Approach to equine neurology Flashcards

1
Q

Neurological examination

A

Mentation/behaviour (from a distance first)

Cranial nerve assessment

Static assessment

Dynamic assessment

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2
Q

Assessment of mental status

A

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

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3
Q

What are behavioural abnormalities indicative of?

A

Forebrain disease

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4
Q

Examples of behavioural abnormalities indicating forebrain disease

A

Yawning

Aimless wandering

Circling

Head pressing

Seizures

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5
Q

Seizure classification

A

Primary (generalised)
- generalised bilateral motor activity

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

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6
Q

Simple focal seizure

A

Normal conciousness

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7
Q

Complex focal seizure

A

Impaired conciousness

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8
Q

Clinical signs of generalised seizure

A

Loss of consciousness

Tonic/clonic muscular spasms

Jaw clamping, paddling legs

Loss of body functions

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9
Q

Cause of ventrolateral strabismus

A

CNIII lesion

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10
Q

Cause of medial strabismus

A

CNVI lesion

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11
Q

Cause of dorsomedial strabismus

A

CNIV lesion

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12
Q

Pupillary light reflex

A

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

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13
Q

PLR pathway

A

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

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14
Q

Afferent arc of vision

A

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

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15
Q

Menace response

A

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

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16
Q

Palpebral reflex

A

Lightly touch at medial canthus to elicit a blink

Testing facial sensation – CN V

And ability to blink - CN VII

17
Q

What are the muscle of mastication innervated by?

18
Q

What is muzzle deviation a classic sign of?

A

CN VII lesion

19
Q

What sign can a CN VIII lesion create?

A

Head tilt towards the lesion

20
Q

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

A

CN V - facial sensation

21
Q

How do you assess tongue tone

A

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

22
Q

Cervicofacial reflex

A

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

23
Q

Parts of a dynamic neurological assessment

A

Straight line

Straight line with head raised

Back up

Serpentine

Obstacles

Tail pull

Tight circles on the spot

Blindfold

24
Q

Ataxia

A

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

25
Paresis
Weakness/deficiency of voluntary movement
26
Spasticity
Stiffness, reduced flexion of joints
27
Dysmetria
Abnormal range of movement
28
Hypermetria
Excessive movement
29
Grade 0 ataxia
Normal strength and coordination
30
Grade 1 ataxia
Subtle neurological deficits only noted under special circumstances but mild
31
Grade 2 ataxia
Mild neurological deficits apparent at all times/gaits
32
Grade 3 ataxia
Moderate deficits at all times/gaits that are obvious to all observers
33
Grade 4 ataxia
Severe deficits with tendency to buckle, stumble spontaenously, and trip and fall
34
Grade 5 ataxia
Recumbent, unable to stand
35
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
36
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
37
Neurological diagnostic tools
CSF taps Endoscopy Imaging - radiography - CT head - MRI head