localization in the nervous system the key to the problem

LOCALIZATION IN THE NERVOUS SYSTEM

THE KEY TO THE PROBLEM

Dr. R. M. HardyDepartment of Small Animal Clinical Sciences

College of Veterinary MedicineUniversity of Minnesota

St. Paul, MN 55108

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I. WHAT NEUROLOGICAL EXAMS WILL AND WILL NOT DOA. They will:

1. Differentiate neurological from musculoskeletal disorders.2. Substantiate that neurological disease does, in fact, exist.3. Localize the problem to one or more major regions of the nervous

system.B. Do not expect neurological exams to:

1. Consistently enable you to identify the etiology for the problem.Ancillary diagnostic approaches are usually necessary for that.

II. SEQUENCE OF EVALUATIONSA. Be systematic and consistent on every exam.B. Evaluate higher centers first.

1. Mental status.2. Gait.3. Posture.4. Postural reactions.5. All the above areas must integrate with either the midbrain or

rostrally.6. Cranial nerve evaluations.7. Spinal reflexes.8. Sensory function.

III. DON'T FORGET A GOOD PHYSICAL EXAMA. Be thorough.B. Don't overlook findings that may help to determine the cause for the

animal's neurological abnormalities.C. Palpate all joints/muscles.D. Check pulses.

IV. MENTAL STATUSA. Often very subjective.B. Owner's observations account for at least 50% of your interpretation.

Consider:1. Attitude.2. Response to commands.3. House training.4. Sleeping habits.5. Other behavioral changes.

C. Direct observation.D. Assessment.

1. Abnormalities in behavior result from diseases affecting CNSarousal sites, i.e. cortex, subcortical nuclei and reticular activatingsystem.



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2. Metabolic diseases can produce identical behavioral changes.a. Hepatoencephalopathy.b. Hypoglycemia.c. Severe acidosis.d. Toxins.e. Drugs.

3. In general, if mental status is normal in patients with neurologicaldisease, the lesion is usually extracranial. Exceptions occur withlesions involving:a. The cerebellum.b. Cranial nervesc. Brain stem nuclei.d. Focal lesions of the forebrain, or reticular activating system.

V. POSTUREA. Observe at rest. Normal animals stand erect, support their weight easily

and can maintain this position for long periods.B. Postural abnormalities include:

1. Head tilt, leaning or falling to one side.2. Body curvature.3. Head or body tremors.

VI. GAITA. This is a skill developed by careful observation of many animals. The

animal should be in an unrestricted area and have good traction.1. Encourage to walk voluntarily.2. If not able to walk voluntarily, support them and see what degree

of voluntary motor control is present.3. Climbing stairs may allow subtle deficits to be identified.

B. Varying degrees of paresis are often most easily detected by visualizingan animal's gait.

C. Ataxia = incoordination of gait and may be associated with:1. A wide based stance.2. Swaying of the trunk from side to side.3. Falling or rolling.4. Leaning to one side while gaiting.5. Hyper or hypometria.6. Crossing of limbs or abnormal abduction of limbs on turning.7. Ataxia can be caused by:

a. Lesions caudal to the midbrain involving both sensory andmotor tracts.

b. Sensory abnormalities alone involving consciousproprioception (CP) pathways.

c. Abnormalities of the vestibular system.



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d Cerebellar lesions.

VII. INTEGRATION OF MENTAL STATUS, GAIT, POSTUREA. Usually indicates whether neurologic disease is present.B. Often suggests whether the primary lesion is intra-or extracranial.C. Completion of the neurological exam aids in finite localization, and

includes:1. Postural reactions.2. Reflex testing.3. Sensory evaluations.

VIII. POSTURAL REACTIONSA. Complex activities performed by the animal following manipulations by

the examiner. Responses are graded based on previous experience withnormal animals.1. Grading of postural reactions.

a. 0 = absent.b. 1 = depressed or weak.c. 2 = normal.

B. The grade assigned is based on the animal's ability to initiate or correct apostural change induced by the examiner.1. The follow-through or motor response is also assessed as the

animal corrects its posture.a. Always repeat the test several times.b. Errors must be consistently reproduced to have significance.

