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Proceedings of the
47th British Equine Veterinary
Association Congress
BEVA
Sep. 10 – 13, 2008
Liverpool, United Kingdom

Next Congress:

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The John Hickman

Memorial Lecture

13.45–15.00

Equine neurology: Watching horses behaving

strangely
Joe Mayhew
Institute of Veterinary, Animal & Biomedical Sciences, Massey University, New Zealand.

Over the last 5 years or so we have learnt much about existing and new disorders in horses from documentation of careful
clinical observations and interventions and from painstaking pathological studies with special emphasis on clinicopathological
correlates. Some of these disorders will be discussed elsewhere in this conference and this paper will highlight a few of
these disorders through which we have added to our understanding of anatomy, physiology and clinicopathological correlates
- the building-blocks for advancing equine neurology.

ACQUIRED CERVICAL TORTICOLLIS ASSOCIATED WITH PARELAPHOSTRONGYLUS TENUIS

The amazingly selective meanderings of these migratory nematode parasites are exemplified by the plight of
Parelaphostrongylus tenuis in some horses that have been elegantly documented4–6. This worm has caused an acute onset
of a lateral deviation of the cervical vertebrae, or scoliosis, which remained static, and was the result of an exquisitely
selective, continuous, cervicothoracic, inflammatory dorsal grey column lesion. Cutaneous hypalgesia to analgesia of the
neck and/or thorax and mild unilateral ataxia and paresis but with no evidence of denervation atrophy in the epaxial muscles
was observed in all affected horses. The scoliosis was clearly argued to be due to loss of afferent cervical proprioceptive
inputs because of the dorsal grey column lesions with some white matter involvement accounting for ataxia and weakness
(Figure 1).

VESTIBULAR SYNDROMES FOLLOWING CERVICAL NERVE ROOT LESIONS

A rather forgotten component to the vestibular system is proprioceptive input from the cranial cervical vertebrae, ligaments
and muscles12,13. Special proprioceptive inputs from the cranial cervical vertebral ligaments and muscles pass via at least

Figure 1: A continuous lesion in the dorsal grey column in the neck (star) causes a segmental interruption of the postural regulation of the
muscle tone in epaxial muscles, resulting in scoliosis of the neck. In addition, it interrupts the proprioceptive and general somatic afferent
input to higher centres resulting in ataxia and hypalgesia. If adjacent white matter is affected, ataxia in pelvic limbs may result.

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Figure 2: The spinovestibular pathway processes special proprioceptive input from the neck to the cauda vestibular nuclei in the medulla
oblongata. Interruption to this system can result in vestibular disease without there being damage to the brain stem.

the C1–3 dorsal spinal nerve roots to ascend the spinal cord via the spinovestibular tract (Figure 2) to the caudal vestibular
nuclei. These nuclei receive no other afferent inputs. Lesions involving these cranial cervical nerves or the vestibulospinal
input to the vestibular apparatus can result in signs of vestibular disease. This certainly can be seen with symmetric lesions
of the dorsal nerve roots of C1–3 when loss of balance, eye deviation and head tilt have been seen.

CERVICAL VERTEBRAL ARTICULAR ULTRASOUND AND ARTICULAR INJECTION

Cervical (peri) articular injections have become a favoured diagnostic and therapeutic tool at least in North America14,19,20.
However, empirical injection of enlarged articular processes without substantive evidence that they are causing a clinical
problem of neck pain alone, neck pain with ataxia and ataxia alone is to be discredited.

ELECTRODIAGNOSTICS: MAGNETIC MOTOR EVOKED POTENTIALS AND QUANTITATIVE ELECTROMYOGRAPHY

Certainly the noninvasive and reasonably innocuous testing for magnetic motor evoked potentials now has received attention
in large animal neurology21 and it appears to be a very sensitive and quite specific electrophysiological test for disruption
of somatic motor pathways in disease states22,23. This and the additional use of more elaborate but error prone
quantitative EMG investigations24,25 should allow more accurate identification of the presence and location of conduction
blocks, and thus functional lesions, in neurological disease states such as wobblers and unusual hindlimb gait abnormalities.

