may be indicated as a salvage procedure in selected cases. limb amputation may be the only possibility. it is not possible to determine immediately whether the lesion is neurapraxic. the severity and the site of the lesion. Failure to match the fascicles in the two segments prevents regenerating axons from reaching their appropriate end-organs. entrapment by inflammatory/fibrous tissue) it should be addressed surgically as soon as possible (fracture repair. abrasion of the dorsal surface of the paw (preventable with adequate foot protection). while awaiting for a possible improvement some complications may occur. the paw should be protected by means of commercially available boots. When the primary cause of nerve injury can be identified (trauma by fractured/dislocated bone.(20) In those instances where limb dysfunction is profound and nerve damage is chronic (no improvement after 3 to 6 months post-injury). splints or special bandages. Treatment of peripheral nerve injury depends on the cause. MRN produces images with higher resolution improving the ability to visualize both normal and abnormal peripheral nerves in various regions of the body.(11) MRI provides fine anatomic detail of soft tissue and can be used to visualise nerve structures. The sutures have to be positioned with no longitudinal and circumferential tension at the repair site.. The surgical repair must be accomplished with the least possible trauma to minimise inflammation and fibrosis.(11) These advanced diagnostic imaging techniques may have an important role in the assessment of peripheral nerve and brachial plexus injuries in companion animals in the near future. . nerve grafts) to perform nerve repair have been described. and paraesthesias with self mutilation. 16) When the nerve lesion is caused by stretch and/or compressive forces associated with a closed traumatic injury. we can state that frequently the greatest diagnostic aid in patients with closed traumatic nerve injuries is the passage of time. In general.g. If the nerve injury produces monoparesis and knuckling such as with radial or sciatic nerve lesions. In veterinary medicine MRI has been successfully used in the diagnosis of peripheral nerve sheath tumors and will certainly have a role in the diagnosis of peripheral nerve injuries. treatment options are quite limited. . DECVN URL: developments in the treatment of peripheral nerve injury include the use of neurotrophic and neurotropic factors to stimulate axonal survival and regeneration (trophic effect) and to direct growing axons to their proper target organ (tropic effect). Luisa De Risio.

DACVIM. BVM&S. UK 18286413 The presentation of neurological disease in camelids.Approach to the Neurologic Camelid: Clinical Neurological Examination. as in other species. Table 1. Differential diagnoses of neurologic disease in South American camelids. MRCVS London. eg EHV-1. varies widely. EEE Trauma without subluxation/ luxation/ fracture* Clostridial myositis Rabies Degenerative Degenerative myelopathy Spondylosis Toxicities Tetanus Botulism Hip problems Rye grass staggers Cerebral hypoxia Peripheral nerve damage Musculoskeletal Bilaterally luxating patellae Nutritional problems Otitis media/interna* Brain abscess Vertebral body abscess Septicaemia/meningitis* Uraemic encephalopathy Hypomagnesaemia Infectious/Parasitic Diseases Meningeal worm (P tenuis infestation)--United States* Metabolic Diseases Pregnancy toxaemia* Hypo/hyperglycaemia Hepatic encephalopathy . These conditions must be differentiated from those of true neurological origin by careful history-taking. Lesion Localization & Diagnostics ACVIM 2008 Claire E. physical examination and use of appropriate diagnostic tests. Whitehead. West Nile. There are many different causes of neurological signs (Table 1) and the clinician must be aware that metabolic and musculoskeletal disease can also present with neurologic signs. MS. Congenital Diseases Hydrocephalus Kyphosis Listeriosis Atlanto-occipital malalignment Traumatic Vertebral body subluxation/luxation* Vertebral body fracture* Viral.

Tremors may also occur with electrolyte imbalances (mainly hypocalcemia and hypomagnesemia). A head tilt may be due to otitis. so that placing reflexes can be tested. The presence of seizures indicates brain involvement. the duration of clinical signs. and assess mental status. myelin disorders. hindlimbs or both can be useful historical information. the lesion is likely to involve the cerebellum.g. circling behavior. with some toxins or with diffuse encephalitis. postural or proprioceptive deficits. These may be difficult to assess in the recumbent animal. deworming programme (parasitic myelopathy). it is usually possible to assist the animal to stand. and of course signalment. In heat stress cases. patients often develop weakness in the forelimbs primarily. Sometimes. knowing whether the problem began with the forelimbs. and changes in the cerebrospinal fluid (CSF) will help establish whether a disease process involves the central nervous system (the technique is described later). it may be hard to distinguish one condition from another clinically..Tick paralysis Ionophore toxicosis Other Hypo/hyperthermia* Mega-oesophagus Brain/spinal cord neoplasia Facial nerve paralysis Gait abnormality Determine Whether the Neurologic Signs are Due to a Lesion in the Nervous System Firstly. and do not discount the possibility that two conditions may be present together. parasitic myelopathy with secondary heat stress in summer. possibly with the use of a sling. Observe the resting animal. especially adults. diet and any dietary changes. However. Look for any head tilt. e. for a recumbent camelid. and also how the problem began. For example. A spinal tap is easily performed in camelids from the lumbosacral space. Determine whether or not a traumatic incident was observed. Localisation of a Lesion Within the Nervous System This is a continuation of the clinical exam. a vestibular lesion or possibly neck pain. especially whether the clinical signs were acute or chronic in onset. When performing the basic clinical examination. whereas patients with parasitic myelopathy develop ataxia and weakness typically in the hindlimbs first. If tremors are present and the head is involved. Hematological and biochemical profiles may help identify metabolic causes. and ataxia. preferably while unstimulated. it is vital to obtain a thorough history of the problem. with alpacas and youngsters. differentiating this from weakness. leaning to one side or head-pressing. but this may be secondary to a metabolic abnormality . whether there have been any seizure episodes. look especially for evidence of cranial nerve deficits.

Assess the animal's gait and ability to turn in circles etc. menace response. single or multiple limb involvement. but may be difficult to assess in camelids with subtle problems since they often resent having their feet touched. Depression. . look for weakness versus ataxia. Hearing may be difficult to test in camelids except by observing their reactions to their environment when unrestrained. The interpretation of data from the neurologic exam aids the clinician in determining the region affected and also whether the lesion is upper or lower motor neuron in origin (Tables 2 and 3). LMN lesions Paresis to paralysis Reduced/absent reflexes Loss of muscle tone UMN lesions Paresis to paralysis Normal or exaggerated reflexes Normal/Increased muscle tone Muscle atrophy appears quickly Muscle atrophy is slow to appear Table 3. Withdrawal reflexes are best tested in camelids by squeezing the digits at the distal end of the digital pad using hemostats. If unilateral. The panniculus reflex is difficult to assess in camelids. and assessment of pupil size and symmetry.such as hypoglycemia or be due to a primary lesion. Absent or reduced reflexes indicate partial or complete loss of sensory or motor parts of the reflex (LMN). patellar reflex. Table 2. pupillary light reflexes. cortical blindness. or if one side of the animal or one half (front or back) is worse than the other. Examination of the cranial nerves should also be performed in the neurologic camelid. partly because of their thick skin but also because they may have be heavily fleeced for much of the year. Observe facial symmetry and determine whether or not ptosis. Lower motor neurons are the efferent nerves that connect the CNS to the muscles. Exaggerated reflexes indicate that there is an UMN defect. If the animal can walk. Palpation of muscle masses is useful in evaluation of muscle atrophy (symmetrical versus nonsymmetrical) and general body condition. Localisation of spinal cord disease based on clinical neurologic features. this is most likely to be due to a peripheral lesion whereas bilateral absence or reduction of reflexes is more likely to suggest the presence of a spinal cord lesion. Various reflexes can be assessed including withdrawal reflexes. gastrocnemius reflex etc. facial sensation. Normal reflexes indicate that sensory and motor function are working normally. Assessment of proprioception can be done. This should include evaluation of the palpebral reflex. or rotation of the globe are present. Characteristics of lower and upper motor neuron lesions. Look for nystagmus or strabismus. these may be evaluated using the Brainstem Auditory-Evoked Response test. while upper motor neurons initiate movements and control extensor muscle tone which is responsible for supporting the body at rest. Where specific hearing deficits are suspected. and slow PLRs (not ophthalmic in origin) may indicate presence of a brain lesion. anal tone. enophthalmos. I do not find this test particularly useful in camelids. whether the problem is unilateral or bilateral.

insert the needle perpendicular to the skin on the midline about 35mm in front of an imaginary line drawn between the two ilia.3 The lumbosacral tap is an easy procedure to perform in camelids and usually requires only a little local anaesthetic whereas the atlanto-occipital tap requires sedation or anaesthesia and is a risky procedure. It helps to anchor the wrist on the animal's pelvis as this is done because the skin is quite thick. based on work in horses. CSF from the lumbosacral space was more likely to have compositional abnormalities in neurological disease and that more useful information would therefore be obtained. Lumbosacral and atlanto-occipital CSF samples were compared in llamas that were experimentally infected with P tenuis. If unsuccessful. the needle needs to be advanced 2-4cm and "two pops" are usually felt as the needle goes through the dura into the subarachnoid space. samples from 3 llamas with suspected meningeal worm were collected simultaneously from the LS and AO spaces: the CSF collected from the LS space showed more significant elevations in protein and cell count. Before the final scrub. In another report. CSF Sample Collection Normally CSF is taken from the lumbosacral space. Collect 2-3ml CSF and split the sample into a plain tube for CSF profile (protein/creatine kinase (CK)/electrolytes etc) and an EDTA tube for cytology (red and white cell counts and differential counts).1 This study concluded that the site chosen would depend on the suspected location of the lesion. inject 0. CSF will be observed in the hub. When the stylet is removed.Spinal cord region C1-5 C6-T2 T3-L3 L4-S2 S1-3 Neurologic features UMN signs to all 4 limbs LMN signs to FL: UMN to HL Normal FL: UMN signs to HL Normal FL: LMN signs to HL Partial LMN signs to HL. The landmarks are the dorsal spinous process of L7 and the two wings of the ilia. further diagnostics will be helpful in reaching a specific diagnosis.5-1ml local anaesthetic at the site using a 22G one inch needle. Using an 18G 3. ensure midline placement and try directing the needle a bit more cranially. A small area is clipped and prepared over the LS space after ensuring that the animal is squarely positioned and the hind legs are pulled forward in order to open up the LS space. Usually the patient will "jump" when the needle penetrates the dura. Welles et al (1994)2 observed rapid deterioration of leukocytes in CSF after collection and advised careful handling and refrigeration .5inch spinal needle in adults (20G in crias). Welles et al (1994)2 stated that. In an adult. incontinence Determine the Cause of the Neurologic Lesion Once the clinician has established that he/she is dealing with a neurologic disease and then determined what neurological deficits are present. These landmarks form a triangle within which an obvious depression can be palpated. Some tests may be done easily in practice whereas others may be limited to specialist or referral facilities.

the protein concentration was only minimally altered. The normal white cell population may be predominantly lymphocytes or neutrophils depending on the amount of blood contamination (more neutrophils with increasing blood contamination). Sodium concentrations should not be reduced too rapidly or cerebral oedema and herniation of the brainstem may occur. Glucose concentration in llama CSF is approximately 40% of serum concentration. normal CK concentration is less than 10 IU/L and white cell count should be less than 3 cells/µl.3. a myelogram may be indicated but is rarely found to be necessary in order to .2. a normal eosinophil count does not necessarily rule out meningeal worm: in experimental infection of llamas with P tenuis. P tenuis infestation is the only parasitic myelopathy so far reported in camelids.2 This compares with cattle in which CSF glucose is approximately equivalent and monogastric species in which it is 60-80% of serum concentrations: rapid changes in serum glucose. fractures or soft tissue injuries as well as demonstrate congenital malformations such as kyphosis. spinal or skull radiographs may be useful. Their method did not indicate that any preservative was used: it is likely that collecting CSF into EDTA tubes will reduce the deterioration of cells. prior treatment with anthelmintics may affect cell counts. Also. Clinical observations suggest that the length of time following initial development of clinical signs until CSF is collected can result in lower percentages of eosinophils seen on cytology. In the absence of blood contamination there should be no eosinophils. Increased protein indicates a disturbance of the blood-brain-barrier and this may occur in any inflammatory disease process including trauma. For more subtle lesions. The most important variables to consider in the CSF are protein concentration and cytology but in certain disease situations other variables such as sodium and glucose may be useful. Increased sodium concentration in the CSF could reflect severe metabolic derangements and may occur in salt toxicity due to unavailability of soon as possible following collection.5 and can be up to 99% of total white cells--eosinophilic pleocytosis with increased protein concentration in the CSF is present in most affected camelids. and in crias with hyperosmolar syndrome. In camelids. meningitis and otitis: if protein electrophoresis shows increased globulin only. These may highlight obvious luxations. Welles et al2 found in their study that in healthy llamas with red cell counts <1400 /µl. this indicates intrathecal synthesis of globulins. Radiographs Depending on the clinical signs.4. the time post-inoculation at which eosinophils increased in CSF varied. and CSF findings. in bacterial meningitis in crias. However. as in stress for example. localisation of lesion. the proportion of eosinophils increases in meningeal worm (parasitic myelopathy)1. Normal CSF protein concentration in camelids is less than 45-50 mg/dl. parasite migration. CK concentration may also be of value in indicating CNS disease although some studies have shown that it may increase due to the presence of epidural fat in the sample. This can cause intense CNS depression and needs to be carefully managed.2 Bacterial infections will decrease CSF glucose and also increase neutrophil count--for example. Two views are essential for cervical films as single view films may not pick up subluxations etc. will take 30mins to 3hours to equilibrate in CSF.

We have found that. 12 thoracic. Am J Vet Res 1994. et al. Rickard LG et al. 5 sacral vertebrae and 10-15 coccygeal vertebrae. especially where the head is involved. DACVIM. et al. MRCVS The Royal Veterinary College Hatfield. Computed Tomography (CT) CT may be required to visualise a suspect area. It may be used to direct the clinician to a particular problem area. 3. J Zoo Wildlife Med 1994. Welles EG. JAVMA 1985. General anaesthesia is required.reach a diagnosis.7(4):124. CT gives a significantly better image of the tympanic bullae than plain radiographs and the extent of soft tissue involvement can be delineated using contrast CT. 4. It is useful to detect denervation and can allow localisation to specific spinal cord segments. This is a good tool for investigating myopathies and neuropathies. Electromyography (EMG) Measures the electrical activity of muscle. Baumgärtner W. MS.187(11):1243. 7 lumbar.55(8):1075. Scarratt WK. 5. although MRI is likely to be preferred if soft tissue or subtle lesions are suspected. et al. 2. et al. Muscle Biopsy Muscle biopsies may be useful if a myopathy is suspected rather than a neuropathy. Ultrasonography May be useful in evaluation of soft tissue injuries and hydrocephalus. It is also useful if a brain mass/abscess or vertebral body abscess is suspected. Prog Vet Neurology 1996. Pugh DG. United Kingdom . References 1.25(3):390. Hertfordshire. in the case of suspected otitis interna. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Claire Whitehead. CT also guides the surgical approach in these cases. BVM&S. Camelids have 7 cervical.17(4):600. Comp Cont Ed 1995.

If the animal no longer greets the owner at the door. The veterinarian will need to be able to perform the tests and more importantly interpret the responses. The evaluation of the gait and posture is crucial in determining if the nature of the gait abnormalities is related to the nervous system or to a musculo-skeletal problem. The mental status cannot be evaluated in the examination room. and goal-directed behaviours. it is the evaluation of the mental status and gait and posture that are the most important to localize the lesion. The brain may not register what the eye sees or the ear hears. that a computer program will soon be available to guide the veterinarian toward lesion localisation. In most cases. The abnormalities can be obvious such as with patients circling compulsively or head pressing. not from observation of the animal. Patients that are blind because of ocular diseases are cautious while walking and rarely do bump into objects. No matter how sophisticated the program. misinterpreted or simply forgotten are reviewed. Thalamocortex: Behaviour The thalamocortex is the site of the intelligence. The masticatory muscles are palpated for symmetry and atrophy. gait and posture. 2001 Joane Parent Canada 18271203 It is likely in this world of technology. Beware of the animal that bumps into objects. The neurological examination is composed of six parts: the evaluation of the mental status. Dogs and cats are excited and/or fearful in the hospital environment. the animal becomes somnolent. There is a decrease or an absence of the animal’s awareness. even if the animal has had time to relax. The animal is unable to relate normally with his environment. The time allowed for this presentation does not permit covering the entire examination. The mental status dictates if the lesion is intra or extra-cranial. However. b. Brainstem: State of consciousness The bulk of the brainstem parenchyma is made of the reticular formation or the so-called Ascending Reticular Activating System (ARAS). 1. the neurological examination will remain pivotal. stuporous or comatose. When this system is affected. The abnormalities of the mental status relate to the brainstem or to the thalamocortex. the evaluation is obtained from the history. MENTAL STATUS The mental status is the most important clue in differentiating intra. a. Even a deaf dog can "feel" the garage door opening. but this is rare. In most cases. the disease is intracranial and involves the brainstem. there may be a more serious problem. This formation is responsible for the arousal of the cerebrum. TRIGEMINAL NERVE The trigeminal nerve has three branches: (1) Ophthalmic (sensory) (2) Maxillary (sensory) and (3) Mandibular (sensory and motor). This may be the fact. 2. ensure that the animal is aware of his surroundings. relying only on the history to bring them out. This adrenaline surge hides the mental changes. However. he is aware of his surrounding because his intelligence (cerebrum and thalamus) is not affected. The owner must be asked specific questions regarding the mental status of the animal: Is the animal as playful? Does he sleep more than before? Is he quieter. spinal reflexes and pain perception.from extracranial disease in the animal with cranial nerve abnormalities. the changes are subtle especially with chronic illness. postural reactions. Only the tests commonly performed poorly. This large nerve innervates the masticatory muscles and provides sensation for most of the head. The history is crucial and must be thoroughly performed. Another example is the older dog becoming deaf.The Neurological Examination WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. The blindness in the patient that collides with objects is central and relates to a brain disease. especially if subtle. lethargic. The . cranial nerves reflexes. Of these. lethargic? If the animal is historically somnolent and this is accompanied by cranial nerve deficits.

towards and away from the examiner. This test should be done gently using cotton swabs (Q-tips) to reveal subtle differences between sides.. It is important to pay attention to details when eliciting it to ensure its absence is real and not the result of poor technique. the limb is positioned in a relaxed flexion to tighten the patellar tendon. If unsure. the cranial nerves V and VII but DOES NOT assess if the information gets to the cerebral cortex. the hind and front limbs. The test must be done with care to enhance subtleties. Touching the lateral canthus and observing for a blink reflex assesses the maxillary branch. 1. is the gait normal? 3. Orthopaedic problems. This latter test provides an evaluation of the cortical response to pain. There are two components to the reflex: the ascending sensory pathway and the descending pathway or lower motor neuron. This reflex is the most often erroneously found to be absent. the trigeminal nerve is the afferent limb (sensory). Touching the canthi and the ears assesses the reflex arc. the examiner lets the animal walk freely on the floor of the examination room while taking the history. Particular attention is given to the foot placement when the animal turns or changes speed. look at the gait again and again. of which type: vestibular. The nasal septum is the only area that consistently elicits a pain response in the domestic species. The evaluation of the ophthalmic branch is assessed by touching the medial canthus (medial corner of the eye where the lid margins meet) and observing for a blink reflex. i. Which limb(s) is/are affected: one limb. To elicit the reflex. the examiner's hand is placed between the limbs and behind or in front of the limbs. If the animal is walking. Is there ataxia? 5. until a consistent response (normal or not) is obtained. Both must be intact for the reflex to be present. the clinician is positioned behind the animal. It is preferable that the medium to large size dog be leash-walked by the owner in the parking lot. the lesion likely involves the sensory pathway and not the lower motor neuron.e. The dog is evaluated at different paces. The questions should not be left unanswered. etc. For the small cat or dog. cerebellar or proprioceptive? 4. Most hospital rooms do not allow a good examination of the gait because of their small size. The animal may or may not blink but the head will be pulled away as a pain response. The animal's weight must be supported with a hand (and forearm in the large dog) between and behind the hind limbs. PATELLAR REFLEXES The patellar reflex (tendinous or monosynaptic reflex) is elicited by tapping the patellar tendon. A series of questions are then answered. or the ipsilateral limbs only? 4. Use a non-slippery floor such as concrete. If there is ataxia. This is evaluated by stimulating the nasal septum. . Touching the base of the ear and observing for a blink reflex assesses the mandibular branch. generalized weakness and patient’s personality may all have an effect on the test. The test results must be taken in the light of the entire examination. If the reflex is absent yet the animal can walk and/or stand. The clinician observes the front limb gait as the animal is coming toward him/her and the hind limb gait as the animal is going away from him/her. 3. The indicated areas to touch are the only ones that consistently give a blink reflex in the normal animal. Start with a gentle stimulus and gradually increase the strength of the stimulus going from side to side. PROPRIOCEPTIVE POSITIONING Performed appropriately. The paw is then slowly knuckled over. both hind limbs. For the evaluation of the front limbs. 5. while the facial nerve (VII) is the efferent limb (motor). In these reflexes. To evaluate proprioceptive positioning of the hind limbs.sensory part of the nerve is assessed mainly through the palpebral reflexes. grass. The flexion of the toes stimulates hundreds of proprioceptors located in the tendons and joints of the toes. GAIT AND POSTURE The evaluation of the gait is important in lesion localization. back yard or sidewalk. proprioceptive positioning (knuckling) is an invaluable tool to evaluate proprioception. Is the animal able to walk? 2. A pet that knuckles does not necessarily have proprioceptive deficits. asphalt.

This is made easy by having the consultations booked with keywords such as 'lameness' or 'stiffness'. Palmerston North. normally the main pad is the first to touch the ground followed by the toes. walking away from you and from the side. physical exam and then lameness examination by beginning with an assessment of the animal's gait. leading to a falsely decreased reflex. WITHDRAWAL OR FLEXOR REFLEXES The withdrawal (flexor) reflexes are difficult to examine objectively because in most of our patients. Veterinary Teaching Hospital. Examine the patient from three directions: walking towards you. The opposite may occur when there is reluctance to fully load the foot. When an animal is lame. observe the length of the stance phase. to alert you there is a case coming up that will need a gait evaluation. a reduction in flexion is common with joint disease. Massey University. Recognising Hind Limb Lameness With a hind limb lameness. The patellar reflex may be absent or decreased in a dog with a cruciate rupture because the tension in the tendon cannot be raised. SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Joane Parent Canada Lameness Examination in Working Dogs AUSTRALIAN VETERINARY ASSOCIATION PROCEEDINGS 2010 Andrew Worth Centre for Service and Working Dog Health and Research. There may be a change from the normal side to side oscillation of the tail to a more vertical oscillation. the swing and stance phases are shortened. or walk them back outside before going near the consult room.6. Then I ask the client to identify the leg they think is affected by pointing it out. The "up" motion of the tail occurs when the affected limb contacts the ground. I like to be able to anticipate lameness evaluations and meet the client in the car park if possible. A normal animal should be able to bring his body to the examiner's hand while flexing the limb. thereby reducing the amount of time spent on the affected limb. We are all familiar with the concept of a 'head bob' for forelimb lameness (the animal raises its head and neck when the lame leg is placed) and 'hip hike' for hind limb lameness (the hip appears to lift over the affected leg). I like to blind myself so without taking any history I observe the gait to form an unbiased opinion. Observe the area of foot contact. it is an invaluable document in the follow up and monitoring of progressive and protracted nervous system diseases. weight is shifted forward by extending the neck and lowering the head. Musculo-skeletal disorders may affect the nature of the flexor and patellar reflexes. I try to meet the owners at their car. New Zealand 24156548 STEP 1: GAIT ASSESSMENT I like to modify the traditional approach of history taking. the form serves as a "check list" ensuring that all parameters have been evaluated. the position of the contact point. A neurological form should always be filled. The front limb reflexes can be used as a comparison for the hind limbs and vice versa. During the examination. polyarthritis and muscle diseases may lead to decreased flexor reflexes because the animal is too weak to withdraw his limb with force. The neurological examination should be done in a methodical and stringent manner every single time paying attention to details. the plane of the stride and whether or not the limb is abducted or adducted during the cycle. Hip dysplasia. ideally outside in good light on a non-slippery surface. the position of the lift point. just so that there is no confusion over the leg that is the cause of concern. The stride length is shortened and the pelvis is tilted in the axial plane so that the hemipelvis on the affected side is more . Although the examination when performed on a regular basis becomes a routine. Note alterations in joint angles. More importantly. Massey University. purposeful movements are still present (so pain perception is as well) and the animal inhibits the response.