C. The following postural reactions may be assessed in dogs and cats.1. Tonic neck responses.2. Placing reactions.3. Proprioceptive positioning.4. Wheelbarrowing.5. Hemiwalking.6. Extensor postural thrust.7. Hopping.

D. Tonic Neck Response.1. Elevating dog's head when it is standing causes increased tone in

forelegs and decreases rear limb tone.2. Ventral neck flexion produces the opposite response.3. Lateral neck flexion causes increased tone on side turned to.4. Abnormalities indicated by failure to respond appropriately.

Weight born on dorsum of paw.E. Placing Reactions.

1. Tactile and visual placing capabilities should be assessed.2. Graded: 0 = absent, 1 = slow, 2 = normal.3. Placing responses are modified by many factors.



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a. Animals positioning.b. How it is held against your side.c. Switch sides if abnormal responses are suspected.

F. Proprioceptive Positioning (CP).1. Early sensory modality to disappear.2. Requires a minimal strength on animal's part if the body is

supported.3. Often only abnormality detected in mild lesions during early

phases.G. Extensor Postural Thrust.

1. Hold animal, head-up, vertically off of floor.2. Slowly lower until rear paws contact floor.

a. Limbs should immediately stiffen to support its weight(reflex action).

b. Animal will take one to two quick steps backward =postural reaction.

H. Wheelbarrowing.1. Elevate rear legs and force animal to walk on its forelimbs.

Response should be rhythmical, symmetrical, strong. The headshould be held erect.

2. If mild motor deficits exist, they may be exaggerated bywheelbarrowing the animal with its head and neck extended. Theanimal may drag its limbs at this point rather than walk normally.

I. Hemiwalking.1. Support animal's weight on one side of its body. Walk laterally,

slowly.



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J. Hopping.1. Try to determine if hopping deficits are during the initiation phase

or the follow through attempt.a. Initiation problems = animal leans too far prior to starting its

hopping action.b. Follow through problems = exaggerated limb movement or

decreased efforts to correct limb position.K. Interpretation of Abnormal Postural Reactions.

1. These are complex motor responses that require intact sensory,motor and brain integration.

2. Problems in initiation usually relate to sensory impairment.3. Follow through problems usually mean motor tracts are involved.4. Taken alone, postural reactions are of little localizing value. Final

localization utilizes reflex testing and sensory evaluations.L. Most Consistently Reproducible Postural Reactions.

1. Some postural reactions are not able to be consistently elicited evenin normal dogs and cats.

2. The following reactions are usually reliable detectors ofneurological problems.a. Conscious proprioception.b. Extensor postural thrust.c. Hopping.d. Wheelbarrowing with head and neck extended.

M. Inconsistently Elicited Postural Reactions.1. Placing - A highly variable reaction.2. Tonic neck and eye.3. Hemiwalking.

IX. SPINAL REFLEXESSpinal reflex testing is one of the most important localizing and prognostic tasksavailable to you. The following reflexes can be assessed in dogs and cats.A. Myotatic (stretch reflexes).B. Flexor (withdrawal). reflex.C. Perineal reflex.D. Panniculus.E. Muscle tone.F. Sensory perception.G. Crossed extensor.H. Grading spinal reflexes can be useful during reassessment of a patient's

neurologic status.1. 0 = absent.2. 1+ = depressed.3. 2+ = normal.4. 3+ = exaggerated.



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5. 4+ = exaggerated with clonus.6. Always use the same instrument and technique and follow a

consistent pattern for performing your exams.I. Thoracic Limb Reflexes.

1. Myotatic responses.a. Biceps tendon.b. Triceps tendon.c. Extensor carpi radialis.d. Dog should be in lateral recumbency, relaxed, and, assess

the "up" limb.e. Biceps and triceps responses are often "absent", i.e. difficult

to elicit, even in normal dogs.f. Extensor carpi radialis reflex is usually detectable in most

animals.2. Flexor response (withdrawal).

a. Noxious stimuli to digits should result in rapid, purposefulflexion of all limb joints.