SCANDINAVIAN KNUCKLING HORSES

This clinical syndrome is one of varying degrees of bilateral sciatic nerve involvement, most horses showing more
prominently signs of peroneal neuropathy and others showing more prominently signs of tibial neuropathy27. Occasional
cases had extensor weakness also indicating femoral nerve involvement. In many cases silage was fed along with poor quality
hay, or there was access to a particular feedstuff. Demyelination may be the underlying lesion compared to the axonal and
myelin (fibre) degeneration seen with many bilateral stringhalt cases. Some milder cases improve but it is not certain
whether this recovery is complete to allow full performance. Peripheral neurotoxins of plant or nonbiological origin would be
the most likely cause of these crippling syndromes27,29,30.

EQUINE MOTOR NEURON DISEASE (EMND)

Acquired equine motor neuron disease (EMND) is a fascinating neuromuscular disorder of horses that does not appear to
have existed prior to 1982 and was first described by the late John Cummings and co-workers from Cornell University in
199033. Hundreds if not thousands of horses now have been definitively diagnosed with EMND in North America and
around the world.
The clinical syndrome expressed depends on the stage of the disease34–36 and is encapsulated by the listing in Table 1.
A clinical truism for the syndrome is that affected horses move better than they stand.

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Table 1: Proportion of major clinical signs recorded for 104 cases of EMND (34, 39).

Clinical sign Occurrence %

Muscle loss 100
Muscle trembling 95
Increased lying down 93
Excellent appetite 90
Shifting weight 90
Extended tail head 76
Lowered head posture 62
Retinal lesions 18

Definitive diagnosis is dependent on the post mortem demonstration of degeneration and loss of cell bodies in the ventral
horn of the spinal cord and in motor nuclei in the brain stem with the exception of those supplying cranial nerves III, IV and
VI. In experimental cases and in naturally-occurring cases of EMND in North America and in Europe, vitamin E deficiency
has been the only consistent nutritional or toxic-related abnormality determined34. Further studies are necessary to explain
the development of hypovitaminosis E and EMND in horses that have adequate access to pasture. Genetic factors for
alterations in amount or activity of the alpha-tocopherol transfer protein, such as the 744 del A mutation of the alpha-TTP
gene operative in some forms of human hypovitaminosis E44,45, will need exploration in this regard.

EQUINE POLYSACCHARIDE STORAGE MYOPATHY (EPSM)

Equine polysaccharide storage myopathy (EPSM) is an autosomal recessive disorder in Quarter Horse and related breeds
that can result in rather exceptional susceptibility to recurrent exertional rhabdomyolysis46–51. Recently, there has been an
association of the disease with a particular microsatellite marker52. However, the morphological diagnostic criteria for
making the diagnosis are variable46,47,53–56. The disease EPSM thus refers to the clinical syndrome of muscle disease,
particularly rhabdomyolysis, with amylase-resistant, sarcolemmal inclusions of acid mucopolysaccharides evident on muscle
biopsy sample. In distinction, where there are clinical signs of myopathy but histological evidence of no or mild myopathic
changes with excess, aggregates or cores of sarcoplasmic, mostly amylase-sensitive polysaccharide (glycogen), then a
distinguishing term such as polysaccharide-associated myopathy should be used. The former is seen particularly as a likely
autosomal recessive trait in Quarter Horses and related breeds and in several other breeds including draught horses,
whereas excess or unusual glycogen storage is seen in association with clinicopathological myopathic syndromes in a wide
variety of breeds48,54 and may be present, histologically, in upwards of 50% of horses54.
The clinical syndromes can likely be ameliorated in many cases with management and dietary modification to include
consistent and appropriate levels of exercise57 and addition of <20% lipid as a source of energy and reduction of soluble
carbohydrates in the animals’ diet48,54,58. Dantrolene sodium may help in altering membrane Ca++ flux to reduce the
outcome of myolysis in these disorders59,60.

