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==[[Cranial Nerve Examination - Horse]]==
 
==[[Cranial Nerve Examination - Horse]]==
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* The cranial nerves are numbered 1-12 from the most rostral to the most caudal.
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* A systematic examination of the cranial nerves can aid accurate identification of the site of a lesion.
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===Cranial Nerve I===
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* Cranial nerve I is the olfactory nerve.
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** Abnormalities are rarely detected in this nerve.
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===[[Neurological Eye Examination - Horse]]===
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====Menace Response====
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* The reflex is assessed by observing the horse blink in response to a visual "threat".
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** The menace reflex is a learned response.
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* When testing the menace reflex, it should be ensured that the hand does not create air movements.
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** These may be sensed, for example by the vibrissae, rather than seen.
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* A positive menace reflex confirms normal function of:
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*# The particular optic nerve (CN II)
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*# The optic chiasm
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*#* Nearly all optic nerve fibres cross at the chiasm in the horse.
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*# Pathways through the thalamus to the occipital visual cortex on the opposite side.
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*# Afferent pathways to the facial nerve (VII) nucleus in the brainstem on the original side.
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*#* It is assumed that the afferent pathway from the visual cortex passes through the cerebellum.
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*#** Horses with cerebellar disease may lack or have diminished menace responses.
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*# The facial nerve on the original side (efferent pathway).
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* '''The menace response therefore assesses both visual pathways and the facial nerve.'''
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====Pupillary Responses====
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* Pupil diameter is controlled by:
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** Parasympathetic function for constriction.
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*** Occulomotor nerve (CN III)
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** Sympathetic function for dilation.
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*** For example, in fear or excitement.
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=====The pupillary light reflex (PLR)=====
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* The PLR is a true reflex; the pathways remain in the thalamus and brainstem, and the stimulus need not be perceived.
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* Shining a light into the eye should result in:
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*# A reflex constriction of the pupil in the same eye.
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*#* The direct response
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*# A partial constriction of the other eye.
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*#* The consensual response
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*#* This is difficult to see in large animals because of the shape of the head.
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* The PLR examines:
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** Optic nerve function
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** The parasympathetic fibres within the occulomotor nerve.
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=====Horner’s syndrome=====
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* Horner's syndrome is a clinical syndrome caused by damage to the sympathetic nervous system.
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* Signs include:
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** '''Ptosis'''
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*** Drooping of the upper eyelid
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** '''Miosis'''
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*** Constriction of the pupil
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** '''Enophthalmus'''
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*** Sinking of the eyeball into the orbital cavity
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** '''Protrusion of the third eyelid'''
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** In horses, Horner's syndrome is often seen in combination with '''regional sweating'''.
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*** Unlike in other animals, sweating in horses is largely dependent on regional increases in blood flow.
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*** Parasympathetic dilation of peripheral blood vessels predominates when sympathetic pathways are interrupted.
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**** This causes regional sweating.
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* The sympathetic supply reaches the eye via the spinal cord; Horner’s syndrome can therefore be caused by spinal cord disease.
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** First order preganglionic fibres originate in the hypothalamus, and pass via the brainstem and cervical spinal cord to the ventral grey matter of the thoraco-lumbar spinal cord.
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** Second order preganglionic neurones exit the spinal cord via spinal nerves.
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*** Preganglionic fibres destined for the head leave the spinal cord at spinal nerves T1-T3.
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** Fibres pass through the thorax, travelling via the cranial stellate ganglion (where they do not synapse), and the vagosympathetic trunk up the neck.
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** Preganglionic fibres then synapse in the cranial cervical ganglion.
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** From here, 3rd order postganglionic neurons pass to:
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*** The eye, via branches of the internal carotid artery.
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*** The skin of the top of the head.
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* The sympathetic supply to the skin the neck caudal to C2 is via segmental cervical vertebral nerves.
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** Cervical vertebral nerves each carry postganglionic sympathetic fibres.
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** These fibres follow the vertebral artery after leving the stellate ganglion.
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** A caudal cervical lesion may therefore affect the sypathetic trunk, causing sweating to C2 but not C2-C8.
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*** I.e. C2-C8 has alternative sympathetic supply, and so is not affected by a lesion of this sort.
