View source for Neurological Eye Examination - Horse

====Menace Response====

* The reflex is assessed by observing the horse blink in response to a visual "threat".
** The menace reflex is a learned response.
* When testing the menace reflex, it should be ensured that the hand does not create air movements.
** These may be sensed, for example by the vibrissae, rather than seen. 
* A positive menace reflex confirms normal function of:
*# The particular optic nerve (CN II)
*# The optic chiasm
*#* Nearly all optic nerve fibres cross at the chiasm in the horse.
*# Pathways through the thalamus to the occipital visual cortex on the opposite side.
*# Afferent pathways to the facial nerve (VII) nucleus in the brainstem on the original side.
*#* It is assumed that the afferent pathway from the visual cortex passes through the cerebellum.
*#** Horses with cerebellar disease may lack or have diminished menace responses.
*# The facial nerve on the original side (efferent pathway). 
* '''The menace response therefore assesses both visual pathways and the facial nerve.'''




====Pupillary Responses====

* Pupil diameter is controlled by:
** Parasympathetic function for constriction.
*** Occulomotor nerve (CN III)
** Sympathetic function for dilation.
*** For example, in fear or excitement.

=====The pupillary light reflex (PLR)=====

* The PLR is a true reflex; the pathways remain in the thalamus and brainstem, and the stimulus need not be perceived.
* Shining a light into the eye should result in:
*# A reflex constriction of the pupil in the same eye.
*#* The direct response
*# A partial constriction of the other eye.
*#* The consensual response
*#* This is difficult to see in large animals because of the shape of the head.
* The PLR examines:
** Optic nerve function
** The parasympathetic fibres within the occulomotor nerve.

=====Horner’s syndrome=====

* Horner's syndrome is a clinical syndrome caused by damage to the sympathetic nervous system.
* Signs include:
** '''Ptosis'''
*** Drooping of the upper eyelid
** '''Miosis'''
*** Constriction of the pupil
** '''Enophthalmus'''
*** Sinking of the eyeball into the orbital cavity
** '''Protrusion of the third eyelid'''
** In horses, Horner's syndrome is often seen in combination with '''regional sweating'''.
*** Unlike in other animals, sweating in horses is largely dependent on regional increases in blood flow. 
*** Parasympathetic dilation of peripheral blood vessels predominates when sympathetic pathways are interrupted.
**** This causes regional sweating.
* The sympathetic supply reaches the eye via the spinal cord; Horner’s syndrome can therefore be caused by spinal cord disease.
** 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. 
** Second order preganglionic neurones exit the spinal cord via spinal nerves.
*** Preganglionic fibres destined for the head leave the spinal cord at spinal nerves T1-T3. 
** Fibres pass through the thorax, travelling via the cranial stellate ganglion (where they do not synapse), and the vagosympathetic trunk up the neck.
** Preganglionic fibres then synapse in the cranial cervical ganglion. 
** From here, 3rd order postganglionic neurons pass to:
*** The eye, via branches of the internal carotid artery.
*** The skin of the top of the head.
* The sympathetic supply to the skin the neck caudal to C2 is via segmental cervical vertebral nerves.
** Cervical vertebral nerves each carry postganglionic sympathetic fibres.
** These fibres follow the vertebral artery after leving the stellate ganglion.
** A caudal cervical lesion may therefore affect the sypathetic trunk, causing sweating to C2 but not C2-C8.
*** I.e. C2-C8 has alternative sympathetic supply, and so is not affected by a lesion of this sort. 
* 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.
** For example, lesions in guttural pouch disease.




====Vision====

* The easiest way to determine blindness in horses is to create an obstacle course. 
** Cover the eyes separately to assess each in turn.
* Ophthalmological examination should be performed if any any of the following are found to be impaired:
** Visual pathways
** Reflexes
** Responses

====Eye position====

* Eye position is controlled by the actions of the extraocular eye muscles.
** These muscles are innervated by:
*** The oculomotor nerve (CN III)
*** The trochlear nerve (CN IV)
*** The abducens nerve (CN VI). 
** '''Dysfunction of these nerves results in strabismus'''. 
* The eyes must move in relation to the position of the head and neck.
** Pathways exist that mediate the movement of the eyes in response to head and neck movement. 
*** Vestibular and neck problems can therefore result in a perceived strabismus.
* Normally, elevation of the head results in ventral movement of the eye.
** The eye is usually fixed on a point in space.
* Lateral head and neck movement results in rhythmic eye movement in response to motion - "doll’s eye vestibular nystagmus". 
** This is similar to a human fixing its eyes on a point out of a window of a moving train. 
** This form of nystagmus is normal.
*** It is characterised by the fast phase being in the direction of movement. 
* Strabismus is relatively easy to asses in the horse due to the elongated shape of the pupil.
** True strabismus is relatively rare in horses.
** Occulomotor nerve dysfunction may result in lateral deviation of the eyeball.
*** Parasympathetic supply is often also interrupted, giving mydriasis. 
** Apparent strabismus may be seen in horses with vestibular disease, since the vestibular system interacts with eye positioning.
*** However, in this scenario eye movements to and away from the apparent direction of strabismus are still possible.


[[Category:Cranial Nerve Examination - Horse|A]]