In trauma cases it is necessary to ascertain the presence of any nerve injury when the CP is altered. This "won't" walk state must be differentiated from "can't" walk. a fracture). marked tissue injury). Helping such an animal to its feet will allow an . This gentle start gains the patient's confidence ahead of potentially painful manipulation later. hence an animal can "choose" not to respond normally. When there is unilateral hip disease. It is important to palpate regional lymph nodes for lymphadenopathy. Lack of an elevated temperature should not be used as an exclusion criteria for joint injection or IMPA. Forelimb Lameness With lameness in a forelimb. A centrally mediated response (vocalisation. it can also be caused by peripheral nerve lesions. cellulitis. and an oscillating motion is seen towards the affected side. You should look for any loss of muscle mass over the scapula and humeral areas and check the thigh circumference and the cranial tibialis muscles. turning to bite. This manoeuvre minimises hip motion by using lateral bending of the spine to achieve forward movement. Onset. which I typically combine with a "pat-down" of the patient.dorsal. Body temperature may be elevated in some disease states (abscessation. When viewed from the rear. History questions: 1. the animal lifts its head when the affected limb bears weight (and appears to dip its head when the sound limb contacts the ground). quantity fed and mineral supplementation important in the younger patient STEP 3: PHYSICAL EXAMINATION Resist the temptation to skip the full physical examination and just move right to the ortho exam. the pelvis of an animal with bilateral hip disease swivels from side to side (Marilyn Munroe style). STEP 2: HISTORY TAKING AND PALPATION OF TOPOGRAPHICAL ANATOMY After the gait assessment comes history taking. the pelvis is tilted sideways.g. The latter is an indicator of long nerve neuropathies (can be seen in Labradors presented with laryngeal paralysis). The neurological examination is most important in the recumbent patient. This tests conscious proprioception and loss of this response is a sensitive indication of spinal cord disease. Ensure you test medial and lateral toes. progression. However. an animal with bilateral cranial cruciate ligament can present recumbent and unable to rise. Diet composition. Test the withdrawal reflex by pinching the skin of the digits.. response to rest 3. While I am taking the history I have my hands on the patient stroking it and looking for asymmetry of muscle and bone. there is also a slight shortening of the opposite hind limb step as the animal hastens to remove weight from the forelimb. STEP 4: BASIC SPINAL NEUROLOGICAL EXAMINATION I next perform a very basic neurological examination at the same time checking for the relative amount to weight the animal is placing on each limb. Identify the problem . Patient's environment and exercise regimen 7. This phenomenon can often cause a misdiagnosis. For example. Testing the myotactic reflexes follows in order to localise a spinal lesion (not performed if above all normal).in the eyes of the owner 2. each paw is lifted (check the amount of weight transferred to the other leg as you do this) and placed on its dorsum (knuckling response). Check for the speed with which the animal replaces the paw. (in one study only 18% of dogs with confirmed polyarthritis were febrile). duration. or the animal has a painful lesion in the limb being tested (e. With the patient standing on the floor or table. Remember too that this reflex is consciously mediated. thus the loss of CP gives us no insight as to upper versus lower motor neuron dysfunction. Concurrent injuries or disease could affect both the prognosis and safety of sedation or anaesthesia required at a later time. Note: When there is shortening of a forelimb stance phase. Any juvenile bone disease 5. trying to move off) indicates the integrity of the nerve pathway (ruling out LMN disease) even if a withdrawal of the limb is not stimulated due to fracture or muscle trauma. Any association with trauma 4. Response to medication or other therapy so far 6. which is typically seen when the reflex is repeated many times over.

biceps insertion traction. Localisation of solitary limb lameness is based around the demonstration of pain and pathology. especially if a potentially genetic disease is present. but not appear overtly lame.assessment of proprioception / myotactic reflexes and withdrawal reactions. The other limbs should not be neglected either. palpation of the inter-tubercular groove during above Findings: Pain on manipulation at stretch of biceps Medial glenerohumeral ligament injury: Shoulder joint laxity / instability Exam: Abduction test of Bardet. but if there is bilateral elbow pain it may not be a viable proposition. Work your way up the limb until swelling or tenderness is noted.bilateral disease. biceps calcifying tenopathy Exam: Biceps retraction testing. This brings me on to one of the real traps for both owners and vets . These would be expected to be normal unless there is major structural disability. evidence of chronicity. rather. grey zone between Sesamoid disease: DDX fracture. develop a systematic approach so that nothing is missed. STEP 5: THE ORTHOPAEDIC EXAM Commences with evaluation of the affected limb and begins distally. palmar / plantar pressure to the MCPJt Findings: Repeatable pain in association with radiographic signs Traumatic joint instability: Requires manipulation +/. Avoid the temptation to immediately focus on the most likely cause of disease. I will complete the examination above and beyond that site then come back to the sore area last to maximise the patient's patience with manipulations. New Zealand . in the latter. Massey University Palmerston North. A common example would be a large breed pup with elbow dysplasia. abnormal > 50 degs. sedation or anaesthesia required Findings: Normal < 30 degs. These dogs may walk with abducted elbows and a short striding gait. If by now I have a focal area of discomfort. Amongst other topics we will cover: Biceps disease: DDX bicipital tenosynovitis. presence of crepitation or effusion and peri-articular thickening indicate presence of pathology and. Due to lesions in both fore or hind limbs some dogs will into appear asymmetrical in gait to the owners. biceps avulsions. This session will concentrate on specific examination and manipulation as it applies to working dogs undergoing lameness assessment. Video and pictorial demonstration will be used to illustrate each step.sedation and stress radiography SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Andrew Worth Centre for Service and Working Dog Health and Research Massey University Veterinary Teaching Hospital. A pup with mildly subluxated hips has a good prognosis. Loss of joint range of motion. fragmentation Exam: Forced flexion of the digits.

demonstrates pyrexia. MRCVS Institute of Comparative Medicine. pointer. PhD. Newfoundland. Weimaraner. associated with bouts when the dog appears unwell. DECVN. Clinically important spinal cord diseases presenting with pain: Meningitis Discospondylitis Intervertebral disc disease* Lumbosacral syndrome* Bone tumour* Vertebral malformations (atlanto-axial subluxation)* * May progress to develop neurological deficits Clinically important spinal cord diseases presenting with neurological deficits: Intervertebral disc disease Fibrocartilaginous embolism Lumbosacral syndrome Trauma Neoplasia Vertebral malformations (atlanto-axial subluxation. BVSc. marked cervical pain and inappetence. CVR. hemivertebrae) Chronic degenerative radiculomyelopathy (CDRM or degenerative myelopathy) in the GSD MENINGITIS Causes of meningitis in dogs and cats include: Immune mediated form commonest: steroid responsive meningitis / arteritis (SRMA) (Bacterial: rapidly fatal) (Viral [distemper]) (Protozoal [Toxoplasma / Neospora]) Breeds affected by SRMA: Large pure breeds (Pyrenean mountain dog.Common Non-Surgical Diseases of the Canine Spine WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. University of Glasgow Glasgow. MVM. . Vizsla) Beagles Clinical Signs of SRMA Typically a waxing and waning course. Faculty of Veterinary Medicine. 2008 Jacques Penderis. UK 18293636 INTRODUCTION The disease of the canine spine can be classified based on whether the primary presenting complaint is spinal pain or neurological deficits.

Discospondylitis is more common in middle-aged large/giant breed dogs. etc. Treatment Treatment of discospondylitis is prolonged (2 to 4 months) and relapses are not uncommon. where annular protrusion into the spinal canal is caused by shifting of the nucleus pulposus material.Diagnosis CSF tap is definitive. and Type II. Brucella titres should be obtained in intact animals in endemic regions. Empirical treatment can be initiated after all samples (urine. degeneration of the disc can lead to protrusion/extrusion. Both Hansen type I and type II disc disease are always preceded by disc degeneration. with evidence of elevated white cell counts. Blood and urine cultures are reported to be positive in 45-75% and 25-50% of cases. accounting for over 2% of all diseases diagnosed in the dog. Analgesia should be provided. May be self limiting after 12-18 months. while systemic signs (fever. It can also be secondary to penetrating wounds. INTERVERTEBRAL DISC DISEASE Intervertebral disc disease is an important cause of canine neurological disease. Disc disease in the dog was first classified by Hansen as: Type I. Advanced imaging (besides MRI) is usually normal and myelography is contra-indicated. traumatic disc extrusion. Males are more commonly affected than females (ratio of 2:1). Cage rest is important to minimize the risk of pathologic fracture. C6-C7 and L7-S1. foreign bodies. Some patients require longer treatment or different drugs. coli. FIBROCARTILAGINOUS EMBOLISM (FCE) . The most common sites affected are mid-thoracic vertebrae. CSF analysis is often normal. Haematology / biochemistry may support inflammation but are nonspecific. usually spread by haematogenous route. respectively. may also occur. DISCOSPONDYLITIS Discospondylitis is a concurrent infection of the intervertebral disk and of the adjacent vertebral bodies (vertebral osteomyelitis). where herniation of the nucleus pulposus occurs through the annular fibres of the disc into the spinal canal. resulting in spinal cord injury with no or minimal residual compression. blood. A third type of disc extrusion. Affected patients typically present with signs of pain or varying degrees of spinal cord dysfunction. Brucella canis and E. This happens when trauma causes rupture of a disc that demonstrated no obvious preceding degenerative changes. disc aspirate) have been taken for culture and sensitivity. Diagnosis Leukocytosis is usually absent. Spinal pain is usually present. Treatment Prednisolone: tapering from an initial immunosuppressive dose for 2 to 4 weeks. Commonly encountered infectious agents are coagulase-positive Staphylococci. primarily consisting of large numbers of non-degenerate neutrophils. but radiographic changes may not appear for up to 3 weeks. With progression. Clinical Presentation Signs are often non-specific in the early stages. Radiographic demonstration of discospondylitis is usually sufficient for diagnosis. Streptococcus species. Continue tapering the dose over 4 to 6 months. Aetiology Discospondylitis is a septic condition. weight loss) are reported in only 30% of cases. Magnetic resonance imaging is the diagnostic procedure of choice.

pudendal. there appears to be a breed predisposition for the development of FCE in miniature Schnauzers. as well as the nerve roots supplied by these spinal cord segments forming the cauda equine. sciatic. 80% of cases occur between 3 and 6 years of age. obturator. but may occur from as early as a few months of age. occasionally. In non-giant breeds. bladder. As there is no residual spinal cord compression there is no need for decompressive surgery or for strict cage rest. Clinical Presentation The onset of FCE is typically peracute and may be associated with a brief episode of pain. pelvic and coccygeal nerves and result in variable involvement of the pelvic limbs. particularly the cervical and lumbar enlargements. but thereafter the disease is non-progressive and pain-free.Aetiology FCE is characterised by ischaemia of the spinal cord secondary to the acute occurrence of emboli. within the arterial and. The nerves affected by lumbosacral syndrome may include the femoral. FCE occurs virtually exclusively in non-chondrodystrophoid breeds and particularly in active medium/large breeds. It may occur in any region of the spinal cord. pelvic limb or tail Tail paralysis Pain-related clinical signs: . However. anal sphincter and perineum. FCE often occurs in association with vigorous exercise or mild trauma (60% in one study). The neurological deficits are usually asymmetrical. consisting of disc-derived fibrocartilage. venous blood supply of the spinal cord. MRI is the most useful imaging modality for making an ante mortem diagnosis of FCE and the primary imaging feature is asymmetrical hyperintensity within the spinal cord on T2-weighted images. Treatment and Prognosis Treatment is by nursing care and early instigation of physiotherapy is very beneficial. tail. and physiotherapy can therefore be started as soon as the diagnosis is confirmed. Clinical Signs The primary clinical signs of lumbosacral syndrome (the presence or absence of the individual clinical signs will depend on the underlying lesion) can roughly be subdivided into 3 categories: Neurological deficits pertaining to the pelvic limbs: Pelvic limb paresis or ataxia Decreased lumbosacral trunk reflexes in the pelvic limb Pelvic limb or hip region muscle atrophy Neurological deficits pertaining to the sacral and coccygeal nerve roots: Decrease or loss of the anal reflex and dilation of the anal sphincter Decreased or absent perineal reflexes Urinary incontinence Faecal incontinence Hypoaesthesia or analgesia of the perineal region. but appears to be more frequent in the cervical and the thoracolumbar regions. Diagnosis Diagnosis is based on the correct history and signalment with no evidence of spinal cord compression. Breed Predisposition FCE occurs in either sex of usually adult dogs. LUMBOSACRAL SYNDROME Lumbosacral syndrome comprises diseases affecting the caudal lumbar (L4-L7) and sacral segments of the spinal cord.

in particular reluctance to jump and climb stairs Nerve root signature (referred pain due to nerve root entrapment) Causes The causes of lumbosacral syndrome are varied and include (based on the DAMNIT classification): Degenerative: lumbosacral stenosis. vertebral arches. spinal synovial cysts Developmental: spina bifida. The disease tends to occur in middle-aged dogs. articular facets. The most common cause of lumbosacral stenosis is a Hansen type-II intervertebral disc extrusion at the level of the lumbosacral junction. In some cases. with an increased incidence in male dogs (with a male to female ratio of 4:1). ventral part of the annulus fibrosus and ventral vertebral body Middle: dorsal portion of the annulus fibrosus. nerve root tumours Inflammatory and Infectious: abscessation. cervical versus caudal lumbar). dermoid sinus. owner's finance. and 2) treat/prevent secondary pathophysiological events. Neoplasia of the spine is classified both with respect to the physical . dorsal longitudinal ligament and dorsal vertebral body Dorsal: pedicles. the stenosis may be lateralised and only affect one intervertebral foramen. (parasitic migration) Trauma: spinal trauma Of these causes of lumbosacral syndrome. with respect to the level of the spinal cord affected (e. boxers and Rottweilers are over-represented.g. often working dogs. discospondylitis. LUMBOSACRAL STENOSIS Lumbosacral stenosis is due to stenosis of the vertebral canal at the level of the lumbosacral junction with consequent compression of the nerve roots. but other causes have been reported. surgeon expertise and preference. TRAUMA Spinal trauma is a common cause of spinal dysfunction and includes endogenous and exogenous causes. sacrocaudal dysgenesis. Affected dogs demonstrate one or more of the features of lumbosacral syndrome.. The choice of treatment (conservative or surgical) depends on severity of the lesion (especially number of vertebral compartments involved). joint capsules. (granulomatous meningoencephalomyelitis). myelodysplasia. Exogenous causes are most often secondary to road traffic accident or fall from a height.Pain over the lumbosacral region Reduced activity. German shepherd dogs. fibrocartilaginous embolism. osteochondritis dissecans Angiopathic: aortic ischaemic myelopathy. ascending and descending syndrome Neoplastic: primary and secondary spinal cord tumours. The condition is most common in large breed dogs. spinous process and interspinous ligament Treatment Assessment of instability: considered unstable if there is a lesion of two or more compartments. transitional lumbar or sacral vertebrae. The aim of spinal trauma treatment is to: 1) prevent further mechanical damage to the spinal cord. (mycotic diseases). NEOPLASIA Neoplasia affecting the spinal cord is common in both dogs and cats and the exact clinical signs depend on the localisation of the lesion. the most important is lumbosacral stenosis. intervertebral disc disease. haemorrhage. Vertebrae can be divided in three anatomical compartments: Ventral: ventral longitudinal ligament. with pain over the lumbosacral region (particularly on palpation and lumbosacral hyperextension) being one of the most consistent clinical signs.

PhD. Due to involvement of the dorsal roots. The clinical signs include paraparesis and urinary/faecal incontinence. The lesion is diffuse and there are therefore no focal localising signs. ataxia and/or upper motor neuron paresis/paralysis. particularly the German shepherd dog.localisation in relation to the meninges and spinal cord (into extradural. intradural but extramedullary and intramedullary). The duration of clinical disease prior to euthanasia on humane grounds is around 6 to 18 months. especially following minor trauma. CVR. CHRONIC DEGENERATIVE RADICULOMYELOPATHY (CDRM OR DEGENERATIVE MYELOPATHY) Chronic degenerative radiculomyelopathy (CDRM) is a degenerative neurological disorder resulting in progressive pelvic limb ataxia and paresis in older large breed dogs. dogs present with a gradual progression of an initial insidious pelvic limb ataxia. Concurrent osteoarthritis will. It is most commonly reported in English bulldogs and can cause paraparesis and urinary and faecal incontinence. Malformations of the Vertebral Arch and Spinal Cord Spina Bifida Incomplete closure of the vertebral arch. but is likely to have a genetic basis. HEMIVERTEBRAE) Atlanto-Axial Subluxation Toy and small breeds such as the Chihuahua and Yorkshire terrier are at highest risk as a result of failure of development of the dens (aplasia or hypoplasia). Clinical Signs Affected dogs are generally over six years of age and the mean age of onset is around 9-years of age. Congenital Syringomyelia and Spinal Dysraphism (Myelodysplasia) Malformations of the spinal cord have been described in Weimaraner and other breeds of dogs. and treatment with NSAIDs may result in apparent temporary improvement. such as focal pain or cutaneous trunci reflex cut-off. Jacques Penderis. exacerbate the abnormal pelvic limb gait. Sacro-coccygeal Dysgensis Reported in the Manx cat as well as pugs and bulldogs. The neurological abnormalities are bilateral and usually symmetrical (although mild asymmetry is not uncommon). however in some cases. the spinal canal can be severely reduced. Clinical signs are those associated with cervical spinal cord compression: pain. Treatment A variety of treatment regimes have been proposed. Faculty of Veterinary Medicine University of Glasgow Glasgow. the patellar reflex is decreased or lost in about 25% of cases. Diagnosis There is currently no in vivo diagnostic test: definitive diagnosis requires neuropathological examination. Malformations of the Vertebral Body and Disc Most of these malformations are incidental findings and do not cause any significant neurological deficits. VERTEBRAL MALFORMATIONS (ATLANTO-AXIAL SUBLUXATION. BVSc. causing compression of the spinal cord. The underlying pathogenesis is unclear. MVM. MRCVS Institute of Comparative Medicine. however. DECVN. Clinically. but there is no reliable evidence to suggest that any of these treatments offer any benefit. United Kingdom . Onset of clinical signs in dogs with the congenital form usually occurs in young animals. although the problem can develop at any age.

Diagnostic Approaches and Treatment British Small Animal Veterinary Congress 2011 Joan R. The terms lower motor neuron (LMN) and upper motor neuron (UMN) are applied to differentiate two basic types of neurological weakness. The aged patient also can be affected by diseases of the muscle. Paraparesis is a non-specific term for bilateral motor dysfunction of the pelvic limbs. Due to the multiplicity of anatomical dysfunctions and the fact that these disorders can mimic and overlap each other. stable or chronic) can be established. degenerative myelopathy.Paraparesis in the Ageing Large-Breed Dog: Other 'Non-degenerative' Causes. In older. University of Missouri. LMN weakness clinically manifests as paresis. Department of Veterinary Medicine. nerve. spasticity and rigidity. osteoarthritis. Neuroanatomical localisation to thoracolumbar spinal cord is specified to the spinal cord areas based upon signs of UMN or LMN limb weakness. Changes in muscle tone that are elicited by passive movements include flaccidity. DACVIM (Neurology) Clydesdale Hall. Onset (sudden or insidious). These areas include the thoracolumbar spinal cord (T3–L3). urethral tone and tail tone. disorders that often overlap with each other include: degenerative lumbosacral stenosis. Weakness is an inability to carry out a desired movement with normal force because of a reduction in strength of the muscles necessary to carry out the movement. hyporeflexia to areflexia and muscle atrophy that is severe and rapid in onset. MO. The term fatigability describes when one or more muscles become weaker with repetitive but normal use and may imply neuromuscular dysfunction. BS. The sacral and coccygeal regions are localised according to LMN signs involving the perineal region. Columbia. spinal cord. neuromuscular junction and muscle disease can all cause abnormal pelvic limb movement in older dogs. large-breed dogs. USA 21494037 Introduction Orthopaedic. DVM. Coates. Clinical History Clinical history is important in defining the location and cause of the disorder. Hansen type II intervertebral disc disease (IVDD) and hip dysplasia. MS. Aged patients often have concurrent orthopaedic and neurological disorders which further complicate the examination process. a diagnostic dilemma is posed to the clinician. Signalment Signalment is important to consider as some breeds are predisposed to specific diseases. paralysis. nerve and neuromuscular junction that can confound the diagnosis of spinal cord disease. bladder function. Disorders that may mimic each other as acute paraparesis . Clinical signs of UMN weakness manifest as general proprioceptive (GP) ataxia and spastic paraparesis/plegia with normal to increased spinal reflexes and muscular hypertonia. College of Veterinary Medicine. and the lumbar intumescence (L4–S2). rate of progression (gradual or rapid) and temporal relation (intermittent/episodic.

A patient with suspected orthopaedic disease should have a neurological examination and vice versa. Often a non-specific clinical sign associated with paraparesis is reluctance to rise. muscle.. myasthenia gravis) and metabolic disorders (e. Paw replacement (proprioceptive positioning) is a non-weightbearing test that is useful for discrimination between orthopaedic and neurological lameness. motor and autonomic dysfunction. spinal cord neoplasia). slowly progressive disease of the long tracts and ganglia of the thoracolumbar spinal cord. Clinical Examination Thorough physical. A stiff or stilted stride is characteristic for an animal with arthritic..g. Presence of spinal hyperaesthesia assists with localisation when present and for determining a differential diagnosis. Exercise intolerance and episodic weakness often are not obvious until exercise. Loss of bladder function usually occurs with paraplegia. more strenuous exercise will exacerbate the paraparesis. Animals with UMN disease will show GP ataxia reflective of a longer spastic stride. nerve roots and intervertebral disc. trauma. orthopaedic and neurological examinations of the patient are crucial to localising the weakness and avoiding unnecessary diagnostic testing and client expense. and endocrine and electrolyte disturbances). Disorders that mimic each other as chronic progressive paraparesis include: hip dysplasia. Disorders causing episodic weakness include myopathy. Spinal hyperaesthesia usually indicates a compressive and/or an inflammatory cause. polyneuropathies. aortic thromboemboli.g. The initial neurological signs consist of GP . Presence of asymmetry is common in vascular and compressive myelopathies (e. Paraspinal structures innervated by nociceptive fibres include the vertebrae. nerve or neuromuscular junction disease. IVDD. Disorders that classically do not manifest spinal cord hyperaesthesia are the degenerative spinal cord diseases. whereas clinical signs will improve with exercise in animals with orthopaedic disease. degenerative myelopathy and Hansen type II IVDD. Gait is evaluated at a slow and fast pace. the extent of spinal cord involvement and the area within the vertebral column affected. Degenerative myelopathy is a non-painful. cardiac and pulmonary dysfunction. degenerative lumbosacral syndrome. gait and posture are evaluated during observation of the patient. Mental status. paresis (weakness) and paralysis (loss of voluntary motor function). Diagnostic Approach and Treatment Spinal Cord Diseases Clinical presentation of thoracolumbar spinal cord disorders commonly manifests as disturbances reflective of sensory..g. bilateral cranial cruciate rupture and early polyradiculoneuritis. The disease commonly occurs in the aged dog of various breeds. IVDD. The degree in severity of motor and sensory deficits from spinal cord disease is dependent upon the rapidity of disease onset. meninges. bilateral cruciate rupture. The extent of muscle atrophy may further delineate presence of LMN disease. intramedullary neoplasia and fibrocartilaginous embolic myelopathy. Abnormal gait descriptions include GP ataxia (loss of proprioception).include: fibrocartilaginous embolism (FCE). discospondylitis. In neurological disease. neuromuscular junction disease (e.

Indications for conservative management include the first episode of clinical signs or when the pain is intermittent. respectively. Prognosis is fair to good if clinical signs improve following early surgical intervention. Both the annulus fibrosus and nucleus pulposus may protrude but the nucleus pulposus is contained within an intact. subluxation. progressive paraparesis include Hansen type II IVDD and degenerative lumbosacral stenosis. Dogs may experience difficulty rising. discectomy. and at this stage the clinical signs are easily confused with hip dysplasia or other orthopaedic disorders. Transverse. Diagnosis is based on myelography and/or cross-sectional imaging (magnetic resonance imaging (MRI) and computed tomography (CT)). Acute onset of clinical signs with Hansen type II IVDD is less common. Abnormal findings on survey radiography include osteochondrosis of the sacral end-plate. Fibroid metaplasia can lead to gradual disc protrusion. sclerosis of the end-plates and bony proliferation of the articular processes. Urinary dysfunction occurs with severe disease. severe pain and severe neurological deficits (in particular incontinence). Degenerative lumbosacral stenosis (DLSS) refers to compression of the cauda equina at the lumbosacral articulation. The most usual clinical sign of DLSS is caudal lumbar pain. . Spinal cord disorders in older dogs exhibiting spinal hyperaesthesia that often result in a slowly. cross-sectional imaging and electrodiagnostic studies. it is relatively common and has been reported in older dogs of various breeds. Both flexed and extended views are used to accentuate any abnormal compression and help establish the presence of a dynamic lesion which may affect surgical treatment. foraminotomy. Diagnosis is determined by survey radiography. The gait is usually short strided. Choices of surgical procedures include dorsal decompression. Hansen type II IVDD occurs in non-chondrodystrophic breeds. transitional vertebrae. Dogs may stand with the pelvic limbs tucked under the caudal abdomen presumably to flex the lumbar vertebral column and lessen nerve root compression. Hansen type II IVDD usually manifests as an insidious UMN paraparesis. and clinical signs occur when the animal is 5–12 years of age. but degenerate annulus. and fixationfusion. and compression from this protrusion results in a slowly progressive focal myelopathy.ataxia/UMN paraparesis. Type II IVDD develops at a slower rate. Prognosis is guarded to fair depending on early surgical decompression. such as German Shepherd Dogs and Labrador Retrievers. Recurring lameness of one or both pelvic limbs is common. Indications for surgical management include failure of conservative management. The recovery rate with conservative management is between 24 and 50%. CT and MR imaging have the advantage of better bone and soft tissue resolution. spondylosis. The management of DLSS is based on an evaluation of the severity and duration of the clinical signs. Prognosis is guarded in dogs with severe neurological deficits and urinary and faecal incontinence for more than a few weeks. Confined rest for 4–8 weeks and pain management are recommended for dogs with an initial episode of only pain. True extrusion of nucleus pulposus into the epidural space usually does not occur but rather a protrusion or bulge of the annulus fibrosus occurs. dorsal and sagittal planes provide determination of lesion extent. Diagnosis is based on ruling out compressive myelopathy with crosssectional imaging and LMN disorders with electrodiagnostic studies. The owner frequently reports that the dog does not jump or has difficulty climbing stairs. Exercise often exacerbates the signs because vascular engorgement within the foramen further worsens the nerve compression (neurogenic intermittent claudication).

Myotatic and flexor reflexes are often decreased or absent. MO . Muscle pain may or may not be evident upon palpation. the stride may show a 'pseudohypermetria' where the paw is flipped out to accommodate. Coates . MG may manifest as an episodic weakness with only pelvic limb involvement. Affected animals can show a shortened stride that progresses to collapse. an enzyme specific for skeletal and myocardial muscle. haemangiosarcoma). Creatine kinase activity.g... Nerve conduction studies may show polyphasia and abnormal waveforms and slow conduction velocities. Many primary muscle diseases are characterised by spontaneous high-frequency discharges. Paraesthesia may be evident depending upon sensory involvement.Other neurological disorders that exhibit spinal hyperaesthesia and present as paraparesis are spinal neoplasia and inflammatory diseases. USA . postural reaction deficits and neurogenic muscle atrophy. Neuromuscular Diseases Myopathy usually presents with generalised weakness and exercise intolerance that can be episodic or persistent. prostatic carcinoma. Muscle biopsy can characterise the myopathy. Electromyography shows spontaneous activity (e. i. A provisional diagnosis can be made by administering intra venous edrophonium chloride (Tensilon test). fibrosarcoma. Diagnosis is often made by nerve and muscle biopsy. DVM. distal symmetrical polyneuropathy). BS.. The neuromuscular junction disorder in older dogs that is most often confused with other paraparetic disorders is generalised myasthenia gravis (MG). Depending upon the severity of atrophy. may be increased. nephroblastoma) or metastatic (mammary carcinoma. myeloma. myotonic and pseudomyotonic. meningioma. Inflammatory disorders include infectious/noninfectious myelitis/meningitis and discospondylitis. i. Joan R. range of joint movement may be limited. Neuropathy is characterised by a flaccid paresis. Muscle palpation with myopathy may reveal severe atrophy or hypertrophy and tremors/fasciculation. In neuropathies with both proximal and distal involvement. Fatigability is noted upon repetitive reflex evaluations. the patient may be unable to walk or may walk with a stilted stride to support its weight.g. intradural-extramedullary: nerve sheath tumour. Strength returns with rest. Spinal neoplasia may be primary (extraduralvertebral: osteosarcoma. DACVIM(Neurology) Department of Veterinary Medicine. If the weakness is distributed more distally (e. Dysphagia.e. Nerve conduction velocities are within normal limits. Cranial neuropathy and muscle fasciculation may also be present. The gold standard test is considered a radioimmunoassay for acetylcholine receptor antibodies. Gait is usually stiff and stilted or bunny hopping. Commonly in myopathic and neuropathic disease. dyspnoea and dysphonia can be clinical signs. Electromyography allows detection of abnormalities within the muscle. College of Veterinary Medicine University of Missouri Columbia. Because of the short half-life (6 hours). positive sharp waves and fibrillation potentials). increased enzyme activity reflects active disease. patellar and blink reflexes. MS. the pelvic limbs are affected first and more severely than the thoracic limbs..e. Electrodiagnostic testing using repetitive nerve stimulation and single-fibre electromyography can further document fatigability. chondrosarcoma.