J. Pelvic Limb Reflexes.1. Myotatic reflexes.

a. Patellar (quadriceps) = highly reliable.b. Gastroenemicus - highly variable.c. Cranial tibial - usually present.

2. Flexor response.a. Lateral stimulus assesses sciatic nerve.b. Medial stimulation assesses femoral nerve.c. Always assess both sides of each rear limb.

K. Crossed Extensor Reflex.1. During the flexor reflex test, the stimulated limb will withdraw

and the opposite limb will slowly go into full extension.2. This response is inhibited in normal spinal cords.3. A positive crossed extensor is an indication of upper motor neuron

disease.4. Do not overinterpret voluntary struggling.

L. Perineal Reflex.1. Tactile stimulation to anal or perineal region leads to anal sphincter

contraction and lowering of the tail (S1,2,3).M. Interpreting Spinal Reflexes.

1. Localize disease to specific regions of the nervous system whenpostural reactions suggest disease exists.

2. Reflexes characterize deficits as affecting either the upper or lowermotor neurons controlling those reflex pathways.

3. Upper Motor Neuron Signs.a. Reflexes are normal or exaggerated.b. Atrophy is mild.



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c. Muscle tone may be normal, increased, or decreased.



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4. Lower Motor Neuron Signs.Hyporeflexia or areflexia.b. Severe (neurogenic) atrophy.c. Hypotonia.d. Interpreting reflexes is difficult until many cases have been

evaluated.5. Flexor Reflex Interpretation.

a. Assesses integrity of the reflex arc.b. Assesses cortical awareness of painful stimuli.c. Must differentiate withdrawal (reflex) from response to pain

(cortex).1) Vocalization.2) Pupils dilate.3) Purposeful withdrawal efforts.

d. Pelvic limb withdrawal.1) Medially assesses femoral nerve (L4-L6).2) Lateral stimulation assesses sciatic (L6-S1).

e. Signs of sciatic palsy.1) Anesthesia on lateral side of paw.2) Withdrawal only elicited on medial aspect of the

paw.3) Limb flexes only at the hip.4) May see exaggerated patellar reflux due to decreased

tone in opposing muscle groups.f. Femoral nerve palsy signs.

(1) Absent withdrawal when tested medially.(2) Limb flexion occurs at the hock and stifle only.(3) Patellar reflex = 0 to 1+.

g. Crossed extensor reflex.(1) Indicates UMN injury is present.(2) Usually associated with more severe lesions of the

cord.(3) Not prognostic for recovery chances.

N. Visceral Function.Abnormalities of micturition and defecation occur with cord injuries.1. Defecation abnormalities.

a. LMNs for anal sphincter are at S1,2,3 cord segments.Assessed by perineal reflex testing.

b. UMN signs = hypertonic sphincter constipation.c. LMN signs = flaccid sphincter, dilated anus, fecal

incontinence.2. Signs of bladder/urethral impairment.

a. Micturition reflex is abolished. Get overdistended bladder,urine dribbling.



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b. LMN signs occur with sacral cord damage (flaccid bladder,overflow incontinence, easily expressed bladder.

c. UMN = distended bladder, spactic sphincters, difficult toexpress.

d. Micturition reflex is lost at about the time voluntary motoractivity is lost.

O. Assessing Muscle Tone.1. Evaluate during the reflex testing.2. Passively manipulate all limbs, palpate muscle groups.3. Graded as >, < or normal.4. UMN lesions most often result in increased tone to muscles distal

to the lesion. Occasionally muscle tone appears normal ordecreased however.

5. LMN lesions involving major muscle groups typically producedecreased tone that is quite obvious.

X. THE SCHIFF-SCHERRINGTON PHENOMENONA. Usually seen following severe, acute lesions involving T-L region of the

spine which produce paraplegia.B. Will see extensor hypertonicity of the forelegs with hypotonia of the rear

limbs.C. Foreleg reflexes and postural reactions are normal, but are difficult to

assess due to "extensor release" phenomena.D. Pelvic limb reflexes are intact in spite of hypotonicity being present.E. Lesions are located between T2 and L4 but most often are near the T-L

junction.F. Signs are transient lasting usually one to two weeks.G. The signs are caused by a loss of spinal interneurons between the thoracic

cord and lumbar cord.H. Does not indicate irreversible damage has occurred.I. Pain perception to the rear limbs is usually absent.

