Neuro Exam of The Horse - Pathology

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Neurological Examination of Horses Overview

Introduction

  • Investigation of neurological disease combines:
    • Case history
    • Neurological examination
    • Neuroanatomical knowledge
    • Experience

Aims of Neurological Examination

  • There are two main aims of neurological examination:
    1. To aid determination of the presence or absence of neurological disease.
    2. To localise the lesion(s) when neurological disease is suspected.

Indications for Neurological Examination

  • Neurological testing may be indicated by:
    1. History
      • For example, the owner reports a seizure-like episode.
    2. Clinical examination
      • For example, an unexplained area of muscle atrophy or patchy sweating.
    3. Information from other tests
      • Particularly negative, confusing or corroborating evidence from these.
      • For example:
        • A horse evaluated for pelvic limb lameness that may in fact have a neurological problem.
        • A horse with altered mentation or depression that has already been found to have abnormal hepatic function.

Approaches to Neurological Examination

  • A methodical approach is necessary, whatever the background, to ensure no aspect of examination is omitted.
  • Two different approaches may be taken:
    1. Systems based
      • The different neurological modalities of the systems are examined in turn.
    2. Anatomic
      • Tests are performed in turn working from head to tail.
  • A combination of the two approaches tends to be used in practice.

Neuroanatomy

  • Certain basic facts must be understood before a decent neurological examination may be performed.

White and Grey Matter

  • White matter consists of myelinated axons of nerve cells.
  • Grey matter is made up of neuronal cell bodies, containing the nucleus.

Afferent and Efferent

  • Afferent pathways relay sensory information from receptors towards the spinal cord or brain.
    • For example:
      • Touch
      • Muscle stretch
      • Vision
      • Balance
  • Efferent pathways relay motor or effector information from the brain or spinal cord to muscles or organs.

Motor Neurons and Motor Reflexes

  • Lower motor neurons are the last link in the efferent pathway.
    • Directly innervate skeletal muscles.
    • Cell bodies are located in the ventral horn of the grey matter of the spinal cord.
    • Their axons run in peripheral nerves and synapse at the neuromuscular junction.
  • Upper motor neurons communicate with lower motor neurons.
    • They:
      • Relay information to lower motor neurons
      • Control the output of lower motor neurons.
    • Upper motor neurons are found in the brain and spinal cord.
  • The term reflex describes a certain sort of nervous pathway.
    • The sequence of events in a reflex is as follows:
      1. Signals are derived from receptors.
        • For example, tendon stretch.
      2. Signals are conveyed directly in sensory (afferent) fibres.
      3. Afferent signals reach the central nervous system.
      4. Effector signals are generated in the CNS.
        • This generally occues via an intermediate neuron, known as the internuncial neuron.
      5. Effector signals are relayed in the lower motor neurons to the muscles.
    • A reflex does NOT require:
      • Conscious perception of the stimulus
      • Ascending or descending upper motor neuron pathways
      • Ascending or descending proprioceptive pathways

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Signalment and History

Signalment

  • The term "signalment" describes the animal's age, sex and breed.
  • The horse's signalemt may be relevant to the neurological examination.
    • For example:
      • A 1 year old thoroughbred colt with ataxia is more likely to have cervical compression than a space occupying lesion.
      • An Arabian foal suffering seizures may have idiopathic epilepsy.

History

  • History is a very important component of the neurological examination.
    • An owner's description of the animal's behaviour or abnormality may both
      • Help direct the neurological examonation.
      • Suggest possible differential diagnoses.
  • For example, a recumbent horse with a history of stumbling or knuckling that has recently fallen:
    • May have underlying cervical vertebral malformation or stenosis, OR
    • It is possible that the onset of pelvic limb weakness may have followed a spate of respiratory disease or an abortions, if the animal has EHV1 myelitis.

Demeanour/ Behaviour

  • The horse should be examined from a distance to assess behaviour and demeanour.
  • Diseases associated with altered mentation or behaviour tend to involve the forebrain.
  • Levels of consciousness are determined partly by the cerebrum and partly by the reticular activating system in the brainstem.

What to Look For

  • Assymetrical changes.
    • These include:
      • Circling
      • Head turning
    • Horses usually circle or turn towards the affected side.
  • Excessive yawning.
  • Head pressing.
    • This is often a sign of severe obtundation, which may be caused by:
      • Diffuse cerebral disease.
      • Metabolic problems, such as hepatic encephalopathy.

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:
    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 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.


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.
        1. Pressure is exerted on the corneal surface through the eyelid.
        2. The opthalmic branch of the trigeminal nerve provides sensory (afferent) input.
        3. Efferent signals are sent via the abducens nerve (CN VI)
        4. 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.

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.

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:
    1. Observing the horse eat and swallow
    2. 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.


Tongue Movement

  • The hypoglossal nerve, CN XII provides motor innervation to the tongue.
  • Normally, a horse resists the 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 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 atrophy is not present in these animals.


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.