Baton Rouge. The brain parenchyma and ventricular system can be differentiated from one another due to differences in soft tissue and fluid X-ray attenuation in CT. PhD. With the widespread availability of CT and MRI. DrMedVet. USA 21493924 Introduction Small animal patients with disease localised to the brain or nasal cavity only have radiographs performed as a screening method when trauma has occurred or skull deformation is present. CT and MRI provide a much better assessment of nasal cavity disease than radiography and are the modalities of choice. it will usually go undetected on CT images. skull radiography for nasal disease is being performed less and less. with hydrocephalus being by far the most common. lissencephaly. brainstem) is extremely difficult to visualise in CT due to beam hardening artefacts in that region. In all other instances cross-sectional imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) are the modalities of choice. If lateral ventricular height of the dorsal horn at the interthalamic adhesion exceeds 0. DECVDI Veterinary Clinical Sciences.Imaging the Head: Seeing What's on the Inside British Small Animal Veterinary Congress 2011 Lorrie Gaschen. MRI pulse sequences allow anatomical details and signal intensities of different tissue types in the brain to be identified. which is not possible in CT. Transverse and sagittal planes of the brain can be examined for the presence of a dilated ventricular system. Arachnoid cysts and quadrigeminal cysts are not uncommon. the anatomy of the caudal fossa region (cerebellum. DVM. Congenital Diseases Hydrocephalus. LA. MRI is the method of choice for detecting most congenital defects. Ultrasonography can be used to detect hydrocephalus in puppies and kittens and is an inexpensive and non-invasive modality that does not require sedation or anaesthesia. Nasal disease is another important indication for imaging the skull.35 cm or if the ratio between the height of the lateral ventricle and the width of the cerebral . MRI is the modality of choice for brain imaging as it allows the best resolution of brain structures for the most accurate localisation of lesions.5–12 MHz probe is adequate. A curved array. meningoceles and Rathke cleft cysts have all been reported. Furthermore. 7. agenesis of various structures. and does not enhance when intravenous iodinated contrast medium is given. Survey radiography is a screening method when skull deformation is present or to identify other bony defects due to the presence of aggressive fungal or neoplastic disease of the nasal cavity. If a lesion does not create a mass effect. The bregmatic fontanelle and foramen magnum windows can be used to examine the brain. The lateral ventricles can be seen in most patients and the third and fourth ventricles as well as the mesencephalic aqueduct in some. Grey and white matter can be distinguished.

The cerebrum may also be affected. ventricular enlargement secondary to loss of brain parenchyma (hydrocephalus ex vacuo) can be distinguished from obstructive hydrocephalus based on enlarged cortical sulci and subarachnoid space. herniation of the cerebellum into or through the foramen magnum. The oedema associated with the inflammation creates this appearance. The condition is characterised by crowding of the caudal fossa. Non-infectious inflammation can also occur.hemisphere (ventricle/ hemisphere ratio) exceeds 0. CT and MRI enable accurate assessment of ventricular size. can be solitary or multifocal. CT can show zones of decreased attenuation (hypodense regions) in the brain. extent of cortical atrophy and the presence of any focal lesions that may account for an obstructive cause of the hydrocephalus. Infectious causes such as canine distemper virus and feline infectious peritonitis are common. Bacterial infections can spread into the brain via a haematogenous route. with MRI being the modality of choice. in severe cases. Cerebellar hypoplasia is another type of congenital defect in both cats and dogs that is best seen with MRI. that can cause mass effect. The most common noninfectious inflammatory neurological disease is granulomatous meningoencephalitis (GME) and it commonly affects the brainstem in middle-aged small-breed dogs. granulomas and tumours of the brain. CT and MRI provide a more thorough approach to identifying the causes of hydrocephalus. MRI shows the distribution of the lesions best. such as cryptococcosis. the ventricles are considered enlarged. compression and. In cats. MRI is the method of choice for diagnosing this disease. Infectious lesions. Both CT and MRI can be used to identify these changes. there is a poor correlation between clinical signs and ventricular size. it is best identified with . Quadrigeminal cysts can also be detected at the foramen magnum with ultrasonography. Acquired Brain Diseases Inflammatory brain diseases are very common in veterinary medicine and are mainly reported in dogs. MRI is required to identify the signal intensity changes associated with infection. Using MRI. Contrast enhancement of the meninges may also occur and is a sign of meningitis. Chiari-like malformations in dogs result in compression of the cerebellum and brainstem and cervical spinal cord malformation such as syringohydromyelia. Because of the inherent disadvantages of CT for showing details in this region of the skull. all lesions have varying degrees of MRI and CT contrast enhancement. One of the difficulties of cross-sectional imaging is the overlap in the appearance of abscesses. The cerebellum appears small with increased amounts of CSF surrounding it. However. Cavalier King Charles Spaniels are most commonly affected but it can occur in other small-breed dogs as well. generally the cerebellum.19. toxoplasmosis is multifocal and contrast-enhancing in MRI. which appear as T2 hyperintensities of the cerebellum and brainstem. Toxoplasmosis and neosporosis are protozoal infections which are often multifocal. resulting in attenuation of the subarachnoid space surrounding the cerebellum. through intracranial extension of extracranial disease (otogenic infections) and foreign body migration.

MRI. It demonstrates none to intense contrast enhancement and is hyperintense on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images and either isointense or hypointense on T1. Another type of inflammation, necrotising meningoencephalitis (NME), is also of unknown aetiology and affects similar dogs to GME. Its appearance is similar to that of GME but it affects the cerebrum more frequently. Specific forms have been described in Pugs and Yorkshire Terriers. Meningoencephalitis can be identified with MRI in some instances. Lesions tend to be localised to the meninges where contrast enhancement can be detected. Enhancement of the cerebrum and cerebellum is also possible. The intracranial vasculature can also be observed with CT and MRI. In CT, intravenous contrast is necessary. In MRI, the vasculature can be assessed with both contrast and non-contrastenhanced magnetic resonance angiography. Aneurysms require angiography to be identified. Cerebrovascular malformations are uncommon as are aneurysms. They can lead to haemorrhage that can be detected with both CT and MRI. However, the underlying malformation requires angiography to make a diagnosis. Infarcts can occur in dogs due to hypothyroidism, hypertension, chronic renal disease, neoplasia, sepsis, fibrocartilaginous infarcts and coagulopathies and protein-losing nephropathy or enteropathy. MRI is required to identify infarcts, and special sequences such as diffusionweighted imaging may be required and can show changes immediately. Haemorrhage appears differently over time on both CT and MRI. Acute haemorrhage is hyperdense on CT. On MRI, signal changes vary from hyperintense to hypo-intense on T1- and T2-weighted images during different stages of haemorrhage and resolution. Intracranial mass lesions are first categorised as to their intra-axial, extra-axial or ventricular locations, then whether they are focal, multifocal or diffuse. Not all masses are tumours. Haematomas and granulomas appear similar to neoplasms. Tumours can be classified according to their location. Meningiomas are extra-axial tumours, typically broad based with meningeal enhancement (dural tail sign) and have expansile growth into the cranium, causing a mass effect and perilesional oedema. They can be seen with both CT and MRI in most cases due to their contrast enhancement. Glial tumours are intra-axial masses that have a variable MRI appearance and variable contrast enhancement. Choroid plexus tumours are ventricular tumours, typically in the third or fourth ventricles and are contrast-enhancing. Lymphoma and histiocytic sarcoma appear as either intra-axial or extra-axial masses hypointense on T1- and hyperintense on T2-weighted MRI images and exhibit contrast enhancement. Because of their variable appearance, they may mimic other tumour types. Pituitary tumours can also be identified on cross-sectional imaging studies. Microadenomas are difficult to see on both CT and MRI studies. Macroadenomas can be identified on both CT and MRI and have a specific location at the sella turcica, expand dorsally and are intensely contrastenhancing. Their anatomical location makes the diagnosis in most cases.

Diseases of the cranial nerves can also be identified mainly on MRI studies. Trigeminal nerve sheath tumours are among the most common. Nasal Cavity Disease Nasal tumours, such as adenocarcinoma, fibrosarcoma, chondrosarcoma, squamous cell carcinoma and lymphoma, affect the nasal cavity and can destroy turbinate bones and invade the brain at the level of the cribriform plate. In endemic areas, fungal agents can lead to similar damage. Both CT and MRI are adequate for diagnosis of aggressive lesions of the nasal cavity. However, rhinitis and inflammation have minimal imaging changes. Biopsy of the nasal cavity is indicated in all cases for a definitive diagnosis.

Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Lorrie Gaschen , DVM, PhD, DrMedVet, DECVDI Veterinary Clinical Sciences Baton Rouge, LA, USA

How I Treat...Back Pain in Chondrodystrophic Dogs
Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine, University of Georgia

Hansen first classified intervertebral disc disease (IVDD) as type I and type II. Hansen type I IVDD is herniation of the nucleus pulposus through the annular fibers and extrusion of nuclear material into the spinal canal. Hansen type I IVDD is commonly associated with chondroid disc degeneration. The disc commonly extrudes through the dorsal annulus, causing dorsal, dorsolateral, or circumferential compression of the spinal cord. Chronic disc extrusion is characterised by extradural fibrous adhesions whilst acute disc extrusion is characterised by extradural haemorrhage and soft disc material. Hansen type I IVDD typically affects small, young, chondrodystrophic dogs and has an acute onset but it can occur in large nonchondrodystrophic dogs, often also having an acute onset. Neurologic dysfunction is a secondary consequence of IVDD. Extrusion of the nucleus causes primary cord injury and associated clinical neurologic signs by concussion and later by compression. Acute and severe disc extrusions cause pannecrosis of the gray and white matter. Sequential haemorrhage, oedema, and neuronal necrosis depend on the severity and type of injury. The treatment for this disc extrusion is often determined by multiple factors including; neurologic status of the dog, delay in presentation for veterinary attention, concurrent medical treatment, concurrent vertebral instability, previous episodes of spinal pain, method of diagnosis of the extrusion, lesion localisation and economics. This means that criteria for such treatment need to remain 'fluid' and therefore specific treatments may differ in similar patient circumstances. The method of diagnosis of IVDD is considered to be an important factor in decision-making. Although myelography is well described in the veterinary literature, common problems encountered such as poor distribution of contrast medium, the presence of spinal cord swelling and neurologic deterioration have led to the belief that it is not the technique of choice in the human field. Computed tomography (CT) can be an adjunctive procedure to myelography to further delineate the extent of a compressive lesion or as a sole technique for detecting IVDD. CT myelography may provide a diagnostic image when there is obstruction of contrast medium flow. CT or magnetic resonance imaging (MRI) are extremely useful for diagnosing foraminal or lateral disc extrusions, as well as the extent of associated extradural and subarachnoid haemorrhage. MR imaging is the best available method for early recognition of disc degeneration in dogs. MR imaging is especially useful as a sensitive, accurate, and non-invasive method for evaluating the caudal lumbar spine and lumbosacral space in dogs. Cerebrospinal fluid analysis should always be performed to rule-out concurrent inflammatory disease. This will be more important with protrusions where the clinical signs may be more chronic progressive in nature and difficult to differentiate from other diseases.

Hansen type I most commonly occur within the thoracolumbar region of chondrodystrophoid breeds. The most common site for Hansen type I IVDD in large nonchondrodystrophic breeds is the interspace between L1 and L2. Functional grading schemes describing hyperesthesia and motor and sensory dysfunction have been used to provide a mechanism for determining treatment for thoracolumbar IVD extrusions. However, the degree of neurologic dysfunction is variable with similar degrees of extrusion and so usually can only be used to assess prognosis rather than treatment options. Advanced imaging studies are again essential. Myelography may provide up to 75% accuracy in the determination of affected space and lateralization of the disc, especially when combined with neurological examination and history. However, CT has been shown to be at least 90% accurate at site localisation and 96% accurate with prediction of lateralization. Similar studies are lacking at present with respect to the MRI in veterinary patients, but my own experience is that this modality offers similar results in terms of localisation accuracy. My indications for non-surgical treatment of this condition are limited to a first-time episode of spinal pain only or financial constraints of the owner. Conservative therapy consists of strict cage rest

for 4-6 weeks, pain relief and/or muscle relaxant use (diazepam). My indications for surgical management of thoracolumbar IVD extrusion are therefore cases with spinal pain only that are nonresponsive to conservative therapy, recurrent disease, cases with neurologic deficits with deep pain, and cases with loss of deep pain perception for less than 72 hours; although I have infrequently had positive experiences with cases that have lost deep pain perception for up-to 7 days duration. The method of choice for surgical decompression is often determined by the imaging study and lesion localisation. With T10-L4 extrusions, I will most often perform a hemilaminectomy at the site of extrusion and extend the defect in the bone cranially and caudally up to a maximum of five intervertebral spaces if necessary until normal epidural fat is identified. For extrusions caudal to L4, I will often perform a dorsal laminectomy and try to combine this with a hemilaminectomy after nerve root visualisation is possible. If there is no deep pain perception present I will perform a durotomy to visualise the spinal cord parenchyma and asses prognosis. I will routinely fenestrate disc spaces T11L3 after decompressive surgery in chondrodystrophoid dogs. Methylprednisolone sodium succinate (MPSS) remains the standard of care in humans. MPSS has been shown to be effective because of its free radical scavenging properties rather than its antiinflammatory effect. In order to obtain this effect, it must be used at high doses and treatment should be initiated within 8 hours of injury. Suggested protocols include initiation of treatment with MPSS within three hours of injury at a dose rate of 30mg/kg given intravenously and followed with either a constant rate infusion of 5.4mg/kg/hr for 24 hours, or second and third boluses of 15mg/kg at two and six hours after the first dose and then a constant rate infusion of 2.5mg/kg/hour for 24 hours. If treatment is initiated between 3 and 8 hours after injury, the recommendation is to continue treatment for 48 hours rather than 24 hours. Delaying initiation of treatment for more than 8 hours has a detrimental effect on outcome in people. As MPSS has both glucocorticoid and free radical scavenging effects, it is postulated that delaying treatment until after the majority of free radical induced damage has occurred is more likely to result in glucocorticoid side-effects. Indeed, although there continues to be wide spread use of glucocorticoids, such as dexamethasone, to treat acute spinal cord injuries in veterinary practice, there is no good evidence that such drugs are beneficial and the side effects have been well documented and at this time they cannot be recommended as efficacious treatments. Recently, substances that fuse membranes ("fusogens") have been proposed as a treatment for acute spinal cord injury. Polyethylene glycol (PEG) is a hydrophilic polymer that targets damaged membranes following intravenous administration and seals membranes preventing intracellular leak of ions and subsequent axonal disruption, restoring axonal conduction. In an experimental model of spinal cord injury in guinea pigs, there was rapid improvement of electrophysiological parameters and of the cutaneous trunci reflex following treatment with PEG. No adverse effects were reported in a phase I trial of PEG completed in dogs with paralysis and loss of pain sensation due to acute disc herniations; 60% of the dogs did recover function but this preliminary study was not blinded and included a historical control group.

(click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt , BVM&S, MRCVS, DACVIM (Neurology), DECVN College of Veterinary Medicine University of Georgia

it is the only differential of peripheral disease that will start to improve in 72 hours with no specific treatment. If the patient is closely monitored over this time course. E. The bacteria commonly responsible for this disease are Staphylococcus spp. Leaning and Falling--Canine Vestibular Dysfunction WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. Streptococcus spp. Platt. Infection of the middle ear can cause vestibular disease due to the production and spread of bacterial toxins into the inner ear. however. DACVIM (Neurology). MRCVS. BVM&S. Therefore.. Clinical signs due to disease of the peripheral vestibular system: Head tilt. or rolling toward or away from the side of the lesion Conscious proprioceptive deficits. central vestibular disease is associated with different aetiologies and a worse prognosis than peripheral vestibular disease. falling. the peripheral component is located in the inner ear and the central component is located in the brain stem and cerebellum. and there is no facial paresis or Horner's syndrome. If the culture results are negative but bacterial otitis interna is suspected. it is essential to approach these cases aiming to primarily further localise the neurological lesion. Up-to 50% of cases of peripheral vestibular disease are due to otitis mediainterna. marked resolution of the nystagmus can be seen. nor does it indicate a specific aetiology. which occurs as a result of the loss of anti-gravity muscle tone on one side of the neck. If there is evidence of facial nerve involvement or Horner's syndrome further ancillary tests should be considered. but this is not specific for this aetiology. rotatory or vertical if present May be depressed or stuporous May have facial paralysis (CN VII) but Horner's syndrome is rare CAUSES OF PERIPHERAL VESTIBULAR DISEASE Idiopathic vestibular syndrome is a common cause of peripheral vestibular disease in the dog. University of Georgia 19506735 INTRODUCTION The onset of a head tilt is a cardinal sign of vestibular disease. 2009 Simon R. circling.Rolling. coli and Pseudomonas spp. falling or rolling toward the side of the lesion If nystagmus is present it is horizontal or rotatory with the fast phase away from the side of the lesion May have concurrent facial nerve paralysis (CN VII) and Horner's syndrome (ptosis. Bilateral vestibular disease may also cause a head tilt if the disease process is not symmetrical but usually does not cause such a sign. then oral enrofloxacin 5 mg/kg every 12 hours for dogs or a combination of oral trimethoprim sulfadiazine (TMP-SDZ) 15-30 mg/kg orally every 12 hours and oral cephalexin 22 mg/kg every 8 hours may be administered. DECVN College of Veterinary Medicine. miosis and enophthalmos) with middle and inner ear lesions Clinical signs due to disease of the central vestibular system: Head tilt. The vestibular system has two functional components. The onset of the vestibular disease may be so acute that is accompanied by vomiting. The infection can directly damage the inner ear with spread to the labyrinth. hemiparesis or hemiplegia on the side of the lesion if unilateral or worse on one side if bilateral Nystagmus may be horizontal. This can be only by diagnosed by ruling out the other causes. Generally. It is the most consistent sign of unilateral vestibular dysfunction. Postural reactions are normal in this disease. Unfortunately. Otitis media-interna. The head tilt may never completely resolve. This will be followed by improved gait over a 7-day period and improvement of the head tilt over a 2-month period. a head tilt is not specific for a brainstem or a peripheral vestibular system lesion localisation.. Antibiotic therapy should be continued for 6-8 weeks. Tear production should be monitored to detect sicca associated with facial nerve (CN 7) . circling.

The vestibular signs may resolve in 1-2 weeks but if antibiotics are prematurely discontinued. strabismus. Doberman. . Nasopharyngeal polyps. Diagnosis may require advanced imaging if physical examination and skull radiographs are not helpful. nystagmus.25 mg/kg once daily for 1-3 days is sometimes given to reduce inflammation and swelling of the vestibular labyrinth. Corticosteroids are usually not required and are avoided if osteomyelitis is present. In acute cases oral prednisone 0. Beagle. ataxia. Polyps are pedunculated masses. Topical treatment of the external ear canal with small amounts of low residue non-irritating antibiotic solutions for a few days may be given but the accumulation of greasy ointments in the middle ear should be avoided.5% acetic acid solution and caustic ear cleaning substances are avoided if possible. Ear hygiene should be monitored but care should be taken when cleaning the external ear canals. they often have a multifocal central nervous system distribution and may also cause profound systemic abnormalities. These include granulomatous meningoencephalomyelitis (GME) and necrotizing meningoencephalitis and can both affect the central vestibular system as part of a multifocal disease. eustachian tube. Neoplasia. Whilst all the above infections can cause vestibular disease. ceruminous gland adenocarcinoma and lymphoma. however. the external and middle ears are gently flushed with saline or a 2. circling. Head trauma may cause the onset of vestibular disease. In cases of concurrent otitis externa and media with a ruptured tympanic membrane. they will frequently have a symmetrical ataxia. Aminoglycosides are contraindicated in otitis interna/media.involvement or antibiotic therapy and artificial tears administered if necessary to prevent keratitis and corneal ulceration. Many learn to compensate by 2-4 months of age but some will remain permanently affected. bacteria and Cryptococcus. They may also be deaf. Tonkinese). these animals may not have a head tilt or nystagmus. Numerous breeds have been associated with congenital vestibular disease (German shepherd. Clinical signs usually begin around 3-4 weeks of age (when the animal begins to ambulate) and may consist of a head tilt. and a side-to-side movement of the head in the horizontal plane. Neoplasia of the structures of the ear includes squamous cell carcinoma. In animals with recurring otitis. The prognosis for each patient not only depends on the infectious etiology but also on the severity of the presenting signs. rolling. or nasopharynx. Trauma. which may be peripheral or central depending upon the severity of the trauma. there is usually no abnormal nystagmus and normal nystagmus cannot be elicited. but thorough rinsing is essential so residual cleaning solution does not irritate the vestibular labyrinth. underlying dermatologic problems such as atopy or hypothyroidism should be investigated and treated. and abnormal head movements. The deafness caused by such drugs is often permanent whereas the vestibular disease may resolve or at least the dog may compensate for the abnormality. Siamese. There are many drugs listed as being ototoxic and can potentially cause both vestibular dysfunction and deafness. Diluted ear cleaning solutions may be necessary in some cases for debris that cannot be cleared by other means. If the abnormality is bilateral. Toxoplasma. CAUSES OF CENTRAL VESTIBULAR DISEASE Inflammatory disease. Surgical intervention: External ear canal ablation and bulla osteotomy in refractory cases. Non-septic otitis media/interna may occur secondary to occlusion of the eustachian tube due to a nasopharyngeal polyp and polyps may occur as a result of chronic middle ear infection or from ascending infection from the nasopharynx. English Cocker. falling. a wide-based stance. Burmese. With bilateral disease. Congenital disease. which arise from the lining of the tympanic cavity. Peripheral vestibular disease may be evident in young animals and attributed to a congenital malformation or degeneration of the inner ear structures. Middle ear haemorrhage subsequent to a trauma may cause peripheral vestibular disease seen with or without facial paresis and Horner's syndrome. There are several inflammatory diseases of unknown aetiology and presumed immune-mediated. Ototoxicity. Recurrence can occur. the clinical signs and infection recur and can be more difficult to treat. The most common topical drug implicated in this scenario is chlorhexidine. neurological as well as systemic. The common infectious diseases responsible for inflammation of the brain and its structures are canine distemper.

endocrine disease. Non-traumatic hemorrhage. In some areas of the country this can result from aberrant parasite migration through the nervous system.g.Neoplasia. In severe cases. neoplasia. and opisthotonus may be present. Metronidazole toxicity. Removal of the drug and supportive care (IV fluid diuresis) usually results in quick recovery. Dosages greater than 30mg/kg/day can result in vestibular disease. SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Simon R. Platt . DACVIM (Neurology). Tumors of the forebrain can also cause central vestibular disease due to caudal transtentorial herniation with secondary compression of the brain stem. respectively. Occasionally. The most common tumours to cause central vestibular disease in cats are meningiomas and lymphomas located at the cerebello-medullary pontine angle. anorexia. and vomiting. MRCVS. Recovery from this disorder can be complete but can depend on the underlying disorder. deficits are permanent. altered mental status. hypertension or may commonly be idiopathic. seizures. Cerebrovascular disease. Ischemia may be embolic or thrombotic and is the most common form of CVD. BVM&S. Dose reductions need to be made in patients with liver and kidney disease as the drug is metabolized and excreted by these organs. nystagmus.. after being on high doses for 7 to 12 days). Clinical signs may include generalized ataxia. DECVN College of Veterinary Medicine University of Georgia . The onset is acute and usually occurs when animals receive high doses for a long duration (e. the other form of CVD. Cerebrovascular disease (CVD) may cause a peracute onset of central vestibular signs. its causes may be due to sepsis. is bleeding into the parenchyma of the brain that may extend into the ventricles.

The increased sensitivity of CT and MRI reveal some disc herniations that are only incidental findings and that are not responsible for causing clinical signs (Figure 1). CSF should be collected from all dogs prior to myelography. Non-chondrodystrophoid breeds are affected less frequently. Survey radiographs may indicate if disc disease is present but are only 60-70% accurate in identifying the exact location. London. THORACOLUMBAR DISC DISEASE Thoracolumbar disc disease is a common disorder in dogs that affects mainly chondrodystrophoid breeds. More information can be found in Small Animal Spinal Disorders. Available from www. . urinary dysfunction may occur with more severe lesions. 2nd edition. Particular emphasis will be on the conditions seen most often in general practicethoracolumbar disc herniations and lumbo-sacral conditions. There is often an associated panniculus reflex cut-off. CT adds accuracy and speed to the evaluation of chondrodystrophoid breeds with disc herniations. A lumbar injection is preferred for myelography because there is often considerable spinal cord swelling. Back pain and neurological deficits in the pelvic limbs are features of thoracolumbar disc disease. PhD. which may be accompanied by depressed or absent deep pain sensation caudal to the lesion. oblique views or a CT myelogram should be used. Peak incidence in these breeds is between three and six years of age. CT is non-invasive as the mineralised disc material shows clearly without the need for contrast even when it is not visible on survey radiographs. by NJH Sharp & SJ Wheeler. the L2/3 and L3/4 sites are shown here. Dipl Mgmt. Figure 1. Either myelography or advanced imaging should be performed for definitive diagnosis. A: CT scan performed prior to myelography. Over 50% of lesions occur at the T1/13 and T13/L1 discs and more than 85% occur between T11/12 and L2/3 inclusive. usually after middle age. Wheeler. FRCVS (Veterinary Neurology) Hertfordshire. 2004 Simon J. Elsevier. UK 18281006 In this lecture. BVSc. shows a centrally located. It is also usually much easier to decide what side(s) the disc material is on from CT or MRI. DECVN. If it is unclear on which side the disc material is located. advances in the treatment of thoraco-lumbar and lumbar spinal conditions will be covered.Update on Spinal Surgery II--Thoracolumbar Spine WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS Approximately 10-15 per cent of dogs show LMN deficits because of lesions between L3/4 and L6/7 discs. mineralised mass that occupies much of the vertebral canal (arrows). Lateral and ventrodorsal images should be taken. which tends to cause cervical myelograms to stop cranial to the lesion. B: Sagittal T2-weighted MRI through the lumbar region of an 11-year-old paraparetic Labrador with disc herniations at T12/13 to L3/4. Neurological deficits range from mild ataxia and paraparesis to paraplegia.

non-surgical therapy is rarely the treatment of choice for dogs with grade 3 lesions or worse. during which time it should only be removed to urinate and defecate. especially following decompression. in L7 in cats and some small dogs. The major long-term problem is that over one-third of dogs will suffer recurrence. A short course of corticosteroids without cage rest does not constitute effective nonsurgical treatment. Clinical problems can arise due to compression of neural structures in the vertebral canal and intervertebral foraminae. Animals that will not rest or are confined inadequately may fail to respond or get worse. The animal must rest quietly in a confined space (traveling cage size) for at least two weeks. Although decompression is the surgical treatment of choice for disc disease it does demand good quality imaging. Corticosteroids provide no overall benefit when used with decompressive surgery. Activities like jumping should be avoided for four to six months. except possibly MPSS for dogs that present within the first eight hours of injury Concomitant fenestration should be performed at the time of the decompression. with between 60-70% recovering in most studies. A satisfactory response should be followed by a further two weeks rest and a gradual increase in activity between the fifth and eighth weeks. Good surgical technique is needed to retrieve as much disc material as possible once the spinal cord has been exposed. Another disadvantage is that the dog can deteriorate during treatment. Any material on the contralateral side must be removed by probing over or under the spinal cord or bilateral decompression may be needed. Patients with marked deficits seen within eight hours of spinal cord injury may benefit from concomitant methylprednisolone sodium succinate (MPSS) therapy. abnormal motion probably leads to degenerative changes such as spondylosis deformans. Decompression is clearly the treatment of choice for dogs with grade five lesions. The prognosis is very good for dogs with grade one. . Strict cage rest is the overriding principle in non-surgical therapy although judicious use of analgesics or anti-inflammatory drugs may also be needed. The rate of recovery is faster after decompression than after either non-surgical treatment or fenestration and there is less likelihood of residual neurological deficits. Minihemilaminectomy removes less bone than a standard hemilaminectomy but only gives good access to the ventral portion of the vertebral canal. Although a useful initial option for some dogs with grade 1 or 2 lesions. and three deficits. Most dogs that recover regain deep pain do so within two weeks. Motion in the normal lumbar spine is greatest at the lumbosacral joint. often due to poor owner compliance. possibly as far as grade 5. In some dogs. This is the minimum time needed for an avascular structure like the anulus fibrosus to repair.Many dogs will recover from moderate neurological deficits following either nonsurgical or surgical treatment. mainly because of the unique anatomical structure of the region. which indicates treatment failure. The vertebral canal in this region contains only cauda equina. These drugs should be withheld when feasible in order to encourage the animal to rest. These degenerative changes then appear to reduce the overall range of motion. two. especially if there are no financial constraints. The spinal cord ends within L6 vertebra in most dogs. osteophyte proliferation and soft tissue overgrowth of the joint capsules. Decompression by hemilaminectomy is the treatment of choice for dogs with spinal cord compression causing persistent or recurrent grade 1 signs and for most with neurological deficits. LUMBOSACRAL DISEASE The clinical signs seen with lumbosacral lesions differ from those seen at other locations of the spine. Imaging usually identifies the affected interspace but determining which side to decompress can be more problematic. as does a lack of improvement within two weeks. The patient must be evaluated regularly for any deterioration. A high proportion of dogs referred for emergency decompression have been treated in the preceding days or weeks using corticosteroids without cage confinement. Pediculectomy also preserves the facet joint and removes less bone than a standard hemilaminectomy. Such treatment can relieve discomfort with a consequent increase in activity.

