Record all observations at the time of the examination.
Repeat the examination at regular intervals using a consistent technique.
Step 1 - Behavior and mental status
The first step of the examination is observation of the horse, preferably in its normal environment: assess the horse's awareness and interaction with the environment, stance, head carriage and foot placement.
Gather information from owner, by observation and by physical examination.
Only the main handler may notice subtle changes in behavior.
Behavioral changes are seen in diseases of the cerebrum.
Changes in mental awareness, including obtundation, stupor, somnolence, lethargy and coma.
Assess horse's response to sensory stimuli and interest in food.
Changes in mental awareness are seen in diseases of the cerebral cortex and of the ascending reticular activating system in the brainstem.
This is also a good stage to observe the horse eat, thus assessing appetite and cranial nerves IX, X and XII.
Step 2 - Head posture and movement
Head tilt with lateral deviation of the poll most often indicates an asymmetric vestibular lesion with the tilt usually to the side of the lesion.
Bilateral vestibular disease → swaying of head.
If head and neck deviated to one side with poll and muzzle in vertical plane, a cerebral lesion is indicated .
Tremors, or jerky movements result from cerebellar disease. Intention tremors may be most obvious while horse is reaching for food.
A head tilt as a result of vestibular disease may be accompanied by circling.
Step 3 - Cranial nerves
Assess bilaterally each of the pairs of cranial nerves.
Cranial nerve nuclei are situated in the brainstem.
Abnormalities in the cranial nerves can result from lesions in the peripheral nerve and its tracts, nuclei in the brainstem or the body part innervated.
Brainstem lesions will typically cause signs of paresis or obtundation.
Peripheral nerve lesions may affect several cranial nerves due to their proximity.
Groups of cranial nerves are commonly affected together, eg fractures to base of skull - nerves III, IV and VI; inner ear disease - nerves VII and VIII and guttural pouch mycosis - nerves IX and X.
Olfaction is very difficult to assess in the horse.
Optic nerve II
Menace responseNeurology: menace reflex - flick hand in front of each eye and horse should blink consistently. This is a learned response and will not be present in neonatal foals, it may be absent in horses with cerebellar disease despite normal vision. Response is mediated by facial nerve (VII)
Shine a bright light into each eye and observe changes in diameter of both pupils swing back and forth to test consensual response.
An immediate direct and consensual constriction is normal.
Midbrain lesions can affect the oculomotor nuclei, eg in swelling of the forebrain, herniation and impingement on the parasympathetic nuclei in the midbrain and on the oculomotor nerves below.
The subsequent uni- or bilateral pupillary dilation in a horse suffering from concussion or coma is a grave prognostic sign.
Oculomotor nerve III, Trochlear nerve IV and Abducens VI
Normal position of eye and its movement.
Follow a similar anatomical course.
Induce 'normal vestibular nystagmus' (a slow phase of eyeball rotation away from the direction of movement of the head followed by a fast phase in the direction of movement) by moving horse's head up and down or from side to side.
A true strabismus resulting from damage to these nerves (rare in horses) will not change during these manipulations .
Strabismus due to vestibular disease will change its position on movement of the head.
The Doll's eye reflex - when the head is lifted the eyes move ventrally to maintain a horizontal gaze - this is normal.
Sensory to head.
Touch ears, medial and lateral canthi (palpebral reflex - this reflex also tests the motor branch of the facial nerve, ie the ability to blink), nostrils and commissures of mouth and observe reflex movements (facial reflexes).
Motor to muscles of mastication - inability to chew, masseter and temporal muscle atrophy in advanced lesions. Check for asymmetry of the muscles of mastication.
Facial nerve VII
Motor to muscles of facial expression.
Facial asymmetry may result from a unilateral lesion - muzzle deviation is typically away from the side of the nerve damage.
May present as corneal ulceration due to inability to close eyelids, ptosis due to paralysis of levator anguli oculi medialis muscle; dyspnea due to collapse of false nostril; drooling of saliva and difficulty in prehension due to lip paralysis .
Hearing and balance.
Abnormal positions of the head and eye and a spontaneous nystagmus.
Blindfolding may exacerbate signs - care should be taken when blindfolding horses with neurological disease as they may fall, it should only be carried out on a soft surface.
Vestibular disease can be classified as central or peripheral.
Central vestibular disease may be accompanied by other cranial nerve signs and changes in mentation → variable nystagmus, including vertical, horizontal or rotatory, and other brainstem signs, eg depression, weakness and ataxia.
