Neurolocalisation, CN Neuropathies

Question 1

opisthotonus with extensor rigidity of forelimbs, but hips are flexed in the HLs

Answer 1

DecereBELLate rigidity

Question 2

rigid extension of neck and all 4 limbs

Answer 2

Decerebrate rigidity = midbrain (or rostral cerebellum)

Opisthotonus = spasm of muscles of neck causing backward arching of the head neck and spine

Question 3

Dog with Altered mentation circles to left (wide); sensory deficits on right side of face and placement deficits in right side paws with normal reflexes and tone in all limbs

Answer 3

Left Forebrain lesion

Contralateral placement deficits

Contralateral facial sensory deficits

Ipsilateral circles/head turn (pleurothotonus)

Gait and muscle tone usually not affected

Question 4

Difference between paresis and plegia

Answer 4

PAresis is weakness/inability to support weight

Plegia = loss of function of motor unit

Question 5

Features of cerebellar ataxia

Answer 5

Dysmetria

Hypermetria (prolonged flexion)

Intentional tremors

Wide base posture at rest with no proprioceptive deficits

Question 6

cause and features of proprioceptive ataxia

Answer 6

spinal cord lesions, which cause disruption of the ascending GP tracts that relay spatial location and degree of muscle contraction of the head neck and limbs

–> incoordination
–> truncal sway,
–> abnormal limb stance and gait with limbs crossing over each other as the animal walks.

Frequently have concurrent paresis because descending (UMN) pathway and ascending GPO pathways are located near each other in spinal cord

Question 7

Features of vestibular ataxia

Answer 7

Loss of orientation of the head with respect to eyes, neck, limbs and trunk. Affected animals may lose their balance, drift, lean or fall or in one direction. Usually towards the lesion
Head tilt TOWARDS lesion (unless paradoxical cerebellar in which case trust the postural deficits)

If peripheral lesion then normal strength and proprioception

In central disease proprioceptive and postural reaction deficits (ALWAYS ipsilateral to head tilt)

Question 8

What controls postural reactions

Answer 8

To maintain normal upright position an increased load on a supporting limb/s requires increased extensor tone - this is accomplished through spinal reflexes, but for smooth coordinated control the sensory and motor systems of the brain must be involved.

Because the pathways for all postural reactions are similar the interpretation of results is the same for all reactions. If hopping and placement are normal abnormalities are unlikely to be found in other reactions

Question 9

Interpretation of paw placement deficits

Answer 9

tests sensation but also motor function required for response

Delay may occur due to lesion affecting ascending tract (ie signal not getting to brain)
But can also be seen due to weakness, peripheral neuropathy preventing normal response)

Question 10

Interpretation of Hopping test

Answer 10

comparison of limb strength and coordination for contralateral limbs. Asymmetry is readily apparent so helps detect unilateral cerebral lesions where deficits are often mild but CONTRALATERAL to lesion. In spinal disease deficits are ipsilateral.

Delayed hopping may indicate a sensory or motor deficit to general proprioception

Poor initiation is seen with sensory deficits and poor follow through with motor

Question 11

Increased tone in all limbs, normal to increased reflexes and proprioceptive deficits
Normal mentation and CN exam

Answer 11

C1-5 lesion, bilateral

Question 12

Reduced withdrawal and tone in right forelimb, normal tone and withdrawal in left
Right forelimb delayed hopping and paw placement

Increased tone in right hind with normal patellar reflex. Reduced paw placement and hopping in right hind.

Normal reflexes and placement/hopping in left hind.

Answer 12

Right lateralising C6-T2 spinal lesion

Question 13

Long strided hindlimb gait scuffing paws
Reduced hindlimb placement/proprioception but increased tone and normal reflexes

FL exam normal

Answer 13

T3-L3 lesion

Mild

Question 14

Bilateral hindlimb paralysis with absent tone and sensation

Absent patellar reflexes and withdrawals absent

Absent anal sphincter tone

Answer 14

Severe L4-S3 lesion

Question 15

Normal FL postural reactions but with rigid extension.

