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:
  1. The particular optic nerve (CN II)
  2. The optic chiasm
     • Nearly all optic nerve fibres cross at the chiasm in the horse.
  3. Pathways through the thalamus to the occipital visual cortex on the opposite side.
  4. 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.
  5. 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:
  1. A reflex constriction of the pupil in the same eye.
     • The direct response
  2. 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.