XI. SENSORY EVALUATIONSA. Objective assessments are difficult.B. Still, they remain your best localizing tool for spinal injuries.C. Assess patients for the presence of:

1. Hyperesthesia.2. Superficial (cutaneous) sensation, pin prick.3. Deep pain.

D. Sensation is assessed during reflex testing.E. Critical to assess animal's awareness, i.e. cortical interpretation of

sensation. Withdrawal without awareness = reflex activity.F. All limbs evidencing paresis or paralysis need sensory testing.



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G. Superficial pain is that elicited by pin prick to skin or pinching skin with ahemostat.

H. Deep pain is crushing type of pain to bone, periosteum, etc. If superficialpain is present, deep pain is always present.

I. Evaluate entire spine for evidence of a localized region of hyperesthenia,decreased sensation and the presence of a panniculus reflex. Theseprocedures will localize lesions within the T-L spine.

J. Panniculus reflex.1. Pinching the skin from T2 to L2 should cause the skin over the back

to flinch or twitch due to panniculus muscle contractions.2. Start caudally and progress cranially when testing.3. The afferent (sensory) part of the reflex depends on intercostal

spinal nerves.4. The efferent (motor) component is from the lateral thoracic nerve

whose nerve cell bodies are located between C8-T1.5. Abnormalities are detected by a failure of the animal to respond to

a skin pinch caudal to the cord lesion.K. Hyperesthesia.

1. Hyperesthesia is an exaggerated response to a mild stimulus.2. Test by using digital pressure all along the spine, caudal to cranial.3. Deep pain fibers are the last sensory modality to be lost due to

their polysynoptic, diffuse organization.4. May be able to detect a line of sensory demarcation one to two

vertebral segments caudal to the location of the lesion.L. Sequence of loss and return to neurologic function.

1. Conscious proprioception is lost first.2. Voluntary motor function is lost next.3. Loss of superficial pain perception accompanies voluntary motor

loss.4. Deep pain perception is the last modality to be lost.

XII. SPINAL CORD SYNDROMESA. Cervical Syndrome (C1-C5) Common causes: Disk disease, cervicalvertebral malformation-malarticulation, meningitis, atlantoaxial subluxation,diskospondylitis.

1. Spastic hemiparesis to tetraplegia2. Hyperreflexia and hypertonia to all affected limbs3. Cervical hyperesthesia or “guarding” against movement4. Depressed postural reactions in all affected limbs5. Bladder incontinence (UMN type)6. +/- respiratory depression7. +/- Horner’s syndrome

B. Cericothoracic syndrome (C6-T2): Common causes: Primary cord tumors,trauma, disk disease, diskospyondylitis



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1. Monoparesis/plegia, hemipresis/plegia, tetraparesis/plegia2. Hypo/areflexia and hypotonia, with atrophy in thoracic limb(s)3. Hyperreflexia and hypertoniawithout atrophy in pelvic limb(s)4. Depressed postural reactions in all affected limbs5. Urinary incontinence (UMN type)6. Hyperesthesia at the level of the lesion7. Hypo/anesthesia below the level of the lesion8. Horner’s syndrome: Meiosis, ptosis, enophthalmos, protrusion

of the 3rd eyelid9. Depressed panniculus reflex (unilateral/bilateral)

C. Thoracolumbar syndrome (T3-L3): Disk disease, spinal fractures,degenerative myelopathy, distemper myelitis, diskospondylitis, metastaticlymphosarcoma in cats, progressive myelomalacia, hemivertebra

1. Spastic weakness/paralysis in the pelvic limbs2. Hyperreflexia and hypertonia without atrophy in pelvic limbs3. Urinary incontinence (UMN type)4. Hyperesthesia at the level of the lesion5. Hypo/anesthesia below the level of the lesion6. Depressed postural reactions in rear limbs7. +/- Schiff-Sherrington posture

