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Major Neurological Syndromes PDF
Major Neurological Syndromes PDF
MAJOR
NEUROLOGICAL
SYNDROMES
I
Reconsideration of neurological syndromes facilitates
topographic diagnosis of lesions wherever they are located in
the central nervous system and/ or peripheral nervous system.
Consequently, neurology must remain equally a science
and an art, therefore presentation of major neurological
syndromes attempts to demonstrate the urgent necessity for
them to be acquired both by the Romanian students and by the
students involved in English programmes, at a time when the
beauty and nobility of clinical neurology must find its well-
defined position in the heap of electronic diagnosis devices.
Rodica Blaa
II
CONTENTS
X. THALAMIC SYNDROMES..89
XVII. COMA239
SELECTIVE REFERENCES.......251
III
I.UPPER MOTOR NEURON SYNDROMES
Hemiplegic gait:
Typical posture during walking:
The forearm and fingers are flexed.
The leg on same side is in extension with plantar
flexion of the foot and toes.
When waking, the patient will hold his or her arm to
one side and drag his or her affected leg in a semicircle
(circumduction).
Recovery of motor deficit of paresis starts with
rhizomelic musculature of lower limb.
Topographic diagnosis:
UMNS at the cortical level (cortical PS):
Hemiparesis is on the opposite side of lesion.
Hemiparesis can be limited only at face and upper limb
or only at lower limb.
Hemiparesis is frequently associated with other
cortical signs (aphasia in the dominant hemisphere,
apraxia, agnosia, jacksonian epileptic seizures,
hemianopsia etc).
Etiology: a) cerebrovascular diseases; b) cerebral
tumor; c) cerebral trauma; d) encephalitis.
UMNS at the internal capsule level (capsular PS):
Hemiplegia is on the opposite side of posterior limb
lesion.
Hemiplegia is equal in both upper and lower limbs.
Spasticity is more precocious and more severe than in
cortical pyramidal syndrome.
Facial paralysis is present on the same side with
hemiplegia (lesion of both posterior limb and genu of
internal capsule.
Recovery of motor deficit is more difficult and more
slowly than in cortical pyramidal syndrome.
Etiology: a) cerebrovascular diseases; b) cerebral
tumor.
UMNS at the brain stem level = alternate syndromes:
Hemiparesis/hemiplegia is contralateral of the lesion.
Paresis/paralysis of one or more motor cranial
nerves (e.g.: III, VII) are ipsilateral of the lesion.
Can be frequently associated with other brain stem
signs (e.g.: vestibular, cerebellar).
Etiology: a) cerebrovascular diseases; b) cerebral
tumor; c) multiple sclerosis.
UMNS at the spinal cord level:
Spinal hemiplegia = half spinal lesion above cervical
enlargement.
Motor deficit is ipsilateral to lesion.
Spinal tetraplegia (quadriplegia):
Complete spinal lesion above cervical enlargement =
bilateral motor deficit.
Spinal crural monoplegia = half spinal lesion below
cervical enlargement (motor deficit affecting lower
limb is ipsilateral to lesion).
Spinal paraplegia = complete spinal lesion below
cervical enlargement (motor deficit is on both lower
limbs).
Etiology: a) spinal cord trauma; b) spinal cord tumor;
c) multiple sclerosis.
II. LOWER MOTOR NEURON SYNDROMES
Glossopharyngeal palsy:
Isolated glossopharyngeal neuropathy is rare as lesions
often involve other cranial nerves in close proximity (VIII,
X, XI and XII).
Quality of speech: a) nasal; b) guttural.
Dysfunction of the secretory parotid gland.
Isolated palsy of ninth nerve can often be asymptomatic,
due to redundant innervations of target structures by the
other cranial nerves.
Clinically:
Difficulty swallowing.
Impairment of taste over the posterior one third of the
tongue for bitter.
Impaired sensation over the posterior one third of the
tongue, soft palate and posterior pharynx.
Absent gag reflex.
Glossopharyngeal neuralgia (GPN):
GPN is a rare pain syndrome, primarily affects the elderly
and is severe and paroxysmal.
Sharp, stabbing pulses of pain in the back of the throat and
tongue, the tonsil and middle ear.
The excruciating pain of GPN can last for a few seconds to
a few minutes.
Paroxysmal pain may return multiple times in a day or
once every few weeks.
Trigger factors:
Swallowing.
Drinking cold liquids.
Talking.
Coughing.
Clearing the throat.
Touching the gum inside the mouth.
GPN can be associated with cardiac dysrhythmia,
bradycardia, hypotension and even asystole and
subsequent syncope.
This effect is similar to that seen in carotid sinus
massage for the treatment of supraventricular
tachycardias (massaging the carotid sinus causes a
hyperstimulation of cranial nerve IX afferent pathway,
resulting in an exaggerated parasympathetic vagal
efferent response).
In an atypical glossopharingeal neuralgia, pain may
radiate in the face, forehead, hypopharynx, larynx and/or
external ear canal.
Etiology:
Microvascular compressions.
Eagles syndrome (cranial nerve IX hyper-excitability
syndrome caused by compression of the nerve against
an elongated of fractured styloid process or a calcified
stylohyoid ligament).
Cerebellopontine angle tumors.
Parapharyngeal space lesions or carcinoma.
Metastasis to petrous temporal bone.
Posttonsillectomy.
Nasopharyngeal carcinoma.
Posterior fossa arteriovenous malformation.
Vagus nerve syndromes:
The vagus nerve exits the brain stem just below the
glossopharyngeal nerve at the pontomedullary junction,
traverses the cerebellopontine angle and exits the cranium
through the jugular foramen.
Innervates all striated muscles of larynx and pharynx
except for stylopharyngeus muscle (innervated by IX) and
tensor veli palatine muscle (innervated by V3).
Sensory input from larynx, pharynx, external auditory
canal, lateral tympanic membrane and posterior fossa
meningeal layers are mediated by the vagus.
Visceral afferent information is conveyed by vagus nerve
from thoracic and abdominal viscera.
Vagus nerve delivers parasympathetic fibers to the
thoracic and abdominal viscera as well, in addition to
larynx and pharynx.
Vagal and superior laryngeal neuralgia:
The two somatic sensory branches of vagus nerve, the
auricular branch and the superior laryngeal nerve can be
the site of a pain syndrome.
Clinically:
Paroxysms of shock-like pain in the side of the thyroid
cartilage, pyriform sinus, angle of the jaw and, rarely, in
the ear.
Occasionally, the pain radiates into the upper thorax or up
into the jaw.
The trigger zone is usually in the larynx and attacks
are precipitated by talking, swallowing, yawning or
coughing.
Swallow syncope or unconsciousness is a rare
complication produced by a vasovagal reflex, with
resulting cardiac inhibition.
Unilateral vagus nerve paralysis:
Hemiparesis of soft palate with hypotonia.
Lueta is deflected by the healthy side of soft palate.
Trouble of swallowing liquids and they will enter the
nasopharinx or trachea.
The vocal cord on the involved side is paralyzed
(recurrent laryngeal nerve paralysis).
Voice is bitonal, hoarse or nasal (recurrent laryngeal
nerve paralysis).
Hemianestesia of soft palate and of the upper third of the
anterior and posterior pillars and corresponding half of
the pharynx.
Loss of velopalatin reflex and of vomiting reflex on the
affected side.
Loss of sensitivity to external auditory meatus and behind
the ear pavilion.
Bilateral vagus nerve paralysis:
Serious disturbances for liquid swallowing.
Pronounced dysphonia that can go up to aphonia.
Autonomic disorders:
Tachycardia or bradycardia.
Severe respiratory disorders with bronchoplegia.
Bilateral recurrent laryngeal nerve paralysis produces
paralysis of both vocal cords, with a whispering voice,
stridor and even death due to tracheal obstruction.
Etiology of uni- and bilateral vagus nerve paralysis:
Meningitis.
Carotid aneurysms.
Neoplasms.
Trauma.
Diphtheria.
Surgery of thyroid neoplasm.
Cervical adenopathy of any cause.
Aortic aneurysm.
Mediastinal tumors.
The brain stem is the posterior part of the brain which is located
caudal to the diencephalon, ventral to the cerebellum and rostral
to the spinal cord.
The brain stem provides the main motor and sensory
innervations to the face and neck (via cranial nuclei and
cranial nerves (CN): III, IV,V, VI, VII, VIII, IX, X, XI and XII).
The brain stem includes:
Midbrain (mesencephalon).
Pons (part of metencephalon).
Medulla oblongata (myelencephalon).
Medial structures of brain stem:
Motor pathway.
Medial lemniscus.
Medial longitudinal fasciculus.
Motor nucleus and nerve.
Periaqueductal gray matter.
Central tegmental tract.
Reticular formation.
Lateral structures of brain stem:
Spinocerebellar pathway.
Spinothalamic pathway.
Sensory nucleus of cranial nerve V.
Sympathetic pathway;
Reticular formation.
The brain stem is an extremely important part of the brain
as the nerve connections of the motor and sensory systems of
the main part of the brain to or from the rest of the body
(corticospinal tract, the posterior column-medial lemniscus
pathway, spinothalamic tract and spinocerebellar tract).
The brain stem plays also an important role in:
Regulation of cardiac and respiratory function.
Pain sensitivity control.
Maintaining alertness, awareness and consciousness;
Regulation of the sleep cycles.
The brain stem syndromes general rules:
Pathways and tracts pass through the entire length of the
brain stem and can be linked to meridians of longitude
whereas the various cranial nerves can be regarded as
parallels of latitude.
