Difference between revisions of "Neuro Exam of The Horse - Pathology"

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==[[Cranial Nerve Examination - Horse]]==
 
==[[Cranial Nerve Examination - Horse]]==
 
* The cranial nerves are numbered 1-12 from the most rostral to the most caudal.
 
* A systematic examination of the cranial nerves can aid accurate identification of the site of a lesion.
 
 
===Cranial Nerve I===
 
 
* Cranial nerve I is the olfactory nerve.
 
** Abnormalities are rarely detected in this nerve.
 
 
===[[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 followinf are found to be imparied:
 
** 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:Neurological Examination - Horse|C]]
 
 
 
===[[Face Sensation]]===
 
 
* Nerve fibres giving sensation to the face are carried in cranial nerve V - the trigeminal nerve.
 
** The trigeminal nerve provides sensory innervation to:
 
*** The skin of the face
 
*** The ears
 
*** The nasal mucosa
 
*** The cornea
 
** There are three divisions of the trigeminal nerve
 
*** The mandibular branch
 
*** The maxillary branch
 
*** The opthalmic branch
 
* Facial sensation is tested by observation for an avoidance response or reflex movement following stimulation.
 
** All the divisions of the trigeminal nerve should be tested. This is achieved by:
 
*** Stimulation within the nostrils
 
*** Stimulation within the ears
 
*** Stimulation between the mandibles
 
*** Testing the corneal reflex.
 
***# Pressure is exerted on the corneal surface through the eyelid.
 
***# The opthalmic branch of the trigeminal nerve provides sensory (afferent) input.
 
***# Efferent signals are sent via the abducens nerve (CN VI)
 
***# The retractor oculi muscle retracts the eye
 
 
====Masticatory muscles====
 
 
* The mandibular branch of the trigeminal nerve carries motor fibres.
 
** It is the only division of the trigeminal nerve that does so.
 
* The muscles of mastication are innervated by these fibres.
 
** The masseter and temporalis muscles are particulaly influenced by the mandibular brach of the trigeminal nerve.
 
*** These muscles of mastication are also the easiest to assess.
 
*** These muscles should be closely examined for signs of atrophy.
 
**** '''Atrophy of the temporalis and masseter muscle indicates damage to the mandibular branch of CN V.'''
 
 
====Facial Expression====
 
 
* The muscles of facial expression are innervated by branches of cranial nerve VII - the facial nerve.
 
* The facial nerve also carries the parasympathetic supply to the lacrimal glands.
 
** Horses with facial nerve dysfunction are therefore prone to corneal ulceration, due to :
 
*** An inability to blink
 
*** Poor or absent tear production
 
 
=====Facial Nerve Dysfunction=====
 
 
* Facial nerve dysfunction is common in the horse.
 
* It is readily identified by one or more of the following:
 
** A lip droop
 
** Muzzle deviation
 
*** Deviation is towards the normal side.
 
** An ear droop
 
* Early or mild dysfunction may be reflected by:
 
** Slight changes to nostril size
 
** Nostril flare
 
** Reduced ear movements in response to audible stimuli
 
* The branch of CN VII supplying the muzzle and nostrils crosses the vertical mandibular ramus and the surface of the masseter muscle.
 
** A lesion to that side of the face, for example a kick, may cause signs confined to the nose.
 
** Alternatively, a more central lesion will give both ear and nostril signs.
 
 
=====The Palpebral Reflex=====
 
 
* The palpebral reflex examines the function of both CN V (afferent) and CN VII (efferent).
 
* The reflex is elicited by lightly touching the eyelids and watching for reflex closure.
 
 
 
[[Category:Neurological Examination - Horse|D]]
 
 
===[[Vestibular System Examination]]===
 
 
====The Vestibulocochlear Nerve====
 
 
* Cranial nerve VIII is the vestibulocochlear nerve.
 
* The vestibulocochlear nerve carries
 
** Auditory, or cochlear, signals.
 
** Balance, or vestibular, signals.
 
* Signals from CN VIII are relayed to the vestibular nuclei in the brainstem.
 
** The nuclei in turn relay information to
 
*** The eyes
 
*** The body and limbs
 
*** Higher centres.
 
* Many efferent signals are controlled in part by cerebellar input.
 
 
====Unilateral Vestibular Disease====
 
 
* Horses with unilateral vestibular lesions often have a head tilt towards the side of the lesion.
 
* 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.
 
** In peripheral diease, the horse may be ataxic but weakness is not normally seen.
 
 
=====Acute=====
 
 
* In the acute stages of vestibular disease, spontaneous nystagmus may be present.
 
** The appearance of nystagmus is different depending on the type of vestibular disease present.
 
*** Central vestibular disease
 
**** Nystagmus often is variable; i.e. rotary, horizontal and vertical.
 
*** Peripheral vestibular disease
 
**** The fast phase of the nystagmus is away from the side of the lesion.
 
 
=====Chronic=====
 
 
* Nystagmus may resolve in more chronic lesions.
 