Consideration of the diagnostic imaging of these patients frequently focuses on the LS joint alone. Instability and malalignment between L7 and S1. Lumbosacral lesions can cause pelvic limb gait abnormalities. Dorsal elevation or attenuation of the column may be seen.6C. The role of instability is unclear and it is difficult to quantify regardless of the imaging technique. Epidural fibrosis. lateral recesses. This can pose a problem for surgical decision-making. These include: Stenosis (multilevel) of the vertebral canal. Cervical injection is preferred. as it avoids the potential for epidural contrast leakage in the area of interest.A number of abnormalities may combine to cause compression of the cauda equina or L7 nerve roots. mild paresis with conscious proprioceptive deficits. trauma and discospondylitis. tail paralysis. Vascular compromise of the spinal nerves. Rotation of the spine and pelvis must be avoided. Diagnosis of lumbosacral disease depends on recognising the historical features and clinical signs and on a careful physical examination. intervertebral foramen and articular processes in cross-sectional images (Figure 2) Figure 2. Osteochondrosis of the sacrum. and incontinence. Many clinically normal dogs have radiographic abnormalities of the lumbosacral junction. occasional dogs with lumbosacral disease will have normal survey radiographs. Same dog as in 10. The main role of survey radiographs is to rule out neoplasia. which should pinpoint the source of pain. Incontinence results from pelvic and pudendal nerve dysfunction. or paraparesis. Hansen Type II disc herniation at the L7/S1 intervertebral space. Subluxation. usually of the joint capsule or ligamentous structures. Pain is common but the signs vary depending on the nature and severity of the neurological impairment. Lameness in performance animals may be exacerbated by work. Conversely. This policy runs the serious risk of missing lesions elsewhere in the vertebral column that are involving the L4-S3 cord segments or ascribing significance to incidental lesions of the LS joint. There may be pain with no deficits. Marked foraminal compression is evident on A: Transverse CT scan and B: 3D reconstruction. Neurological localisation of a patient will indicate a lesion of L4-S3 spinal cord segments. or LMN neurological deficits. Urinary incontinence is usually LMN in nature with dribbling of urine and a bladder that is easily expressed by manual pressure. but low back pain is quite different from that seen in thoracolumbar lesions. Soft tissue proliferation. . for example by the patellar reflex. CT is particularly useful as it shows the vertebral canal. It is advisable that the patient be anaesthetised or sedated heavily when radio-graphing the lumbosacral joint. Dogs with chronic degenerative lumbosacral lesions may present with non-specific clinical signs. osteophytosis or thickening of the articular processes. lameness. It may be possible to define the location more accurately. Myelography can therefore be useful to assess the low lumbar region and the rest of the spinal cord.

Transverse images provide the best visualisation of disc or foraminal anatomy. The choice of surgical procedure is then between dorsal laminectomy. in working dogs and those with marked pain or neurological deficits. Further indications for surgery include CT or MR findings of increased soft tissue suggestive of epidural fibrosis. Surgical treatment is indicated when nonsurgical treatment has failed. One potential disadvantage of MRI is over-diagnosis. There is loss of signal in the lumbosacral disc but minimal compression of the cauda equina (arrowhead). relieve pressure on neural tissues. distraction and fusion. T2-weighted MRI of the lumbosacral spine of a seven-year-old Labrador with lumbosacral pain. This may be successful if pain is the main clinical sign. FRCVS (Veterinary Neu Hertfordshire. PhD. U . Figure3. There are a number of similarities between lumbosacral disease and caudal cervical spondylomyelopathy. it does not address instability if this is a contributing factor. Most dogs are treated initially with rest and anti-inflammatory medication. Decompression of the cauda equina and spinal nerves can be achieved by dorsal laminectomy. A: Image made with the spine in flexion. or a combination of the two. Distraction of the dorsal aspect of L7 and S1 is achieved using screws placed through the articular processes of L7/S1 and into the body of the sacrum. or a large disc herniation. Wheeler. There is severe compression at L7/S1 caused by both disc and ligamentum flavum (arrowhead). BVSc. severe pain. which can be combined with foraminal decompression or even facetectomy. The anulus fibrosus should be excised once the cauda equina is retracted laterally when there is marked bulging of the disc. even by expert neuroradiologists (Figure 3). Simon J. Laminectomy often provides rapid relief of pain with improvement of mild gait abnormalities and minor neurological deficits.MRI provides better soft tissue resolution than CT as well as an ability to acquire images in multiple planes without image degradation. Definitive criteria for these procedures are lacking. Dipl Mgmt. Redundant joint capsule can also be removed. Click on the image to see a larger view. Routine fenestration may also be warranted. and prevent abnormal motion. A rationale can therefore be made for lumbosacral distraction and stabilisation. earlier detection of disc degeneration and evaluation of the entire lumbar spine in a single sagittal examination. B: Image from the same dog made with the spine in extension. namely to open the vertebral canal and intervertebral foramen. Decompression by laminectomy can be combined with fixation and fusion. The principle is the same. DECVN. Fusion is promoted by removing the articular cartilage from the facet joints and by a cancellous bone graft. especially if it enhances with contrast. especially for dogs with marked neurological deficits. This can be combined with dorsal laminectomy.

. A few neurons terminate in the fastigial nucleus and the flocculonodular lobes of the cerebellum. Anatomy The vestibular apparatus is contained within the petrosal portion of the temporal bone (in what is also known as the inner ear). Perilymph is secreted by arterioles of the periosteum surrounding the labyrinth and drains into the subarachnoid space through the perilymphatic duct. trunk and limbs in reference to the position of the head. medial. the semicircular canals and the cochlea. The Vestibular Nuclei There are four vestibular nuclei (rostral. PhD Ryan Veterinary Hospital. School of Veterinary Medicine. University of Pennsylvania USA 18283394 The vestibular system is responsible for maintaining an animal's balance and normal orientation relative to the earth's gravitational field.H. The vestibular neurons then enter the medulla between the caudal cerebellar peduncle and the spinal tract of the trigeminal nerve and terminate in the vestibular nuclei. These interneurons are facilitatory to ipsilateral extensor muscles. Efferent Fibres Fibres from the lateral vestibular nucleus descend in the ipsilateral ventral funiculus and synapse on interneurons in the ventral grey column forming the vestibulospinal tract. Vite. The MLF controls the position of the limbs and trunk with respect to the position of the head. The bony labyrinth consists of three communicating fluid-filled portions: the vestibule. It comprises a membranous and bony labyrinth. They are inhibitory to ipsilateral flexor muscles and to contralateral extensor muscles. DVM. The Path of the Vestibular Neurons The vestibular neurons travel with the vestibulocochlear nerve. Fibres from the medial vestibular nucleus descend in the dorsal portion of the ventral funiculus through the cervical and craniothoracic spinal cord segments. lateral and caudal) which are in the lateral wall of the fourth ventricle. forming the medial longitudinal fasciculus (MLF). The vestibular nuclei receive afferents from the vestibulocochlear nerve and from the fastigial nucleus of the cerebellum. These fluid-filled regions contain perilymph. This system maintains the position of the eyes.Vestibular Diseases in the Dog and Cat: Old and New Diagnostic Methods British Small Animal Veterinary Congress 2006 C. a fluid with ionic composition similar to cerebrospinal fluid. They enter the skull through the internal acoustic meatus.

The strabismus may not be noted until the head is elevated or returned to the horizontal plane Abnormal nystagmus with the slow phase directed toward the side of the lesion There are normal and pathological causes of nystagmus. The labyrinth initiates the slow phase. post-rotatory nystagmus is depressed when the patient has been rotated away from the side of the lesion. The MLF controls eye position with respect to the position of the head. the following signs characterise vestibular system dysfunction: Loss of balance Vestibular ataxia characterised by regularly falling toward the side of the lesion Abnormal posture characterised by leaning. It may be seen when the head is not moving (spontaneous or resting nystagmus) or it may be induced by moving the head into different positions (induced nystagmus). . and the fast phase is elicited by the brain stem. Post-rotatory nystagmus occurs after rotating the head. In cases where vestibular system involvement is present but signs are mild. It has a fast and a slow phase. Acute Vestibular or Cerebellar Signs Regardless of whether the lesion is located centrally or peripherally. If peripheral vestibular disease is present. ataxia may be accentuated by blindfolding the animal. and/or rolling toward the side of the lesion Head tilted toward the side of the lesion. and nystagmus may be accentuated by placing the animal on its back. The fast phase of the nystagmus is in the opposite direction of the direction in which the head was moved. with the fast phase being in the direction of head motion. ataxia and head tilt may be accentuated by lifting the animal off the ground. (A head tilt exists when an imagined horizontal line running through both ears is tilted from the horizontal plane) Ventral strabismus of the eye on the side of the lesion. neck and body. IV and VI. turning of the head. Abnormal nystagmus is associated with disease of the vestibular system.Fibres of the MLF also project rostrally to cranial nerves III. Abnormal nystagmus is associated with pathology. Cerebellar Involvement The caudal cerebellar peduncle is the pathway for afferent vestibular neurons projecting to the cerebellum. Physiological nystagmus is nonpathological and is associated with movement of the head.

deep otic examination or thyroid testing. Burmese and Tonkinese cats have also been affected. enrofloxacin or trimethoprim/sulfa +/-bulla osteotomy are recommended Idiopathic labyrinthitis. Spontaneous recovery is common Other causes. Imaging of the osseous bullae and/or deep otic examination may confirm middle ear disease. Akitas and other dogs. these animals are treated with antibiotics until a definitive diagnosis is made. Normal tear production is generally present over the eye affected with an abnormal palpebral blink response. The direction of the nystagmus is usually horizontal or rotary and is unchanged when the position of the head is altered. Inner Ear/Vestibular Nerve Disease of the inner ear or vestibular nerve results in only the signs listed above. Compulsive circling is associated with disease of the cerebral hemispheres and diencephalon. Computed tomography (CT) and magnetic resonance imaging (MRI) are more sensitive at diagnosing middle ear disease than are plain film radiographs Evidence of infection of the inner ear alone is rarely visible on either CT or MRI images. German Shepherd Dogs. Diseases of the inner ear/vestibular nerve include: Otitis interna/media. Treatment with cephalosporins. Siamese. Polyneuropathy. Localising Signs of Vestibular System Dysfunction to the Peripheral or Central Portions of the Vestibular System Vestibular system dysfunction may result from disease of the inner ear. Antibiotics are recommended but may not be necessary. tumours and trauma involving the inner ear or vestibular nerve may result in vestibular system dysfunction. Auditory dysfunction is rarely recognised. If disease also affects the middle ear. occasionally. Hypothyroidism may be associated with polyneuropathy and. vestibular signs resolve only after the institution of thyroid hormone supplementation. Smooth Fox Terriers. In general. images of the bullae. Dobermans. Signs of vestibular dysfunction are generally present at birth. Aminoglycosides at high doses may result in deafness and signs of peripheral vestibular dysfunction Medulla/Cerebellum . signs of CN VII dysfunction (drooping lip and ear and absent palpebral blink) and a Horner's syndrome may result. no loss of balance and no abnormal nystagmus. Older dogs and cats of any age may be affected. No abnormalities are found on blood work. With compulsive circling there is no ataxia.A common mistake is to attribute compulsive circling to disease of the vestibular system. Cocker Spaniels. Congenital vestibular syndromes have been described in Beagles. The presence of neurological deficits in addition to the ones listed above helps to determine where the lesion is located. medulla or cerebellum. CN VII dysfunction and Horner's syndrome do not occur.

C. In general. storage disease and demyelination Exceptions to the Rules of Localisation Bilateral involvement of the inner ear may result in a wide-based stance and swaying of the body. De Lahunta. 1983. hemiparesis and postural reaction deficits may occur. A. Analsysis of traditional and novel neurological examination techniques for the diagnosis of vestibular dysfunction in dogs. Disease of the cerebellum and medulla occasionally results in head tilt. when the animal is lifted off the ground a severe loss of balance is evident. Intramuscular thiamine hydrochloride (25-50 mg) can resolve the signs Infarction of the medulla or cerebellum may be suspected on the basis of cerebrospinal fluid abnormalities and images of the brain Other causes of chronic progressive signs of central vestibular dysfunction include: cerebellar hypoplasia. Troxel. cryptococcosis. neosporosis. In these instances. CH. Inflammatory and neoplastic causes commonly result in vestibular dysfunction due to involvement of the medulla and/or cerebellum: Canine distemper virus infection.H. Due to involvement of the upper motor neurons and the proprioceptive system. USA . K. DVM PhD University of Pennsylvania PA. Drobatz.Disease of the medulla may result in changes in mental status due to involvement of the ascending reticular activating system. requiring a week or more of hospitalisation. results in recovery although months may be required before all signs resolve Thiamine deficiency may result in vestibular system dysfunction. Vestibular system--special proprioception. However. Dysmetria. M. Philadelphia: WB Saunders. without evidence of nystagmus or strabismus. Due to involvement of other brain stem regions. parasitic migration and other meningoencephalitides may result in vestibular system dysfunction Neoplasia may be suspected on the basis of cerebrospinal fluid abnormalities and images of the brain Metronidazole intoxication at doses greater than 30 mg/kg will frequently result in an acute onset of vestibular system dysfunction with vertical nystagmus and. depriving the animal of tactile or visual sensory information causes a worsening of the signs of vestibular disease. seizures. Journal of the American Veterinary Medical Association (in press). and head and neck tremors may result from disease of the cerebellum. 238-254. rotary or vertical and may change when the position of the head is altered. menace deficits ipsilateral to the side of the lesion. Supportive care. In: Veterinary Neuroanatomy and Clinical Neurology (second edition). References 1. dysfunction of cranial nerves V-XII may occur ipsilateral to the side of the lesion. Vite. cerebellar abiotrophy. occasionally. strabismus and slow phase of the nystagmus directed away from the side of the lesion (paradoxical vestibular syndrome). granulomatous meningoencephalomyelitis. toxoplasmosis. 2. Vite. the postural reaction deficits remain ipsilateral to the side of the lesion. The direction of the nystagmus may be horizontal.

palate and pharyngeal mucosa. Nasopharyngeal diseases arise from tissues within. caudal nasal ethmoturbinates. auditory tubes. The nasopharynx is dorsal to the soft palate and extends from the choanae to the larynx. some or all of clinical signs listed may be present. localises disease to the caudal nasal cavity or nasopharynx. it is usually possible to localise upper respiratory disorders to the sinonasal cavity. Table 1.Diagnostic Investigation of Feline Nasopharyngeal Disease WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. middle-ears. including the base of the skull. Sinonasal cavity disease: Nasal discharge Epistaxis Sneezing* Facial distortion Caudal nasal cavity/nasopharyngeal disease: Inspiratory dyspnoea Stertor (inspiratory)* Excessive swallowing Gagging Paroxysmal reverse sneezing* Coughing Sneezing Nasal discharge Epistaxis Halitosis Dysphonia Concurrent otitis externa/head shaking Concurrent media/interna (OMI) Laryngeal disease: Stridor (inspiratory)* Cough Dysphonia Gagging Retching Dysphagia CLINICAL SIGNS OF CAUDAL NASAL CAVITY/NASOPHARYNGEAL DISEASE An obstructive respiratory pattern characterised by a normal or mildly increased respiratory rate and inspiratory dyspnoea. For each category. A stertor is a snoring or snorting sound that results from turbulent air-flow caused by . Localisation of feline upper respiratory disorders. 2007 Vanessa Barrs 18287655 Presentation for upper respiratory signs is common in feline practice. bordering or contiguous with the nasopharynx. larynx or caudal nasal cavity/nasopharynx (Table 1). Localising signs are asterisked. together with stertor. From the findings of a thorough history and physical examination including careful observation of the respiratory pattern.

Differential diagnoses of caudal nasal cavity/nasopharyngeal disease. This sonorous respiration is characteristic of caudal nasal cavity/nasopharyngeal disease. Other signs that may be present are listed in Table 1. In cats with nasopharyngeal disease and OMI. and in certain geographical regions such as Australia. head-shaking. in cats with nasopharyngeal disease and OMI there may be intracranial extension of infection through the internal acoustic meatus. A mucoid effusion develops in the tympanic bullae. Rarely. Neoplasia Lymphoma Carcinoma Other Inflammatory Nasopharyngeal polyp Nasopharyngeal stenosis Infectious Mycotic nasopharyngeal diseases Cryptococcosis Aspergillosis Atypical bacterial infections Mycobacteria Accumulation of excessive nasal secretions Infectious/inflammatory rhinosinusitis Sinonasal cavity disease Foreign body Congenital Choanal atresia Palatine defects The most frequent causes of nasopharyngeal disease in cats are neoplasia.g. .4-5 Neoplasia Of neoplastic diseases lymphoma is by far the most common.3 AETIOLOGIES Once disease has been localised to the caudal nasal cavity/nasopharynx. resulting in signs of central nervous system dysfunction. mycotic granulomatous infections. the following differential diagnoses should be considered: Table 2. Nasal discharge is present in some cats due to obstruction of nasopharyngeal drainage by a mass lesion or because of concurrent sinonasal cavity disease. followed by carcinomas.2 Rupture of the tympanic membrane from polyp growth or infection can cause otitis externa and clinical signs of head-shaking..2. cryptococcal granuloma).1.airway obstruction rostral to the larynx. Cats with nasopharyngeal disease may develop otitis media/interna (OMI) from occlusion of the pharyngeal openings of the auditory tube by a mass lesion (e. or ear-scratching/grooming. signs of peripheral vestibular disease. especially cryptococcosis.g. This is often complicated by secondary ascending bacterial infection with oropharyngeal flora. OMI may also develop because of direct involvement of the tympanic bullae in the disease process (e.. non-infectious inflammatory disease. nasopharyngeal polyp). Horner's syndrome and/or facial nerve palsy may occur. ipsilateral to the affected bulla.

Infectious Infectious agents that cause granulomatous disease are a differential diagnosis for feline nasopharyngeal disease. may enter the nasopharynx during incomplete vomition. The first stage includes non-invasive investigations. Foreign Bodies Nasopharyngeal foreign bodies. performed with the patient under general anaesthesia. prolapse of the nictitating membrane. including fungi and bacteria. nasopharynx.Inflammatory Nasopharyngeal polyps are the most common inflammatory cause and are thought to occur in response to ascending oropharyngeal viral infection. partial or complete. and membranous or bony. ocular discharge and exposure keratitis). during attempts to swallow or during regurgitation in oesophageal motility disorders. These pedunculated growths arise from the mucosa of the tympanic bullae or auditory tube and protrude into the nasopharynx. In severe infections turbinate destruction may be permanent. such as plant or food material. Unilateral. . signs of rostral nasal cavity or sinus infection may be subtle or absent. In cats this is thought to occur secondary to viral or bacterial upper respiratory infections. Infection with Feline Herpesvirus causes epithelial necrosis and osteolysis of nasal turbinates. palate and cribriform plate. membranous choanal atresia has recently been described in a Himalayan cat. Preliminary investigations by the author's group have shown that in contrast to canine sinonasal aspergillosis which is typically caused by Aspergillus fumigatus. Cryptococcal infections that originate in the caudal nasal cavity can develop into mass lesions that obstruct one or both choanae.9 In other species the choanal obstruction may be unilateral or bilateral. resulting in presentation for stertor. infections in cats involve other species of Aspergillus including Neosartorya sp. often with secondary bacterial infection. stertor and oral cavity lesions including palatine ulceration and/or mass lesions in the pterygopalatine fossa.8 This newly recognised clinical syndrome in cats is characterised by a retrobulbar mass (exophthalmos. DIAGNOSTIC INVESTIGATION Diagnostic investigation of cats with nasopharyngeal disease is relatively straightforward and should be conducted in two stages.3 Acquired nasopharyngeal stenosis (NPS) is characterised by the presence of a web of fibrous scar tissue (cicatrix) that spans the nasopharynx caudal to the choanae and has a small central aperture. Importantly. Congenital Choanal atresia is a congenital anomaly characterised by developmental failure of the caudal nasal cavity to communicate with the nasopharynx. Excessive Nasal Secretions Any cause of sinonasal cavity disease.6-7 Acquired NPS has also been described in other species secondary to caustic burns. Identification of nasopharyngeal involvement is important clinically. or rarely. since biopsy of nasopharyngeal lesions is a reliable method of obtaining tissues for definitive diagnosis through fungal culture and histopathology. including infectious and inflammatory rhinosinusitis can cause accumulation of nasal secretions in the caudal nasal cavity/ nasopharynx. Polyps may also extend through the tympanic membrane into the horizontal ear canal. It occurs as an inflammatory response to mucosal ulceration of the nasopharynx. oropharyngeal surgery or reflux of gastric contents through the nares during general anaesthesia. This distinctive constellation of clinical signs reflects the propensity of sinonasal cavity aspergillosis in cats to invade contiguous tissues including the orbit. resulting in chronic rhinosinusitis. Sedation may be required for some procedures.5 Nasopharyngeal involvement is common in sino-orbital aspergillosis infections of cats. and should be considered as a differential diagnosis for chronic unilateral nasal discharge. through the internal acoustic meatus of the tympanic bulla into the cranial vault. The second stage includes imaging and biopsy collection.

4. there may be extension of growth through the tympanic membrane into the horizontal ear canal. miosis.. Step 3 (LCAT) should always be performed since fungal infection may not be detectable on swabs of the rostral nasal cavity. enophthalmos. fleshy masses and otitis externa may be observed. Computed tomography (CT) is more sensitive than radiography. The most common neoplasm implicated was nasopharyngeal lymphoma.11 However. head tilt.g. diagnosis also requires cytological evidence of inflammation or the presence of abundant organisms. A large nasopharyngeal mass will cause ventral deviation of the soft-palate and can be palpated dorsal to the soft-palate. nasopharynx. sequentially. Signs of peripheral vestibular disease in cats with OMI include vomiting. is low. prolapse of the nictitating membrane) ipsilateral to the affected bulla may be seen concurrently. 5. and/or lysis of paranasal bones . metastatic pulmonary neoplasia. Chronic otitis media is more readily detected as mild bony reaction and thickening of the tympanic bulla wall. Thoracic Radiography: Thoracic radiography is useful to screen for lower respiratory tract involvement in the primary disease process. Diagnostic Imaging: The nasal cavity. Furthermore. e. In cats with OMI the tympanic membrane may be discoloured or bulging. It is important to distinguish between peripheral vestibular disease and central vestibular disease in all patients since intracranial extension of infection from the middle-ear can occur. some large nasopharyngeal masses can be digitally massaged into the oropharynx for biopsy or removal. Exceptions include infection with Bordetella bronchiseptica or Actinomyces sp. which may be primary pathogens. If radiography is used views should include lateral skull.Stage 1 1. under general anaesthesia: 1. Pink. Soft Palate Inspection: The soft-palate should be inspected during induction of general anaesthesia and intubation. using curved extraction forceps by grasping the rostral stalk of the polyp. severe destruction of both maxillary turbinates and ethmoturbinates. Recurrence is common and ventral bulla osteotomy is often required. Haemorrhage is usually minimal. Aspiration Cytology & Microbial Culture: Where present. dorsoventral occlusal view or open-mouth ventrodorsal view and rostrocaudal open-mouth or rostro 10° ventro-caudodorsal oblique view. a third of cats with nasopharyngeal disease were found to have effusive bulla disease on CT. pulmonary cryptococcosis. the following diagnostic investigations should be performed. ataxia and spontaneous nystagmus in the absence of postural reaction deficits. Stage 2 If definitive diagnosis is not obtained using these non-invasive procedures.10 On CT. 2. middle-ear involvement in cats with caudal nasal cavity/nasopharyngeal disease is more common than previously thought. The diagnostic imaging modality used will depend on availability. In cats with nasopharyngeal polyps. circling. Bacterial culture of superficial nasal swabs is usually unrewarding since normal flora is present and bacterial infections are usually secondary to underlying disease. destruction of maxillary turbinates is commonly seen in cats with inflammatory or neoplastic sinonasal disease. Recently. The sensitivity of radiography for the detection of acute otitis media. and to perform in vitro susceptibility testing of the fungal pathogen. A positive titre is indicative of active infection. After intubation. Serology: A latex cryptococcal antigen agglutination test (LCAT) detects the presence of cryptococcal antigen in serum. Facial nerve palsy and components of Horner's syndrome (ptosis. frontal sinuses and tympanic bullae should be assessed in patients with caudal nasal cavity/nasopharyngeal disease. Since the nasal cavity of healthy cats can be colonised with Cryptococcus sp. particularly where unilateral. Nasopharyngeal polyps can be removed with firm traction. ventrodorsal skull. as identified by loss of aeration of the bullae. 2. Cytology and fungal culture of nasal swabs is useful for the detection of Cryptococcus sp. Neurological Examination: A neurological examination should be performed in any cat with nasopharyngeal disease and suspected middle-ear involvement. Nasopharyngeal masses are most easily identified as soft-tissue opacities dorsal to the soft-palate on a lateral skull radiograph. enlarged local lymph nodes (mandibular or retropharyngeal) or facial soft-tissue masses should be aspirated. Otoscopy: Thorough otoscopic examination should be performed to visualise the integrity of both tympanic membranes. 3.