Flaccid paralysis of HLs with increased reflexes

Answer 15

Schiff Scherrington Phenomenon

–> severe T3-L3 lesion causing spinal shock resulting in disruption of normal UMN input to the HLs so appears as LMN

Question 16

components of neurological exam

Answer 16

sensorium and behaviour,
posture and gait,
postural reactions,
muscle mass,
tone,
spinal reflexes and cutaneous sensation
AND cranial nerves.

Question 17

What is the crossed extensor reflex

Answer 17

seen when performing the withdrawal response

Extension of the contralateral limb –> abnormal response indicating UMN lesion

Question 18

Pathway of PLR

Answer 18

Light detected by retina
–> signal in optic nerve (both medial and lateral branches)
–> medial branch crosses to other side of brain
–> both synapse on occulomotor nerve nucleus in midbrain (both sides)
–> activation of parasympathetic fibres in occulomotor nerve
–> stimulation of the ciliary ganglion (parasympathetic input to iris)
–> pupil constriction in response to ACh
(sympathetic NS causes dilation) in both eyes

Does not assess vision but response to light which is a reflex not involving the cerebrum.

So can have blindness (ie signal not geting to forebrain with normal PLR if the lesion is caudal to CN3 nucleus)

Question 19

What can cause both direct and consensual PLR to be absent in one eye

Answer 19

Lesion of the optic nerve or retina –> signal not getting into brain

Question 20

Pathway of vision and subsequent menace response

Answer 20

Retina
–> optic nerve medial and lateral branches
–> optic chiasm
–> medial branch goes to contralateral lateral geniculate nucleus (and lateral branch goes to ipsilateral)
–> relay information to cortex via the optic tract
–> integration of visual stimuli from both eyes and mediates reactions

–> stimulates response via motor cortex
–> input to facial nerve nuclei in brainstem
–> LMN input to eyelids causing blink

Question 21

What lesions can cause Menace deficit

Answer 21

Retinal or optic nerve as no visual input (ipsilateral)

Forebrain lesion will cause deficits on CONTRALATERAL side to lesion (due to decussation)

Optic tract lesion
After decussation so deficit is greatest on contralateral side.

Facial nerve neuropathy - will not blink but menace still present and vision normal

Question 22

Cause of absent direct and consensual PLR in an eye with normal PLR direct and consensual in other eye

Answer 22

Occulomotor nerve lesion or parasympathetic innervation loss will be unilateral deficit on affected side (both with direct and indirect stimulation) but the opposite eye will have consensual constriction and direct constriction

Question 23

How does vestibular system maintain balance and eye position

Answer 23

inner ear sensors detect movement in 3 dimensions (semicircular canals), rotary movement (ampulla) and linear acceleration (utricle)
–> in put to sensory afferent of vestibular nerve
–> peripheral vestibular ganglion (in internal acoustic meatus) –> efferents to brain

Pons and medulla
–> send signals to spinal extensors ipisilateral to the increased firing )
–> increased tone on side of increased firing

–> signals to CN III, IV VI nuclei to control eye movement
–> fast phase of movement is same direction as head movement.

Cerebellum also recieves input from vestibular efferent
–> projections that inhibit the action of afferents to the spinal cord negative feedback to prevent excessive tone)

Question 24

Cause of nystagmus in vestibular disease

Answer 24

loss of input from affected side –> interpretation in brain as increased input from opposite side

–> fast phase nystagmus AWAY from lesion

Question 25

Why does cerebellar vestibular disease cause paradoxical changes

Answer 25

Cerebellar inputs on the spinal cord projections normally inhibit the action of the vestibular afferents to regulate extensor tone

–> loss of this inhibition –> increased extensor tone on same side to lesion so fall to other side.

Question 26

How to differentiate central from peripheral vestibular disease

Answer 26

presence of proprioceptive deficits only seen in central disease.