HYPERKALAEMIC PERIODIC PARALYSIS (HYPP)

Young-adult (2–3 years), mostly male Quarter Horse and Quarter Horse-related breeds have been reported to be affected
with this autosomal dominant disease61. Homozygous animals are more severely affected than heterozygotes49. The owner
notices intermittent episodes of muscle trembling over the body or face, sometimes with intermittent projection of the
nictitating membrane, that may lead to involuntary recumbency. Other premonitory signs include yawning, lowering of the
neck, swaying and disinterest in food and water. During a mild episode the horse is alert, appears distracted and reluctant
to move, and may stumble as if weak. In a fulminant episode fasciculations or muscle tremor, particularly involving the flank,
shoulders and neck and sometimes the face, progress to staggering, buckling, marked muscle spasms and paraplegia may
precede involuntary recumbency. A severe episode, perhaps following forced exercise or KCl provocation, results in severe
tremor and tetany of many muscles with recumbency and sweating. An episode may last several minutes to hours, typically
less than an hour, with full and usually rapid recovery occurring.
The clinical syndrome in this inherited channelopathy is distinct but does closely resemble the acquired channelopathy
induced by lolitrem-B in perennial ryegrass staggers.

STIFF HORSE SYNDROME

Recently, a stiff horse syndrome similar to stiff person syndrome has been recorded. Clinical signs appear to wax and wane
and range from mild muscle stiffness to sudden and often violent muscle contractions. Generally there is an insidious onset.
Between episodes the horse may appear normal although, if present, the generalised muscle stiffness may persist.

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Exercise intolerance associated with mild to moderate muscle stiffness may be the only initial clinical sign. This may easily
be attributed to a primary myopathy, with pain on muscle palpation, although serum muscle enzyme concentrations remain
in the normal range. Components of the syndrome bear resemblance to such disorders as tetanus, equine motor neuron
disease, hyperkalaemic periodic paralysis, exertional myopathies and especially the acquired channelopathies associated
with the mycotoxicoses such as perennial ryegrass staggers.
The most useful diagnostic test is detection of antibodies against GAD in serum and cerebrospinal fluid and, although
some cases have had high anti-GAD titres, several strongly suspected cases have been negative on this test.
The overall message really is that with the array of enigmatic movement and postural disorders encountered in equine
neurology that appear to be variations on the themes of stringhalt, shivering and claudication72–74, a broad approach to
delving into possible aetiological mechanisms should be taken that includes the possibility of immune associated
neurotransmitter derangements such as SPS.

GRASS SICKNESS
Grass sickness or equine dysautonomia has been described since the early 20th century and since then has had quite a
devastating effect on equine populations in parts of Western Europe75–78.
Per-acute colic with gastrointestinal stasis and rupture, anorexia with mild signs of colic and ileus, to chronic cachexia
covers the general spectrum of syndromes seen with this very unusual disease. Moderate tachycardia, indifference to food,
difficulty swallowing, excessive salivation, depressed gastrointestinal sounds, abdominal distension and usually mild colic are
very often present to varying degrees. Muscular tremor and patchy sweating may be primary signs or may reflect the
dehydration, electrolyte imbalances and colic that occur. Posturing with all feet close together as a weak patient does, ptosis
and especially rhinitis sica are very distinctive signs when present.
No definitive clinical diagnostic test exists. As the clinical signs of Horner’s syndrome are symmetric, ptosis can be
difficult to detect. However, a recently described aid to clinical diagnosis is the observance of a rapid reversal of ptosis with
0.5 ml of 0.5% phenylephrine eye drops89. The resulting marked difference in degree of ptosis and particularly in eye lash
angle can be spectacular.