5. leaving the caudal edge intact. Garosi. A 10 ml aliquot of sterile saline is flushed vigorously through one naris into the ventral nasal meatus. A cuffed endo-tracheal tube. during nasopharyngeal more predictive of sinonasal neoplasia than inflammatory disease.2 Vanessa Barrs Valentine Charlton Cat Centre. Diagnostic tissue specimens dislodged during this procedure can be retrieved from the packing material in the pharynx for cytology. Australia Use. whilst occluding the other naris. the orbit and calvarium in cats with neoplasia or filamentous fungal infections. The University of Sydney NSW. In cats with suspected sinonasal cavity disease rhinoscopy should be performed after nasopharyngeal endoscopy. to facilitate superior access to the rostral nasopharynx. but not all cats.5% bupivacaine facilitate a decreased plane of general anaesthesia in some. the soft-palate can be incised longitudinally. MRI after intravascular contrast administration is superior for evaluation of intracranial softtissues.3 3. Alternatively. 4. In patients with suspected otogenic intracranial infection. culture and histopathology. Harvesting of biopsy samples utilising this flushing technique obviates the need for endoscopic biopsy and often yields larger biopsy specimens than can be obtained using endoscopy alone. fine-needle aspirates of mass lesions through the softpalate can be obtained for cytological analysis. UK 18283942 . to check patency and dislodge foreign material or masses. though rarely necessary for diagnostic purposes. and then repeated on the other side. DVM. Cup biopsy forceps are useful to obtain 'blind' tissue biopsies from the nasal cavity. should be used. Haemorrhage. CT is also useful to document involvement of extrasinonasal structures including facial soft-tissues. with adequate insufflation to seal the trachea and protect from aspiration of lavage solution. The pharynx is packed with sterile swabs to prevent aspiration and to trap flushed material. Large nasopharyngeal mass lesions may be visualised by retraction of the soft palate with a spay hook. a size 5 or 6 Fr urinary catheter is inserted via each ventral nasal meatus into the nasopharynx. Care should be taken not to advance biopsy forceps caudal to the medial canthus of the eye. Regional anaesthesia of the pharynx with 2% topical lignocaine gel and maxillary nerve blocks using 0. although mild. CT is generally superior to magnetic resonance imaging (MRI) for evaluation of destructive lesions in bony structures contiguous with the nasopharynx. Other Procedures: Where endoscopic visualisation of the nasopharynx is hampered by excessive secretions or haemorrhage. Visualisation of the Nasopharynx: The patient is placed in dorsal recumbency with an intraoral gag in place. When the choanae are clearly visualised endoscopically. to prevent inadvertent penetration of the cribriform plate. Mass lesions in the choanae/nasopharynx can be biopsied using endoscopic biopsy forceps. Visualisation of the choanae requires retroflexed nasopharyngeal endoscopy. Faculty of Veterinary Science. Nasal Cavity Lavage: Flushing saline from the nasal cavities into the nasopharynx is useful to dislodge foreign bodies and diagnostic fragments of friable tumours or granulomas. Misuse & Abuse of MRI ACVIM 2005 Laurent S. DECVN. MCRVS Newmarket. Suffolk. is common during rhinoscopy and can impair visualisation of the nasopharynx.

Unfortunately. . When compared with other imaging techniques. magnetic resonance imaging). diffusion. Other pulse sequences used for small animal MRI include fluid-attenuated inversion recovery (FLAIR) (used to suppress CSF signals in order to examine lesions of the brain parenchyma which are near to the ventricle or subarachnoid space). MRI is now more readily available to the veterinary community and considered as an "indispensable tool" in most referral practices. MRI also has the benefit of the absence of ionizing radiation risk. T2weighted images are used for identifying regions of increased free water (regions of edema. Gadolinium-enhanced T1-weighted images allow for identification of regions within the CNS where the blood-brain barrier is not intact. T1weighted images are useful for visualizing anatomy. cellular infiltration or inflammation). MRI is the preferred imaging method for humans with central nervous system disease. The possibilities are nearly endless. susceptibility.0 Tesla. Consequently. The advances made in diagnostic imaging have made this discipline more "understandable" and accessible to every practitioner. the demand from pet owners for diagnostic modalities such as MRI has increased. partial volume and signal drop-off artifacts. Compared to man. signal void. The clinician must therefore still rely on clinical acumen to choose appropriate diagnostic tests and interpret results of these. Common MRI artifacts are important to recognize and include motion. advances in therapy seem to lag behind the progress made in the availability of this diagnostic imaging technique. Other than the risks associated with this general anesthesia (especially in patients with severely compromised brain function). The most common pulse sequences used to image the brain and spinal cord are those based upon the spin-echo. multiplanar capability and absence of ionizing radiation risk when compared to other imaging techniques. Numerous MRI radiofrequency pulse sequences have been designed in order to improve soft tissue contrast resolution. computed tomography. these diagnostic tests often lack specificity in determining the exact nature of the disease process.INTRODUCTION The past ten years has seen a dramatic increase in the availability of sophisticated neurodiagnostic tests (electrodiagnosis. With unlimited media availability provided by the internet. their relatively high sensitivity. there is no conclusive evidence for irreversible or hazardous bioeffects related to short-term exposures of human beings to static magnetic fields up to 2. most practitioners and veterinary students considered neurology as the "dark side" of veterinary medicine.and perfusionweighted (use for early detection of infarction) and fat-saturation techniques. gradient echo (increased sensitivity of blood products and calcification). A precise localisation of the problem within the nervous system (anatomic diagnosis) and understanding of the suspected disease process (differential diagnosis) are the keys to a successful management. The advantage of using such technology is undeniable in terms of diagnostic capability and progress in the understanding of complex neurological problems. MRI IN THE CONTEXT OF CLINICAL NEUROLOGY Until recently. the general public has become more informed and sometimes more critical of what can or cannot be done for their beloved companion. despite and sometimes because of. MR imaging does require that the veterinary patient be anesthetized. Its main advantages rest on its highly accurate soft tissue resolution. Unfortunately.

neoplastic. or anatomic site. etc. while it is usually of insufficient sensitivity to measure the specific chemical responsible for the disorder. narcolepsy or diseases classified as "movement disorders"). antibody titers. a good understanding of disease process mechanism. these secondary chemical changes may be specific for the disorder. MRS is also of use in the investigation of intrinsic metabolic disease where. Magnetic resonance techniques may still hold the key to non-invasive specific histological diagnosis. The combined results of sequences might in some cases be strongly suggestive of a specific pathological process. shape. are increasingly recognized in dogs or cats with the advance of neuro-imaging. stereotactic or surgical). anomalous or trauma) and (c) intra-cranial functional brain disease (mainly diseases caused by abnormal neurotransmission or ion channel disorders such as primary epilepsy. cerebrovascular accidents. Initial hopes that MRI signal intensity would be diagnostic for specific pathologic processes have not been borne out.MR imaging is likely to add information to that obtained by conventional imaging techniques when 1) the area of the suspected lesion cannot be evaluated using other means. b) intra-cranial structural brain disease (cerebrovascular. MRI has excellent soft tissue contrast resolution and high sensitivity to many disease processes affecting the brain. coagulation profile. the interpretation of the imaging findings relies on the clinical understanding of the suspected disease process (differential diagnosis). it can detect the secondary chemical pathological changes. 3) a lesion is evident on other imaging techniques but more 3-D information is required for example for treatment planning. INVESTIGATION OF BRAIN DISEASES Because of its excellent soft tissue resolution. inflammatory or infectious. 2) the information produced by conventional imaging techniques is limited. In some situations. Magnetic resonance spectral patterns have been shown in man to be distinct for different tumor types and grades. The validity and utility of MRS in canine patients with brain tumors as well as patient with intrinsic metabolic disease is currently being analyzed at the Animal Health Trust. Diseases that affect the brain are divided into a) extra-cranial disease (toxic or metabolic). Previously considered uncommon. the use of other diagnostic tests (cerebrospinal fluid analysis. . metastatic work-up. Elimination of extra-cranial causes of brain disorder is a pre-requisite to MRI evaluation of brain disease. Signal intensity on MRI scans is a reflection of subtle biochemical and biophysical tissue properties. Response to radiation therapy is also reflected by MRS patterns. and in particular brain infarcts. However. MRI imaging of the brain is indicated in the diagnostic work-up of animals with neurological signs of brain disease. and/or histological diagnosis after tissue biopsy (ultrasonographic guided. Magnetic resonance spectroscopy (MRS) provides metabolic information about brain tumors beyond what is obtained from anatomic images. As a result. The improved resolution of imaging methods has made the identification of small pathological process such as lacunar infarcts possible. These infarcts are now clearly the most common category of infarcts in man and dogs.). pathological processes such as inflammatory mass and neoplasia share some MRI characteristics as well as similarities in origin. Radiologists and neurologists have long tried to correlate histopathological results and MR signal intensity using combination of sequences to distinguish non-neoplastic from neoplastic disease (and to further classify different types of neoplastic disease). degenerative. In many cases.

plain radiography and myelography have been the techniques of choice for the investigation of spinal cord disease. . edema. myelography provides no information about the spinal cord parenchyma other than whether it is compressed. The main limitations of MRI in these cases are mainly technical (choice of adequate imaging plane and sequences). neoplasm) and b) non-compressive diseases (spinal cord malformation. b diseases for which the parenchymal changes can only been seen microscopically (especially degenerative disease such as degenerative myelopathy).The absence of abnormalities on MRI evaluation of the brain could indicate a) incorrect anatomical diagnosis (disease affecting parts of the nervous system other than the brain). syringo-hydromyelia. MRI offers the double advantage of showing spinal cord parenchymal changes (such as those associated with inflammation. or c) diseases causing very subtle parenchymal changes that might not be detected with a low strength magnet (vascular disease such as fibrocartilaginous embolism or inflammatory disease of the spinal cord). MRI evaluation of the spinal cord can be extremely time-consuming. or d) functional brain disease (primary epilepsy and movement disorders). However. c) diseases causing very subtle parenchymal changes that might not be detected with a low field magnet (small infarct or hemorrhage and degenerative disease). infarct or neoplasia) and allowing transverse images (greatly assisting with the localization of the compressive tissue). Common indications of MRI in investigation of peripheral nerve disease include the investigation of a) cauda equina syndrome (very often technically difficult using myelography and epidurography). and can lead to over-diagnosis of incidental changes such as mildly herniating discs. field of view allowed. Diseases affecting the peripheral nervous system can affect one single peripheral nerve (mono-neuropathy) or multiple peripheral nerves (polyneuropathy). MRI evaluation of the spinal cord could be normal in the case of a) incorrect anatomical diagnosis (particularly with neuromuscular disease. without an accurate anatomic diagnosis (suspected spinal cord segments affected). operator-dependant (detailed knowledge of anatomy) and inherent poor specificity in differentiating neoplastic from non-neoplastic disease processes. displaced or swollen. and c) cranial nerve neuropathy. b) toxicity or metabolic disease affecting the brain function without causing macroscopic parenchymal changes (hepatic encephalopathy. especially in large dogs. INVESTIGATION OF SPINAL CORD DISEASES Diseases affecting the spinal cord are broadly divided into a) compressive diseases (disc herniation. electrolyte imbalance or hypoglycemia). the spinal cord and brainstem. degenerative diseases and vascular accident). spinal malformation. Traditionally. vertebral fracture/luxation. accurate positioning of the animal and setting of different imaging planes). Suspected spinal cord disease is a common indication for MRI in small animals. b) brachial plexopathy. Unfortunately. INVESTIGATION OF NERVE AND MUSCLE DISEASES The peripheral nervous system consists of 12 pairs of cranial nerves and 36 pairs of spinal nerves that extend from. inflammatory/infectious CNS disease. or to. MRI also has the benefit of being safer than conventional myelography as a subarachnoid injection is not required. brain disease or disease affecting other spinal cord segments than the ones imaged). Other limitations are mainly technical (magnetic field strength.

INVESTIGATION OF VASCULAR RELATED NEUROLOGICAL DISORDER In addition to stroke. image contrast is the result of blood motion. UK . Garosi. is easy to use and do not need contrast medium injection. congenital portosystemic shunt (hepatic encephalopathy) and other vascular malformations (such as caudal vena cava malformation) as possible cause of exerciseinduced weakness and collapse. MCRVS The Animal Health Trust Kentford .Newmarket. magnetic resonance angiography or MRA) can non-invasively assess the vascular system. Two techniques can be used 1) time of flight (TOF) MRA and 2) contrast MRA.e. In addition to its use for tissue evaluation. MRI has proven useful adjunctive diagnostic procedure for cases of polymyositis where diagnosis is elusive. TOF may be used in either a 2-D (sensitive to slow-flowing blood) or a 3-D sequence (high spatial resolution and sensitive to fast-flowing blood). and a muscle biopsy is the only manner in which a definitive diagnosis can be made. Image data can be collected during the whole measurement cycle. In all MRA techniques. MR imaging (i. However. Contrast MRA is based on the use of paramagnetic contrast agents in combination with gradient-echo sequences. The MRI signal intensity of normal muscle is intermediate between that of fat and cortical bone. Although less invasive. Paramagnetic contrast media strongly enhance the MR signal due to T1 shortening. demonstrating arterial and venous contrast pass. MRI studies in man and in dogs have showed a good correlation between uniform hyperintensity on T1-W and T2-W images showing enhancement after contrast medium administration and muscle inflammation identified histopathologically. DECVN.Electromyography is better than MRI for muscle disease evaluation. one of the main limitations of MRA is its lower resolution compared with conventional angiography which becomes progressively worse as the vessel luminal size decreases.. Laurent S. vascular-related neurological disorders include aortic thrombo-embolism (ischemic neuromyopathy). The TOF MRA can be implemented on every MR system. particularly if a specific anatomic localization cannot be reached by other means. DVM.

Since the wobbler dog is a clinical diagnosis the clinician should always be aware of the differential diagnoses. Also cervical instability may already be evident on the neutral views but may be evoked by stress views (flexion. and the static or dynamic nature of the spinal cord compression. Basset Hound) or middle-aged to older animals (6–8 years. . Degenerative lesions include intervertebral disc degeneration (IVDD) and Hansen type II fibrinoid disc herniation (protrusion).The Wobbler Dog: A Surgical Dilemma WSAVA/FECAVA/BSAVA World Congress 2012 Björn P. Myelography followed by computed tomography (CT) (myelo-CT) and scanning in different positions may also be very informative. DVM. extension and linear distraction and compression). C7–T1) and in the Great Dane more vertebrae can be affected (C4– T1). The Netherlands 23011744 Caudal cervical spondylomyelopathy (CCSM) causing wobbler syndrome is a condition of young dogs (1 year. In the Dobermann usually one junction is involved (C5–C6. tapered cranial cervical apertura. The neurological deficits can eventually progress to the thoracic limbs and evolve into tetraparesis and tetraparalysis. Myelography with stress views (Figure 1) demonstrates the effect of the dynamic compression: unstable vertebrae. but specifically with CCSM the dynamic component of the disease may be missed when MRI is only performed in a neutral position. end-plate sclerosis and collapsed intervertebral disc space. proprioceptive deficits. vertebral body deformation and asymmetry of the articular facets. lymphoma of the vertebral body) in a Dobermann may give exactly the same appearance of wobbler dog as CCSM. Great Dane. CCSM is usually a progressive disease that has a slow onset but neurological deficits may also progress acutely bringing the dog down. C6–C7. Stress views are essential to provide the localisation. Cervical radiography under sedation or anaesthesia of the C4–T1 region may show spondylosis. forelimb lameness and mild cervical pain. PhD. Dobermann. The clinical signs in the wobbler dog can typically be a mix of upper motor neuron disease (spinal cord) and lower motor neuron disease (compression of nerve roots that contribute to the plexus brachialis). ligament hypertrophy and disc protrusion contribute to a ventral and/or dorsal component in the spinal cord compression. The cervical instability shows the dynamic component of the disease: compression on the spinal cord worsens in extension and lessens in flexion. Wobbler syndrome (syndrome = the clinical description of a complex of signs) is characterised by posterior paresis and ataxia. DECVS Yalelaan. Meij. vertebral body malformation. Anatomical abnormalities include stenosis of the cranial apertura of the cervical vertebral canal. With the availability of magnetic resonance imaging (MRI) many clinicians have replaced myelography with MRI. Discospondylitis (infection of the intervertebral disc usually caused by Staphylococcus) or neoplasia (e. Utrecht. Rottweiler)..g. ligamentous hypertrophy of the dorsal longitudinal ligament (ventral to the spinal cord) and the ligamentum flavum (dorsal to the spinal cord) and joint capsule proliferation.

Figure 1. Neutral (A). flexion (C) views. extension (B). . Myelography in an 8-year-old Dobermann with caudal cervical spondylomyelopathy at C6–C7.

Surgical techniques that have been performed in the past include: distraction with a cylindrical cortical allograft kept in place with a plastic Lubra plate. the cervical region needs also to be stabilised but here we have a paradox: the cervical region is a highly flexible region and surgical techniques to stabilise the unstable cervical junction are prone to surgical failure. Arthrodesis of the cervical vertebrae is promoted by packing cancellous bone around the affected cervical junction.. stability or both. since the disease is progressive there may come a decision point to proceed for surgical treatment. However. the paradox between a highly flexible cervical spine and rigid implants remains. type II disc degeneration and dorsal longitudinal ligamentous hypertrophy. The dilemma in surgery has several aspects. distraction with Steinmann pins or screws and fixation with a polymethyl methacrylate (PMMA) bridge. In the case of a dynamic component. Cervical locking plates and interbody titanium cages or smart devices will probably offer a better way to treat cervical instability and promote fusion than the techniques reported in earlier days. physiotherapy (hydrotherapy or exercises for proprioception) and administration of non-steroidal anti-inflammatory drugs or corticosteroids.The Surgical Dilemma In mild cases of wobbler syndrome medical treatment is the first strategy. When spinal segments have been fixated and fused another problem arises in the so-called adjacent segment disease ('domino effect'): stabilisation of one junction may relocate the stress to the next weak link in the chain. Another dilemma is the time point in the disease process to advise surgery: in many textbooks it says that the aim of surgery is to slow down or stabilise the neurological deficits but in that view it may be the best approach to stabilise early in the disease onset. myelo-CT or MRI findings usually determine which surgical technique is chosen as the best treatment option. as interbody fusion is obstructed by metal implants or PMMA plugs. Conservative treatment consists of a chest harness for life. e. . Linear distraction of cervical vertebral bodies results in decompression at the site of the dynamic lesion and (temporary) fixation of the vertebral bodies allows fusion to take place which is promoted by cancellous or corticocancellous bone grafts harvested from the proximal humerus. Ventral decompression ('ventral slot') is indicated in static ventral compressive spinal cord lesions but these are rare in the true wobbler dog. in addition to decompression. cervical instability. This will usually lead to some clinical improvement and may slow down the progression. screw and washer technique (Figure 2) and the modified distraction-stabilisation technique using an interbody PMMA plug.g. However. The myelographic examination. bodyweight reduction when applicable. Fusion of cervical vertebrae by the surgical techniques listed is usually by ventral spondylosis. The ideal spinal fusion would be direct continuous bone bridging at the level of the vertebral bodies and techniques to stimulate this are now reported or under development. Harrington rod distraction device. Ventral distraction and stabilisation is indicated in one or multiple dynamic ventral compressive spinal cord lesion(s). The goals of surgical treatment are decompression. When a dynamic component has been diagnosed a surgical technique such as ventral decompression that only deals with static compression may not be sufficient. exercise regulation (omit exercises that worsen the ataxia from the daily pattern).

the screw and washer technique (eight out of 10 dogs) and following dorsal laminectomy in a Great Dane. Harrington rod distraction device (four dogs). dorsal (hemi)laminectomy (one dog) and screw and washer (10 dogs). ventral decompression ('ventral slot'. Dorsal decompression (e. Clinical and neurological stabilisation or improvement was seen with the Steinmann pin and PMMA technique (two of three dogs).Figure 2. e. by continuous dorsal laminectomy) is indicated in static or dynamic dorsal compressive spinal cord lesions. At Utrecht University 23 dogs (21 Dobermanns and two Great Danes) were surgically treated for CCSM. Complete surgical arthrodesis by spondylosis of the cervical vertebrae was observed with . three dogs). osteophytes around articular facets or interarcuate (flaval) ligamentous hypertrophy. Steinmann pins and PMMA bridge (three dogs).g.g.. The surgical procedures included Lubra plate and cortical graft (two dogs). Myelography in an 8-year-old Dobermann with caudal cervical spondylomyelopathy at C5–C6.. The Lubra plate and Harrington rod techniques had a high rate of surgical implant failure and the procedures were abandoned. The ventral decompression technique resulted in neurological worsening in two of three dogs. Before (A) and after screw and washer fixation (B).

The Netherlands . DVM.the screw and washer technique. DECVS Utrecht. Meij. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Björn P. PhD. However. with long-term follow up it was seen that the vertebral bodies collapsed on the washer and the screw tip touched the opposite cortex close to the spinal canal.

These data are not available for the European countries. P53 mutations and MDM2 gene amplification were observed in a subgroup of canine soft tissue sarcoma. DECVS. DACVS Professor. The annual incidence of STS in the United States is estimated to be 35/100. In general. EPIDEMIOLOGY Little is known about the pathogenetic cause of STS in dogs and cats. Extensive classification schedules are available from human literature and are simplified to fit into the companion animal situation. STS is defined as a malignant tumour of the extraskeletal connective tissues. A classification by localisation. Because soft tissues are estimated at 40% proportional body weight. retrievers seem predisposed to development of soft tissue sarcomas of the head (oral cavity/mandibular/maxillary region) with often a low grade histologic appearance but high aggressiveness. is at present unknown. The presence of foreign bodies or material (such as vaccinations) may induce chronic stimulation of the tissues and promote neoplastic transformation. however. infiltrative and locally aggressive tumours that have a variable metastatic potential. Radiation has also been associated with sarcoma formation. STS are fleshy (the Greek word 'Sapkoua' or 'sarkoma' is often translated as flesh-like mass). support or connect other anatomic structures and are present in any part of the body. foreign bodies. These tissues. For example. although sarcoma formation after extracorporal therapeutic radiation seems to be rare. is complicated by overlapping patterns of dedifferentiation or by the inability to recognize the appearance of the cell of origin. . CLASSIFICATION All soft tissues are exposed to the risk of benign or malignant tumour formation. dependent on original tumour location. grade and tumour stage seems more logical and may prove more useful at present. It is unclear if trauma causes an owner to be more aware of problems in that area or if trauma is an initiating cause in STS. In general.000 for dogs and 17/10000 for cats at risk. with an overrepresentation of the older animal. although certain breeds seem to be afflicted with tumours more commonly than others.g. however. An example of this is the parasitic infestation of Spirocerca lupi and the incidence of oesophageal cancer.Sarcomas of Soft Tissues WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. all of mesoderm origin. Utrecht University. Any classification schedule. parasites and radiation have been associated with STS in both species. most studies report medium to large breeds to be affected more commonly. and communality in diagnostic and therapeutic approach. chronic trauma. splenic hemangiosarcoma) will be discussed in the representative chapters.. Cats are afflicted less frequently (7% reported for skin and subcutaneous tissues). it is not surprising that numerous soft tissue tumours arise with regularity. Whether STS predisposition is caused by a breed-specific genetic abnormality or by a high inbreeding coefficient due to the popularity of the breeds. and variation in biological behaviour. Head Soft Tissue Surgery. Utrecht 18274255 INTRODUCTION Sarcomas of soft tissues (STS) are common in companion animals and pose a therapeutic and diagnostic challenge for the practising veterinarian. Visceral and other organ-specific STS (e. Still. familial predispositions have not been reported. Changes in genetic make-up. 2006 Jolle Kirpensteijn. surround. with ubiquitous localisation possibilities. INCIDENCE STS are common tumours and comprise from 15% (skin and subcutaneous tissues) to 35% (spleen) of all canine tumours. No sex or breed predilections have been found. Department of Clinical Sciences of Companion Animals. vaccinations. similarities in clinical presentation. STS are often grouped together because of their shared mesodermal origin. STS form an assembly of tumours of different histogenetic origin. Faculty of Veterinary Medicine. This chapter will describe the common STS in dogs and cats. Trauma was associated with the incidence of STS.

Incisional. grade and presence of local or distant metastases. Experienced pathologists may apply a different weight to the respective factors in different types of STS to assess tumour grade. this is based upon the presence of a pseudocapsule of atrophic remains of surrounding tissue and wedged tumour cells. regional lymph nodes (N). site. Muscle actin. In evaluating soft tissues. For example. Tumour staging is based on four parameters: histological grade (G). the poorer the prognosis . MRI has many advantages over CT imaging. Some peripheral nerve sheath tumours have been reported to be sensitive to the touch. this provides a solid indication for further diagnostic work-up. rate of growth of the tumour often does not predict the biologic behaviour correctly. DIAGNOSIS The diagnostic plan for STS is not essentially different from any other tumour type. Tumour grade is determined by degree of differentiation. warranting evaluation of these lymph nodes. Although many STS are not well-diagnosed by FNAB because of their limited exfoliative character. metastasis to regional lymph nodes in the limb or inguinal area. Proper imaging should be performed of more centrallylocated lymph nodes along the lymphatic tract. cellularity and matrix formation. A pulmonary CT scan is preferred above plain radiographs. For example. Chronic traumatic inflammation as cytologic diagnosis of FNAB should fit with history and site. Sufficient tissue. The higher the stage of the disease. FNAB of the regional lymph node and CT or MRI imaging techniques. however. In all other cases an incisional biopsy is preferred. The easiest method of biopsy is fine needle aspiration (FNAB). TNCB is the easiest and fastest method and requires minimal sedation. undifferentiated STS may spread to regional lymph nodes. Although haematogenous spread of STS is more common. radiographs of the chest for possible metastatic spread. Moreover. The prognostic effect of localisation of the tumour is most likely dependent on the difficulty of complete excision. desmin. Normal tissue should be incorporated in the biopsy specimen to evaluate peripheral infiltration of the tumour. Clinically. synovial cell sarcomas are often reported to spread through the lymphatics. in general. The most important factors in STS evaluation are the determination of tumour grade and tumour stage. vimentin. Additional biopsy specimens should be obtained in all cases. so additional diagnostics are necessary. there are indications that splenic metastases are not uncommon in cases with synovial cell sarcomas. excisional or thick needle core biopsy (TNCB) specimens should be obtained. Pain is associated with location. STS often are solid masses that seem well-circumscribed and encapsulated. In human sarcomas. A clinical differentiation between benign and malignant is not possible. and cytokeratins for synovial cell sarcomas specifically. Adjunctive diagnostic evaluations should include routine blood work. Tumour grade is determined through histological evaluation and varies among grade I (low grade or well differentiated) to grade III (high grade or poorly differentiated). Incisional biopsies should always be performed in such a manner that removal of the scar is possible in future radical excisions or adjunctive radiation therapy protocols. electron microscopic and biogenetic markers will improve the ease of classification in the future. Multiple core biopsies should be performed and submitted to the pathologist. peripherally-located tumours are more easily detected and often smaller than more centrally-located STS. is often better acquired by incisional or excisional biopsies. factor VIII actigen and lysozyme are suggested to be useful for the differential diagnoses of STS. should be followed by ultrasound examination of the internal iliac area. cellular pleiomorphism. The physical appearance is noticed depending on the location of the tumour and. In case of any doubt and in particular also if cytology indicates mesenchymal proliferation in absence of an inflammatory response. However. while infiltration through this pseudocapsule and through fascia leads to attachment to deeper structures. is often not available or cost-effective. however. In addition. radiographs of the local tumour site for possible underlying bone infiltration. the tumour grade has a major impact on tumour staging. many other tumour types can be excluded as well as some inflammatory processes. tumour size (T). and distant metastasis (M). in particular if infection can be demonstrated while overlying skin is intact. Factors reported to be of prognostic importance in canine STS are size. Excisional biopsies are only advantageous when adequate margins can be obtained. as well as mitotic index and amount of tumour necrosis. pressure of the tumour or tumour invasion. in cases of suspected or proven metastasis to the regional lymph node.Advances in histochemical. ultrasound of the tumour. and this method should be used as the first step in the diagnosis.