D. Lumbosacral syndrome (L4-S3): Pelvic fractures and luxations,fibrocartilagenous emboli, lumbosacral stenosis, disk disease, sacrococcygealdysgenesis

1. Flaccid paresis/paralysis of pelvic limbs and tail2. Urinary incontinence (LMN type)3. Hypo/areflexia with hypotonia and atrophy in pelvic limbs4. Dilated anal sphincter, depressed/absent anal reflex5. Depressed bulbocavernosus reflex6. Fecal incontinence

` 7. Depressed postural reactions in pelvic limbsXIII. BRAIN SYNDROMES

A. Pontomedullary Syndrome1. Spastic weakness/paralysis in:

a) all four limbs (i.e., tetraparesis/tetraplegia) orb) limbs on the same side of the body (i.e.,

hemiparesis/hemiplegia)2. Normal/increased reflexes and muscle tone in all limbs3. Postural reaction deficits in limbs on the same side, or in all

limbs4. Multiple cranial nerve deficits

a) jaw paralysis, decreased facial sensation (CN V)b) depressed palpebral reflex (CN V, VII)c) facial paralysis (CN VII)\d) head tilt, falling, rolling nystagmus (CN VIII)



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e) pharyngeal/laryngeal paralysis (CN IX, X)f) tongue paralysis (CN XII)

5. Irregular respirations6. Mental depression

B. Cerebellar Syndrome1. Spastic, goose-stepping gait in all limbs, especially thoracic, with

preservation of strength2. Truncal ataxia3. Intention tremors of head, eyes4. Broad based stance5. Postural reactions delayed with exaggerated responses6. Menace deficit (ipsilateral), with normal vision7. Anisocoria (contralateral pupil dilated)8. +/- Opisthotonus (rare)9. +/- Vestibular signs (rare)

C. Vestibular SyndromeCentral Peripheral

1. Loss of balance Yes Yes2. Head tilt Yes Yes3. Falling/rolling Yes Yes4. Nystagmus Yes Yes

Horizontal Yes YesRotatory Yes YesVertical Yes NoPositional Yes No

5. Strabismus Yes Yes6. Cranial nerve deficits V, VI, VII-possible VII-possible7. Horner’s syndrome No Possible8. Cerebellar signs Possible No9. Mental depression Possible No

10. Hemiparesis with ipsilateral Possible Nopostural reaction deficits

D. Midbrain Syndrome1. Spastic weakness/paralysis in:

a) all four limbs (i.e., tetraparesis/tetraplegia) orb) limbs on the contralateral side of the body

(i.e. hemiparesis/hemiplegia)2. Increased reflexes and muscle tone in limbs on the contralateral side,

or in all limbs (all limbs may be held in rigid extension, i.e.,opisthotonus.

3. Postural reaction deficits in limbs on the contralateral side, or in alllimbs

4. Mental depression or coma5. Ipsilateral deficits of CN III (oculomotor)



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a) ventrolateral strabismusb) dilated pupil unresponsive to light, with normal visionc) drooping of the upper eyelid (ptosis)

6. Hyperventilation7. +/- Bilateral miosis8. +/- Obstinate progression/head pressing (cats)

E. Hypothalamic Syndrome1. Normal gait2. Altered mental status (disorientation, lethargy, or coma)3. Change in behavior (aggression or hyperexcitability)4. Abnormal movement/postures

a) trembling, pacing, wandering, hiding, tight circling, headpressing

5. Bilateral deficits of CN II (optic), at the level of the chiasma) visual impairmentb) dilated pupilsc) depressed pupillary reflexes

6. Abnormal temperature regulation (hyperthermia, hypothermia,poikilothermic)

7. Abnormal appetite (hyperphagia/obesity, anorexia/cachexia)8. Endocrine disturbances

a) diabetes mellitusb) diabetes insipidusc) hyperadrenocorticismd) acromegaly/excess growth hormone