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* Lesions occuring post- cranial cervical ganglion result in sweating of the face and the area of skin at the base of the ear down to about C1.
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** For example, lesions in guttural pouch disease.
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====Vision====
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* The easiest way to determine blindness in horses is to create an obstacle course.
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** Cover the eyes separately to assess each in turn.
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* Ophthalmological examination should be performed if any any of the followinf are found to be imparied:
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** Visual pathways
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** Reflexes
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** Responses
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====Eye position====
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* Eye position is controlled by the actions of the extraocular eye muscles.
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** These muscles are innervated by:
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*** The oculomotor nerve (CN III)
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*** The trochlear nerve (CN IV)
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*** The abducens nerve (CN VI).
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** '''Dysfunction of these nerves results in strabismus'''.
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* The eyes must move in relation to the position of the head and neck.
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** Pathways exist that mediate the movement of the eyes in response to head and neck movement.
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*** Vestibular and neck problems can therefore result in a perceived strabismus.
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* Normally, elevation of the head results in ventral movement of the eye.
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** The eye is usually fixed on a point in space.
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* Lateral head and neck movement results in rhythmic eye movement in response to motion - "doll’s eye vestibular nystagmus".
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** This is similar to a human fixing its eyes on a point out of a window of a moving train.
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** This form of nystagmus is normal.
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*** It is characterised by the fast phase being in the direction of movement.
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* Strabismus is relatively easy to asses in the horse due to the elongated shape of the pupil.
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** True strabismus is relatively rare in horses.
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** Occulomotor nerve dysfunction may result in lateral deviation of the eyeball.
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*** Parasympathetic supply is often also interrupted, giving mydriasis.
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** Apparent strabismus may be seen in horses with vestibular disease, since the vestibular system interacts with eye positioning.
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*** However, in this scenario eye movements to and away from the apparent direction of strabismus are still possible.
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[[Category:Neurological Examination - Horse|C]]
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===[[Face Sensation]]===
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* Nerve fibres giving sensation to the face are carried in cranial nerve V - the trigeminal nerve.
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** The trigeminal nerve provides sensory innervation to:
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*** The skin of the face
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*** The ears
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*** The nasal mucosa
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*** The cornea
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** There are three divisions of the trigeminal nerve
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*** The mandibular branch
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*** The maxillary branch
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*** The opthalmic branch
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* Facial sensation is tested by observation for an avoidance response or reflex movement following stimulation.
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** All the divisions of the trigeminal nerve should be tested. This is achieved by:
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*** Stimulation within the nostrils
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*** Stimulation within the ears
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*** Stimulation between the mandibles
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*** Testing the corneal reflex.
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***# Pressure is exerted on the corneal surface through the eyelid.
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***# The opthalmic branch of the trigeminal nerve provides sensory (afferent) input.
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***# Efferent signals are sent via the abducens nerve (CN VI)
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***# The retractor oculi muscle retracts the eye
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====Masticatory muscles====
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* The mandibular branch of the trigeminal nerve carries motor fibres.
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** It is the only division of the trigeminal nerve that does so.
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* The muscles of mastication are innervated by these fibres.
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** The masseter and temporalis muscles are particulaly influenced by the mandibular brach of the trigeminal nerve.
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*** These muscles of mastication are also the easiest to assess.
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*** These muscles should be closely examined for signs of atrophy.
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**** '''Atrophy of the temporalis and masseter muscle indicates damage to the mandibular branch of CN V.'''
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====Facial Expression====
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* The muscles of facial expression are innervated by branches of cranial nerve VII - the facial nerve.
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* The facial nerve also carries the parasympathetic supply to the lacrimal glands.
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** Horses with facial nerve dysfunction are therefore prone to corneal ulceration, due to :
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*** An inability to blink
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*** Poor or absent tear production
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=====Facial Nerve Dysfunction=====
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* Facial nerve dysfunction is common in the horse.
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* It is readily identified by one or more of the following:
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** A lip droop
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** Muzzle deviation
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*** Deviation is towards the normal side.