** However, it may return with changes in head position.
 
*** I.e. positional nystagmus.
 
* Visual accomodation improves ataxic movements.
 
** However, these may return dramatically on blindfolding.
 
 
====Bilateral Vestibular Disease====
 
 
* An observable head tilt may not be present.
 
* Movements are likely to be markedly ataxic.
 
** This is probably due in part to involvement of ascending proprioceptive and descending motor pathways that run through the brainstem.
 
 
[[Category:Neurological Examination - Horse|E]]
 
 
===[[Pharyngeal and Laryngeal Function]]===
 
 
* The pharynx and larynx are innervated by:
 
** CN IX - the glossopharyngeal nerve
 
** CN X - the vagus nerve
 
** CN XI - the accessory nerve
 
* Pharyngeal and laryngeal function is best studied by:
 
*# Observing the horse eat and swallow
 
*# Endoscopy
 
 
====Laryngeal Dysfunction====
 
 
* Left recurrent laryngeal hemiplegia is the most common dysfunction in horses.
 
** The left recurrent laryngeal nerve is a branch of the vagus nerve.
 
** Horses are known as "roarers".
 
 
====Pharyngeal Dysfunction====
 
 
* Pharyngeal paralysis in horses is commonly associated with peripheral disease.
 
** Especially guttural pouch disease.
 
*** Endoscopy of the guttural pouches should be therefore be performed in horses that are dysphagic.
 
 
 
[[Category:Neurological Examination - Horse|F]]
 
 
 
===[[Tongue Movement]] ===
 
 
* The hypoglossal nerve, CN XII provides motor innervation to the [[Tongue - Anatomy & Physiology|tongue]].
 
* Normally, a horse resists the [[Tongue - Anatomy & Physiology|tongue]] being retracted from the mouth.
 
** The horse will quickly return the tongue after it is pulled out to the side.
 
* Horses with hypoglossal weakness appear differently.
 
** The [[Tongue - Anatomy & Physiology|tongue]] may protrude from the mouth.
 
** Chronic unilateral hypoglossal lesions may result in unilateral tongue atrophy.
 
** Bilateral hypoglossal lesions may result in difficulty prehending food.
 
* Horses with cerebral dysfunction may have signs corresponding to tongue weakness.
 
** However, [[Tongue - Anatomy & Physiology|tongue]] atrophy is not present in these animals.
 
 
 
[[Category:Neurological Examination - Horse|G]]
 
  
  

Revision as of 16:01, 9 March 2011

Neurological Examination of Horses Overview


Neurological Examination Initial Observation - Horse

Cranial Nerve Examination - Horse

Body, Spinal Cord and Limb Neurological Examination - Horse

Conscious Proprioception Testing

  • It is possible to test a horse’s conscious proprioception by altering the position of the limbs in space.
    • Horses should normally replace their limbs to the normal position within a few seconds.
      • There is a degress of individual variability, however, and the test can be difficult to interpret.
  • Tests can also be performed by walking or trotting a horse and then suddenly stopping.
    • The animal should be observed to see how quickly it replaces its legs in a normal position.

Gait

  • Gait is a combination of higher control of motor function and unconscious proprioception.
  • During assessment of gait, the examiner is looking primarily for evidence of ataxia and/ or weakness.
    • Each leg should be assessed in turn.
  • Defects may be graded on a five-point scale (the Mayhew scale).
    • 0 is normal and 5 is recumbent.

Ataxia

  • Defects in unconscious proprioceptive pathways result in ataxia.
    • These pathways originate in muscle spindle stretch receptors and golgi tendon organs.
    • Impulses are relayed via peripheral nerves to the spinal cord.
    • Signals then ascend in pathways to the cerebellum.
      • Primary cerebellar diseases in horses are rare, but classically cause incoordination of the head and limbs.
        • Weakness is not a prominent feature.
        • The cerebellum communicates with the vestibular nuclei, and so cerebellar diseases may sometimes present with vestibular signs.
  • Manifestations of ataxia:
    • Exaggerated movements - hypermetria
    • Reduced movements - stilted hypometric movements
    • Both exaggerated and reduced movements - dysmetria.
  • Animals may also
    • Sway
    • Place their feet abnormally
      • Horses cross or weave their feet, with abnormal abduction or adduction.
  • Signs of spinal ataxia may be exaggerated by lifting the horse's head.
    • This is beacuse it removes the horizon.
    • Similar responses can be generated by walking up and down slopes.
  • Circling the horse can also reveal ataxia.
    • The horse may plant its feet and rotate around them without placing them properly.
    • Outward rotation of the pelvic limbs is also a common sign.
      • The term for this is "circumduction".
  • Unconscious proprioception may also be tested by backing the horse.
    • Normal horses back with a diagonal gait.
    • Horses with spinal ataxia will often pace when backing.