9. SeizuresF. Cerebral Syndrome

1. Normal gait2. Altered mental status (apathy, depression, disorientation, lethargy,

coma)3. Change in behavior

a) loss of trained habitsb) failure to recognize ownerc) aggressiond) hyperexcitability

4. Abnormal movements/posturesa) pacing, wandering, circling, or head pressingb) twisted head and trunk (pleurothotonus)

5. Postural reaction deficits in contralateral limbs6. Visual impairment (e.g., bumping into objects, contralateral menace

deficit) with normal pupillary light reflexes7. Seizures8. +/- Papilledema9. +/- Irregular respiration



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G. Paroxysmal Syndrome1. Episodic seizures2. Episodic sleep3. Episodic syncope4. Episodic muscle cramping5. Episodic weakness6. Episodic tetany7. Episodic myoclonus

XIV. CRANIAL NERVE EVALUATIONSA. Useful in localizing and confirming diseases involving the brain.B. Cranial nerves III to XII have their nerve cell bodies within the brainstem.C. Testing involves assessing reflexes mediated through individual cranial

nerves.D. When abnormalities are identified in isolated cranial nerves, it localizes a

disease process to a specific region in the nervous system and mustinvolve either the nerve cell body or peripheral nerve branch of thecranial nerve.

E. It is valuable prognostically to determine if lesions are central (nerve cellbody) or peripheral (nerve fiber).

F. Signs associated with central lesions.1. Abnormal mental status.2. Upper motor neuron signs to the limbs are also present.

G. Olfactory nerve (I).1. Infrequently tested difficult to assess.2. Complaints of poor appetite and reduced effectiveness in hunting

dogs.3. Use non-irritating oils (clove) alcohol, acetone, food.4. Requires that bilateral disease exists (anosmia).

H. Optic nerve (II).1. Several cranial nerves are evaluated simultaneously.

a. Optic = sensory.b. Oculomotor (III) - motor to pupil and extraocular muscles.c. Trochlear (IV) motor.d. Abducens (VI) motor.

2. Visual system testing involves assessing:a. Vision.b. Papillary light reflexes.c. Ocular movements.

3. Visual testing can be evaluated in several ways.a. Obstacle testing, strange environment, bright and decreased

illumination.b. Menace reaction: cotton balls thrown at the dog's eye. Blink

response.(1) Be careful of air currents.



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(2) Test each half of the visual field. Nasal field (whichlooks laterally) is most important one.

(3) Be careful of wind currents which may stimulate thecornea (V) and induce a blink reflex.

(4) Assess integrity of two cranial nerves during this testII and VII as well as cortical awareness.

c. Always do a complete ophthalmic exam if visual deficits aredetected.

4. Absent menace response is not always associated with optic nervepathology.a. Severely depressed animals menace poorly.b. Very young animals have a poorly developed menace

response.c. Cerebellar lesions may impair the menace reaction.

5. Pupillary light reflex assesses cranial nerves I and III.a. Oculomotor nerve carries somatic motor as well as

autonomic fibers. Parasympathetic nerves that controlpupillary constriction travel within the III nerve to innervatethe iris.

b. Sympathetic nerve fibers innervate the iris dilators.c. Direct and consensual light responses will determine which

pupil is abnormal.d. Interpretation of visual pathway lesions.

(1) Extensive unilateral or bilateral retinal, optic nerve orchiasmal lesions cause blindness and markedmydriasis if the lesions are bilateral, or slightmydriasis if the lesion is unilateral.

(2) Direct and consensual pupillary light responses areabsent when the affected eye is tested.

(3) Pupillary light reflex is normal when the unaffectedeye is tested.

6. Lesions involving parasympathetic fibers to the eye cause thefollowing findings.a. Unilateral LMN disease of cranial nerve III causes anisocoria

(mydriasis) on the affected side with normal vision.b. The affected eye is dilated, and does not respond to light.

The consensual response in the affected eye will be normal,i.e. light shown in affected eye causes the opposite eye toconstrict.

c. The unaffected eye has opposite response, i.e. direct =normal, consensual = absent.

d. Lesions involving the peripheral nerve of III are usuallyassociated with unilateral signs.