Malignant Peripheral Nerve Sheath Tumours (PNST) Malignant PNST contain a group of tumours with varying nomenclature. body of the octopus) leaves these tumour extensions (cf.. a low to moderate rate of metastasis is seen in most fibrosarcomas (the subgroup of oral cavity/mandibular/maxillary fibrosarcomas is the exception to the rule). however.GENERAL CONSIDERATIONS STS pose a problem to the veterinarian mainly because they tend to be locally aggressive. Included in this group are neurofibrosarcoma and malignant schwannoma. The most common location is the subcutaneous tissues of the distal extremities in de dog. Synovial cell sarcoma and undifferentiated sarcomas are more frequently of high grade and have a relatively high rate of metastasis. FSA. The canine. For instance. High grade tumours. but are most commonly seen in the skin and subcutaneous tissues and the oral cavity. most commonly associated with young dogs. whilst diagnostic surgical biopsies depict a low histological grade. They can occur anywhere in the body. has an aggressive biological behaviour. Low to moderate rate of metastasis is seen in (mostly low grade) hemangiopericytoma and the closely related malignant peripheral nerve sheath tumour. Most recurrences will occur within 2 years after primary tumour removal. The recent more complete pathological differentiation in subtypes. these last subtypes have a moderate rate of metastasis. It is unclear at this moment what the cell of origin is in these tumours (i. located in the oral cavity. are currently grouped under the nomenclature malignant peripheral nerve sheath tumours (PNST) instead of under FSA. such as synovial cell sarcoma and rhabdomyosarcoma have an higher incidence of lymphatic spread especially in late stages of the disease. Per definition. Invasion of these tumours into the spinal cord is not uncommon and may be seen in over half of cases of high histological grade. Similarly. i. PNST can occur anywhere in the peripheral nerve system. Complete surgical excision is often impossible because of localisation or size of the tumour. Among STS subtypes there exists considerable variation. Overall metastatic rate is estimated to be 20%. however. this appears based on a link between subtype and frequency distribution of histologic grade. and mandibular and maxillary region.e. tentacles) in the patient. the tumour homeostasis is disrupted and fast growing tumour cells thrive causing fast tumour regrowth. Recurrence is caused because STS tend to spread into deeper or surrounding tissues by invasion or extension next to natural anatomic structures. Education and communication should be directed in the future to achieve these goals of early detection and complete removal. will decrease the total number of 'pure' FSA in dogs and cats. Before surgery. Recurrence is common after incomplete resection and is the primary reason to refer STS to the Utrecht University Surgical Oncology Service. PNST located in the closer proximity to the vertebrae (including those in the region of the plexus brachialis) often will cause nerve compression and signs of pain and neurological deficit. In part. except for embryonal rhabdomyosarcoma (high rate). Rhabdo or leiomyosarcomas are relatively less common. FSA are tumours derived from the fibrocytes. 40-60%. These finger-like outgrowths of the tumour are often compared to the tentacles of an octopus. fibrocytes or Schwann cells).. is a tumour that should be mentioned specifically. HISTOLOGICAL SUBTYPES Fibrosarcoma Fibrosarcoma (FSA) was the most commonly diagnosed STS. This tumour. a diverse group of tumour types derived from fibroblast associated with nerves. neuroFSA. Feline FSA occur often on the limbs in older animals without a sex or breed predilection. PNST are locally aggressive and metastasise rarely (in less than 20% of the dogs). Cutting of the tumour mass (cf. histologically-low-grade-and-biologically-high-grade. and liposarcomas are rare. Shelling out STS is the most common cause for recurrence. FSA are relatively more common in the cat than in the dog and have a locally-aggressive behaviour. Through this. Metastasis rate is dependent on tumour grade. Early detection and diagnosis of the original STS will facilitate complete removal and prevent recurrence. Metastases spread by haematogenous routes and lymph node involvement is reported to be rare. . a CT-scan (or MRI) of the region is advised.e.

subcutis or deep-seated tissues. Dermal/subcutaneous HSA have been reported in certain breeds (Whippet. These tumours are often soft to the touch. The tumours have a soft and cystic like appearance and may coincide with peripheral oedema. There appears to be some influence of hair length and skin colour. Although often described in young animals. and more HSA of ventral smooth and hairless skin. Therefore. less subcutaneous types. Older dogs (with boxers predisposed) are affected. indicating peripheral nerve origin. are superficial tumours. with assessments of less than a 25% rate of metastasis. Biological behaviour is characterised by local infiltration and early metastasis. The majority of the cutaneous HSA. they can affect dogs and cats of all ages. Strictly dermal HSA without invasion have a fair prognosis. Multifocal manifestation of HSA is not only seen with visceral forms. but have a low (<15%) rate of metastasis. malignant tumours derived from fat cells. HSA commonly are located in body cavities and are of extreme aggressiveness (see related chapter). pointers) and may be associated with exposure to ultraviolet light. Lymph fluid may 'sweat' through the skin of affected sites. Somewhat less common. and HPC consists of 5% of all skin and subcutaneous tumours. yet are locally aggressive (infiltrative). often located in the ventral-abdominal or preputial region. Infiltrative lipomas can only be distinguished from benign lipomas if muscle invasion is present histologically. in which tumour grade is the most important predictor of behaviour. Predilection sites include abdomen. Clinically. and many will stain positive for the immunohistochemical marker S100. and associated with longer survival times (median survival 780 days) than the hypodermal (stage II) and deep muscular (stage III) located tumours. Dogs with short hair coats and lightly pigmented skin have more dermal type of HSA. are poorly defined and often occur in the ventral region of the body. Infiltrative lipoma is a form that is described in the dog and is comparable with the human well-differentiated liposarcoma. Blood Hound. tumourous blood vessels is not rare. some authors group HPC under PNST. The deep muscular HSA have a larger size. Myxosarcoma Myxosarcoma are FSA containing connective tissue cells that produce intracellular mucin. but behave similarly to other FSA. Infiltrative lipomas are often observed in the muscles of the front and hind legs. they originate of capillaries in dermis. HPC often have a slow rate of growth. respectively). though proof is lacking for this histogenetic origin. Saluki. however. do not have an anatomical predilection.Haemangiopericytoma (HPC) Haemangiopericytomas (HPC) were believed for long to stem from pericytes (cells with contractile properties surrounding small blood vessels). HPCs form a whorl-like growth pattern at histological examination without visible connection with nerves. and generally have a shorter survival (median survival 172 and 307 days. they appear more attached to the deeper structures and less encapsulated. Behaviour of extracavitary HSA depends on location and size. but also sometimes at dermal/subcutaneous sites. Lymphangiosarcomas are invasive and have a high metastatic potential . The ventral thorax and abdomen is a predilection site of the cat. Liposarcomas are observed in older animals and may be associated with foreign bodies or obesity. Haemangiosarcoma (HAS) HSA are common tumours that arise from endothelial cells of blood vessels. Biological behaviour of HPCs is similar to that of PNST. posing a major problem in the therapy. Liposarcomas are often firmer than 'normal' lipomas. Rupture of bad-quality. prepuce and hind legs. They have an infiltrative behaviour and are difficult to remove locally because of their infiltrative nature. Liposarcoma Liposarcomas are rare. Lymphangiosarcoma Lymphangiosarcoma are rare tumours of the lymph vessels. with or without knowledge by the owner of a pre-existing lump in the same area. Most HPC's are located on the extremities. including muscle or even bone. High rates of metastasis are seen with invasive lesions and with those of deeper anatomical location. Dermal (stage I) HSA are small tumours. and may lead animals to be presented with haematoma.

In these cases a more conservative surgery is planned (e. reflecting the mixed differentiation. a tumour from the striated muscle cells. respectively. spleen and liver. but can only be performed in combination with adjunctive therapy modalities such as radiotherapy. Recurrence rates of 60-70% are reported in marginally-excised. Two forms have been described: the first occurring in the urogenital tract of young dogs (mainly bladder) and is referred to as juvenile-type or botryoid rhabdomyosarcoma. Surgery Surgery is only successful if large margins of normal tissue are obtained. SCS are locally aggressive and metastasise late in the disease process. is not associated with an increased risk of metastases. the origin of the tumour cell is not clear (synovial cell versus periarticular connective tissue cell). Although most STS tend to recur within a year after surgery. . with either one being epithelial-like. as a result. Clinical signs may relate to obstruction or bleeding due to ulceration.g. limb spare). again depending on tumour grade. The recurrence rate decreases when the surgery is performed by more experienced oncologic surgeon. Local invasion of underlying bone is common in later stages of the disease and is easily recognisable on routine radiographs by punched-out bone lesions. a repeat surgery is more complicated if the STS has recurred and failure is more likely. SCS metastasise to lymph nodes. Wide surgical excision is often complicated by the anatomic localisation of the tumour to important structures. The objective local failure rate for marginal excisions (peel-out or shellingout STS) in humans is 86%. knowledge of innovative reconstruction techniques and better understanding of the pathophysiological properties of the tumour. Multiple leiomyosarcomas are possible and warrant thorough examination of the abdomen before or during the surgery. Transformation of benign leiomyomas to leiomyosarcomas has been suggested but not scientifically proven. In general. Metastasis rates of up to 50% have been reported. are unknown in dogs and cats. Histologic typing may divide those with onecell population (monophasic) from those with two-cell populations (biphasic). however. the other mesenchymal. The tumour invades the bone at the attachment of the joint capsule or tendons to the bone. Recurrence.. with or without adjunctive therapy. these rates. as of yet. The surgical goal is to completely remove the STS and. myocard and rarely other skeletal muscle locations Rhabdomyosarcomas are locally aggressive and metastasise early. lungs. It is the authors' opinion that the incidence of metastases depend more on tumour grade than on the type of surgery performed. Synovial Cell Sarcoma Synovial cell sarcoma (SCS) are tumours that arise from tenosynovial tissue and are often associated with lameness. Immunohistochemistry often demonstrates a positive signal for both cytokeratins as well as for desmin. An example of this type of surgery is the amputation of a limb. Also. however. The second form occurs in the older animal and is described affecting the tongue. tendons or bursae have been described. based on large numbers. Predilection sites are the stifle and elbow joint but other locations near joints. pharynx. Rhabdomyosarcoma Rhabdomyosarcoma. a large margin of normal tissue is sacrificed. canine haemangiopericytomas and STS. but should be interpreted with caution. Leiomyosarcomas are infiltrative tumours that metastasise late in the disease process. Paraneoplastic hypoglycaemia has been associated with leiomyosarcoma. They can occur in any part of the body. Experience often correlates to a more radical surgery. lobulated masses most commonly associated with the digestive tract from oesophagus to rectum or the urogenital tract. TREATMENT Surgery is the primary therapy of STS. The first surgery has the largest chance for complete removal. adequate follow-up of 2 to 3 years is necessary. chemotherapy and immunotherapy. Extrapolation from human data is tempting. in this tumour type. with margins of 2-3 cm normal tissue advocated. Failure rates after wide local excisions and more radical excisions (such as amputations) were 49% and 14% in humans. The owner should be made aware of the increased chance of recurrence compared to radical excision. Limb-sparing surgeries are an alternative. is relatively rare in the dog. but are described as firm.Leiomyosarcoma Malignant transformation of smooth muscle cells are the origin of leiomyosarcoma.

however. Radiation therapy is associated with acute-onset and with chronic side effects. Interleukin-2. Chemotherapy is used for palliation in macroscopic and may be of limited benefit in eliminating microscopic local or metastatic disease in STS. Photodynamic Therapy Photodynamic therapy was used after surgery in dogs with HPC and appeared to have no advantage over other forms of therapy in regards to preventing recurrence. and most dogs experienced local failure or metastatic disease. including anthracyclines (doxorubicin. Combination therapy of an anthracycline with vincristine and cyclophosphamide appear more effective in a limited series of STS. References 1. Most cats of the first group had incomplete (dirty) surgical excisions. et al. achieving identical results compared to radical excision (80-90% at 2 years). More randomised studies using large populations evaluating the effect of chemotherapy are necessary. Kirpensteijn J. The scientific data supporting the efficacy of these protocols in dogs and cats are currently missing. mitoxantrone). Complications. Radiation is more effective with minimal (microscopic) disease than with more bulky disease. A pilot study in 17 dogs showed a recurrence free percentage at two years of approximately 70%. The Netherlands . was combined with marginal surgery in a pilot study of 17 dogs with MPNST and is currently tested in a double-blind prospective study. Multidrug chemotherapy protocols. Forrest. The radiation therapy is used to treat the microscopic disease left behind after marginal excision of the tumour bulk. and limited efficacy decrease the applicability of this therapy type in dogs with STS. DECVS & ACVS Faculty of Veterinary Medicine Utrecht University Utrecht. Surgical excision and radiotherapy did not increase median tumour-free and survival times compared to complete excisions in feline FSA. however. Intraoperative radiotherapy has been described to cause STS formation in approximately 20% of dogs treated. Chemotherapy Chemotherapy can be used to treat local and systemic disease. have been advocated as the most successful. Of STS-subtypes. Immunotherapy The treatment of STS with immunotherapy is under review at Utrecht University. while fractionated radiotherapy as a sole therapy using megavoltage irradiation yields a one-year control of about 50-60%. a cytokine and immunostimulant. Radiation in combination with surgery results in increased disease free intervals. The addition of whole body hyperthermia was not associated with a better local tumour control. Radiation has also been used in combination with local or whole-body hyperthermia. (J Vet Med Intern 2000) showed a median time to recurrence after incomplete excision of STS and radiotherapy of 798 days. HPC seems relatively sensitive. Two-year recurrence free rates of approximately 30% were described. including delayed wound healing and infection. The initial results from the pilot study are encouraging. Rutteman GR. BSAVA Manual 2003 SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Jolle Kirpensteijn.Radiation Therapy Conventional techniques of radiation are rarely successful.

DrMedVet. DECVS University Veterinary Teaching Hospital Sydney. Cats with pelvic fractures should routinely undergo abdominal and thoracic radiographs and blood analysis. that is the acetabulum. the ilial body and the sacroiliac joint. ilial body fractures. and are also crucial to diagnose or rule out concurrent spinal (e. NSW. Camperdown. Cats with neurological deficits and/or extreme pain should also undergo surgery to explore for possible nerve entrapment within the fracture fragments. Pelvic fractures are classified into sacroiliac luxations.or bilateral stabilisation. Injury to the pudendal and coccygeal nerves (flaccid tail) is also common and is usually caused by concurrent sacrococcygeal fractures or luxations.. a neurological examination is performed with emphasis on the sciatic. Haematuria is common in cats with pelvic fractures. Surgical stabilisation is generally indicated in fractures that involve the weight-bearing elements of the pelvis. the pudendal and the coccygeal nerves. and other fractures. Unilateral surgery is often sufficient in cats with an intact pelvic floor because reduction and . Many patients have concurrent injuries to the thorax and abdomen. the question arises whether to perform uni. Sciatic nerve or pelvic plexus injuries occur in more than 10% of cats with pelvic fractures and are most commonly associated with sacroiliac luxations and ilial fractures. The following combinations of injuries are common: Ilial body and pelvic floor fracture Ilial body fracture and contralateral sacroiliac luxation. the degree of pelvic canal narrowing and the presence or absence of neurological deficits. Australia 19884963 Introduction Pelvic fractures account for 20-30% of feline fractures. with/without pelvic floor fracture Pelvic Fractures--When to Repair The decision for conservative or surgical treatment depends on the localisation of the fractures. Orthogonal radiographs of the pelvis are performed to identify and classify the pelvic fractures. Besides a thorough physical and orthopaedic examination. Because the pelvis is ringshaped. In cases with bilateral injury of the weight-bearing parts of the pelvis. It can be caused by injury to any part of the urinary system. with/without pelvic floor fracture Unilateral sacroiliac luxation and pelvic floor fracture Bilateral sacroiliac luxation. pelvic floor fractures and fractures of the pelvic margin. acetabular fractures. It can also be severe enough to cause anaemia. and although it is often self-limiting the patients must be monitored closely for signs that indicate urinary tract trauma that requires medical or surgical intervention.g. at least two fractures/luxations are present in most cases. sacrococcygeal) or hip joint injury.Pelvic Fractures in Cats: When and How to Repair British Small Animal Veterinary Congress 2010 Katja Voss.

Fractures of the non-weight-bearing parts of the pelvis (pelvic floor. Sacroiliac Luxations Sacroiliac luxations are most commonly repaired by insertion of a lag screw across the joint.7 mm screws and plates with adequate instrumentation is needed for surgical stabilisation of pelvic fractures. Lateral plating is associated with a relatively high incidence of screw loosening that can result in medial displacement of the caudal fragment and subsequent pelvic canal narrowing. Insertion of the screws is more difficult than with lateral plating (using a C-guide helps). Screw holding power is especially a problem in the ilial wing where the bone is very thin. which has been shown to reduce the incidence of screw loosening and the degree of pelvic canal collapse as compared to lateral plating. Stabilisation of sacroiliac luxation has also been described using positional screws inserted through a ventroabdominal approach. The ventroabdominal approach has the advantage of the surgeon being able to stabilise bilateral sacroiliac luxations via a single approach. Inserting the cranial plate screws across the sacroiliac joint or placing two plates parallel to each other are options to improve bone purchase. . They are bent slightly more concave than necessary to facilitate restoration of pelvic canal width. but guidelines have recently been published that facilitate adequate screw placement. The size of the area for safe screw insertion is very small in cats. Plates can also be placed along the dorsal rim of the ilium.stabilisation of one hemipelvis automatically results in adequate reduction of the lesion of the other hemipelvis. The sacroiliac lag screw should penetrate at least 50-60% of the width of the sacrum to prevent screw loosening. The animals should then be re-radiographed to monitor for progression of healing and for signs of pelvic canal narrowing. The approach can also be extended cranially or caudally to repair intra-abdominal injuries or concurrent fractures of the pelvic floor. ischium) are generally treated conservatively with cage rest and pain management. Pelvic canal narrowing of more than 40% is likely to result in chronic obstipation or constipation. The plates are typically positioned on to the lateral surface of the ilium. Anatomical reduction also helps to enhance fixation stability. Unilateral fractures of the ilium and sacroiliac luxations can also be treated conservatively if they are not or only minimally displaced. the ilial wing. The caudal screws are usually inserted first so the caudal fragment can be used to help lever the fracture into reduction before inserting the cranial plate screws. Ilial Fractures Plate osteosynthesis is used to stabilise most ilial fractures. Pelvic Fractures--How to Repair A selection of 1. using a dorsolateral approach.5 mm to 2. It is advantageous to have an oscillating drill mode available to reduce the risk of iatrogenic damage to nerves during drilling. Cats with bilateral injuries and concurrent fractures of the pelvic floor have instability of both hemipelvises and often require bilateral fracture/luxation repair.

These can be stabilised with two or three interfragmentary lag screws or 'skewer pins' that are placed perpendicular to the fracture and create interfragmentary compression. and using a figure-of-eight wire to create interfragmentary compression. and iatrogenic nerve injury. Gentle manual expression of the bladder or placement of an indwelling urinary catheter and/or application of enemas may be required to avoid urinary and faecal retention in patients that are not ambulatory in the immediate postoperative period. whereas longer plates are required for oblique and multifragmentary fractures. This counteracts the tendency of the caudal fragment to rotate distally. and a figure-ofeight wire that is placed around the free ends of the pin and is tightened laterally. but residual lameness is observed in up to 30% of cats with sacroiliac luxation repaired with a lateral lag screw. Long oblique fractures of the ilium are common in cats. Postoperative Treatment and Prognosis Postoperative treatment consists of adequate pain management and cage confinement for 2-4 weeks that is followed by restriction of activity for another 3-6 weeks. In kittens younger than 12 weeks of age.but the longer screws purchase more bone. NSW. Plate osteosynthesis is the most widely applied stabilisation method. Acetabular physeal fractures are occasionally seen in kittens. Prognosis after acetabular fractures depends on fracture type and ability to restore the hip joint during surgery. A 'skewer pin' consists of a K-wire driven across the fracture. These can be repaired using a screw and tension band technique that involves placing one screw cranial and caudal to the fracture. Screws placed at the level of the acetabulum are aimed medially to exit the medial cortex of the pelvis. Katja Voss. The decision to perform a femoral head and neck excision is sometimes only made intraoperatively. Avascular necrosis of the skin around the back and tail sometimes develops due to skin avulsion at the original trauma. Although cats can have an acceptable limb function after femoral head and neck excision. The prognosis is good to excellent in cats with ilial fractures. Australia . Acetabular Fractures Acetabular fractures must be reduced and stabilised surgically to avoid development of severe coxarthritis and chronic pain. pelvic canal narrowing with subsequent obstipation. An approach to the hip joint using a trochanteric osteotomy gives the best exposure of the acetabulum. Dorsal plating is also a very good technique for long oblique fractures. Complications after pelvic fracture surgery include implant loosening. The prognosis is good for kittens older than 16 weeks. this technique is a salvage procedure and should only be used for non-reconstructable fractures. there is a possibility of premature fusion of the acetabular bones resulting in abnormal hip development. DrMedVet. Short plates with a minimum of two screws cranial and caudal to the fracture can be used in simple transverse fractures. Perfect plate contouring is necessary to obtain anatomical reduction. DECVS University Veterinary Teaching Hospital Sydney Camperdown.

The localisation rather than the disease process is most responsible for the presenting clinical signs. CVN. This type of disc herniation is more commonly reported in nonchondrodystrophic dogs. Republic of Ireland 23011648 Intervertebral Disc Disease Intervertebral disc disease (IVDD) in the dog is the most common neurological disorder requiring nursing care. This type of disc herniation is more commonly reported in chondrodystrophic dogs. Dachshund. The nucleus pulposus has a gel-like consistency and its function is to absorb shock and dissipate forces evenly over the IVD structure. Beagle. The clinical presentation of an animal with IVDD varies with the site of the lesion. Dublin. the changes the compression produces within the spinal cord (intramedullary changes secondary to hypoxia). paresis or paralysis. the more compression the worse the clinical signs). Dogs with a Hansen type II herniation/protrusion are affected by a slow degenerative process of the annulus fibrosus. DAVN (Small Animal). leading to degeneration and mineralisation of the nucleus pulposus. loss of deep pain sensation. leads to spinal cord compression. The nucleus has a decreased ability to absorb shock and once the annulus fibrosus of the intervertebral disc ruptures.. .. Patients with IVDD can present with pain. RVN. The annulus fibrosus hypertrophies and bulges into the vertebral canal and. the mechanical displacement of the spinal cord (i. Belfield. over time.Neurological Conditions: Case Studies WSAVA/FECAVA/BSAVA World Congress 2012 Gillian Calvo. It occurs most frequently in the chondrodystrophoid dogs (e. A1 DipHE. Compression of the spinal cord in disc disease is caused by either a disc extrusion or a disc protrusion (Figures 1–3). Basset Hound. Pekingese. University College Dublin.g. Cocker Spaniel) but also affects the nonchondrodystrophoid breeds. Dogs with a Hansen type I herniation/extrusion show premature ageing of the nucleus pulposus. the nucleus pulposus extrudes ('explodes') into the spinal canal causing compression of the spinal cord. urinary and occasionally faecal incontinence. the onset of the problem and associated with this the dynamic force of the compression (acute speedy disc herniations usually cause more clinical signs compared to a gradual slow compression). the mechanical displacement of the spinal cord and the duration of clinical signs. ataxia.e. A normal intervertebral disc (IVD) consists of a nucleus pulposus in the middle surrounded by the annulus fibrosus. French Bulldog. Cert Canine Hydrotherapy University Veterinary Hospital.

Disc extrusion (Hansen type I). Figure 2. .Figure 1. Normal disc.

Patients with cervical disc disease can present with varying degrees of neurological deficits and functional abilities. Disc protrusion (Hansen type II). Cervical Disc Disease Cervical disc disease is a common condition in chondrodystrophic breeds with Hansen type I disc extrusion and nonchondrodystrophic breeds with Hansen type II disc protrusions. more severe in acute versus chronic presentation Low head carriage. Clinical presentation: Neck pain. reduced movement of the head Pain on palpation of the spine and neck muscles Reluctance to eat due to pain when lowering head to the bowl Potentially kyphosis (hunched back) .Figure 3.

Neurological deficits: All four limbs are affected. Exception: monoparesis or lameness of only one thoracic limb due to compression of the nerve root (nerve root signature) Ataxia.B. Surgical decompression of cervical disc disease is commonly achieved with a ventral slot technique (Figure 4: disc herniation causes ventral compression of the spinal cord at C6–7. or tetraplegia (no voluntary movement) Symmetrical or asymmetrical +/. Figure 4. It is uncommon to have reduced / absent deep pain sensation in cervical disc disease. Figure 5: ventral slot at C5–6). .Proprioceptive deficits in all limbs Upper motor neuron (UMN) bladder Potential respiratory deficits in tetraplegic patients N. ambulatory or nonambulatory tetraparesis (voluntary movement present). C6–7 cervical disc extrusion.

. Surgical decompression of thoracolumbar disc disease is usually achieved with a hemilaminectomy technique (Figure 6: L1–2 disc extrusion. The area of the spinal cord commonly affected by thoracolumbar disc disease is T11 to L2 vertebrae. C5–6 ventral slot. Figure 7: L1–2 left-sided hemilaminectomy). Type I disc extrusions are most frequently seen. Thoracolumbar Disc Disease Thoracolumbar disc disease is a common condition in chondrodystrophic breeds but also occurs in nonchondrodystrophic breeds.Figure 5.