Establishing of intersect between meridians of longitude
and parallel of latitude it is possible to establish the site of the
lesion.
Lesions of medial structures: a) contralateral weakness; b)
contralateral proprioception/vibration loss; c) ipsilateral
internuclear ophthalmoplegia; d) ipsilateral cranial nerve
function loss.
Lesions of lateral structures: a) ipsilateral ataxia;
b) contralateral pain/temperature loss; c) ipsilateral
pain/temperature loss of face; d) ipsilateral Horner
syndrome.
Lesions of the four CN of medulla oblongata: a) glosso-
pharingeal (IX) ipsilateral pharyngeal sensory loss; b)
vagus (X) ipsilateral palatal weakness; c) spinal accessory
(XI) ipsilateral shoulder weakness; d) hypo-glossal (XII)
ipsilateral weakness of tongue.
Lesions of the four CN of pons: a) trigeminal (V) ipsilateral
facial sensory loss; b) abducens (VI) ipsilateral eye
abduction weakness; c) facial (VII) ipsilateral facial
weakness; d) auditory (VIII) ipsilateral deafness.
Lesions of two CN of midbrain: a) oculomotor (III) eye
turned out and down; b) trochlear (IV) eye unable to look
down when looking towards nose.
Alternating syndromes:
Ipsilateral = affected CN.
Contralateral = affected trunk and limbs.
Almost all brain stem syndromes are induced by vascular
lesions (infarcts).
A small part of the brain stem syndromes are of tumoral
nature.
Medulla oblongata syndromes:
Lateral and rostral medullary syndrome (retroolivar
Wallenberg syndrome) = posterior inferior cerebellar
artery syndrome:
Ipsilateral:
Facial hemihypoalgesia and hemithermoanesthesia
syringomyelic dissociation (nucleus and tract of
CN V).
Cerebellum:
The largest part of the metencephalon.
Situated with brain stem in the posterior cranial fossa;
Present behind the pons and medulla oblongata.
Separated from pons and medulla oblongata by the cavity of
fourth ventricle
Covered by tentorium cerebelli.
Connected:
To the midbrain by superior peduncle.
To the pons by middle peduncle.
To the medulla oblongata by inferior peduncle.
Cerebellum promotes the synchrony and accuracy of
movement required for purposeful motor activity.
The cerebellar modulation and coordination of muscular
are important in: a) skilled voluntary movement; b)
movements of posture; c) equilibrium.
Cerebellum receives a tremendous number of inputs from
the spinal cord and from many regions of both the cortical
and subcortical brain.
In this way, the cerebellum receives extensive information
from somesthetic, vestibular, visual and auditory sensory
systems, as well as from motor and nonmotor areas of the
cerebral cortex.
Longitudinally, the cerebellum consists of two large
hemispheres, which are united by midline vermis.
Transversally, the cerebellum is divided in:
Flocculonodular lobe (archicerebelum, vestibulo-
cerebellum);
Anterior lobe (paleocerebellum, spinocerebellum).
Posterior lobe (neocerebellum, cerebrocerebellum).
Vestibulocerebellum (archicerebellum) is phylogenetically
the oldest division of the cerebellum and receives input from
the vestibular system and projects back to the vestibular and
reticular nuclei, which in turn projects to the spinal cord and
oculomotor nuclei.
The vestibulocerebellum is important for equilibrium and
for control of the axial muscles that are used to maintain
balance in face of gravity.
The vestibulocerebellum also controls eye movement and
coordinates movements of the head and eyes.
Spinocerebellum (paleocerebellum) receives extensive
somato-sensory input from the spinal cord, auditory, visual
and vestibular systems.
The vermis projects to the fastigial nucleus and from there
influences cortical and brain stem components of the
medial descending systems (axial and girdle muscles).
The intermediate part of cerebellar hemispheres projects
to the interposed nuclei (globose and emboliform) to
control the lateral descending systems (distal muscles of
extremities).
The spinocerebellum receives a continuous flow of
somatosensory information regarding the status of the
musculo-skeletal system, as well as concurrent
information from cortical areas about motor commands.
Cerebrocerebellum (neocerebellum), which occupies the
lateral zone of the cerebellar hemispheres, is phylogenetically
late in development and is particularly well represented in
primates.
This region receives, via the pontine nuclei, most of its
input from sensory, motor and premotor areas of cerebral
cortex.
Most of the outputs of the cerebrocerebellum are to the
dentate nucleus, which in turn projects to the cerebral
cortex.
The cerebrocerebellum is thought to function in the
planning and initiation of voluntary movements.
It is necessary for achieving in rapid limb movements,
especially those involving fine dexterity of the distal
extremities and movements at multiple joints.
Although the divisions of the cerebellum that are on
phylogenetic criteria and comparative anatomic studies
correspond reasonably well to by the locus of the termination
of major afferent projections, this congruence is not total.
Considerable overlap exist between the regions defined by
the anatomic sites of afferent terminations.
Moreover, the physiologic effects of activating afferent
sources project far beyond the boundaries ascribed to
these regions.
In addition, it should be recognized that many symptoms of
cerebellar dysfunction simply defy limitation to any one
division of the cerebellum.
For instance, lesions in certain cerebral and brain stem
areas may likewise interrupt the flow of information to or
from the cerebellum, causing gait disturbance similar to
that seen in disease of the cerebellum itself.
Cerebellar syndromes:
Disturbances:
Postural instability.
Delayed initiation and termination of motor.
Inability to perform continuous, repetitive movements.
Errors in smoothness and direction of a movement.
The lock of coordination or synergy of movement,
especially complex movements.
The lock of motor plasticity or learning.
General rules:
If only one side of the cerebellum is affected, the
symptoms are unilateral and ipsilateral to the lesion.
Lesion of the cerebellum produce errors in the planning
and execution of movements, rather than paralysis or
involuntary movements.
If symptoms predominate in the trunk and legs, the lesion
is near the midline.
If symptoms are more obvious in the arms, the lesion is
in the lateral hemispheres.
The most severe disturbances are produced by lesions in
the superior cerebellar peduncle and the deep nuclei.
Many of the symptoms of cerebellar disease improve
gradually with the time if the underlying disease process
does not itself progress.
Almost all patients with cerebellar lesions have some
type of gait disturbance.
Speech disturbances occur only with bilateral damage.
Signs and symptoms similar to those produced by
cerebellar lesions can appear with disorders that affect
structures adjacent to the cerebellum or affect the
afferent or efferent connections of the cerebellum.
Cerebellum is responsible for monitoring both motor and
nonmotor functions.
Ataxia:
Difficulty regulating the force, range, direction, velocity,
duration and rhythm in smooth performance of voluntary
acts.
Defective timing of sequential contraction of agonist/
antagonist muscle.
Usually persists despite visual cues (unlike ataxia due to
posterior column disease affecting the spinal cord).
Gait ataxia:
Unsteady during ambulation.
Waking with broad-based gait.
Lower center of gravity.
Decrease in the normal, free-flowing arm swing.
Walking heel-to-toe or running the heel of one foot
dawn the shin of the other leg while standing or
waking or lying down if difficult.
Limb ataxia:
Dysmetria = difficulty in bringing a limb smoothly and
accurately to a specific target in space (inability to
control range of movement).
Hypermetria = an involved limb may overshoot its
target.
Hypometria = an involved limb may undershoot its
target.
Asynergia = decomposition of movement = lack of
synergy of various muscles while performing complex
movements (because of errors in the timing and
sequencing of their component parts, may deteriorate
into a series of successive simple movement, rather
than one smooth coordinated movement.
Dysdiadochokinesia = inability to perform rapid
alternating movements, such as rapid supination and
pronation of the forearm.
Intention tremor (kinetic tremor) = rhythmic,
alternating, oscillatory movement of a limb as it
approaches a target, with excessive rebound when
an opposed motion is suddenly released.
Truncal ataxia:
Swaying of the trunk.
Staggering gait.
Difficulty in sitting unsupported.
Bulbar ataxia:
Loss of motor coordination caused by a lesion in the
medulla oblongata..
Cerebellar dysarthria = abnormalities in articulation and
prosody: scanning, slurring, staccato, explosive, hesitant,
garbled speech.
Oculomotor dysfunction:
Pendular nystagmus.
Gaze-evoked nystagmus.
Upbeat nystagmus.
Rebound nystagmus.
Optokinetic nystagmus.
Opsoclonus.
Skew deviation.
Occular bobbing.
Muscle hypotonia:
Usually accompanies acute hemispheric lesions and tends
to decrease with time.
More noticeable in upper limbs and proximal muscles.
Refers to a decreased resistance to passive stretch as
might occur with passive limb movement.
In early and severe cases, a distinct flabbiness of muscle
can be palpated and the muscle accommodates greater
stretch without discomfort.
Pendular deep tendon reflex.
Inability to stop a rapidly moving limb.
Although hypotonia is not as conspicuous as ataxia, it can
exacerbate the symptoms produced by ataxia.
Macrography:
Writing may be larger than normal.
Lack of poise:
Inability to carry out motor activities against the force of
gravity.
Particularly evident during rapid changes in body position or
in direction of movement.
Unsteadiness of gait or an inability to sit or stand without
swaying or falling.
Delays in the initiation and termination of movement.
Intentional movements, such as grasping or pointing, may be
slowed in both the buildup and the relaxation of force.
The movement of an affected limb is delayed and slowed.
Nonmotor deficits:
Cerebellar cognitive affective syndrome:
Executive function (impairments of set-shifting,
abstract reasoning, verbal fluency and working
memory.