ATYPICAL MYOPATHY
Several hundred cases of highly fatal, atypical myopathy or myoglobinuria have been reported in young, adult, grazing
horses mostly from Europe but also North America and Australasia90–93. Horses may be found dead or more often
showing various signs of reluctance to move, stiff and short strides, apparent sedation and fine muscle tremors. They
quickly become laterally recumbent and urine becomes dark with myoglobin staining although more sub-acute cases do
occur90. Plant, bacterial and fungal toxins have all been considered as possibilities but the cause or causes remain
completely unknown90. Clinicians suspecting cases are urged to log on to the atypical myopathy alert site and complete
the appropriate forms in an effort to unravel the epidemiology of this dastard disease: (dominique.votion@ulg.ac.be);
(http://www.ivis.org/reviews/rev/votion/chapter.asp?LA=1#forms).

COMPLEX REGIONAL PAIN SYNDROME

Cases of complex regional pain syndrome have been reported in horses98 in which the localised profound allodynia has been
so debilitating as to prompt decisions for euthanasia. Interestingly, sometimes following a perineural anaesthetic block is
performed in the limb of a horse there is a regional strip of reflex vasodilation and sweating proximal and distal to the
injection site. The regional distribution of this sympathetic response outside the resulting analgesic area is similar to that
seen around the trigger point of horses having complex regional pain syndrome.

FLUPHENAZINE TOXICITY
The long acting phenothiazine drugs perphenazine and fluphenazine have caused an interesting syndrome of fluctuant
somnolence and compulsive activity that can consist of adopting abnormal postures and displaying incredibly frantic,
repetitive movements99–103. Thus an affected horse may stand fixated by an object and appear to watch unapparent
images move, stand with the forelimbs placed well forward and the head flexed between the knees, and perform tonic
repetitive movements such as incessant pawing with one limb, head swinging and pseudo-rubbing on objects. Recumbency
without somnolence and seizure-like activity also occurs. Anticonvulsant and narcotic drugs are indicated to help control the
signs102 and possibly anticholinergic drugs such as benztropine and diphenhydramine can be considered100,103.

GRANULOMATOUS MENINGOENCEPHALOMYELITIS (GME)

A collection of cases demonstrating disseminated, multifocal, granulomatous lesions are documented in large animal internal
medicine and dermatology literature and are referred to by several terms including idiopathic generalised granulomatous

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disease, eosinophilic granulomatous disease, equine sarcoidosis, multisystem granulomatosis, systemic granulomatous
disease and equine histiocytic dermatitis; the former definition being preferable for many reasons104–108. In one case of
idiopathic systemic granulomatous disease in an aged mare, there was a multifocal granulomatous encephalomeningitis, and
neurological signs consisted of a rapid progression of somnolence, head pressing, excitement, seizures and recumbency109.
Subacute leukoencephalitis and necrosis was accompanied by necrotising vasculitis and large perivascular accumulations of
lymphocytes, macrophages, some neutrophils and multinucleated giant cells. Several other very similar isolated cases have
been seen in horses by the author and have been documented110.
In general, it is accepted that equine idiopathic generalised granulomatous disease is a programmed immune response
to chronic environmental antigens107,111. On the other hand, with further cytological specification some of the apparently
inflammatory meningoencephalitides may more closely resemble diffuse lymphoma, meningeal sarcoma or
microglioma111, 112. Drawing a likeness between this idiopathic generalised granulomatous disease in horses to Vicia
villosa (hairy vetch, fodder vetch) toxicity113–116 is enticing. This is particularly so as firstly these plants contain numerous
phytolectins that bind lymphocytes117 and secondly nonsuppurative, granulomatous leukoencephalitis has been detected
histologically in one horse with this disease114.

SCLEROSING PANENCEPHALITIS
Sclerosing panencephalitis occurs in at least 2 specific diseases in man, namely subacute sclerosing panencephalitis
associated with modified measles virus DNA and progressive multifocal leukoencephalopathy associated with a papovavirus.
A novel case of sclerosing panencephalitis has been documented in a mature horse showing progressive multifocal
asymmetric signs including blindness, hypermetric ataxia and multiple asymmetric cranial nerve dysfunction over
approximately 12 weeks118. Lymphocytic encephalitis, necrosis, demyelination and prominent fibrillary and gemistocytic
astrogliosis dominated the lesions widespread throughout the neuropil and meninges of the brain. Although a diffuse
astrocytoma could result in some of the cellular characteristics it was concluded that this was primarily a panencephalitis.
A search for viral DNA in future cases is warranted.

