Approach to equine neurology

Question 1

Neurological examination

Answer 1

Mentation/behaviour (from a distance first)

Cranial nerve assessment

Static assessment

Dynamic assessment

Question 2

Assessment of mental status

Answer 2

Consciousness

Ascending reticular activating system (CNS and cerebral hemispheres)

Alert -> depressed -> stupor -> semi-comatose -> comatose

Assess response to external stimuli
○ General environment
○ Specific e.g. skin pinch

Question 3

What are behavioural abnormalities indicative of?

Answer 3

Forebrain disease

Question 4

Examples of behavioural abnormalities indicating forebrain disease

Answer 4

Yawning

Aimless wandering

Circling

Head pressing

Seizures

Question 5

Seizure classification

Answer 5

Primary (generalised)
- generalised bilateral motor activity

Focal/partial
- localised part of the cerebral cortex
- can be simple or complex

Question 6

Simple focal seizure

Answer 6

Normal conciousness

Question 7

Complex focal seizure

Answer 7

Impaired conciousness

Question 8

Clinical signs of generalised seizure

Answer 8

Loss of consciousness

Tonic/clonic muscular spasms

Jaw clamping, paddling legs

Loss of body functions

Question 9

Cause of ventrolateral strabismus

Answer 9

CNIII lesion

Question 10

Cause of medial strabismus

Answer 10

CNVI lesion

Question 11

Cause of dorsomedial strabismus

Answer 11

CNIV lesion

Question 12

Pupillary light reflex

Answer 12

Pupillary constrictor muscles innervated by parasympathetic fibers of CN III
§ Both pupils should constrict in response to light

Pupillary dilator muscles innervated by sympathetic fibers

Rostral colliculi detection responsible for dazzle reflex (subcortical reflex)
§ Horse blinks/withdraws head

Pupil should constrict in response to bright light source

Question 13

PLR pathway

Answer 13

Photoreceptors of retina -> optic nerve

Optic nerves join at optic chiasm – 90% fiber decussation in the horse to contralateral optic tract

Fibers go to dorsal geniculate body, then to the visual cortex

20% of the fibers in the optic tract go to the pretectal nuclei and control pupillomotor function rather than to visual cortex

From pretectal region, some pupillomotor fibers cross again to the contralateral parasympathetic CN III nuclei
□ This explains consensual/indirect stimulus to contralateral pupil – why shining a light in one eye elicits a bilateral response

More fibers project to the rostral colliculi and elicit dazzle response
□ Does not involve vision, subcortical reflex

Question 14

Afferent arc of vision

Answer 14

optic nerve to optic chiasm, to contralateral visual/occipital cortex for perception

Question 15

Menace response

Answer 15

efferent arc ipsilateral facial nucleus

Tests CN II, visual cortex, CN VII

Care not to create air current

Response, not reflex! Care RE foals – develops after birth

Cerebellar disease may disrupt transmission between occipital cortex and facial nucleus

Question 16

Palpebral reflex

Answer 16

Lightly touch at medial canthus to elicit a blink

Testing facial sensation – CN V

And ability to blink - CN VII

Question 17

What are the muscle of mastication innervated by?

Answer 17

CN V

Question 18

What is muzzle deviation a classic sign of?

Answer 18

CN VII lesion

Question 19

What sign can a CN VIII lesion create?

Answer 19

Head tilt towards the lesion

Question 20

Which cranial nerve is tested by touching the face lightly with a pen?

Answer 20

CN V - facial sensation

Question 21

How do you assess tongue tone

Answer 21

Can assess by pulling tongue out of the side of the mouth – most horses will really resist this

Question 22

Cervicofacial reflex

Answer 22

Tap with a pen at level of C1-C2

Spinal nerves at C1 and C2 and tests CN VII as effects grimace response at corner of mouth

Question 23

Parts of a dynamic neurological assessment

Answer 23

Straight line

Straight line with head raised

Back up

Serpentine

Obstacles

Tail pull

Tight circles on the spot

Blindfold

Question 24

Ataxia

Answer 24

Incoordination of motor movements

Loss of proprioception - reduced awareness of limb placement.
§ Conscious proprioception - abnormal limb position at rest
§ Unconscious proprioception - abnormal limb placement or movement when moving

Question 25

Paresis

Answer 25

Weakness/deficiency of voluntary movement

Question 26

Spasticity

Answer 26

Stiffness, reduced flexion of joints

Question 27

Dysmetria

Answer 27

Abnormal range of movement

Question 28

Hypermetria

Answer 28

Excessive movement

Question 29

Grade 0 ataxia

Answer 29

Normal strength and coordination

Question 30

Grade 1 ataxia

Answer 30

Subtle neurological deficits only noted under special circumstances but mild

Question 31

Grade 2 ataxia

Answer 31

Mild neurological deficits apparent at all times/gaits

Question 32

Grade 3 ataxia

Answer 32

Moderate deficits at all times/gaits that are obvious to all observers

Question 33

Grade 4 ataxia

Answer 33

Severe deficits with tendency to buckle, stumble spontaenously, and trip and fall

Question 34

Grade 5 ataxia

Answer 34

Recumbent, unable to stand

Question 35

UMN

Answer 35

Determines, coordinates, and recruits use of muscle
§ Initiation and regulation

Cell bodies in brainstem (unconscious), cortex (conscious)

Messages to tracts in spinal cord

Control of voluntary movement

Clinical signs depend on location/severity of lesion
§ Paresis: can’t recruit enough muscle/not coordinated
§ Hyperreflexia

Question 36

LMN

Answer 36

Directly stimulates contraction of muscles

Cell bodies in spinal cord gray matter and brainstem

Messages via tracts in spinal cord

Clinical signs dependent on degree of loss

Paralysis/paresis with atrophy

Areflexia

Question 37

Neurological diagnostic tools

Answer 37

CSF taps

Endoscopy

Imaging
- radiography
- CT head
- MRI head