Spatial cognition (visual-spatial disorganization,
impaired visual-spatial memory).
Language (dysprosodia, agrammatism, mild anomia).
Emotional, personality and behavioral changes:
Disinhibited and inappropriate behavior (anxiety,
hyperactivity, impulsiveness, irritability, dysphoria,
apathy).
Lowering of intellectual function.
Archicerebellar syndrome:
Disorders cause disturbances of locomotion and
equilibrium, with permanent truncal and gait ataxia.
Patients with isolated flocculonodular lesions lose their
ability to stand or to walk without swaying or falling and
trend to fall even when sitting with their eyes open.
When the effects of gravity are reduced by the patient
lying in bed or being physically supported, movements
may be completely normal.
Abnormalities of posture and station (e.g.: head tilt) and
eye movements also occur.
Eye movement disorders (nystagmus, disturbances of
vestibulo-ocular reflexes.
Tremor is not evident and muscle tone remains normal.
Paleocerebellar syndrome:
The cardinal feature is involvement of legs.
The gait is wide-based and ataxic, with small hesitant
steps.
Spinocerebellar ataxia reflects a more general deficit in
the control of the muscles of ambulation, where
vestibule-cerebellar ataxia reflects a particular
inability to control the leg muscles in the presence of
the force of gravity.
Muscle hypotonia.
Neocerebellar syndrome:
Damage of the lateral cerebellar hemispheres and
dentate nucleus disturbs skilled coordinated
movements and speech.
Errors in direction, deviation from proper course,
dysmetria, dysdiadochokinesia and intention tremor all
may be present, especially in movements of upper
extremities.
The gait may actually be normal, reflecting the relative
sparing of the axial muscles and lower limbs.
Intentional movements, such as grasping or pointing, may
be delayed in their initiation and slowed in both the
buildup an relaxion of intended force.
Stretch reflexes and muscle tone are often diminished,
resulting in flabbiness, lock of check and pendular deep
tendon reflexes.
Dysarthric speech may occur with bilateral involvement
and can be pronounced.
Oculomotor disturbances may also occur.
Pancerebellar syndrome:
Bilateral signs of combination of all cerebellar syndromes.
Etiology:
Although cerebellar disorders as a whole are not very
common, a wide variety of factors, both inherited and
acquired, can adversely affect cerebellar function.
Inherited or idiopathic degenerations:
Spinocerebellar ataxia: (e.g.:Friedriechs ataxia)
Cerebellar ataxia: (e.g.: olivopontocerebellar atrophy).
Developmental disorders:
Arnold-Chiari malformations.
Dandy-Walker malformation.
Congenital cerebellar hypoplasia.
Nutritional disorders:
Vitamin B1 (thiamine) deficiency.
Vitamin B12 (cobalamin) deficiency.
Vitamin E deficiency.
Neoplastic disorders:
Astrocytoma.
Medulloblastoma.
Cerebellar metastasis.
Tumors of the cerebellopontine angle.
Paraneoplastic cerebellar degeneration.
Infections:
Creutzfeldt-Jakob disease.
Cerebellitis with viruses, bacteria, fungi, parasites.
Vascular disorders:
Cerebellar infarction.
Cerebellar hemorrhage.
Intoxications:
Drug-induced cerebellar syndrome.
Recreational or accidental exposure to volatile
solvents.
Poisoning with heavy metals.
Injury due to physical or mechanical trauma:
Trauma of the head, particularly in the area of the
occiput.
Metabolic disorders:
Inherited and acquired disorders of lipids, urea cycle,
pyruvate and lactate metabolism.
Demyelinating disorders:
Multiple sclerosis.
X. THALAMIC SYNDROMES
SNr.
SNr bears a strong resemblance, both structurally and
functionally, to the GPi.
SNr is an important processing center in basal ganglia.
The neurons in SNr are mainly GABAergic.
The main input to the SNr derives from striatum and
comes by two routes, direct and indirect pathways.
The direct pathway consist of axons from striatum that
project directly to SNr.
The indirect pathway consists of three links: a) a
projection from striatum to the GPe; b) GABAergic
projection from GPe to the STN; c) glutamatergic
projection from STN to SNr.
Striatal activity exerts an excitatory (or rather
disinhibitory) effect on SNr neurons via direct
pathway, but an inhibitory effect via indirect pathway.
GABAergic neurons in SNr convey the final processed
signals of the basal ganglia to the thalamus and
superior colliculus.
SNr inhibits DAergic activity in the SNc via axon
collaterals.
The GABAergic neurons of SNr spontaneously fire
action potentials.
The purpose of these spontaneous action potentials is
to inhibit targets of the basal ganglia and decreases in
inhibition are associated with movement.
SNc.
The most prominent function of the SNc is fine motor
control.
SNc is heavily involved in learned responses to stimuli.
SNc is important in spatial learning, the observations
about ones environment and location in space.
Temporal processing is also an important function of
SNc.
SNc has been suspected of regulating the sleep-wake
cycle (insomnia, REM sleep disturbances).
Akinesia/bradykinesia:
Akinesia means the absence or failure of movement.
Bradykinesia means slowness of movement.
Together they are the terms used to definite the
difficulty PD patients have in initiating and executing a
motor plan.
The nature and severity of akinesia/bradykinesia
worsen over the course of illness.
Early on, hypokinesia (falling short of the mark when
executing a movement) is nearly always present, later
progressing to bradykinesia (slowed movements) and,
finally, to akinesia.
Early signs may be confined to distal muscles
(micrographia, decreased dexterity, impaired
sequential finger movements).
Particularly difficult for patients are sequential actions,
such as alternating pronation-supination of the hand
and complex motor acts, such as buttoning a shirt.
Quick repetitive movements, such as repeated
opposition of the forefinger and thumb, will typically
show a rapid decrease in amplitude and frequency.
In more advanced stages, patients have difficulty rising
from a chair and display a generalized slowing of
voluntary movements.
Inability to perform simultaneous actions.
Difficulty rolling in bed or rising from a seated
position.
Facial and vocal manifestations of bradykinesia
(hypomimia, masked facies, hypophonia, monotonic or
festinating speech, palilalia, dysarthria, dysphagia and
sialorrhea) are often apparent to the clinician before
the formal examination has even begun.
Rapid fatigue with repetitive movements.
Akathisia (an unpleasant desire to move).
Freezing.
Bradykinesia probably plays a greater role than
rigidity in determining a patients degree of disability.
Postural instability:
Postural instability with associated gait disorder is
usually the last of the four cardinal sings to appear.
Postural instability proves to be the most disabling, least
treatable manifestations of PkS.
No single factor is alone responsible for postural
instability and gait disturbances (it stems from a
combination of changes in postural adjustment, the
loss of postural reflexes, rigidity and akinesia).
Loss of postural reflexes often occurs early but is
rarely disabling until years later.
The patients adopt a stooped posture with flexion of
the neck and trunk.
The arms held in an adducted position with elbows
flexed.
Once a patient starts to lose the ability to make rapid
postural corrections, a tendency to fall forward or
backward becomes evident (pull test with
retropulsion).
The earliest sign of gait disturbance is often decreased
arm swing, but over time patients also begin to walk
with short, shuffling, uncertain step.
Gait initiation and turning become particularly
difficult.
Once walking has begun, the loss of postural reflexes
and stooped posture combine to produce a festinating
gait (in effort to retain balance, the patient walks faster
and faster in a shuffling manner, as the legs try to catch
up with the bodys forward momentum).
Although the gait is unsteady, the base is usually
minimally or not at all widened and truncal ataxia is
absent.
Freezing is a phenomenon distinct from other forms of
akinesia because it is during ambulation and it proves
most troublesome.
Patients freeze especially when starting to walk (start
hesitation), attempting to turn or approaching a
narrow or crowded space (doorways, corners, closets,
a sidewalk with heavy traffic).
Sitting en bloc represents a special form of freezing
in which a patients literally falls into a chair.
Kinesia paradoxica (opposite of freezing) is the term
used to describe sudden short periods of relatively
effortless mobility experienced by a few patients.
Musculoskeletal deformities:
Deformity of the hands and feet are common in PD.
The parkinsonian hand display ulnar deviation,
flexion of metacarpophalangeal and distal
interphalangeal joints and extension of the proximal
interphalangeal joints (striatal hand).
The great toe can be tonically extended with
remaining toes curled claw-like.
Coincident with rigidity, mild scoliosis may be seen,
concave contralateral to the affected side.
Later, kyphosis becomes prominent and contributes to
the disabiling postural changes of advanced disease.
Pain and sensory symptoms:
Although peripheral nerve diseases is not associated
with PD, pain and sensory complaints are surprisingly
common.
Pain is often proportional to the degree of motor
dysfunction an may be take the form of muscle cramps,
stiffness, dystonia, radiculopathy or arthralgias.
Paresthesias, numbness, burning or tingling may occur
at any stage of the disease, independent of the degree
of motor manifestations.
Autonomic dysfunction.
Bowel and bladder symptoms:
Urinary difficulties include hesitancy, urgency and
increased frequency.
Constipation.
Sexual dysfunction is a frequent compliant and may
involve both loss of libido and impotence.
Episodic sweating occurs in some patients.
Orthostatic hypotension with dizziness and fainting
is uncommon in PkS.
Dermatologic problems:
Chronic seborrhea leads to greasy skin, particularly on the
face.
Sleep disorders:
Excessive daytime somnolence.
Sleep fragmentation.
Total sleep time is reduced.