ANATOMY OF THE SPHENOPALATINE SINUS

Disorders of the equine sphenopalatine sinus, including empyema and neoplasia, have been reported to cause damage
to cranial nerves II and V. However, the clinical anatomy of these sinuses has only recently been well described in
horses119. There is much variation between individual horses in sphenopalatine sinus anatomy. The sphenoidal sinuses
are small in young horses and become larger and more complex with age. Variation in the extent that the sphenopalatine
sinus extended into the basisphenoid bone also occurs. The septum dividing left and right sphenoidal sinuses is frequently
not midline, but always intact. The sphenoidal and palatine sinuses communicate in most horses. In such cases, what
could accurately be termed the (combined) sphenopalatine sinuses usually drains directly into the caudal maxillary
sinuses. Additionally, in 5 out of 16 cases, some compartments of the sphenoidal sinus also drain into the ethmoidal
sinus. The dorsal and lateral walls of the sphenoidal sinus are very thin and directly adjacent to cranial nerves II, III, IV,
V and VI and major blood vessels. Therefore, many combinations of cranial nerves and blood vessels can be damaged
with disorders involving the sphenopalatine sinus with degrees of blindness, strabismus, anisocoria and facial analgesia
being seen.

LATERAL DIGITAL MYOTENECTOMY FOR STRINGHALT

Stringhalt, also known as springhalt and Hahnentritt (‘rooster kick’), is an anciently recorded disease that is characterised by
a sudden, apparently involuntary, exaggerated flexion of one or both hindlimbs during attempted movement. The hindlimb
motion may be as mild as a slightly excessive flexion to violent movements during which the fetlock or toe will contact the
abdomen, thorax and occasionally the elbow with attempted strides leading to a peculiar bunny hopping and plunging gait.
The form that usually occurs as outbreaks is seen in Australia120, New Zealand121, United States122,123, Chile124 and
Japan125 and thus will be referred to as bilateral, plant-associated stringhalt. Usually there is symmetrical or slightly
asymmetrical involvement of the pelvic limbs, with prominent distal muscle atrophy in severe cases. The thoracic limbs are
also affected in severe cases with knuckling of the forelimb fetlocks, prominent extension of more proximal joints and atrophy
of the distal musculature, in association with prominent stringhalt in both hindlimbs. Bilateral stringhalt has been associated
with exposure to several plants notably Hypochoeris radicata, Taraxicom officinal and Malva parviflora (mallow
weed)120,121,123. These are related species of flat weeds, Taraxicom officinal being the common dandelion. It is interesting
that size and age may be predisposing factors in at least bilateral stringhalt, in so far as older and taller horses tend to
become affected126 in preference to smaller horses such as ponies and native Chilean breeds124.
The pathological lesions present represent a distal axonopathy preferentially affecting large diameter axons in long
nerves126,127. This explains the muscle atrophy but there must also be selective involvement of γ-efferent fibres to account

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for the movement disorder with abnormal input via the 1a-afferent fibres to the α-efferent neurons resulting in inappropriate
firing of lateral digital extensor and other muscles.
Although palliative, removing a section of the myotendinous region of the lateral digital extensor muscle relieves the
syndrome quite spectacularly in many cases128,129.