Weakness

  • Weakness usually manifests as toe dragging, stumbling, or knuckling over.
    • It is a good idea to look closely at the horse’s hooves to see if any are abnormally worn.
  • Weakness may be caused by dysfunction of either the upper or lower motorneurons.
    • Lower motor neuron weakness.
      • Accompanied by:
        • Muscle flaccidity
        • Muscle atrophy if chronic
      • May sometimes appear similar to lameness.
    • Upper motor neuron weakness.
      • Presents as a lack of control of limb muscle movement.
      • Tested most easily tested by pulling the tail during walking.
        • Pulling the tail while stationary probably primarily tests lower motor neuron control and muscular strength of the pelvic limb.


Site of Spinal Lesions Determination - Horse

  • If there are no brain or brainstem signs, an animal with ataxia or weakness is most likely to have a lesion in the spinal cord.
  • The spinal reflexes used in small animals to assess specific segments are not very useful in adult horses.
    • However, withdrawal reflexes are useful in recumbent horses with severe lesions.
      • A stimulus is applied to the distal limb and the reflex results in limb withdrawal.

Cervical Lesions

  • Cervical lesions occur from C1 to C5
    • C6 and C7 may also be included.
  • Horses with defects in all four legs are most likely to have a cervical lesion.
  • The pelvic limbs tend to be more severely affected than the thoracic limbs.
    • This is due to the topographical arrangement of the white matter tracts in the spinal cord.

Effects on Reflexes

  • Cervicofacial reflex
    • The cervicofacial reflex is tested by lightly stimulating the skin of the lateral neck.
      • In an intact reflex movement of the lips should be observed.
      • This reflex varies widely between individual horses.
      • This is not intact in cervical lesions.
  • Withdrawal reflexes
    • Only of use in recumbent horses.
    • In cervical lesions, reflexes in both thoracic and pelvic limbs may be exaggerated.
      • This is due to a loss of upper motor neuron inhibition.

Brachial Lesions

  • Brachial lesions occur from C6 to T2.
  • Signs of a spinal lesion at this level differ in the thoracic and pelvic limbs.
    • Thoracic limbs
      • Lower motor neuron signs
        • Weakness
          • May be mild
          • May manifest unwillingness to take the weight on the other thoracic limb when one is picked up.
        • Muscle atrophy
      • Withdrawal reflex in recumbent animals may be reduced.
    • Pelvic limbs
      • Ataxia
      • Upper motor neuon weakness
        • For example, swaying and stumbling.
      • Withdrawal reflex in recumbent animals may be exaggerated.

Thoraco-lumbar Lesions

  • Thoraco-lumbar lesions occur in the segments T3 to L3 of the spinal cord.
  • In an animal that has pelvic limb ataxia and weakness but no thoracic limb involvement, the lesion will be between T2 and L3.
    • I.e. caudal to the brachial plexus.
    • The animal should be closely examined for symmetry over the gluteals and pelvic limbs.
      • If there is symmetry, the lesion is likely to be at this level.
      • If there is no symmetry, the lesion is likely to be more caudal, and involve the pelvic outflow.
  • Asymmetry may be detected in the cutaneous trunic reflex.
    • This is tested by lightly stimulating the skin of the lateral thorax.
  • The withdrawal reflex in the pelvic limb may be exaggerated.
  • Flexibility of the thoracolumbar spine may be assessed.
    • The skin of the longissimus musculature is firmly stimulated, and observed for:
      • A lordotic movement over the thorax and cranial lumbar region, and
      • A kyphotic movement over the caudal lumbar region and gluteals.

Lumbosacral Lesions

  • Lumbosacral lesions occur between the segments L4 and S3.
  • Horses with such lesions may:
    • Exhibit atrophy of one or more muscles of the pelvic region, and so
    • Be easy to pull over when standing, and
    • Be unwilling or unable to take weight on the affected side when the other limb is lifted.
  • More caudal lesions may:
    • Affect the anal and perineal reflexes.
      • These are tested by lightly stimulating the skin surrounding the anus and observing for a reflex contraction of the anal sphincter.
    • Cause paresis of the tail.
  • The withdrawal reflex may be reduced or absent in the pelvic limb.

Sacral Lesions

  • Damage to the savral spinal cord can affect bladder function and control of defaecation.

Bladder Incontinence

  • The bladder is reflexely controlled, via higher order neurones in the caudal brainstem and cerebrum, by the:
    • Pelvic nerve
      • Parasympathetic fibres leave the spinal cord in the sacral segments and combine to form the pelvic nerve.
        • These fibres innervate the smooth detrusor muscle of the bladder wall.
    • Pudendal nerve
      • The pudendal nerve innervates the striated muscle of the bladder neck.
  • During micturition, the bladder is evacuated as:
    • The striated muscle is relaxed.
    • Stimulation of the pelvic nerve causes the detrusor smooth muscle to contract.

Faecal Incompetence

  • Lesions in the sacral region may also be manifest as faecal incompetence.
    • In horses, problems are usually caused by defects in the lower motor neurons in the pelvic nerve.
      • Faeces is retained.