Male PD patients have rapid eye movement (REM)
sleep behaviour disorder, in which excessive motor
activity occurs during dreaming.
Pathophysiology of PD.
Bradykinesia and rigidity are result of degeneration of
DA-ergic nigrostriatal tract which leads to the
preponderance of activity in the indirect pathway
(hyperactivity in the indirect pathway and
hypoactivity in the direct pathway) with consecutive
increase of inhibitory basal ganglia output to the
thalamus (increased tonic inhibition of thalamocortical
neurons by excessive output from GPi/SNr may reduce
the responsiveness of cortical mechanisms involved in
motor control).
Tremor is a result of oscillatory activity in motor areas
of the basal ganglia or of the thalamus output nuclei
which lead to rhythmic activity in thalamocortical
cells and in turn may lead to oscillations in
corticospinal projection neurons.
Cognitive and behavioral disturbances reflect
disruption of nondopaminergic (serotoninergic)
pathways.
Pain and sensory symptoms possible reflects a role for
the basal ganglia in sensory processing (altered
striatal input to sensory centers in the thalamus).
Autonomic dysfunction can be the consequence of the
Lewy body neuropathology described within the
myenteric plexus and partial or complete loss of
autonomic innervations.
Unified Parkinsons Disease Rating Scale (UPDRS):
Contains six sections:
The first is a limited assessment of mentation,
behaviour and mood.
The second is assessment of activities of daily living in
both on and off state, determined by history.
The third is a detailed motor examination based on the
widely used Columbia scale.
The fourth is a questionnaire assessing complications,
focusing principally on fluctuations and dyskinesias.
Myoclonus:
Myoclonus (Mc) is a movement disorder:
Mc is a brief jerk caused by neuronal discharges.
A myoclonic jerk consist of a single muscle discharge but
can be repetitive, giving rise to a salvo of muscle activity.
Myoclonic jerks mai occur alone or in sequence, in a
pattern or without pattern.
Mc is caused by rapid contraction (positive Mc) and
relaxation (negative Mc) of the muscle.
Both forms often share the same etiology, coincide in the
same patients and can even affect the same muscle group.
It is important to realize that different patterns of Mc are
often combined in the same subject.
Mc can be classified from various point of view:
Clinical presentation:
Spontaneous.
Action.
Reflex.
Clinical distribution:
Generalized.
Multifocal.
Segmental.
Focal.
Neurophysiological origin:
Cortical.
Brain stem (reticular).
Spinal cord.
Epileptic myoclonus:
Cortical reflex Mc.
Reticular reflex Mc.
Primary generalized epileptic Mc.
Photic cortical reflex Mc.
Juvenile myoclonic epilepsy.
Progressive myoclonic epilepsy.
Etiology:
Physiological.
Essential.
Symptomatic (associated with epilepsy or associated with
other causes).
Normal Mc:
Hiccups: Mc of the diaphragm.
Hypnic jerks: involuntary myoclonic twitch during
hypnagogia just as a person is beginning to fall asleep
or during the non-REM sleep, often causing awaken
suddenly.
Essential Mc:
Essential Mc occurs in the absence of the epilepsy or
other apparent abnormalities in the brain or nerves.
The EEG should be normal.
Familial cases as well as sporadic cases are seen.
The Mc is generalized, appears to occur seldom at rest
and is clearly induced by action.
Reflex Mc:
Somesthetic, visual and auditory stimuli,
independently and in combination may trigger Mc.
Such Mc is focal or generalized in distribution.
Action Mc:
Action Mc occurs during active muscular contraction
and affects both posturally acting muscles and prime
action.
Action Mc may be focal or segmental, but the most
common distribution is multifocal or generalized.
Negative Mc (astreixis):
Negative Mc is present only during active muscular
contraction and in fact is almost always combined with
positive action Mc.
Negative Mc are two major clinical presentation: a)
asterixis; b) postural lapses.
Spontaneous Mc:
Spontaneous Mc may be focal, multifocal or
generalized.
It may be sporadic and occur unpredictably or coincide
with specific movements, such as in normal people
with nocturnal myoclonus or in patients with early
morning myoclonic epilepsy.
In other instances, it may be almost continuously
present, as in patients with metabolic
encephalopathies or Creutzfeldt-Jakob disease.
Orbitofrontal cortex:
Especially areas 10, 11, 12 and 47 Brodmann.
It has extensive connections with other association
cortices, primary motor, primary sensory, olfaction,
gustatory, visual streams, striatum and other
subcortical areas
It is involved in: emotional impulse control, arousal,
personality, reactivity to the surroundings and mood.
Orbitofrontal circuit connects the frontal monitoring
systems to the limbic system
A particular area Anterior cingulate gyrus (areas 24
and 25 Brodmann) appears to be most associated with
mood (particularly depression and mania).
Premotor cortex (supplemental motor area, secondary
motor cortex, area 6 Brodmann):
It is immediately anterior to the motor cortex.
It has many of the same connections as motor cortex.
Its output is to motor cortex, with a smaller output to the
brain stem and spinal cord.
This region receives input from sensory association cortex
as well as feedback from the basal ganglia via the VA and
VL of the thalamus.
Frontal eye field (inferior area 8 Brodmann):
It is located just inferior and rostral to the premotor
cortex.
Its activity in this region results in conjugate horizontal
gaze of the eyes away from the stimulus.
This receives input from the medial dorsal nucleus of the
thalamus as well as other areas of the cerebral cortex.
It makes output to the superior colliculus and the para-
median pontine reticular formation (PPRF).
Broca area:
Broca area has two executive language regions.
The first and main executive region is found on the
inferior third frontal gyrus (opercular and triangular
portions of inferior frontal gyrus areas 44 and 45
Brodmann).
Localized in the dominant hemisphere is involved in
the coordination or programming of motor
movements for the production of speech sounds (does
not directly cause movement to occur).
In the nondominant hemisphere, Broca area is
involved in the ability to generate inflections of voice.
Visually perceived words are given expression in writing
through a second executive language area.
Motor area (precentral gyrus, primary motor cortex,
Brodmann area 4):
It is in the precentral gyrus and is the origin of most of the
corticospinal tract and a large number of corticobulbar
fibers.
There is a very-defined somatotopic organization of motor
cortex.
Cortical motor homunculus is a visual representation of
the concept of the body within the brain.
The homunculus is like an upside-down motor map of
contralateral side of the body.
The resulting image is a grotesquely disfigured human
with disproportionately huge hands, lips and face in
comparison to the rest of the body.
Because of the fine skills harvest found in these
particular parts of the body, they are represented as
being larger on the homunculus.
Specific movements tend to be represented (such as
elbow flexion) rather than specific muscle.
Motor area has projections to the thalamus and basal
ganglia.
Thalamus (VL nucleus) makes significant input to the
motor cortex.
The precentral gyrus receives significant input from
sensory cortical areas as well as from the premotor cortex.
Frontal lobe syndromes:
Effects of frontal lobe disease may be summarized as
follows:
Effects of unilateral frontal lobe disease, either left or
right:
Contralateral spastic hemiplegia.
Slight elevation of mood.
Increased talkativeness.
Tendency to joke.
Lock of tact.
Difficulty in adaption.
Loss of initiative.
If entirely prefrontal: a) no hemiparesis; b) grasp and
suck reflexes or instinctive grasping may be released.
Anomia with involvement of orbital parts.
Effects of dominant frontal lobe disease:
Motor speech disorder with agraphia, with or without
apraxia of lips and tongue.
Apraxia of left hand.
Loss of verbal associative fluency.
Perseveration.
Changes seen in first section of frontal lobe disease.
Effects of bifrontal disease:
Bilateral hemiplegia.
Spastic pseudobulbar palsy.
If entirely bilateral prefrontal: a) abulia; b) akinetic
mutism; c) lack of ability to sustain attention and solve
complex problems; d) rigidity of thinking; e) bland
affect; f) social ineptitude; g) behavioral disinhibition;
h) inability to anticipate; i) labile mood; j) varying
combinations of grasping, sucking, decomposition of
gait and sphincteric incontinence.
Motor cortex syndromes:
Contralateral hemiparesis.
Hemiparesis is with faciobrachial prevalence.
Rarely, hemiparesis is with lower limb prevalence.
Hemiparesis is frequently associated with other cortical
signs (aphasia in the dominant hemisphere, apraxia,
agnosia, jacksonian epileptic seizures).
Broca aphasia = expressive aphasia = motor aphasia =
non-fluent aphasia = anterior aphasia.
Lesion in frontal suprasylvian region (44 & 45
Brodmann areas) in dominant hemisphere.
Speech is telegraphic, meaning that articles,
conjunctions, prepositions, auxiliary verbs (function
words) and morpho-logical inflexions ( e.g.: plurals,
past tense), are omitted.
Speech output (sentences) is severely reduced and
limited to short utterances of less than four words and
restricted to noun-verb combinations.
Syntax and morphology are affected
Speech is laborious and clumsy.
Comprehension relatively preserved (the person may
understand speech relatively well and be able to read or
write beyond an elementary level).
Repetition is impaired.
Associated signs: right arm and face weakness.
Pure word mutism (aphemia, pure motor aphasia of
Djrine):
The patient looses all capacity to speak while retaining
perfectly the ability to write, to understand spoken
words, to read silently with comprehension and to
repeat spoken words.
Facial and brachial paresis may be associated.
Lesion is anterior and superior to Broca area.
Transcortical motor aphasia:
The patient is unable to initiate conversational speech,
producing only a few grunts or syllables.
Comprehension is relatively preserved, but repetition is
strikingly intact.