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** An ear droop
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* Early or mild dysfunction may be reflected by:
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** Slight changes to nostril size
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** Nostril flare
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** Reduced ear movements in response to audible stimuli
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* The branch of CN VII supplying the muzzle and nostrils crosses the vertical mandibular ramus and the surface of the masseter muscle.
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** A lesion to that side of the face, for example a kick, may cause signs confined to the nose.
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** Alternatively, a more central lesion will give both ear and nostril signs.
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=====The Palpebral Reflex=====
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* The palpebral reflex examines the function of both CN V (afferent) and CN VII (efferent).
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* The reflex is elicited by lightly touching the eyelids and watching for reflex closure.
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[[Category:Neurological Examination - Horse|D]]
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===[[Vestibular System Examination]]===
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====The Vestibulocochlear Nerve====
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* Cranial nerve VIII is the vestibulocochlear nerve.
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* The vestibulocochlear nerve carries
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** Auditory, or cochlear, signals.
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** Balance, or vestibular, signals.
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* Signals from CN VIII are relayed to the vestibular nuclei in the brainstem.
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** The nuclei in turn relay information to
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*** The eyes
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*** The body and limbs
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*** Higher centres.
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* Many efferent signals are controlled in part by cerebellar input.
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====Unilateral Vestibular Disease====
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* Horses with unilateral vestibular lesions often have a head tilt towards the side of the lesion.
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* If nystagmus is absent, determining whether a horse with a head tilt is also weak is helpful in deciding whether vestibular disease is central or peripheral.
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** In peripheral diease, the horse may be ataxic but weakness is not normally seen.
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=====Acute=====
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* In the acute stages of vestibular disease, spontaneous nystagmus may be present.
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** The appearance of nystagmus is different depending on the type of vestibular disease present.
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*** Central vestibular disease
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**** Nystagmus often is variable; i.e. rotary, horizontal and vertical.
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*** Peripheral vestibular disease
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**** The fast phase of the nystagmus is away from the side of the lesion.
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=====Chronic=====
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* Nystagmus may resolve in more chronic lesions.
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** However, it may return with changes in head position.
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*** I.e. positional nystagmus.
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* Visual accomodation improves ataxic movements.
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** However, these may return dramatically on blindfolding.
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====Bilateral Vestibular Disease====
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* An observable head tilt may not be present.
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* Movements are likely to be markedly ataxic.
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** This is probably due in part to involvement of ascending proprioceptive and descending motor pathways that run through the brainstem.
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[[Category:Neurological Examination - Horse|E]]
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===[[Pharyngeal and Laryngeal Function]]===
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* The pharynx and larynx are innervated by:
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** CN IX - the glossopharyngeal nerve
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** CN X - the vagus nerve
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** CN XI - the accessory nerve
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* Pharyngeal and laryngeal function is best studied by:
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*# Observing the horse eat and swallow
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*# Endoscopy
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====Laryngeal Dysfunction====
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* Left recurrent laryngeal hemiplegia is the most common dysfunction in horses.
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** The left recurrent laryngeal nerve is a branch of the vagus nerve.
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** Horses are known as "roarers".
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====Pharyngeal Dysfunction====
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* Pharyngeal paralysis in horses is commonly associated with peripheral disease.
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** Especially guttural pouch disease.
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*** Endoscopy of the guttural pouches should be therefore be performed in horses that are dysphagic.
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[[Category:Neurological Examination - Horse|F]]
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===[[Tongue Movement]] ===
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* The hypoglossal nerve, CN XII provides motor innervation to the [[Tongue - Anatomy & Physiology|tongue]].
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* Normally, a horse resists the [[Tongue - Anatomy & Physiology|tongue]] being retracted from the mouth.
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** The horse will quickly return the tongue after it is pulled out to the side.
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* Horses with hypoglossal weakness appear differently.
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** The [[Tongue - Anatomy & Physiology|tongue]] may protrude from the mouth.
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** Chronic unilateral hypoglossal lesions may result in unilateral tongue atrophy.
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** Bilateral hypoglossal lesions may result in difficulty prehending food.
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* Horses with cerebral dysfunction may have signs corresponding to tongue weakness.
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** However, [[Tongue - Anatomy & Physiology|tongue]] atrophy is not present in these animals.
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[[Category:Neurological Examination - Horse|G]]
       
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