Clinical presentation of patient: Pain on palpation of the thoracolumbar spine Kyphosis Reluctance to exercise / run or jump Reluctance to be lifted and occasional associated pain .Figure 6. L1–2 disc extrusion. Figure 7. L1–2 left-sided hemilaminectomy.

voluntary urination is lost when the patient loses the ability to ambulate Loss of deep pain perception in the pelvic limbs and tail with severe spinal cord lesions N.Neurological deficits: Ataxia/paraparesis of pelvic limbs or paraplegia of pelvic limbs (in most severe cases) Symmetrical or asymmetrical (one pelvic limb is more affected) Proprioceptive deficits in the pelvic limbs Upper motor neuron (UMN) bladder: as a general rule. Lumbosacral Disc Disease Lumbosacral disc disease is most commonly seen in mature large breed dogs caused by a Hansen type II disc protrusion. Surgical decompression of lumbosacral disc disease is usually achieved with a dorsal laminectomy technique (the dorsal spinous process and the dorsal roof of the spine is removed). especially difficulty jumping into the car +/.B. The thoracic limbs are not affected by thoracolumbar disc disease and therefore should remain neurologically intact. patients are usually ambulatory Tail paralysis in most severe cases Symmetrical +/.Proprioceptive deficits in the pelvic limbs .Urinary and faecal incontinence Neurological deficits: Weakness of pelvic limbs (paraparesis) and tail with a crouched gait. Clinical presentation of patient: Pain on palpation of the lumbosacral spine Crouched gait Low tail carriage Reluctance to exercise/run or jump.

g..B.Lower motor neuron (LMN) bladder N. Nursing the Patient Mattress and padded. Assess/monitor the patient for: Pain: pain score at least once daily Urine abnormalities: colour. odour Decubital ulcer formation Progress in physiotherapy (deterioration in limb/ bladder function?) Respiratory compromise (especially in patients with cervical disease). Loss of superficial sensation (e. i. chewing limbs or penis) and/or deterioration in deep pain perception or complete loss. Bladder management (patientdependent choice of bladder management): Monitoring and expression of bladder every 4–6 hours (UMN bladder!) Intermittent catheterisation of bladder every 4–6 hours Indwelling urinary catheter drainage every 4 hours and clean with Hibitane twice daily if in situ If a UTI (urinary tract infection) develops. acrylic bedding (Vetbed) in recumbent/partially recumbent patients. . absorbable bedding that draws urine away from the patient.e. Subtle changes are often picked up by the veterinary nurse during nursing and are part of the overall assessment of the patient. The thoracic limbs are not affected by lumbosacral disc disease and therefore should remain neurologically intact. Conservative treatment requires close monitoring to recognise changes in the neurological signs. antibiosis should be based on urine culture results via cystocentesis.. Increased respiratory noise is an indication of lung disease especially in recumbent patients. Nursing Care for Post-Surgical Disc Disease Patients Surgical treatment may alter those deficits and functional abilities and a repeat of the original neurological examination is performed postoperatively once the patient has recovered from the anaesthetic and has received suitable analgesia.

and a treatment plan is established. increase circulation..9% solution if pneumonia is suspected or diagnosed.g. If recommended by the veterinary surgeon. Often a combination of multiple techniques is applied. If assistance with walking is required use a hoist. The benefit of physiotherapy is to reduce pain especially with regard to muscle spasms.. The first step in the physiotherapy process is to identify whether physiotherapy is indicated in the presented patient. Physiotherapy begins as soon as possible after surgery. Cold Therapy (Cryotherapy) Acute stages of inflammation e.Nebulisation and coupage every 4 hours with sodium chloride 0.g. Tetraparetic patients: use of harness or leads looped between the front legs instead of leads around the neck (surgery in the ventral neck area!). Where possible. The selection of the appropriate treatment method for the individual patient is based on the diagnosis and the initial assessment. proprioceptive reeducation (body's awareness of movement and where the various parts of the body (e. Rehabilitation and Physiotherapy Rehabilitation is the process of restoring the maximum function. After 24–48 hours or when the veterinary surgeon feels the patient is stable enough. Paraparetic patients: if assistance with walking is required use a pelvic harness or sling as required. encourage lymphatic drainage and increase nerve conductivity. independence and quality of life following illness or injury. post-surgery or trauma . the paw) are located in relation to each other (spatial orientation)) and coordination and balance exercises can commence. or a harness for the thoracic and pelvic limbs or a sling. take the dog out 3–4 times a day. Initial assessment includes a history and a thorough examination of the musculoskeletal system to identify any problems the patient may have. Tetraparetic recumbent patient: turn every 4 hours if unable to turn completely unaided. objective outcome measures are used to monitor progress. use protective boots to avoid scuffing of nails and toes. Based on these findings treatment goals (short-term and long-term) are determined taking into account the abilities of the patient and the expectations of the owners. Suitable analgesia is required for effective physiotherapy to take place. Physiotherapy Treatments A wide variety of techniques and modalities are available. including muscle strengthening and active assisted exercises.

Commercial heat packs are available which regulate and maintain temperature for the duration of treatment improving effectiveness. vasodilation. This technique is advisable and particularly beneficial over the dorsal neck and shoulder musculature following cervical decompressive surgery. Heat Therapy (Thermotherapy) Used once the acute phase is over (> 72 hours) Hot packs are applied for 15–20 minutes every 3–4 hours Can be easily made by filling disposable gloves with hot water. Massage Massage has multiple beneficial effects for the patient: Pain relief (removal of noxious chemicals and release of endogenous endorphins) Increase in circulation (aids healing due to increasing oxygen supply to tissue. Cold therapy is most effective during the acute phase of inflammation and provides analgesia. increases cellular metabolism and aids in connective tissue mobility prior to exercise. This technique is beneficial prior to massage on muscles in spasm as it encourages relaxation and ultimately pain relief. reduces blood flow (vasoconstriction) and controls bleeding and reduces muscle spasms. increase in venous and lymphatic return) Mobilisation of adhesions and tissues (using friction and effleurage) Improving proprioceptive awareness due to manual stimulation of the body Preparation of muscle for exercise and reduction of muscle fatigue following exercise Reduction of tension and anxiety Improves the bond between the patient and the therapist (or the owner) .Apply cold packs on the incision or trauma site for 15–20 minutes every 4–6 hours (up to every 2 hours in severe injuries) the first 24–48 (or 72 hours) hours after surgery Cover ice packs with a damp towel and never apply ice directly to skin to avoid intolerance and ice burns. Always check the temperature on yourself before applying to the patient. reduces inflammation and oedema formation.

the therapist provides the force to move the joints Active. enhance function. trampolines. reduce the risk of injury. ball-playing. Balance is the ability to adjust the equilibrium either when standing or during movement. optimise overall health and enhance fitness and wellbeing. ligaments. articular cartilage and blood vessels ROM exercises are beneficial to maintain joint flexibility and joint homeostasis Therapeutic Exercise Exercises represent the final element in achieving maximum recovery. dancing and standing on the physioball. postures or activities intended to prevent long-term physical impairment. Proprioception is the sense that indicates whether the body is moving and also where the various parts of the body are located in space and in relation to each other (spatial orientation). strength exercise to increase the muscle mass only accompanies the rehabilitation plan rather than being a main focus in the recovery. recovery of balance and proprioception is most important in the rehabilitation.It also allows you to assess for any muscle pain and atrophy. muscles. balance pads. Range of Motion Movement of a joint through the maximum motion possible Passive. Dogs with . whereby the patient provides the force to move the joint themselves Passive range of motion (ROM) includes moving the joint into flexion to the first point of resistance. changes of direction when running. General exercise include exercises that require response to changes in the surface such as wobble boards. joint capsule plus fluid. infection. tendons. open wounds or areas of malignancy. i. Sufficient strength needs to be built up for the neurological patient to perform exercises focusing on balance and proprioception. However. Proprioception is very well developed in sporting and working dogs due to the increased demand. In all dogs with neurological dysfunction or proprioceptive deficits resulting in joint injury or surgery. detect tissue sores or decubital ulcers Massage should not be performed over areas of acute inflammation. Therapeutic exercise is the systematic performance or execution of planned physical movements. then similarly into extension and this is repeated in a rhythmic manner 15–20 times holding each stretch for 10 seconds to enable surrounding soft tissues to adapt/stretch in response Using a cycling motion in the limbs simulates normal gait pattern Moving a joint through its full ROM involves the nerves..e. The sense of proprioception decreases with age and is often impaired especially after injury to the nervous system.

It is not advisable to use this method with patients who are unable to bear their own weight as inadequate support of the spine occurs due to abdominal pressure causing flexion of the lumbar spine. Swimming is also used to build up muscle strength with the buoyancy support of the water. post ventral slot) requiring support on all four limbs can be walked with the aid of a hoist for maximum support (Figure 10) or an 'A' frame for less support (Figure 11). Depending on the ability of the patient. . Care must be taken in hemilaminectomy patients that the pelvic sling does not cause skin trauma or put pressure on male genitalia especially the testes. Figure 8. Building up flexibility and endurance (stamina) is usually not part of the initial or medium-term rehabilitation plan for neurological patients but is in orthopaedic patients. Assisted Exercise The patient is unable to perform any movement and thus requires an external force to perform passive movement. These stages range from 'assisted' exercise to 'active-assisted' exercise to 'free-active' exercise and finally 'resistance' exercise.g. Active-Assisted Exercise Active-assisted exercises are used with patients who have some control over their body and limb function but require reeducation in proprioception and gait. Patients with cervical disease (e.weakness require support using harnesses or physioballs to stand or walk. Pelvic harness. the patient moves through different stages of the therapeutic exercise as coordination and strength improves. Assisted walking using a pelvic harness (Figure 8) for patients after a hemilaminectomy. This includes ROM exercises. Abdominal support slings (Figure 9) can be used in patients who require minimum help on the hindlimbs.. or a hoist after a ventral slot can provide sufficient assistance for the patient to go for walks.

. Figure 10. Mechanical hoist. Abdominal support sling.Figure 9.

Figure 11. strengthening and proprioception exercises against gravity and bodyweight can be initiated: . 'A' frame. Free-Active Exercise Once patients are weightbearing and have sufficient coordination.

Sit to stand exercise Downward pelvic pressure Alternate limb lifting Corner tapping/hip swaying Trotting poles (Figure 12) / Cavaletti poles (Figure 13) A wobble board (Figures 14 and 15) can be used for proprioception training. Trotting poles. Figure 12. Figure 13. This exercise should be done once the animal is reasonably strong and just needs 'fine tuning'. . Cavaletti poles. coordination and balance.

Wobble board. Figure 15.Figure 14. . Wobble board.

e. Figure 16. using additional weights in the free exercise is implemented. limb strength and coordination. distal limb weights or sledge pulling. The resistance of water means 'treading' water for the patient is more difficult than if treadmill therapy is used dry (Figure 16). Interval training is generally performed with short timed sessions on the treadmill with or without water. This can be achieved by using a rucksack with weights. The use of water also helps to support the patient during the treatment.g. Hydrotherapy has been shown to help relieve muscular pain and especially muscle spasm due to its moderately warm water temperature (28°C) however a thermal spa would be more beneficial in achieving muscular relaxation (35°C). The buoyancy of the water helps to support the patient's bodyweight and relieves pressure on the joints. balance and coordination.Resistance Exercise This exercise goes a step further than the free-active exercise as additional resistance.. Underwater Treadmill Active walking can be encouraged to improve limb strength. Hydrotherapy Hydrotherapy can be used to improve general cardiovascular fitness. . Underwater treadmill.

Gillian Calvo. Department of Companion Animal Clinical Sciences Oslo. Dublin. DAVN(Small Animal). DVM. DECVO Norwegian School of Veterinary Science. CVN. Cert Canine Hydrotherapy University Veterinary Hospital University College Dublin Belfield. DHE. RVN. 2004 Ellen Bjerk s. Republic of Ireland Ocular Examination WORLD SMALL ANIMAL VETERINARY ASSOCIATION WORLD CONGRESS PROCEEDINGS. Norway 18281027 Examination of the eye includes History General examination Inspection Control of vision Examination of outer structures Schirmer tear test . PhD. A1.

can be placed on the cornea after topical anaesthesia. the microscope providing . heterochromia. and also in connection with the inherited disease Collie Eye Anomaly. and obstacle course under different light conditions. in dogs vision is obscured by the sclera. a gonioscopy lens. The pupil is round in dogs and large felines. The pupil will stay apparently dilated. The most commonly used gonioscopy lenses are the Barkan lo-vac and the Koeppe lens. Directing the light from an angle allows localization of the opacities.Fluorescein staining Tonometry Examination of deeper structures Electrophysiology Imaging Vision should be assessed before pupil dilation through menace response. The most common congenital malformation is persistent pupillary membranes. Iris in the two eyes may be of different colors. The iris contains small irregular folds. Iris cysts may be present in the anterior chamber. The optimal instrument for examination of the lens. Especially in the cat. The cysts can be differentiated from tumours by their round and often transparent appearance. Haemorrhage in the anterior chamber may be seen in connection with tumours and inflammations. often dependent on coat color. This is seen as holes in the iris. Pigmentation of the iris varies. and the iris should be clearly visible. is a slit-lamp biomicroscope. Inspection of the iridocorneal angle may be indicated as part of a breeding program in certain breeds. Normally the iris rests on the anterior lens capsule. more rarely iris colobomas. In cats the angle is easily visible. Gonioscopy findings of the two eyes are similar in almost all normotensive dogs. Repeated application may be indicated in some dogs. and the width of the angle as well as the appearance of the pectinate ligament is noted. Lens Initial examination is performed by directing light into the eye to allow the reflex from the fundus (retroillumination). biconvex in the cat. Larger exudates of leucocytes and fibrin may form sterile aggregates (hypopyon) with or without red blood cells present. THE ANTERIOR CHAMBER AND IRIS The anterior chamber should only contain clear fluid. This instrument consists of two parts. This lecture is restricted to examination of intraocular structures. in bleeding disorders. Uveitis with increased cell content of the aqueous humour may cause opacity of the fluid. Subluxation or luxation of the lens causes a deepening of the anterior chamber and also a characteristic shivering of the lens when the eye moves (iridodonesis). If uveitis is present. the effect of Tropicamide may be poor in the affected eye. falling cotton ball. Especially in older dogs of small breeds. which may cause some discomfort in bright weather. Gonioscopy is also indicated when an intraocular tumor is present and as a means of differentiation between primary and secondary glaucoma in breeds predisposed to primary glaucomas. however. GONIOSCOPY Many dog breeds are predisposed to glaucoma. The whole iridocorneal angle should be examined. the iris may be more or less atrophied. pupillary light reflexes. EXAMINATION OF THE POSTERIOR SEGMENTS Pupil dilatation The most common medication for diagnostic use is Tropicamide. Opacities may be seen as darker areas through the pupil. immune complexes may sometimes be seen ventrally on the inside of the cornea as small brownish spots. In mild cases the aqueous look dusty (Tyndall effect). or major parts of the iris may be lacking. An extra curved lens. One drop is applied in the eye and in a normal eye maximum dilation is achieved after approximately 20 minutes.

the surface with the steeper curvature should face the examiner. most indirect ophthalmoscopy lenses are aspheric with two different curved surfaces. Binocular vision also facilitates localisation of opacities within the lens. The optic disc is situated at the horizontal midline in the lower part of the tapetum. which can be directed into the eye at different angles and with a slit-formed light beam. Normal easily distinguished variations include the suture lines of the lens. To prevent image distortion. distribution of blood vessels and myelination of the optic disc. and the examiner tries to neutralise the movements of light across the animal's fundus by adding lenses of varying strength in front of the animal's eye. but orientation is more difficult than with the indirect one. a stronger lens provides a wider field of view. Non-tapetal fundus is mostly darkly pigmented. Thus. and retinoscopy may be indicated in some behavioural problems. pigmented dots representing remnants of the pupillary membrane are not infrequently observed. On the posterior lens capsule occasional small dots representing remnants of the tunica vasculosa lentis may be seen. The panoptic direct ophthalmoscope may represent a better tool than the traditional one. The degree of myelination around the nerve fibres decides the size and shape of the optic disc. Given lenses of equal power. This is termed tigroid fundus. Given equal lens diameters. size of tapetum. direct and indirect. brighter vessels from the underlying choroid can be seen extending radially towards the periphery. or a modified indirect ophthalmoscope with the use of as focal light source and a lens. and on the anterior lens capsule small. The retinoscope is held with one hand at a fixed distance from the animal's eye. the tapetum is present in the cat. In direct ophthalmoscopy the effective field of vision is determined by the illuminating system. and the light source. A central cupping of the disc is often present. . In indirect ophthalmoscopy the field of view is determined by the ratio of lens diameter and focal length. In miniature breeds the tapetum can be limited to a minor area above the optic disc. This is often seen in eyes with a blue iris ("wall eye" or "china eye"). Most direct ophthalmoscopes project a beam of light about one disc diameter. the direct ophthalmoscope is a good tool for close examination of details. Examination of the retina includes description of the optic disc. a larger lens provides a wider field of view. Only small reflective islets of tapetal tissue may be seen in some dogs. The color of the tapetum in dogs older than 12 weeks varies from yellow to bluish-green. tapetum and nontapetum. monocular indirect ophthalmoscope as a hand-held indirect ophthalmoscope. Albinotic fundus is tigroid fundus also lacking choroidal pigmentation. There are substantial normal variations in fundus color. Retinoscopy Retinoscopy is performed to evaluate the animal's refractive status. retinal vessels. 3-5 retinal veins from the periphery of the retina merge to form a vessel ring on the optic disc. Normally. If the retina is poorly pigmented. Except from some white animals. for instance in examining the optic disc. In puppies less than 8-12 weeks old the differentiation of the retinal layers are not yet complete. The visual field is restricted. The tapetum is a triangular reflective layer situated in the dorsal half of the fundus. or may even be totally absent. where the light source sits on a headband. A streak retinoscope represents a practical.10-20 x enlargements enables visualisation of small structures. Cat discs are poorly myelinated and appear smaller than in the dog. About 20 small arterioles extend radially from around the disc. Options for indirect ophthalmoscopy include the binocular indirect ophthalmoscope. Familiar myopia has been described in some dog breeds. although not very sophisticated tool for veterinary ophthalmology. nuclear rings and small remnants of the hyaloid artery. the degree of pigmentation varying according to coat and iris color. and it is difficult to examine the peripheral retina. if the animal is nearsighted or far-sighted. that is. Ophthalmoscopy There are two principles for ophthalmoscopy. and using a direct ophthalmoscope may be compared to peeping through a keyhole: You get a detailed view within a small field of vision. and the whole fundus appears blue with no visible tapetum. but must be distinguished from pathologic changes (colobomas).

This Nurse Masterclass Series will cover the management of the neurosurgical patient. the arterial phase. After pupil dilation a contact electrode is placed on the retina and a reference electrode as well as a ground electrode on the head. as in cataracts. ERG can be used to establish an early diagnosis of photoreceptor disease. the arteriovenous phase. and after light adaptation. both regarding anesthesia. PhD. One common mistake is to use too small amount of fixation fluid. representing either a filling defect or a masking effect. Histology For histology the eye should be taken out as soon as possible after death. Meij. the capillary phase and the venous phase. Preference for fixation fluid may vary. Changes can present as either hypofluorescence. Fluorescein angiography is a dynamic method to explore the fundus vasculature and tissues. There are many types of ERG equipment available. Radiography. removing as much extraocular tissue as possible before fixation. basic aspects on advanced imaging techniques for the neurosurgical patient. but may be more indicated in central neuro-ophthalmic disease affecting vision. MRI (magnetic resonance imaging) and CT (computer tomography) are also routinely used. The following stages are recorded: The choroidal phase.Electroretinography Electroretinography (ERG) registers the response from the retina to light stimuli. The retina is stimulated with light of different wavelengths before. aw well as other intraocular conditions. DECVS Yalelaan. The Netherlands 23011846 Introduction Canine and feline neurosurgical patients are challenging. the amount should be about 10 x the size of the eye. Norway Management of the Neurosurgical Patient WSAVA/FECAVA/BSAVA World Congress 2012 Björn P. or in changes in periocular structures. preparation of the dog and . dark adaptation and recording. then less frequently during the following 3-5 minutes. Ellen Bjerk s. DECVO Norwegian School of Veterinary Science Department of Companion Animal Clinical Sciences Oslo. DVM. fundus photography as well as fluorescein angiography represent useful tools. or hyperfluorescence representing leakage of dye from vessels. Utrecht. The important factor is to standardise examination methods. Ultrasound and other imaging techniques Ultrasound is indicated to record space-occupying lesions and retinal detachment. one should discuss with the pathologist who performs the examination of the eye what to use. It should be carefully dissected. Items that will be covered are assessment of neurological deficits. neovascularisation or a "window effect" where the choroidal vasculature is seen through the retinal pigment epithelium. For recording or diagnosis of retinal disease. The animal should be anesthetised for the procedure. DVM. to distinguish blindness caused by photoreceptor disease from blindness from other causes and also to evaluate the function of the retina where it cannot be visualised. PhD. both for the nurse technician and for the veterinary neurosurgeon. during and after dark-adaptation. especially in cases where the fundus cannot be visualized. Serial photographs are taken the first 20 seconds after intravenous injection of a 10% fluorescein sodium solution.

Grading of neurological deficits is based on postural reactions (proprioception = positional stance in space). decreased proprioception. Neurological Examination The neurological examination (and not imaging!) is the only examination that can give functional information on the spinal cord in a paretic or paralysed dog. spinal trauma. The Masterclass is aimed at the experienced nurse technician with advanced skills and a learning ambition that goes beyond the standard surgeries. caudal cervical spondylomyelopathy ('wobbler syndrome'). spinal tumours. ambulatory (able to walk from A to B) Grade 3 = severe paresis. By following this Masterclass the nurse technician will gain new knowledge in the field of the management of the neurosurgical patient which will allow him/her to contribute significantly in the surgical success of these patients. special considerations during neurosurgery and the short-term postoperative neuro-care which will be the primary responsibility of the nurse technician. voluntary motor function (standing and walking from A to B) and conscious nociception (= pain recognition by the brain). This is especially the case for dogs with intervertebral disc disease (IVDD) that are presented with paresis (reduced voluntary movements) or paralysis of the pelvic limbs (respectively paraparesis and paraparalysis). both pre. Neurological grading: Grade 0 = normal Grade 1 = spinal pain. degenerative lumbosacral stenosis ('cauda equina syndrome'). The Masterclass will cover a variety of neurological disorders that require neurosurgical intervention such as: intervertebral disc (IVD) degeneration and herniation. The veterinarian will usually do a neurological grading of the neurosurgical patient. no neurological deficits Grade 2 = paresis. neurosurgical instrumentation. no proprioception. The nurse technician plays an essential role in the management of the neurosurgical patient. surgical brain tumours including pituitary adenomas and surgery of the peripheral nerves.and for neurosurgery. non-ambulatory (able to stand but not able to walk from A to B) . rehabilitation and physiotherapy of the patient. In case of neurological deficits of all four limbs this is called tetraparesis or tetraparalysis/tetraplegia. But the nurse technician may also be involved in the long-term postoperative care.

When the patient has been stabilised and the organs have been taken care of. it is essential to support the spine. In general. The first line of treatment is directed at the life-threatening diseases and not at the spinal fracture. will lead to low-quality radiographs and may pose a greater risk of dislocation of vertebrae. nurse technicians should be able to learn to grade patients using this grading system which will help the veterinary surgeon in the diagnostic work-up and decision tree when to wait. onset of disease. although many other factors. such as breed. anaesthesia is mandatory when imaging spinal fractures. and especially grades 4 and 5 necessitate diagnostic work-up and immediate treatment to prevent further damage to the spinal cord. The pitfalls are omitting to examine these patients for other ailments and failing to do a proper neurological examination the first time the animal enters the clinic. contusion of the heart). bladder rupture). imaging should be performed as soon as possible. and the staff should transfer the cushion (with dog) from table to . In the end. conscious nociception absent With some practice.. There are usually other trauma than the traumatised spine and these patients may have thoracic trauma (pneumothorax. non-ambulatory (not able to stand and not able to walk from A to B). no proprioception. However. sedation or anaesthesia will take away muscle tone and therefore may contribute to spinal instability. no bladder function. which may worsen and even transect the spinal cord. with a vacuum support cushion or a stretcher with braces). conscious nociception present Grade 5 = paralysis. decreased bladder function. In case of grade 5. diaphragmatic herniation. The grading may be hampered by the inability to examine the animal due to pain. The pain should be dealt with immediately with intravenous analgesics and the patient should be immobilised as well as possible (e. abdominal trauma (haemoabdomen. Grading should be documented and dated in the medical records. Extreme caution should be taken when giving these patients muscle relaxants since the muscle tone around the spine may be the last stabilising factor in fractures of multiple vertebral compartments.g. On the other hand. aetiology. duration of deficits. shock. the prognosis is extremely poor for functional recovery when conscious nociception is absent for a period longer than 48–72 hours. bodyweight and the owner's motivation will influence the final prognosis. no proprioception. Also the grading will help to follow the success of treatment over time. non-ambulatory (not able to stand and not able to walk from A to B). when to treat or when to refer. preferably in a vacuum cushion. However. The Spinal Trauma Patient The spinal trauma patient may have other organ failures besides an unstable spine and should be approached with the greatest care and special considerations. Grading can also be used for the prognosis: in general the prognosis will worsen with increasing grade. grades 1 and 2 can be treated conservatively (with medication) whereas grades 3. Dogs with spinal fractures are usually extremely painful (when not completely paralysed) and are usually brought in on stretchers. when animals are handled without care. hypovolaemia or other limb fractures. as it provides analgesia and allows the production of high-quality radiographs.Grade 4 = paralysis. this presents another dilemma: imaging of the awake patient is usually not possible due to the pain.

Contrast radiography includes myelography and epidurography.g. Radiography of the spine is best performed under sedation to produce highquality radiographs. the contrast agent may leak into the brain and cause convulsions when the dog wakes up from anaesthesia. MRI is able to visualise oedema of spinal cord parenchyma and is diagnostic for spinal cord infarction or fibrocartilaginous thromboembolic myelopathy (FCE). In contrast to CT. caudal cervical spondylomyelopathy (wobbler disease). discospondylitis. e. and a contrast agent e.g. the result of an acute type 1 extrusion of nucleus pulposus in chondrodystrophic dogs (e. This may be prevented by elevating the head after contrast injection. Flexion/extension. These imaging techniques are a neurosurgeon's delight! CT is a radiographic technique producing transverse slices of the spine or skull. French Bulldog) that severely damages the spinal cord and starts a . degenerative lumbosacral stenosis. T2.. Indications for MRI are IVDD. The developments in veterinary neurosurgery have been advanced by imaging techniques such as computed tomography (CT) and/or magnetic resonance imaging (MRI). and a radioreceiver that receives radio-signals. spinal cord tumour and pituitary and brain tumours. Myelography is performed under anaesthesia and the contrast agent is injected in the subarachnoid space around the spinal cord between the skull and C1. radio-transmitter that excites the protons.table and not the dog itself.. Pituitary tumours are enhanced by a contrast agent because the pituitary gland is outside the blood-brain barrier. wobbler disease). e. Imaging of the Neurosurgical Patient Radiography and contrast radiography are still considered valuable diagnostic techniques to diagnose conditions that require neurosurgery. traction and axial compression views of the cervical region are indicated for confirmation of the diagnosis CCSM. Myelography may show extradural compression by a spaceoccupying lesion (like a herniated disc). Indications for CT are spinal fractures. T1. Brain tumours are enhanced by a contrast agent because of damage to or loss of the blood-brain barrier by the tumour. gadolinium). Oblique views when aiming for optimal ventrodorsal or lateral views make precise radiographic interpretation of the spine very difficult due to overlapping bony structures. IVDD. all staff should be informed that the patient has a spinal fracture so accidental traction on the spine in different directions will not occur.g. degenerative lumbosacral stenosis (cauda equina disease). Also. discospondylitis. MRI is a technique that depends on the magnetic dipole of the hydrogen proton. in case of caudal cervical spondylomyelopathy (CCSM. Myelography is able to image the dynamic nature of a disc herniation. or between L4 and L5 or L5 andL6. Also..g. relaxation times. Especially with cervical myelography.. MRI involves: A hardware component (magnetic field. The software component that generates pulse sequences (timing diagram) through mathematical calculations (Fourier transformation) on the radio-signals. The contrast agent (magnetisation or spin density of tissue. spinal cord tumour and pituitary and brain tumours. skull fractures.