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e. Lesions affecting the nucleus of III causes bilateral pupillaryabnormalities due to the close proximity of these nuclei.

f. Central lesions involving III are also associated withmydriasis and strabismus.

g. Central lesions also are associated with altered mentalstatus, gait and posture.

7. Lesions involving the sympathetic nerves to the pupillary dilatorscause:a. Meiosis on the affected side, ptosis, enophthalmus and

protrusion of the 3rd eyelid = Horner's syndrome.b. Sympathetic fibers to pupillary dilators originate in the

hypothalamus, descend within the cord to T1,T2, synapse,exit the spinal cord and enter the vago-sympathetic trunk.A second synapse occurs in the cranial cervical ganglion andpost-synaptic fibers follow branches of the carotid arteryuntil they innervate the iris.

8. Control of eye movements involves cranial nerves III, IV(Trochlear) and VI (Abducens).a. Eyes normally maintain a central position when the head is

moved.b. Deviation from normal central ocular position = strabismus.

(1) Fixed strabismus = ocular position is always offcenter regardless of head position.

(2) Positional nystagmus = abnormal eye location iselicited by changes in head position.

c. Normal ocular nystagmus.(1) Occurs when the head is moved up and down or left

and right.(2) Fast phase of the nystagmus is towards the direction

the head is moved.(3) Noting normal ocular nystagmus assesses the

integrity of cranial nerves III, IV and VI.9. Interpreting abnormal eye movements

a. Fixed strabismus is most often associated with localinquiries to the LMN of the extraocular muscles.(a) Trochlear palsy - dorsolateral strabismus, rare.(b) Abducens palsy - medial strabismus, rare.(3) Oculomotor palsy - leads to ventrolateral palsy, ptosis

and mydriasis.b. Positional strabismus.

(1) Usually due to abnormalities of UMN control overextraocular muscles, mediated via the vestibularsystem.



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(2) Usually see ventrolateral strabismus if head and neckare elevated.

(3) Vestibular injury may abolish the "dolls eye" reflex.Eyes will remain fixed and central during headmovements.

I. Trigeminal Nerve (V)1. Both sensory and motor branches exist.2. Sensory distribution is to face, cornea, eyelids, pinna, tongue and

nasal passages.3. Assessing trigeminal sensory function.

a. Pin prick to face, lips, nasal passages (V and VII).b. Tongue withdrawal (uses V and XII).c. Palpebral (blink) reflex. Be sure dog does not see your

finger approaching its face. Assess nerves V and VII.4. Assessing trigeminal motor function.

a. Motor to the muscles of mastication. Requires bilateraldisease for jaw weakness to be apparent.

5. Interpreting abnormal responses to trigeminal nerve testing.a. Loss of sensory and motor function to all branches is usually

seen with proximal peripheral nerve injury.(1) Motor and sensory nuclei are separated centrally.(2) Trigeminal motor and sensory branches are separated

peripherally.b. Complete sensory loss with no other signs suggests the

injury is peripheral since the trigeminal sensory nucleus isdiffusely organized within the brain stem.

c. Central lesions affecting the trigeminal nucleus areassociated with mental disease, and UMN signs to the limbs.

d. Bilateral trigeminal motor defects result in an inability toclose the jaw. Motor loss with no sensory deficits impliesthe lesion is centrally located since motor nuclei are discretewithin the brain stem.

e. Unilateral motor V injuries do not affect jaw function.Muscle atrophy will be noted clinically.

J. Facial Nerve Evaluations (VII)1. Assess along with 5th cranial nerve.2. Examine face, ears, eyes, lips for symmetry.3. Taste fibers to the rostral 2/3 of the tongue run with CN VII. Can

be tested using atropine on a cotton swab.4. Assessment of VII function.

a. Acute LMN palsy causes drooling, tearing, absent palpebralreflex, food falls from the side of the mouth, palpebralfissures will be slightly wider than normal, the lower liddroops.



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b. With chronic facial palsy muscle contracture develops, signsget less severe and the face will deviate (be pulled) towardsthe affected side.

c. Many dogs with unilateral or bilateral facial palsys arehypothyroid. Always check thyroid function.