This type of aphasia occurs in two clinical context:
In a mild or partially recovered Broca aphasia in which
repetition remains superior to conversational speech.
In states of abulia and akinetic mutism with frontal
lobe damage.
Several cases have resulted from infarctions in the
watershed zone between the anterior and middle cerebral
arteries.
In the nondominant hemisphere, lesions of the regions of
the brain that are analogous to Broca area affect to
generate inflexion of voice (aprosodia).
Apraxia.
Left frontal lesions, especially near supplementary motor
and premotor cortices, can cause limb apraxia without
loosing knowledge or understanding of the movement.
There is often a concomitant apaxia of speech (buccofacial
apraxia).
Callosal apraxia also may occur with anterior cerebral
artery stroke, causing unilateral left-limb apraxia.
Constructional apraxia localizes to the right hemisphere
or to the frontal lobes.
Orbitofrontal syndrome:
The orbitofrontal syndrome is the most dramatic of all
frontal lobe disorders.
The predominant behavioral change is social disinhibition
(personality change):
Ignore social conventions and exhibit undue
familiarity, talking to strangers and touching or
fondling others without permission.
The patients are tactless in conversation and may
make uncivil or lewd remarks.
The patients are impulsive, responding immediately
and unpredictably to changing environmental
circumstances.
The patients lack empathy and are unsympathetic to
the needs of others.
The patients lock conscientiousness and fail to
complete assigned tasks.
The patients are unconcerned about the consequences
of their behavior and may engage in activities that
endanger themselves or others.
Risk assessment is poor.
Mood alterations accompany the orbitofrontal syndrome.
Lability and irritability are the most common changes
(patients rapidly shift from happiness to anger or
sadness).
Anger can often be relieved by redirecting the patients
attention to some new activity.
Hypomania or mania may accompany orbitofrontal
dysfunction, characteristic if the lesion affects the right
hemisphere.
Involvement of orbitofrontal cortex (OFC) is often
implicated in addictive behavior in addition to nucleus
accumbens and amygdala.
Addicted individuals show deficits in orbitofrontal, striatal
and thalamic regions.
Conscious and unconscious components are hypothesized
to serve as mechanisms responsible for maintenance drug
addiction.
In addition, hypoactivity in the OFC in the alcoholics is
further supported by blunted metabolism in the OFC to
response to both serotoninergic and GABA-ergic agents.
Patients with inferior mesial lesion tend to manifest
anterograde and retrograde amnesia and confabulation.
Frontomedial syndrome (anterior cingulate syndrome):
The frontomedial syndrome:
Marked by apathy.
Emotionally, the apathetic individuals is unmotivated
to initiate new tasks and there is a disinterest in
establishing or accomplishing goals.
Cognitively, the apathetic individuals fails to formulate
or implement plans and activities.
N.B.: The patient with a left unilateral lesion may have
transcortical motor aphasia characterized by transient
mutism recovering to a nonfluent verbal output with
preserved repletion and comprehension.
Motorically, apathetic individuals have reduced
activity (they may sit for a long periods without
participating in conversation or activities).
The grasp reflex is commonly present; a) contact
grasp; b) traction grasp; c) magnetic grasp.
In the most extreme form of apathy (bilateral lesions of
anterior cingulate):
Permanent akinetic mutism:
Wakeful state;
Prominent apathy;
Indifference to pain, thirst or hunger;
Lock of motor and psychic initiative;
Spontaneous movements;
Verbalization and respond to commands;
Such individuals will eat if fed;
The patients are not paralyzed;
The patient may be incontinent.
A severe but less enduring defect in retentive memory
has been observed with infarction of septal gray matter, a
cluster of midline nuclei at the base of frontal lobe, just
below the interventricular septum and including the
septal nucleus (connected with the hippocampus and
amygdala), nucleus accumbens and paraventricular
hypothalamic gray matter.
The amnesic syndrome that follows ruptured anterior
communicating aneurysm is due to a lesion involving
these nuclei.
N.B.: The frontomedial syndrome must by distinguished
from locked-in syndrome or catatonia.
Opercular syndrome (anterior opercular syndrome, Foix-
Chavany-Marie syndrome):
Rare disorder due to bilateral lesions of opercular cortex
surrounding the insula.
Loss of voluntary control of facial, pharyngeal, lingual,
masticatory and sometimes ocular muscle activity.
Decreased gag reflex.
Absence of emotionalism.
Frontal lobe epilepsies (FLE):
FLE are a focal type of epilepsy originating from an
epileptic focus anywhere within the frontal lobe.
Complex and varied patters in the spread of seizure
discharges explain the variability in the clinical and EEG
manifestations of FLE.
General characteristics:
Generally short seizures.
Complex partial seizures arising from frontal lobe,
often with minimal or no postictale confusion.
Rapid secondary generalization (more common in
seizures of frontal lobe than of temporal lobe
epilepsies).
Prominent motor manifestations which are tonic or
postural.
Complex gestural automatisms frequent at onset.
Frequent falling when the discharge is bilateral.
Seizures from the motor cortex:
Simple focal motor-clonic or tonic-clonic seizures with
or without jaksonian march and their localization
depend on the side and topography of area involved.
In cases of lower prerolandic area there may be speech
arrest, vocalization or dysphasia, tonic-clonic
movements of the face on contralateral side or
swallowing.
Generalization of the seizure frequently occurs.
In the rolandic area, partial motor seizures without
march or jaksonian seizures occur, particularly
beginning in the contralateral upper extremities.
In the case of seizures involving the paracentral lobule,
tonic movements of ipsilateral foot may occur as well
as the expected contralateral leg movements.
Post ictal (Todd paralysis) is frequent.
Seizures from the supplementary motor area:
Hyper motor seizures (sudden and explosive) of
bizarre bilateral, asymmetric tonic posturing and
movements.
Complex gestural automatisms.
Extreme motor restlessness.
Complex motor automatisms and agitation.
Frenetic complex motor automatisms of both arms and
legs.
Intensity affective vocal and facial expression
associated with powerful bimanal-bipedal and axial
activity..
Repetitive rhythmical and postural movements
accompa-nied by bizarre vocalization.
Complex motor automatisms with kicking and
thrashing.
Complex and global gesticulations.
Anterior frontopolar region:
Forced thinking.
Initial of contact and adversive movements of head
and eyes.
Contraversive movements.
Axial clonic jerks and fall.
Autonomic signs.
Dorsolateral region:
Tonic or, less commonly, clonic movements.
Versive eye and head movements.
Speech arrest.
Orbitofrontal region:
One of complex partial seizures.
Initial motor and gestural automatism.
Olfactory hallucinations and illusions.
Autonomic signs.
Opercular region:
Mastication, salivation, swallowing, laryngeal
symptoms, speech arrest, epigastric aura, fear,
gustatory hallucinations and autonomic phenomena.
Simple partial seizures, particularly partial clonic facial
seizures, are common and may be ipsilateral.
Cingulate region:
Complex partial seizures with complex motor gestural
automatisms at onset.
Autonomic signs are common, as are changes in mood
and affect.
Other types of frontal lobe seizures:
Epilepsia partialis continua Kozhevnikov
Frontal absences.
forced thinking and forced acts.
Gelastic seizures
Lesions of frontal lobes:
Degenerative:
Pick disease.
Alzheimer disease.
Dementia with Lewy bodies.
Frontotemporal dementia.
Amyotrophic lateral syndrome with dementia.
Vascular:
Anterior cerebral artery occlusion medial frontal
syndrome.
Anterior cerebral artery/communicating anterior
artery aneurysm rupture orbitofrontal syndrome.
N.B.: some patients develop infarctions in the basal
forebrain.
In addition to the akinesia and personality changes,
patients may develop a striking confabulatory amnesia
that is severe and permanent and that resembles
Wernicke-Korsakoff syndrome.
Mild anomia may be present.
Finally, a syndrome of affective depression may occur
after strokes affecting predominantly the left frontal
lobe.
Bilateral cerebral artery infarct is associated with a
syndrome of quadriparesis (legs worse than arms) and
akinetic mutism.
Occlusion of the artery of Heubner may cause
infarction of the head of the caudate nucleus and may
result in an agitated confusional state that evolves to
akinesia, abulia and mutism, along with personality
changes.
Infarction of the anterior branches of the upper
division of the middle cerebral artery which supply
parts of the lateral prefrontal cortex may be
characterized by planning deficits, impairment of
working memories and apathy.
Borderzone infarctions between the distribution of
the anterior and middle cerebral arteries are
characterized by the man-in the barrel syndrome
with proximal weakness at the shoulder and hip.
Traumatic:
Closed head injury orbitofrontal contusion,
diffuse axonal injury to white matter fibers.
Middle cerebral artery occlusion lateral
convexity.
Binswanger disease hemispheric white matter.
Demyelinating:
Multiple sclerosis white matter (especially peri-
ventricular).
Metachromatic leucodystrophy white matter
(begins frontally).
Marchiafava-Bignami disease corpus callosum
(anteriorly).
Neoplastic:
Meningioma subfrontal orbitofrontal.
Meningioma convexity lateral convexity.
Meningioma falcine medial frontal.
Glioblastoma, oligodendroglioma, metastasis local with
diffuse edema.
Infectious:
Creutzfeldt-Jakob disease focal onset with rapid spread.
Syphilis prefrontal.
Herpes encephalitis orbitofrontal and temporal.
Inflammatory:
Systemic lupus erythematosus or other inflammatory
disorders diffuse.