T13–L1. in addition. L1–2. potassium). T12–13. As soon as they are awake the first neurological examination is done to assess brain function. L2–3) disc disease in chondrodystrophic dogs (e. C3–4. In cats with acromegaly (the pituitary tumour produces excess growth hormone (GH)) that are undergoing pituitary surgery the same considerations are taken into account as for dogs with Cushing's disease but. is visible on T2-weighted MRI as a hyperintense signal in the spinal cord parenchyma. Therefore continuous monitoring of glucose levels is imperative in the postoperative phase and short-acting insulin medications should be administered to prevent hypoglycaemic events.negative spiral of oedema. Infusion with mannitol is used to lower the intracranial pressure. The hormonal substitution therapy in dogs after hypophysectomy includes thyroxine. Degenerative lumbosacral stenosis in nonchondrodystrophic dogs (e. Apart from the routine monitoring devices. In the ICU. In case of pituitary surgery in dogs for tumours that cause Cushing's disease (the pituitary tumour produces excess adrenocorticotropic hormone (ACTH)) the postoperative monitoring includes electrolytes (sodium. it is imperative in brain surgery to have some type of monitoring of blood pressure and possibly also intracranial pressure. cortisone and desmopressin (a synthetic vasopressin analogue).g.g. A 'cold' brain requires less oxygen. Brain and pituitary surgery requires some type of magnification (operating loupes) or an operating microscope.. the dogs are stimulated to drink immediately after surgery to regulate their water balance. also for the assisting nurse technician. French Bulldog. Disc herniations are usually type 2 (protrusion) herniations of the annulus fibrosus and . Dachshund). The temperature of the surgical unit should be kept below room temperature. ischaemia and spinal cord necrosis (called myelomalacia). myelogram. In the cervical region a ventral approach is used called a ventral fenestration (incision of the annulus fibrosus) and decompression (ventral slot of the vertebral bodies). The Brain Patient The patient that undergoes brain or pituitary surgery requires special care. the veterinary surgeon usually requires on hand all the available imaging data (radiographs. In the thoracolumbar area a left or right-sided approach is used called hemilaminectomy and lateral fenestration. these cats usually have insulin-dependent diabetes mellitus which will resolve quickly after surgery. During neurosurgery. Postoperative neurosurgical care is done in the intensive care unit and patients are kept sedated for some hours after brain surgery before waking them up. C4–5) and thoracolumbar (T11–12. German Shepherd Dog). Also preoperative planning and three-dimensional (3D) measurements on sizes of space-occupying lesions and tumours are an enormous help for the surgeon. CT and MRI) for localisation of the correct surgical approach and intraoperative feedback of surgical findings in relation to the imaging findings. Neurosurgical Indications and Procedures The following diseases are the most common indications for neurosurgery: Intervertebral disc disease (IVDD) with cervical disc disease (C2–3.. Disc herniations are usually type 1 (extrusion) herniations of the nucleus pulposus.

A head stand. a vacuum cushion and/or surgical tape is used to stabilise the head during the surgical procedure. Spinal cord tumours. Atlanto-axial instability in miniature dogs (e. or cervical locking plates. In this disease.. Foot pedal-controlled burring is preferred over hand console-controlled burring since this adds to stability of the burr in the surgeon's hand. The pituitary tumour is usually approached by the oral route to the brain via a transoral. irrigation can be automatically integrated in the hand burr but continuous lavage with saline from a syringe by the nurse technician is just as efficient and more reliable than equipment! Copious lavage is a prerequisite in neurosurgery to . Dobermann). Craniotomy approaches can be combined or modified to improve exposure to various aspects of the cerebral hemispheres and cerebellum. The mandible is reflected downwards and the approach to the base of the skull is through the soft palate. The location of the tumour dictates the approach. Caudal cervical spondylomyelopathy (wobbler disease) in non-chondrodystrophic dogs (e.g. vertebral plates or pin-PMMA fixation technique. Also. followed by dorsal fenestration of the disc and nucleotomy (removal of the nucleus pulposus). The nurse technician should be aware of postoperative respiratory depression and apnoea in this condition since the respiratory centre is close to the surgical field and may be temporarily affected.g. Brain tumours. unilateral or bilateral transfrontal sinus craniotomy. The most common approach is the ventral approach with lag screw fixation. Pituitary tumours. The approach is dependent on the localisation but usually the approach is not a standard technique. lumbar and lumbosacral area spinal tumours are best approached by dorsal laminectomy. In the thoracolumbar area. pins and polymethylmethacrylate (PMMA). Tumours of the neurocranium can be approached through craniotomy. The dogs and cats are in sternal recumbency and the maxilla is supported on a metal bar attached to the operating table. The term craniectomy is used when the bone flap that is created during craniotomy is not replaced..g. Some of these patients need to be ventilated postoperatively for some time. The most common approaches to the calvarium are: rostrotentorial transparietal or transtemporal craniotomy with or without osteotomy of the zygomatic arch. Chihuahua). the type 2 disc herniation is usually more dynamic in nature and requires decompression but also stabilisation using a variety of techniques such as screw and washer. The advantage of an electrical burr is that the speed of rotations can be fine-tuned. In the lumbosacral area the most common approach is dorsal laminectomy. caudotentorial craniotomy. Special Considerations During Neurosurgery Neurosurgical instrumentation for the approach and detachment of muscles include periosteal elevators and Gelpi retractors. or suboccipital craniotomy. through the nasopharynx and through the sphenoid bone. Laminectomies are performed with an electrical or air-powered burr unit. The surgery is considered a contaminated surgery because the approach is through the mouth and nose.nucleus pulposus. In the cervical area and thoracolumbar. Lubra plates. dorsal laminectomy leads to an unstable spine which requires some type of fixation afterwards e. transnasal microsurgical trans-sphenoidal hypophysectomy. Most craniotomies are performed with the cat in sternal recumbency..

Bipolar electrocautery has the advantage over monopolar electrocautery that the current will pass between the tips of the bipolar forceps and will not affect the adjacent muscle tissue or nerves (or spinal cord).g. swimming and exercises for proprioception. Urine weakens the skin barrier and enables bacteria to enter through the skin and cause redness and infection. During most neurosurgical procedures some type of magnification is required to assess the condition of nerves. Typically a nurse technician can assist and speed up this phase of the surgery. the spinal cord. Long instruments are preferred which keeps the hands out of the surgical field.g. Especially in spinal cord and brain tumour surgery. This can be kept to a minimum by precauterising muscular attachments with bipolar electrocautery before cutting the attachments. Bedding of the patient should be kept dry. As long as the animal is not urinating spontaneously and has to be catheterised. Rehabilitation of the paralysed patient may include frequent bathing. etc. exercising standing with support bags. spinal cord or brain and to assess the sharp margins between normal and affected tissue. Pain medication postoperatively may include non-steroidal anti-inflammatory drugs (e. oral tramadol or fentanyl patches). hydrotherapy with an underwater treadmill. Postoperative recovery of conscious nociception is fast (24–48 hours). In monopolar electrocautery the current goes from the tip of the monopolar to the contact plate which may cause unwanted twitching and movements of the surgical field. During neurosurgery haemostasis is primarily controlled by bipolar electrocautery. This may even take up to 2 weeks after surgery. the surgeon is moving on the cutting edge between normal and affected (tumour) tissue. carprofen) and/or morphine-like substances (e. wheelchair walking. In neurosurgery it may not be possible to take safe margins with tumour excision so the aim is tumour management by debulking (cytoreduction) rather than complete tumour excision. nerves and brain are explored with fine ball-tipped neurosurgical probes. muscle massage. Canine rehabilitation should start on the first day after surgery whenever possible and practical. The paralysed patient requires intensive care and its owner requires guidance. The animal should be turned at regular intervals. Paralysed patients frequently have no voluntary urination. The use of postoperative steroids after laminectomies is highly controversial. there is an indication to treat with systemic antibiotics.provide cooling during burring. A referral letter is made to inform the physiotherapist on the medical history and to provide a channel for feedback on follow-up. 'Bladder' management requires catheterisation or frequent attempts to empty the bladder by manual abdominal pressure. This requires a different mindset than in standard tumour surgery. Once the surgeon has entered the spinal canal or the bony calvarium.. Animals that soil the perineal region with urine and faeces in the postoperative period run a great risk of development of decubitus ulcers or dermatitis in the perineal region.. clean and soft at all times. The veterinary surgeon may refer the animal to an animal physiotherapist within the practice or outside. recovery of motor . to remove the bone shavings and to keep the surgical field free of blood. Approaches to the spine require detaching of muscular attachments and this causes profuse bleeding. Rehabilitation of the Neurosurgical Patient Neurosurgery is only the first step in recovery of the patient off its legs.

Lateral or accessory canals are uncommon in dogs and cats.function may take 6 weeks and recovery of postural reactions (proprioception) may take up to 6 months! Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Björn P. DVM. located within the tooth. Sandringham 20183764 Anatomically the tooth is divided into the crown. Lateral canals provide passage between the central pulp cavity and periodontal tissues in locations other than at the apex. PhD. Meij. (the portion visible above the gum line) the neck (the junction) and the root (the portion under the gingiva enclosed in the socket). The Netherlands Root Canal Therapy in the Dog AUSTRALIAN VETERINARY ASSOCIATION PROCEEDINGS 2009 Rod Salter. emerges from the tooth and connects with the periodontal ligament at the apex. MACVSC (Veterinary Dentistry) Melbourne Veterinary Dentistry and Oral Surgery Service. The apex of the tooth is the tip of the root. DECVS Utrecht. The pulp. The pulp is composed of soft connective vascular and nerve . BVSC.

fibroblasts. Sooner or later the bacterial infection will be extensive and will spread throughout the canal. The odontoblastic layer covers the periphery of the pulp chamber. Innumerable dentinal tubules perforate the dentin at right angles to the pulp and contain cytoplasmic extensions from the odontoblasts called Tomes fibbers. . or it can be idiopathic in origin. a layer of cementum gradually covers the dentin and the pulp chamber and root canal narrow. Pulp tissue consists of four layers. Physiologically the pulps functions are formative. Vessels that pass through the apical foramina are distributed throughout the pulp. lies next to the odontoblastic layer in mature teeth. At best. and defensive.tissue. Weil's basal layer (cell-poor layer). The dental pulp is a blood-rich organ. Then bacteria and/or bacterial by-products and other irritants from necrotic tissue will diffuse from the root canal into the periapical tissues with resultant development of a periapical inflammatory lesion. After the root lengthens. the pulp system harbours bacteria and their by-products. Teeth sustaining minimal trauma and teeth with immature apexes have more chance of pulpal survival than do teeth that have been subjected to severe trauma or teeth with closed apexes. elastic fibbers. Pulpal insult can result from extension of the inflammatory process through the dentinal tubules. Pulpal tissues produce dentin. Severity of trauma and the degree of apical closure are important factors in the recovery of the pulpal tissue from physical trauma. and nerves. The odontoblasts function to produce dentin throughout the vital life of the tooth. the defences will temporarily halt or slow their spread or tissue destruction. The dentinal tubules and the odontoblastic process narrow toward the periphery of the tooth. nutritive. As regards pathophysiology the pulps response to injury is via inflammation. which ceases entirely after pulpal death. Pulpal damage also occurs as a result of trauma (pulpal exposure resulting from coronal fracture or intradental haemorrhage without pulp exposure). fibrocytes. through localisation of blood-borne bacteria in hyperaemic pulp. collagen fibbers. The pulp provides nutrients to the surrounding tissues during and after development. a consequence of excessive pressure within the pulp space. Continued severe irritation results in pulpal death because hyper vascularity and swelling in a closed space effect necrosis once arterial inflow ceases. with each odontoblast enclosed and remaining vital in its dentinal tubule that extends to the dentinoenamel / dentinocemental junction. Pulp also contains lymph vessels. tapering to an almost closed structure at the enamel junction cemental wall. or as a result of periodontal disease in combination periodontic-endodontic lesions. the opening at the apex narrows. The cellular content of the dentinal tubules is significant in endodontic treatment inasmuch as open dentinal tubules can lead to pulpal disease. respectively. The pulp does not have the capability to rid itself of these damaging bacteria as they are located within both the pulp and the dentinal tubules. Pulpal disease passes from reversible hyperaemia to an irreversible pulpitis and ends in suppurative pulpitis and necrosis. As maturation occurs. resulting in thicker dentinal walls and narrower pulp cavities as the teeth mature. Periapical inflammation and abscess formation are extensions of the pulpal inflammatory response. Microorganisms present in dentin and canals constitute the main sources of dentin microbial irritants of the dental pulp and periapical tissues. or iatrogenic factors. by direct dentinal insult from topical irritants. blood vessels. With increasing age and exposure to physiologic functioning. penetration by bacteria from such factors as caries or external resorption. the pulp connects with the surrounding periapical tissue through a wide opening. Pulpal disease decreases dentinal deposition. sensory. in which the apex is not yet fully developed. It contains odontoblasts. Most vessels are thin walled with large lumens. The sensory function of the pulp is a response to pain via nerves that enter the apical foramen. It is this tissue that responds most dramatically to any insult or injury to the dentition. As a consequence of pulp exposure to the oral cavity. In young animals. additional layers of dentin are added. A cell-rich layer is located between the cell-poor layer and the fourth layer which is the central pulp. with processes extending into the dentinal tubules.

The pulp is encased in rigid walls therefore. a small increase in tissue pressure as a result of increased capillary permeability causes passive compression and even complete collapse of the venules at the site of pulpal injury. In cases of dental attrition and abrasion. its . macrophages. At this stage the condition is no longer painful and it can go unnoticed for a considerable period of time. bradykinin. Increased capillary permeability due to inflammation causes movement of fluid from the vessels into the tissue. Potential pulpal antigens include bacteria and their by-products. Sooner or later. Depending on the severity of irritation. Soon thereafter. cold and pressure. the colour may eventually diminish and the tooth will return to its normal appearance. which will proceed to total necrosis. In addition to nonspecific inflammatory preparations. Affected teeth may first present with a pink or blue tingeing of the tooth. As a consequence of these releases. With progressive wear. plasma cells and mast cells as well as various classes of immunoglobulins indicate that mediators of immunologic reactions also participate in pathologic changes during pulpal pathosis. In contrast. Clinically significant is the usual absence of noticeable symptoms to the patient. lymphocytes. closure or sealing off of inflamed pulps induces rapid and total pulp necrosis and periapical pathosis. which directly or through dentinal tubules can initiate different types of immunologic reactions. the destruction of the pulp often proceeds without the knowledge of the patient the owner or the vet! Injury to pulp tissue results in cellular damage and release of nonspecific mediators of inflammation. If exudate produced during irreversible pulpitis is absorbed or drains through caries or an exposure into the oral cavity. The pain eventually disappears as sclerosis and calcification of the dentinal tubules occur.Secondary dentin is formed by the odontoblasts after root formation has been completed. Pulp pathology can range from a transient inflammation (reversible pulpitis) to irreversible pulpitis. regardless of the severity or progress of inflammation. The formation of tertiary dentin results from irritation of odontoblastic processes within the dentinal tubules. the infection spreads through the apical delta and causes a periapical periodontitis. In addition to liquefaction necrosis. and emigration of leucocytes at the site of injury. The presence of potential antigens and the identification of immunocompetent cells such as PMN leukocytes. bacterial invasion and obliteration of the blood vessels cause pulp necrosis. however. the tertiary dentin may become clinically evident as a brown spot in the centre of the occlusal surface. A periapical granuloma is visible on radiograph as a round radiolucent area. At this stage the condition is painful and facial soft tissue swelling may be evident. vascular stasis. The formation of secondary dentin is the tooth's response to the stimuli of the normal aging process. The brown colour is explained by the irregular nature of the tertiary dentine which causes it to stain easily. such as histamine. pulpal necrosis is delayed and the radicular pulp may remain intact for long periods. This can be differentiated from an exposed pulp chamber by probing with a dental explorer. an exudate forms in the pulp. The dentinal tubules which continuously "harbour" bacteria and necrotic material ensure the contamination is continuous and persistent. ischemic necrosis of dental pulp can occur as a result of traumatic injury and disruption of blood supply. Pain is manifested by sensitivity to heat. which in turn progresses to a periapical granuloma or a periapical abscess. The pulp tissue in essence reacts to numerous various irritants like other connective elsewhere in the body. If irreversible destruction has occurred. and arachidonic acid metabolites. pulp exposure may occur if tertiary dentin formation cannot keep pace with the rapid wear. With severe dental abrasion. Thus. the formation of tertiary dentin will usually seal off the pulp cavity. Tertiary dentin is produced by the odontoblasts that are directly affected by the irritation. Blood vessel obliteration occurs because the narrow root canal does not allow for the swelling associated with an inflammatory reaction. Complicated dental fractures cause pulp exposure. the colour changes to a purple-gray as the pulp dies and the blood cell components are degenerated. If the pulpitis is reversible. Dentin exposed by uncomplicated dental fractures is initially painful because of the presence of intradentinal nerve fibers and fluid movement through the tubules. The continuous deposition of dentin results in a progressive reduction in the size of the pulp chamber and root canal. immunologic responses can also initiate and perpetuate pulpal diseases. Haemorrhage occurs and an acute pulpitis ensues which is very painful. there is increased vascular permeability. If removal of fluid by venules does not keep up with filtration of fluid from capillaries. reactions.

and host resistance. seeking new nutrients. this barrier generally takes the form of granulation tissue. There are three major goals of veterinary endodontic therapy that should be attained for reasonable assurance of success: 1) Initially the entire contents of the pulp chamber and canal should be removed with endodontic files and irrigation. This results in the classic periapical lucency on radiographs. in acute periapical disease abscess formation is more common. or on the lingual or palatal surface. pathogenicity of the organism. Before the endodontic system can be dressed. root pathology. a cure can only be affected if the cause is removed. 2) Using endodontic files. the canals should be cleaned and enlarged so as to give the canal a slight funnel shape. Preoperative radiographs should always be taken to assess the shape and location of the canals. Coronal access is made with a variety or burs including #l or #2 round bur. However. Sterilization involves irrigation of the root canal to disinfect the canal and remove pulp tissue remnants and dentin debris. Access sites: Canine teeth: Fracture location can play a role. Initial penetration through the enamel should be perpendicular to the enamel. degree of organism challenge. Injury to periapical tissues usually results in cellular damage and release of nonspecific as well as specific immunologic mediators of inflammatory reactions Once the pulpal tissue becomes infected. The objectives of endodontic therapy are to relieve pain. The periapical tissues have good collateral circulation. and 3) The apex (or apices) of the treated tooth should be sealed and the canal packed with an endodontic filling material. prevent further infection. Since endodontic diseases originate from an infected or affected pulp. Preparation: Coronal access: This should be well planned to gain straight line access to the root canal. and then angled toward the apex once into the dentin." Dr. As the apical periodontal ligament is the only directly associated soft tissue in this situation. Root canal therapy has many advantages over extraction. Standard root canal therapy is less traumatic for the patient and more aesthetically pleasing to the owner than surgical extraction. . and avoid complications associated with extraction. In more chronic cases. bacterial involvement will eventually extend to these tissues. The best reason is that the tooth is saved rather than resorting to "toothenasia". This phase is concerned with the debridement of the root canal system and shaping of the root canal in preparation to receive a specific type of filling." The preparation phase means proper coronal access. and periapical tissues. on the facial surface. and host response. Check depth and angle with a radiograph. Obturation is the development of a fluid-tight three dimensional seal at the apical foramen and total obliteration of the root canal. and the coronal end sealed against further invasion of organisms. although it may take purulent or cystic forms at the apex. restore and maintain function. This then constitutes "The Endodontic Triad. 1975. but usually 2-4mm coronal to the gingival margin. and periapical pathology. remove infection. attention must be given to the tissues surrounding the pulp. organisms will continue to invade. I Wolch. This is to eliminate the avenues of leakage from the oral cavity or periradicular tissues into the root canal system. periapical pathology of pulpal origin can range from slight inflammation to extensive tissue destruction. or a #330 pear bur. and the cost of root canal therapy is similar to that of surgical extraction. and the installation of intracanal medication for staged treatment. Chronic proliferative changes at the apex stimulate dissolution or resorption of periapical bone. any unsupported or fractured tooth structure should be removed to provide a clear view of the remaining sound tooth structure. PULPECTOMY / ROOT CANAL THERAPY Although the objective of endodontic therapy is the management and treatment of the injured pulp. "In the treatment of any disease. Incisor teeth: Through the fracture site. Whether an acute or chronic process develops depends on the severity of trauma. it is axiomatic that the root canal must be thoroughly and carefully debrided and obturated.duration. which allows the building of a defensive barrier in an attempt to confine the pathogens and their toxins within the root canal system and periapical tissues..

about 1 mm distal to the buccal groove on the buccal aspect of the crown. establish the working length with a small file and endostop. Be careful to avoid furcation perforation. Continue preparation by locating the canals with a pathfinder or small size endodontic file. increments. With the Step-back technique. Talk to the supplier and find what works best for you. It has a good effervescent action. and withdrawn. and may help seal the dentinal tubules. The Gates Glidden drills are used for coronal and midroot preparations. Sodium hypochlorite (bleach) is an antimicrobial that helps dissolve organic debris. The cut is made during retraction of the reamer. Step (crown)-down technique: Preparation begins coronally and is advanced apically using smaller and smaller instruments. the distal root. twisted clockwise ¼ turn. 3. There are two basic approaches. and may improve the canal sealer interlock. A K-reamer has half as many twists as a K-file. Prevention of perforation of this area demands that you follow the principles of access preparation. Throughout the debriding or filing process. Fully rotate with the canal to engage the pulp tissue. Larger files can be used longer. and bends. and some antimicrobial properties. and don't use in small canals. Barbed broaches are used for pulp extirpation. Be sure to protect the oral tissue when irrigating with this product. Instrumentation and recapitulation continues until clean shavings emerge on the file and the desired canal shape is achieved. They are used to prepare the coronal portion of the root canal. The goal is a continuously tapered preparation of the root canal. The goal is to leave as much tooth structure as possible while removing enough to allow easy instrumentation. The working length is not established first. General file principles: Use 1 to 3 times and then replace. Root canal irrigants should be used frequently during the process of instrumentation. dislodges dentin chips and debris. have a thorough knowledge of tooth anatomy and the use of radiographs. The smear layer is a combination of organic and inorganic debris crushed into a fine paste along the walls of the pulp cavity. Many instrument aids are available. The file resembles a wood screw. Never force or allow broach to bind against the walls. Prepare the apical portion of the canal first with recapitulation using progressively larger files. and Peeso reamers. The advantages of removing the smear layer are improved removal of bacteria. Maxillary 4th premolar teeth: Mesial roots: Transcoronal approach. the root canal must be recapitulated.Mandibular teeth: Mesial root: Through the mesio-occlusal pit on the lingual side. The smear layer is created by instrumentation. about ½ way from the gingival margin to the cusp on the buccal aspect of the crown. I. and penetration and retraction with the file. 2. and the distal root on the occlusal surface. This confirms the patency of the canal. and cuts only in one direction--retraction. K-type reamers. Hedstrom files. Inspect the files for unraveling. Cleaning and shaping the canal involves the use of a variety of instruments including barbed broaches. K-type files. The disadvantages of removing the smear layer are that it may help occlude the apex and lateral canals. With the Step-down technique (crown-down technique)--Prepare proper access and locate the canal. Hedstrom files have an excellent cutting effect. Confirm the working length radiographically. Both of these cut by being tightly inserted into the canal. twists. the flutes are locked in the dentin. The step back is done in 1 mm. soften the dentin and remove the smear layer. Gates-Glidden drills. or is accessible via the transcoronal approach. If used with rotation. and are easily fractured if turned or twisted. A smaller diameter file is intermittently inserted to the measured apical length and the small bits of debris that are packed into the apex are removed to insure total canal debridement. Discard if defective! Gates Glidden Drills and Peeso Reamers are engine driven instruments used on a slow speed contra angle handpiece. Step-back technique: Preparation is begun at the apex working back up the canal coronally with larger and larger instruments. Hydrogen peroxide can be used in conjunction with bleach. Gates Glidden drills tend to separate near the shank. Chelating agents lubricate the file. Hybrid approaches. The coronal 2/3 of the canal is enlarged first using files and . A furcation is the site where 2 roots separate from the crown. The palatal root can be accessed separately if necessary.

If persistent haemorrhage is encountered when drying the canals. and therapeutic sealers such as calcium hydroxide. Heated instruments are penetrated into the gutta percha. and tapered. and 55mm. Two basic obturation techniques are vertical and lateral compaction. and removed. consider 2-stage therapy. Secondary vertical compaction also occurs. there is vital pulp tissue remaining. and 4) Final obturation. or by using endodontic files or gutta percha points to place the cement into the canal. Use heated pluggers to soften and prefit cold pluggers to condense the gutta percha. They come in various lengths. Prepare the sealer and place into the canal. a body shape that is smooth. Large pluggers are used to compact the gutta percha. The depth of penetration is measured using an endostop on the spreader. allowed to remain 1 minute as gutta percha is compacted laterally and somewhat apically. irrigate again with bleach and water. and the canal is free of pulp remnants and debris. The process is repeated with a smaller plugger until the apical gutta percha mass is compacted. left 2-3 seconds to allow heat transfer. the spreader is inserted. The canal may be filled by utilizing a Lentulo spiral filler on a reduction gear contra angle. The goals of either technique is an apex that is clean with "natures" shape basically unchanged. bacteriostatic. The spreader is returned to the canal to laterally compact again. the master cone is seated in the canal. The process is continued until the canal is fully obturated and a radiograph is taken to confirm the fill. with the standard sized corresponding to file sizes. fine. non-eugenol based such as epoxy resins and glass ionomers. or conventional.5mm). With vertical compaction. sets slowly. Midsize pluggers are used to compact the gutta percha. medium and coarse. radio opaque. When satisfied with the shape of the canal. Many types and sizes of spreaders and pluggers are available. with the 25mm at the same sizes as files. That point is dipped in sealer and inserted into the canal. Gutta percha is the most commonly used material to obturate root canals. Spreaders have pointed tips. Auxiliary points that seat to penetration depth are chosen. in extra fine. With lateral compaction. The spreader is removed using rotation and coronal gutta percha is removed. The ability to achieve this is highly dependent on the quality of the canal preparation. It should fit to working length or shorter (. Root canal sealers fill the space gutta percha is unable to fill. If this happens. not stain. and complete the procedure 3-4 weeks later. Kfile or injection) as a temporary filling. Proceed with either lateral or vertical compaction. The ideal characteristics are: tacky when mixed to provide good adhesion to the canal wall. The apical portion if prepared last. that are more tapered and pointed. The goal of obturation is a 3 dimensional fill and a tight seal. and pluggers have flat tips. Most of these come as a powder and liquid spatulated together to thicken consistency and are then introduced into the prepared root canal. contact the walls in the apical portion and demonstrate slight resistance to removal.Gates Glidden burs. haemorrhage from the periapical tissues. These are available in 25 and 55 mm lengths. or root resorption present. You are ready for obturation when the canal is clean and shaped to an optimal size and is dry. Dry the canal. then dry with paper points. This minimizes binding of files in the coronal 1/3 of the canal. Seat the master cone. place calcium hydroxide intracanal medication (paste filler. and soluble in common solvents. tissue tolerant. The master cone is selected based on the final apical file used. Failure to fully obdurate and seal the canal will lead to endodontic failure. 2) Working length. . will not shrink upon setting. Most root canal sealers are eugenol based (zinc oxide-eugenol). Excess sealer will extrude out the access point. Spreaders and pluggers are used to compact gutta percha into the prepared root canal. Heated instruments are again inserted to selectively remove coronal gutta percha. A minimum of 4 films are taken during a procedure: 1) Preoperative. The cone is grasped with cotton pliers at a position that approximates the working length. continuous flowing. 3) Master cone placement. The fit is confirmed radiographically.

SPEAKER INFORMATION (click the speaker's name to view other papers and abstracts submitted by this speaker) Rod Salter. place bonding agent. Follow-up radiographs should be taken at 1 and 3 years if there was no periapical lucency present. Coronal leakage through improperly placed restorations can result in endodontic failure. Place an intermediate layer to prevent contact of the composite with any remaining sealer. BVSc. Place a final layer of unfilled resin or composite sealant and cure. vertical compaction. MACVSc (Veterinary Dentistry) Melbourne Veterinary Dentistry and Oral Surgery Service Sandringham . Vertical compaction does fill accessory canals with a significantly greater incidence. Acid etch the dentin and enamel. Additional film intervals are based on the results of the first follow-up films. Remove the gutta percha from the access preparation. place composite and light cure. and initially at 6 to 9 months if periapical lucency was present. and smooth the composite.There is no statistical difference in filling efficiency between lateral vs. Final radiographs should be taken after the restorative is placed. clean excess sealer from the walls.