Approach to equine neurology Flashcards
Neurological examination
Mentation/behaviour (from a distance first)
Cranial nerve assessment
Static assessment
Dynamic assessment
Assessment of mental status
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
What are behavioural abnormalities indicative of?
Forebrain disease
Examples of behavioural abnormalities indicating forebrain disease
Yawning
Aimless wandering
Circling
Head pressing
Seizures
Seizure classification
Primary (generalised)
- generalised bilateral motor activity
Focal/partial
- localised part of the cerebral cortex
- can be simple or complex
Simple focal seizure
Normal conciousness
Complex focal seizure
Impaired conciousness
Clinical signs of generalised seizure
Loss of consciousness
Tonic/clonic muscular spasms
Jaw clamping, paddling legs
Loss of body functions
Cause of ventrolateral strabismus
CNIII lesion
Cause of medial strabismus
CNVI lesion
Cause of dorsomedial strabismus
CNIV lesion
Pupillary light reflex
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
PLR pathway
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
Afferent arc of vision
optic nerve to optic chiasm, to contralateral visual/occipital cortex for perception
Menace response
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
Palpebral reflex
Lightly touch at medial canthus to elicit a blink
Testing facial sensation – CN V
And ability to blink - CN VII
What are the muscle of mastication innervated by?
CN V
What is muzzle deviation a classic sign of?
CN VII lesion
What sign can a CN VIII lesion create?
Head tilt towards the lesion
Which cranial nerve is tested by touching the face lightly with a pen?
CN V - facial sensation
How do you assess tongue tone
Can assess by pulling tongue out of the side of the mouth – most horses will really resist this
Cervicofacial reflex
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
Parts of a dynamic neurological assessment
Straight line
Straight line with head raised
Back up
Serpentine
Obstacles
Tail pull
Tight circles on the spot
Blindfold
Ataxia
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
Paresis
Weakness/deficiency of voluntary movement
Spasticity
Stiffness, reduced flexion of joints
Dysmetria
Abnormal range of movement
Hypermetria
Excessive movement
Grade 0 ataxia
Normal strength and coordination
Grade 1 ataxia
Subtle neurological deficits only noted under special circumstances but mild
Grade 2 ataxia
Mild neurological deficits apparent at all times/gaits
Grade 3 ataxia
Moderate deficits at all times/gaits that are obvious to all observers
Grade 4 ataxia
Severe deficits with tendency to buckle, stumble spontaenously, and trip and fall
Grade 5 ataxia
Recumbent, unable to stand
UMN
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
LMN
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
Neurological diagnostic tools
CSF taps
Endoscopy
Imaging
- radiography
- CT head
- MRI head