Parietal lobe:
Parietal lobe extends from the central sulcus (Rolando
fissure) anteriorly to the imaginary parietal-occipital fissure
posteriorly, above temporal lobe (Sylvian fissure).
There is a parietal lobe in each hemisphere and one is not
completely a mirror image of the other, especially in the
functional level.
Each lobe shows three parts: a) the postcentral gyrus; b)
the superior parietal lobule; c) the inferior parietal lobule.
The inferior lobule includes the angular and
supramarginal gyri.
From the medial aspect, the parietal lobe contains:
The postcentral gyrus part of paracentral lobule.
Part of cingulate gyrus.
Precuneus.
Primary sensory strip (postcentral gyrus) = Brodmann
areas 3, 1 & 2.
Secondary sensory area (superior parietal lobule, sensory
associated areas) = 5 &7 Brodmann areas.
Supramarginal gyrus = 40 Brodmann area.
Angular gyrus = 39 Brodmann area.
Afferents:
Ventral posterior nucleus of thalamus.
Commissural fibers from the opposite somatic sensory
cortex through the corpus callosum.
Short association fibers from the adjacent primary
motor cortex (collaterals of corticospinal fibers).
Efferents:
Association fibers pass to the ipsilateral motor cortex
and to area 5 and area 40 Brodmann.
Commissural fibers pass to the contralateral
somesthetic cortex.
Projection fibers descend to the ventral posterior
nucleus of the thalamus of the same side and the
posterior column and spinal posterior gray horn of the
opposite side.
The first function of the parietal lobes is to integrate
sensory information to form a single perception
(cognition).
The dominant lobe is particularly important for:
Perception, interpretation of sensory information.
Formation of idea of a complex meaningful motor
responses to the stimuli.
Language, mathematical operations, body image
(supra-marginal gyrus and angular gyrus).
The nondominant lobe is especially important for visual-
spatial functions.
The posterior parietal cortex receives somatosensory
and/or visual input, which then, through motor
signals, control movement of the arm, hand, as well as
eye movements.
The parietal-temporal-occipital (PTO) junction is an asso-
ciation area located in the cortex of human brain, which
includes portions of parietal lobe (Brodmann areas
39 angular and 40 supramarginal), temporal lobe
(Brodmann area 37 fusiform) and occipital lobe
(Brodmann area 19 peristriate).
This association area one of three in the cortex is
responsible for the assembly of auditory, visual and
somatosensory information system.
Meaning is assigned to stimuli in PTO, which outputs
to numerous other areas of the brain. Notably the
limbic and prefrontal areas, which are involved in
memory.
In the dominant hemisphere, the PTO is involved in
language recognition (reading, listening and writing).
In the nondominant hemisphere, the PTO identifies
the spatial characteristics of objects and is involved
in spatial awareness.
Parietal lobe syndromes:
Either hemisphere:
Hemianesthesia (pseudo-thalamic syndrome).
Tactile inattention.
Unilateral muscular atrophy.
Hemiataxia.
Homonymous incongruent hemianopsia.
Unilateral visual inattention and disorientation.
Neglect of one half of body and extrapersonal space.
Constructional apraxia.
Dominant hemisphere:
Bilateral idiomotor apraxia (motor apraxia, kinesthetic
apraxia limb-kinetic apraxia):
Loss of ability to carry out, on command, a complex or
skilled movement, though the purpose thereof is clear
to the patient.
Bilateral ideational apraxia:
Loss of ability to conceptualize, plan and execute the
complex sequence of motor actions involving the use
of tools or objects in everyday life.
The patient has lost the perception of the objects
purpose.
Disturbance in the idea of sequential organization of
voluntary actions.
Cannot perform a series of acts although able to
perform individual components of the series.
Loss of conceptual knowledge associated with objects
and overall goal of the activity sequence.
Disorder of language.
Tactile agnosia (bimanual asteriognosis).
Visual autotopagnosia.
Dyslexic types of aphasia (conduction aphasia, lesions in
supramarginal gyrus):
Severely defective repetition.
Paraphasia in repletion and in spontaneous speech.
Normal comprehension.
Impaired writing spontaneous and to dictation.
Errors in spelling, word choice and syntax.
Pain asymboly.
Gerstman syndrome (angular syndrome):
Dysgraphia/agraphia (deficiency in the ability to
write).
Dyscalculia/acalculia (difficulty in learning or compre-
hending mathematics).
Finger agnosia (inability to distinguish the finger on
the hand).
Left-right disorientation (inability to distinguish right
from left).
Nondominant hemisphere:
Topographic disorientation.
Topographic memory loss.
Dressing apraxia ( lesions in inferior parietal lobule).
Constructional apraxia ( lesions in inferior parietal
lobule).
Hemiinattention.
Contralateral neglect a part of the body.
Anton-Babinski syndrome:
Asomatognosia (inability to recognize part of ones
body).
Anosodiaphoria (indifference to illness).
Anosognosia (denial of illness).
Spatial neglect.
Apraxia of eye opening.
The individual typically has difficulty putting together
puzzle.
Bilateral parietal lobe:
Blint syndrome:
Bilateral damage to the posterior superior watershed
area of parietooccipital junction (Brodmann areas 7 &
19).
Paralysis of visual fixation.
Optic ataxia (the inability to guide the hand toward an
object using visual information).
Ocular apraxia (inability to voluntarily control gaze
and inability to carry out familiar movements when
asked to do so).
Spatial disorientation
Inability to execute voluntary movement in response
to visual stimuli.
Despite normal field of view and normal acuity, the
patients perceives only one object, from which he can
hardly move his eyes, while all other objects are not
recognized.
Simultanagnosia inability to perceive the visual field
as a whole (inability to perceive simultaneous events
or objects in ones visual field (difficulty integrating
components of visual scene).
Pure cases are extremely rare, often associated with
alexia, prosopagnosia, visual field deficits.
Agraphias:
Pure agraphia:
Aphasic agraphia:
Spelling and grammatical errors abound.
Special forms of agraphia caused by abnormalities of
spatial perception and praxis.
Constructional agraphia:
Words are formed clearly enough but are wrongly
arranged on the page.
Words may be superimposed, reversed, written
diagonally or haphazard arrangement, or from right to
left.
With right parietal lesions, only the right of the page is
used.
Usually one finds other constructional difficulties as
well, such as inability to copy geometric figures or to
make drawings of clocks, flowers, or maps.
Apraxic agraphia:
Language formation is correct and the spatial
arrangements of words are respected, but the hand
has lost its skill in forming letters and words.
Handwriting becomes a scrawl, losing all personal
characters.
Apraxias:
An inability to use body parts successfully.
An inability to carry out learned skilled, purposeful
movements to command or in imitation, despite intact
motor and sensory systems, good comprehension, normal
volition normal cognition and full cooperation.
The subject cannot produce the correct movement in
response to verbal command, nor imitate correctly a
movement performed by the examiner, nor perform a
movement correctly in response to a scene or object,
nor handle an object correctly.
Apraxias result from disconnections of the posterior
speech area from the association areas lying anterior to
the primary motor cortex, and from disconnections of the
visual association areas from these motor association
areas.
Auditory disorders:
Cortical deafness appears in bilateral lesions of Heschl
gyri.
Lesions of the secondary (unimodal association) zones of
auditory cortex Brodmann area 21 and part of
Brodmann area 22 have no effect on the perception of
sounds and pure tones.
However, the perception of complex combinations of
sounds is severely impaired (auditory agnosia).
Amusia is a form of the auditory agnosia and appears
in lesions of nondominant hemisphere.
Nondominant hemisphere is important for
recognition of harmony and melody (in the absence of
words), but that the naming of musical scores and all
the semantic (writing and reading) aspects of music
require integrity of dominant temporal and probably
the frontal lobes as well.
Auditory illusions (paracusias) :
Sounds or words may seem strange or disagreeable.
Sounds or words may seem to be repeated, a kind of
sensory perseveration.
Auditory hallucinations:
Elementary (e.g.: murmurs, blowing, sound of running
water or motors, whistles, clangs, sirens).
Complex (e.g.: musical themes, choruses, voices).
Hearing may fade before or during hallucinations.
In temporal lobe epilepsy, the hallucinations may
occur alone or in combination with visual or gustatory
hallucinations, visual distortions, dizziness and
aphasia.
Vestibular disturbances:
If the cortical vestibular area is destroyed on one side, the
only clinical effect may be subtle change in eye
movements on optokinetic stimulation (mere often a
result of parietal damage).
Epileptic activation of this area may occur vertigo or
sense of disequilibrium.
Pure vertiginous epilepsy does occur but is a rarity.
Area V3:
Dorsal V3 (anatomically located in Brodmann area 19)
is normally considered to be part of the dorsal stream,
receiving inputs from V2, may play a role in the
processing of global motion.
Ventral V3 has much weaker connections from the V1
and stronger connections with the inferior temporal
cortex.
Area V4:
It is the third cortical area in the ventral stream,
receiving strong feedforward input from V2 and
sending strong connections to the posterior
inferotemporal area and has weaker connections to
V5.
It is the first area in the ventral stream to show strong
attentional modulation.
Like V1, V4 is tuned for orientation, spatial frequency
and color.
Unlike V1, V4 is tuned for object features of
intermediate complexity (simple geometric shapes).
V4 is not tuned for complex objects such as faces, as
areas in the inferotemporal cortex are.
Area V5, also known as visual area middle temporal (MT),
is a region of extrastriate visual cortex that is thought to
play a major role in the perception of motion, the
integration of local motion signal into global percepts and
guidance to some eye movements.