Deficits are always IPSILATERAL to lesion so help with localising cerebellar lesions also (which will have paradoxical head tilt in opposite direction)

Question 27

Head tilt to left
Nystagmus fast phase to left
Falling or small circles to left

Proprioceptive deficits in right FL and HL

Answer 27

Cerebellar vestibular lesion on RIGHT

Question 28

head tilt and circling to left
Nystagmus fast phase to right
No proprioceptive deficits

Answer 28

Left peripheral vestibular lesion

Question 29

DDx for peripheral vestibular localisation

Answer 29

ACUTE NON PROGRESSIVE idiopathic (canine and feline - both recover spontaneous in most cases much more common in dogs 39% of vestibular cases), congenital, head injury,

ACUTE PROGRESSIVE - otitis media or interna (49% of all peripheral cases), inflammatory polyp (cats > dogs), ototoxic medications, neoplasia

CHRONIC PROGRESSIVE - hypoTH (causes defect in energy metabolism), primary aural neoplasia, otitis media, inflammatory polyp

Question 30

DDx for central cerebellar vestibular lesion

Answer 30

MUO, thiamine deficiency (cats - also affects optic nuclei), hypoglycemia, hypoTH, trauma, infectious (CDV, FIP, bact, Toxo), metronidazole toxicity, cerebrovascular accident (most often cerebellum due to less blood supply DDx hypertension)
Post-GA vestibular syndrome in cats
COMS/syringomyelia, arachnoid cysts

Question 31

Cause of ventrolateral strabismus and mydriasis

Answer 31

CN 3 lesion

Question 32

Cause of medial strabismus and inability to retract globe

Answer 32

CN 6 lesion

Question 33

Cause of dropped jaw and loss of facial sensation

Answer 33

bilateral trigeminal n lesion
most likely idiopathic neuropathy as bilateral disease would be huge brainstem lesion

Question 34

DDx for masticatory muscle atrophy

Answer 34

Trigeminal neuritis, intracranial brainstem lesion, TMJ injury, retrobulbar abscess, MMM,

Question 35

What could cause loss of left side facial sensation and motor function (3)

Answer 35

Unilateral peripheral trigeminal nerve lesion on left

RIGHT sided intracranial lesion of forebrain or LEFT sided brain stem lesion

Question 36

What nerve dysfunctions can result in pharyngal weakness, dysfunction or laryngeal dysfunction

Answer 36

CN X - recurrent laryngeal nerve motor and sensory innervation to the pharynx

CN IX sensory and motor to pharynx so can cause dysfunction of swallowing but not lar par

Question 37

What nerves may contribute to development of megaoesophagus

Answer 37

CN X vagus

CN XII hypoglossal - also causes tongue atrophy

Question 38

Unilateral miosis (not dilating in dark) with protrusion of TEL and ptosis

Answer 38

indicates Horners

Need to differentiate as 1st, 2nd or 3rd order

Question 39

Horner’s symptoms with concurrent UMN changes and GP deficits in ipsilateral limbs

Answer 39

indicates central lesion most likely

Question 40

Expected findings of topical phenylephrine test in different Horner’s locations

Answer 40

Central - no dilation, not hypersensitive probably because still get some sympathetic input

2nd order (preganglionic) - no dilation, not hypersensitive probably because still get some sympathetic input

Postganglionic - dilation within 20 minutes even with very dilute sample

Question 41

DDx for optic nerve lesion

Answer 41

Optic neuritis → perform fundic exam and see optic disc swelling
(can be primary dz or part of MUO or secondary to systemic infection/neoplasia)
64% responded to immunosuppression in recent series

• Retinal Dystrophy or SARD
• Retinal degeneration of thiamine deficiency
• Enrofloxacin toxicity in cats causes bilateral retinal degeneration
• Degenerative change to optic nerve

Question 42

DDx for trigeminal n lesion localisation

Answer 42

Idiopathic Trigeminal neuropathy
Most likely if bilateral disease and no other neurological signs
→ impairs motor function but may not affect sensation. A result of nonsuppurative inflammation and demyelination → axonal atrophy.
→ ipsilateral muscle atrophy if unilateral
DDx neuritism masticatory myositis, TMJ injury, retrobulbar abscess, peripheral nerve sheath tumour (if unilateral)

Question 43

Recent series on feline vestibular disease found:

Answer 43

otitis and idiopathic most common cause

Thiamine deficiency presents as bilateral signs and more common in females

Other DDx, post-TECA, FIP, polyps, neoplasia

Spontaneous recovery reported in most of the idiopathic cases