TEMPOROHYOID OSTEOARTHROPATHY
Temporohyoid osteoarthropathy (THO) with proliferative osteopathy involving the temporal bone, temporohyoid joint and hyoid
bone, is reported only in adult horses and may be sub-clinical or may result in evidence of difficulty chewing or more often
neurological syndromes, notably various combinations of facial and vestibulochoclear nerve dysfunction. Some of the cases
have bilateral disease as determined by endoscopic and radioimaging studies, although the clinical signs are most often
unilateral130–134.
The cause of temporohyoid osteoarthropathy is unclear although to this author a traumatic origin is most plausible in
most cases135 with chronic otitis media/interna accounting for a select few cases. Regardless of the aetiology of the
osteoarthritis, clinical signs can occur from either the osteoarthritis itself or from fractures of the adjacent temporal bone
and rarely basilar bones, due to partial or complete fusion of the joint.
Physical examination findings may include difficulty chewing, pain on external palpation of the parotid area, head shaking
and behavioural problems especially when being ridden131,132,134,136. Once the joint is partly fused, sudden forced head
jerking, falling, teeth floating, nasogastric intubation and sudden prolonged vocalisation can cause periarticular fractures of
the petrous temporal bone resulting in combinations of an abrupt onset of facial and vestibular nerve dysfunction.
Endoscopic examination of the guttural pouch is probably superior to plain radiographic imaging in confirming the presence
of the disease by revealing enlargement of the proximal stylohyoid bone due to osteoarthritis when compared to the opposite
side. In acute or progressive cases having ill-defined endoscopic and plain radiographic imaging findings, gamma scintigraphy
should be considered as a diagnostic aid. Monitoring brain stem auditory evoked potential recordings is a very noninvasive
procedure that may assist in refining the prognosis in individual cases137 and following progress of the disease.
Several cases have improved with the passage of time only to show further signs relative to facial and vestibular nerve
dysfunction in weeks to months time. These would seem to be ideal candidates for unilateral surgical disunion of the hyoid
apparatus. Initial surgical disunion of the hyoid apparatus was performed by removal of a mid-shaft portion of the stylohyoid
bone138. To reduce the temporary difficulties in swallowing encountered and to reduce the possibility of other real and
potential complications of this surgery the technique of ceratohyoidectomy was proposed and used with success135,136.
Except with major cranial fractures and if eye problems cannot be resolved135, the outlook for survival with residual
neurological deficits is quite good. Of 33 cases of temporohyoid osteoarthropathy132, 20 cases survived for which there
were longer term follow-up details. Of these, 70% returned to previous level of use although more than 50% of the 20
horses still had evidence of facial nerve deficits and/or vestibular dysfunction. Thus, in spite of some optimistic suggestions,
if full athletic performance without neurological dysfunction is required then the prognosis with or without surgical
intervention has to be fair to guarded for these cases.
Cases of THO have given us a better insight into the ability of horses to accommodate to vestibular dysfunction and to
survive with degrees of facial paralysis.

POST ANAESTHETIC CEREBRAL NECROSIS

An newly defined unexpected complication of apparently routine general anaesthesia in some mature horses is diffuse and
severe cerebral necrosis resulting in signs of diffuse encephalopathy immediately or some hours to days after recovery from
anaesthesia139,140. There is cerebral oedema and laminar neuronal cortical necrosis, and with time gliosis and small
perivascular mononuclear cuffs, most prominent in the watershed zones between major vascular supplies in the
occipitoparietal lobes. These lesions are associated with generalised signs predominantly consisting of somnolence to
dementia, central blindness, wandering compulsively, pushing against objects and ataxia. One patient with this tentative
diagnosis that recovered showed prominent muzzle and ear twitching141, very reminiscent of patients suffering from
bacterial meningitis and from West Nile viral meningoencephalitis.
There certainly must be a compromise to cerebral circulation or metabolism and circumstantially it is related to the
general anaesthetic procedure, but no consistent perturbations predominate139,142.

CONCLUDING COMMENTS
Being a biology watcher does have its rewards in equine neurology. Over the last 5–10 years by making accurate
observations, recording of findings and publishing clinical results we have a better insight into the pathophysiology of
diseases, the application of better therapy and improved accuracy of diagnosis and prognosis. Hopefully this discourse on
some of the interesting aspects of several equine neurological diseases will stimulate others to share their experiences.

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REFERENCES AND FURTHER READING

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