Occipital lobe syndrome:
Clinical effects of occipital lobe lesions:
Visual field defects:
Homonymous hemianopsia = loss of vision in
corresponding halves of visual fields:
a) if the field defects in the two eyes are identical
(congruous), the lesion is likely to be in the calcarine
cortex and subcortical white matter of the occipital
lobe;
b) if the field defects are incongruous, the visual fibers
in the optic tract or in parietal or temporal lobe are
more likely to be implicated;
Insular lobe.
Insular lobe (insula, insular cortex) is a portion of the
cerebral cortex folded deep within the lateral sulcus between
the temporal lobe and the frontal lobe.
The cortical area overlying it towards the lateral surface of
the brain is the operculum (formed from parts of the
enclosing frontal, temporal and parietal lobes)
Operculum is believed to be involved in consciousness.
The insular cortex is divided into two parts:
The larger anterior insula receives: a) a direct
projection from the basal part of ventral medial
nucleus of the thalamus; b) a particularly large input
from the central nucleus of amygdala.
The anterior insula is interconnected to regions in the
temporal and occipital lobes, opercular and
orbitofrontal cortex.
The smaller posterior insula connects reciprocally
with the secondary somatosensory cortex and receives
input from spinothalamically activated posterior
inferior thalamic nuclei.
Left insular cortex has a relationship with cerebellar
system.
Functions of insular lobe:
The insular cortex:
Aids interoceptive awareness of body states, such as
the ability to time one own heart beat.
Correlates with increased accuracy in the subjective
sense of the inner body and with negative emotional
experience.
Involved in the control of blood pressure, particularly
during and after exercise.
Is where sensation of pain is judged as to its degree.
Processing vestibular sensations.
Noninteroceptive perceptions include: a) passive
listening to music; b) laughter and crying; c) empathy
and compassion.
It contributes to hand and eye motor movement,
swallowing, gastric mobility and speech articulation.
Altered sexuality:
Hypersexuality.
Hyposexuality.
Etiology:
Encephalitis (autoimmunity).
Cerebrovascular diseases.
Tumor.
Corpus callosum
There are three structures that interconnect the cerebral
hemispheres:
The anterior commisure, a structure that interconnects
the olfactory system and part of the limbic system.
The posterior commisure (hippocampal), a structure that
interconnects parts of the limbic system.
The corpus callosum, a large structure that mediates
interconnection between a large number of cortical
processing areas.
Corpus callosum (CC):
CC is a wide, flat bundle of neural fibers beneath the
cortex in the human brain at the longitudinal fissure.
CC connect the left and right cerebral hemispheres and
facilitates interhemispheric communication.
CC is consisting of 200-250 millions contralateral axonal
projections.
The posterior portion of corpus callosum is called the
splenium.
The anterior is called the genu (knee).
Between anterior and posterior portions is the truncus
(body) of the corpus callosum.
The part between the body and splenium is often
markedly thinned and thus referred to as the isthmus.
The rostum is part of corpus callosum that projects
posteriorly and inferiorly from the anterior most genu.
Thinner axons in the genu connect the prefrontal cortex
between the two hemispheres.
Thicker axons in the midbody of the corpus callosum and
the splenium interconnect areas of the premotor,
supplementary motor regions and motor cortex, with
proportionally more corpus callosum dedicated to
supplementary motor regions.
Temporal lobe:
Temporopolar.
Anterior temporal:
Middle temporal.
Posterior temporal.
Areas supplied:
The bulk of the lateral surface of the hemisphere
except for the superior inch of the frontal and parietal
lobes ( supplies by ACA) and the inferior part of the
temporal lobes (supplies by PCA).
Superior division supplies rolandic and prerolandic
areas (location of Brocas area).
Inferior division supplies lateral temporal and inferior
parietal lobes (location of Wernickes area).
The penetrating branches of MCA supply:
Putamen.
Part of the head and body of caudate nucleus.
Outer globus pallidus. Posterior limb of the internal
capsule.
Corona radiata.
MCA ischemic syndromes:
Occlusion of MCA by a thrombus is relatively infrequent.
Most MCA occlusions are embolic.
Main trunk occlusion of either side yields:
Contralateral hemiplegia.
Eye and head deviation toward the MCA infarct.
Contralateral hemianopia.
Contralateral hemianesthesia.
Loss of consciousness may occur.
Main trunk occlusion involving dominant hemisphere:
Global aphasia.
Idiomotor apraxia.
Agraphia
Main trunk occlusion involving nondominant hemisphere:
Anosognosia.
Superior division of MCA (more frequent) infarct lead to:
Contralateral deficit with significant involvement of the
upper extremity and face, sparing partially of the
contralateral leg and foot.
Broca aphasia (dominant insula and operculum).
VA ischemic syndromes:
The results of VA occlusion are quite variable.
When there are two good-sized arteries, occlusion of one
may cause no recognizable symptoms and signs.
If the subclavian artery is blocked proximal to the origin of
left VA, exercise of the arm on that side may draw blood
from the right VA and BA, down the VA and into the distal
left subclavian artery sometimes resulting in the
symptoms of vertebrobasilar insufficiency (subclavian
steal syndrome).
Subclavian steal syndrome (a demand for blood flow to
the arm is met by siphoning effect on the blood within the
ipsilateral VA causing it to flow in retrograde fashion):
Vertebrobasilar insufficiency: a) moderate posterior
headache; b) dizziness or vertigo; c) syncope; d)
ataxia; e) motor deficits; f) visual disturbances.
Symptoms and signs in the left arm: a) diminished or
absent radial pulse; b) transient weakness on exercise;
c) claudication; c) paresthesias; d) coldness; e)
pain.
Initiation or exacerbation of symptoms by physical
exercise.
If the occlusion of the VA is so situated as to block the
branches suppying the lateral medulla (PICA) a
characteristic syndrome may result (lateral medullary
syndrome Wallenberg syndrome).
When the vertebral branch to the anterior spinal artery is
blocked, flow from the other (corresponding) branch is
usually sufficient to prevent infarction of cervical cord.
Rarely, occlusion of the VA or one of its medial branches
produces a medial medullary syndrome.
Occlusion of a VA low in the neck is usually compensated
by the anastomotic flow to the upper part of the artery via
the thyrocervical, deep cervical and occipital arteries or
reflux from the circle of Willis.
Basilar artery (BA):
BA is formed by the two VAs joining each other in the midline.
It ascends along the ventral aspect of the pons.
It ends at pontomidbrain junction where it divides into
two posterior cerebral arteries.
Facial weakness.
Ipsilateral cerebellar ataxia.
Ipsilateral Horner syndrome.
Paresis of conjugate lateral gaze.
Contralateral loss of pain and temperature sense of arm,
trunk and leg (lateral spinothalamic tract).
If the AICA occlusion is close to the origin of the artery, the
corticospinal fibers may also be involved, producing a
contralateral hemiplegia.
If the AICA occlusion is distal, there may be cochlear and
labyrinthine infarction.
Posterior cerebral artery (PCA):
PCAs are paired vessels, usually arising from the top of the BA
and curving laterally, posteriorly and superiorly around the
midbrain.
In about 70% of persons, both PCAs are formed by the
bifurcation of BA and only thin PCoAs join this system to
the ICAs.
In 20 to 25% of the persons one PCA arises from the BA in
the usual way, but the other arises from the ICA.
In the remainder (5 to 10%) both PCAs arise from
corresponding ICA.
The PCA is divided into P1 and P2 segments by the PCoA.
Penetrating branches to the mesencephalon, subthalamic,
basal structures and thalamus arise primarly from the P1
segment and PCoA.
The P2 segment bifurcate into posterior temporal artery
and internal occipital artery.
The interpeduncular branches of the PCA arise just above
the BA bifurcation and supply: a) the red nuclei; b) the
substantia nigra bilaterally; c) medial parts of the cerebral
peduncles; d) oculomotor and trochlear nuclei; e)
reticular formation of the upper brainstem; f)
decussation of the brachia conjunctivae (superior
cerebellar peduncles); g) medial longitudinal fasciculi;
h) medial lemnisci.
The thalamoperforate branches (paramedian thalamic
arteries) of the PCA arise more distally, near the junction
of the PCA and PCoA and supply the inferior, medial and
anterior parts of the thalamus.
The thalamogeniculate branches of the PCA arise still
more distally and supply: a) geniculate body; b) the
central and posterior parts of thalamus.
The medial branches of the PCA supply: a) lateral part of
the cerebral peduncle; b) lateral tegmentum and corpora
quadrigemina; c) pineal gland.
Posterior choroidal branches of the PCA run to: a)
postero-superior thalamus; b) choroid plexus; c)
posterior parts of the hippocampus.
Cortical branches of PCA supply: a) inferomedial part of
the temporal lobe; b) medial occipital lobe, including
cuneus, precuneus and visual Brodmann areas 17, 18 and
19.
PCA ischemic syndromes:
Occlusion of the PCA:
Can produce a greater variety of clinical effects than
occlusion of other artery, because both the upper
brainstem, which is crowded with important structures
and the inferomedial parts of temporal and occipital lobes
lie within its domain.
Obviously the site of the occlusion and the arrangement of
the Circle of Willis will in large measure determine the
location and extend of the resulting infarct.
Occlusion proximal to the PCoA may by asymptomatic or
have only transitory effects if the collateral flow is
adequate.
Even distal to the PCoA, an occlusion may cause relatively
little damage if the collateral flow through border-zone
from anterior and middle cerebral arteries is sufficient.