K. Cranial Nerve VIII = Cochlear Branch.1. Difficult to assess hearing objectively.

a. Response to sudden noises.b. History is best clue.c. Loss must be severe before problems are appreciated.d. Auditory evoked potentials can be utilized in specialized

diagnostic centers.L. Cranial Nerve VIII - Vestibular Branch.

1. Function maintain the equilibrium of the head and/or body inspace.

2. Diseased animals have abnormal postures and gait.a. Head tilt towards the affected side is common.b. The trunk is often flexed towards the affected side.c. Patients often circle to one side.d. In early cases they will fall towards the affected side.e. Rolling along the floor until they hit a support object will

occur.f. Often vomiting is noted in acute vestibular injuries due to

nausea.3. A ventrolateral strabismus will frequently be evident if the head

and neck are extended and elevated.4. Nystagmus is often present.

a. Nystagmus is described by the direction of its fast phase.Usually both fast and slow components exist and this istermed jerk nystagmus.

b. Nystagmus that is equal in speed in its side to side motion =pendular nystagmus and is most often associated withcerebellar diseases and blindness.

c. Assess nystagmus initially while the animal is quiet and atrest. If nystagmus is present, it is termed resting or constantnystagmus.

d. The head is next moved laterally and up and down to elicitnormal ocular nystagmus. If abnormal nystagmus is elicitedby such manipulations it is termed positional nystagmus.Changes in body position (lateral, on back, etc.) may alsoinduce a positional nystagmus.

5. Normal vestibular nystagmus.a. Assesses an animal's response to rotational forces.b. The fast component is towards the direction moved.



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c. The nystagmus should cease rapidly once rotation isstopped.

d. This normal response may be depressed when the animal isturned towards the side of the lesion.

e. If no nystagmus is elicited on testing, it is turned a "dollseye" response and is abnormal.

6. Localizing a lesion to the peripheral portion of CN VIII or itscentrally located nucleus is prognostically valuable.a. Central lesions are located in the brain stem.b. Peripheral lesions involve receptors to the inner ear or

damage to CN VIII from the brain to the cochlea.c. Central VIII lesions often carry a poor prognosis.

7. Signs supporting central vestibular disease.a. Signs are static or progressive.b. Signs of mental disease are often present.c. Postural reactions are abnormal.d. Multiple other cranial nerves are involved (V, VI, VII).e. Nystagmus that is vertical in direction or that changes

direction in response to changes in head position is usuallydue to damage to vestibular nucleus.

8. Signs supporting peripheral vestibular injury.a. Patients usually improve with time.b. Mental status is normal except for disorientation.c. Postural reactions are normal, but awkward.d. Associated cranial nerves may include VII, and Horner's

syndrome may be present.e. Nystagmus characteristics.

(1) Usually horizontal or rotatory.(2) Fast phase is towards side opposite the lesion.(3) The direction of the nystagmus does not change with

changes in head position.M. Glossopharyngeal Nerve - IX.

1. Motor to pharynx and palate, test via gag reflex.2. Sensory branches innervate the caudal 1/3 of the tongue.

N. Vagus Nerve - X1. Motor function to the pharynx, larynx, thoracic and abdominal

viscera. Functions to allow normal swallowing, gagging, andvocalization.

2. Signs of vagal lesions.a. Voice changes.b. Dyspnea (laryngeal plegia).c. Regurgitation (megaesophagus) requires bilateral nerve

injury.O. Spinal Accessory Nerve - XI.



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1. Motor to neck muscles: trapezius, sternocephalicus,branchiocephalicus.

P. Hypoglossal Nerve - XII.1. Motor to intrinsic and extrinsic muscles controlling the tongue.

Test by inducing the animal to lick.2. Signs of disease.

a. Acutely, the tongue deviates towards the diseased sidewhen extruded.

b. Chronically, fibrosis, atrophy and contracture deviate thetongue towards the affected side.

c. Can grasp the tongue and assess its strength.



localization in the nervous system the key to the problem

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