PCA ischemic syndromes can be classified in: a) central and
peripheral territory of PCA; b) anterior-proximal, cortical and
bilateral cortical.
Central territory PCA syndromes:
Thalamic syndrome (contralateral).
Thalamoperforate syndrome (crossed cerebellar ataxia
with ipsilateral third nerve palsy).
Weber syndrome.
Paresis or paralysis of vertical eye movement.
Contralateral:
Ataxic tremor.
Postural tremor.
Intention tremor.
Chorea.
Hemiballismus.
Decerebrate attacks.
Peripheral territory PCA syndromes:
Contralateral homonymous hemianopsia.
Bilateral occipital lobe lesion, possibly with involvement
of parieto-occipial region:
Bilateral homonymous hemianopia.
Achromatopsia.
Failure to see to-and-from movements.
Inability to perceive objects not centrally located.
Apraxia of ocular movements.
Inability to count or enumerate objects.
Memory defects.
Topographic disorientation.
Prosopagnosia.
Simultagnosia.
Unformed visual hallucinations.
Metamorphopsia.
Teleopsia.
Illusory visual spread.
Palinopsia.
Distortion of outlines.
Anterior-proximal PCA syndromes:
In these syndromes are involved:
Interpeduncular branches.
Thalamoperforate branches.
Thalamogeniculate branches.
Thalamic syndrome (Djerine-Roussy) = thalamo-
geniculate arteries syndrome.
Central midbrain and subthalamic syndromes = inter-
peduncular arteries syndromes:
Weber Syndrome.
Paresis of vertical gaze.
Stupor or coma.
Contralateral ataxic tremor.
Movement disorders.
Anteromedial inferior thalamic syndromes = thalamo-
perforate syndromes:
Extrapyramidal movement disorders (hemiballismus
or hemichoreoathetosis).
Deep sensory loss.
Hemiataxia or tremor may be added in various
combina-tions.
Vascular amnesia is induces by occlusion of
paramedian thalamic branches.
Cortical PCA syndrome:
Homonymous hemianopsia (macular or central vision
may be spared because of collateralization of occipital
pole from distal branches).
Visual hallucinations in the blind parts of visual fields.
Metamorphopsia and palinopsia.
Alexia with or without agraphia.
Anomia (amnestic aphasia).
Visual agnosia.
Color dysnomia.
Bilateral cortical PCA syndromes:
These may occur as a result of successive infarctions or
from a single embolic occlusion of the upper BA, especially
if the PCoAs are unusually small.
Extensive lesions:
Total blindness of cortical type.
Bilateral homonymous hemianopsia.
Unformed visual hallucinations.
The papillary reflexes are preserved.
Optic disc appears normal.
Prosopagnosia (bilateral mesiotemoporo-occipital
lesions).
Anton syndrome = the patient is unaware of being
blind and may deny it even when it is pointed out to
him.
Balint syndrome (bilateral occipitoparietal border-
zone lesions).
Korsakoff amnestic-like syndrome (bilateral lesions
that involve inferomedial portions of temporal lobes).
Etiology:
Subarachnoid hemorrhage.
Bacterial meningitis (including tuberculosis
meningitis).
Viral meningitis.
Meningoencephalitis.
Parasitic meningitis.
Aseptic meningitis.
Neoplastic meningitis
XVI. INTRACRANIAL HYPERTENSION.
Anatomophysiology of awareness.
Awareness implies that the individual is not only alert but
is cognizant of self and surroundings.
Interaction of the CC and RF is required for the individual
to be awake.
Anatomophysiology of attention.
Attention to specific aspects of the perceived universe
depends on both awareness as a general property and on
the specific anatomical structures that mediate the
sensory phenomena involved.
In order to attend to a particular stimulus, the pathways
required for its perception must be functional.
Each primary sensory modality has one or more principal
cortical regions the must function in order to attend to a
stimulus.
Attention enables an awake and alert individual to select
a task or a stimulus to process from a number of
alternatives to select a cognitive strategy to carry it out
(the ARAS is thought to facilitate this process by
enhancing the perception of differences between
competing stimuli).
Coma.
Coma is a state of unconsciousness, lasting more than six
hours in which a person:
Inability to be aroused.
Cannot be awaked.
Fails to respond normally to painful stimuli, light and
sound.
Lock a normal sleep-wake cycle.
Does not initiative voluntary actions.
A person in a state of coma is described as being comatose.
Etiology nonstructural or structural causes:
Nonstructural causes.
Metabolic and endocrine derangements:
Hypothermia and hyperthermia.
Hypoglycemia.
Diabetic ketoacidosis.
Hyperosmolar nonketotic coma.
Renal failure uremia.
Reyes syndrome.
Hyponatremia/ hypernatremia.
Panhypopituitarism.
Myxedema.
Adrenal cortical failure (addisonian crisis).
Porphyria.
Hypertensive encephalopathy.
Nutritional.
Wernickes encephalopathy (thiamine deficiency).
Vitamin B12 deficiency.
Burn encephalopathy.
Septicemic/toxic shock.
Hypoxic brain injury:
Asphyxiation.
Drowning.
Anoxemic anoxia (cardiac arrest).
Anemic anoxia (hemorrhagic shock).
Toxic brain damage:
Alcohol.
Carbon monoxide.
Cyclosporine.
Drug overdose.
Opiates.
Barbiturates.
Benzodiazepine.
Inflammatory/infectious processes:
Meningitis.
Encephalitis.
Postinfectious encephalomyelitis.
Vasculitis:
Cerebral lupus
Neurosarcoidosis.
Neoplastic:
Leptomeningeal carcinomatosis.
End stage of dementing processes ( persistent vegetative
state is more usual).
Epilepsy:
Convulsive status epilepticus.
Nonconvulsive status epilepticus.
Postictal state.
Structural causes:
Traumatic brain injury:
Diffuse brain injury
Epidural hematoma.
Subdural hematoma.
Intracerebral hematoma.
Penetrating brain injury.
Intracranial hemorrhage.
Subarachnoid hemorrhage.
Spontaneous subarachnoid hemorrhage.
Aneurysm rupture.
Arteriovenous malformation rupture.
Tumor hemorrhage.
Spontaneous hemorrhage.
Intracerebral.
Cerebellar.
Brain stem.
Infarction.
Cerebral.
Cerebellar.
Brain stem.
Intracranial infection.
Subdural empyema.
Focal encephalitis (herpes simplex).
Cerebral abscess.
Brain tumor.
Primary neoplasm.
Secondary neoplasm.
Hydrocephalus.
Obstructive.
Communicating.
Pathophysiology.
Diffuse lesion of both cerebral hemispheres (cortical gray
matter and subcortical white matter).
Bilateral diencephalic damage (especially to the
paramedian dorsal thalamus).
Damage to the paramedian gray matter anywhere from
the posterior hypothalamus to the tegmentum of the
lower pons.
When the respiratory centers in the lower medulla are
damage, apnea ensues.
The irreversible destruction of critical brain stem areas
usually follows catastrophic supratentorial events that
cause brain herniation and subsequent compression and
ischemia of the brain stem.
Eye opening
Spontaneous open with blinking at baseline..4
Opens to verbal command....3
Opens to pain, not applied to face..2
None.... 1
Best verbal response
Oriented...5
Confused conversation, able to answer question.4
Inappropriate words, words discernible..3
Incomprehensible speech.2
None.1
Maximum Score..15
Respiratory pattern.
Normal pattern.
Cheyne-Stokes: periodic increase and decrease of rate and
depth, followed by an expiratory pause and then a
repeated pattern seen with diencephalic pathology and
bilateral hemisphere dysfunction (nonspecific).
Hyperventilation: raises suspicion of hypoxia or metabolic
coma with acidosis, such as with ethylene glycol,
methanol, salicylates and lactic acidosis (central
neurogenic hyperventilation may occur with midbrain
damage).
Cluster breathing: periods of rapid irregular breathing
separated by periods of apnea it is similar to Cheyne-
Stokes respiration but without the crescendo/
decrescendo pattern or regularity of the latter (this is seen
with high medullary or low pontine lesions.
Apneustic breathing: deep inspiration followed by breath
holding, then long slow expiration at a rate of 6 breath per
minute (implies pontine damage basilar artery
occlusion).
Ataxic (Biots) breathing: irregular and disorganized
breathing (occur with medullary dysfunction and is
usually preterminal).
Pupil examination.
Pupillary size, shape and reaction are integral components
of the assessment of conscious state.
Equal-sized and reactive pupils in a comatose patient
indicate a metabolic or toxic cause, with exception of
anoxia, anticholinergics, glutethimide and botulinum
toxin, which cause fixed, dilated pupils (narcotics cause
small pupils that react sluggishly).
Unequal-sized pupils:
Imply a structural lesion of the brain or cranial nerves.
One caveat is that direct ocular trauma may produce
mydriasis.
A pupil that dilates after a cerebral insult is indicative
of changing intracranial pathology with increasing
tension on the ipsilateral oculomotor nerve resulting
from uncal herniation through the tentorial hiatus.
Dilated nonreactive pupils from the time of an injury
imply irreparable brain damage or bilateral optic
nerve injury.
The Horners syndrome implies disruption of the
sympathetic nervous system input to the pupil an may
follow carotid occlusion or dissection, among other
causes.
Bilateral pinpoint pupils occur with pontine lesions that
leave the parasympathetic nerves unopposed.
Bilateral fixed and dilated pupils (7 to 10 mm) occurs with
medullary injury, with post-tonsilar or central herniation,
after anoxia or with hypothermia (< 32o C).
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