Peripheral vestibular disease may be accompanied by facial asymmetry due to the close anatomical association with the facial nerve. Changes in mentation are not usually present. Normally a horizontal nystagmus with the fast phase away from the lesion.
Hearing deficits are difficult to detect in horses - test response to a handclap. Brainstem auditory evoked response tests are available in a limited number of institutes and allows for direct analysis of hearing capabilities.
Glossopharyngeal nerve IX and Vagus X
Dysphagia - glossopharyngeal → sensory to pharynx and vagus → motor to pharyngeal muscles. Dysphagia may be caused by central or peripheral disease.
Gag reflex - observe horse eating, stimulate and observe with endoscope.
Larynx - vagus supplies afferents and efferents.
'Roaring' due to recurrent laryngeal nerve damage. Absent thoracolaryngeal (slap) test Larynx: slap test.
Change in phonation.
Accessory nerve XI
Paralysis of trapezius or cranial sternocephalicus muscles → atrophy.
Hypoglossal nerve XII
Motor to tongue and epiglottis.
Grasp tongue and pull out side of mouth (test both sides) - most horses will normally retract tongue Botulism.
Step 4 - Examination of the neck and trunk
Perform an overall examination for muscle atrophy.
Examine skin sensation and spinal reflexes.
Note central perception of horse to applied stimuli.
Observe any abnormal sweating on the neck and trunk.
Head and neck
Test skin sensation over neck with a blunt probe.
Tap lightly along the skin over the brachiocephalicus cervical vertebrae to elicit the local cervical response - twitching of skin and brachiocephalicus.
Cervico-facial response (tap between C1-C3) - ipsilateral ear twitch, eyelid closure and retraction of commissure of mouth.
Move head and neck up and down to test for signs of pain and for range of movement.
Test skin sensation and spinal reflexes.
Tap with a blunt instrument over thorax for cutaneous trunci responses (twitching and central sensory perception).
Run a blunt instrument from the withers to the caudal lumbar area on each side of the spine to extend thoracolumbar vertebral column.
Thoracolumbar flexion is produced by running a blunt instrument over the rump.
Spinal reflex tests involving the limbs are impossible in the standing horse:
In the recumbent horse, assess the patellar and withdrawal reflexes. Use a large plexor, eg twitch handle.
CARE when doing this to ensure no one is in danger zones for being kicked.
With horse in lateral recumbency hold upper pelvic limb partially flexed.
Strike the patellar tendon with heavy object, eg hoof testers should elicit stifle extension.
Reflex requires an intact femoral nerve and spinal cord segments L3-L5.
Roll horse over to test opposite limb.
Flexor (withdrawal reflex):
Pinch skin of distal limb with hemostat and flexion of leg should be stimulated.
Requires intact spinal cord segments L6, S1 and S2 for the pelvic limb and C6-T2 for the thoracic limb.
Observe for cerebral response - some form of objection to the stimulus.
Use the responses to decide if an upper motor neuron lesion (hyper-reflexive), or a lower motor neuron lesion (hypo-reflexive) is present.
Test skin sensation of the limbs.
Especially important in recumbent horses.
Tail tone and perineal reflexes
This area is involved in a number of equine neurologic conditions, specifically cauda equina syndrome Polyneuritis equi.
Difficulty passing feces/urine or colic signs may be observed by the owner if cauda equina syndrome is present.
Abnormal carriage of tail. Cauda equina results in a flaccid tail, whereas motor neuron disease can result in a raised tail.
Assess skin sensation.
Gently stimulate perineum, should lead to reflex contraction of anal sphincter and elevation or depression of tail .
Step 5 - Gait and posture
Gait is predominantly controlled by the brainstem, spinal cord, and peripheral nerve and muscle function.
Gait must be assessed thoroughly.
Use stress tests to demonstrate mild abnormalities.
Observe and grade (from 1-4) for the following abnormalities:
Hypometria or spasticity.
Deficits are just detectable at walk but are worsened by pertuberations.
Deficits easily detected at walk and exaggerated by pertuberations - backing, circling, neck extension.
Deficits prominent at walk with a tendency to buckle or fall.
Spontaneous stumbling, tripping or falling.
Examination of gait
Observe horse at walk and trot and when backing, circling and pivoting on a tight circle.
If gait abnormality not readily apparent, it may be helpful to observe horse walking up and down a slope, walking over small obstacles, walking with the head and neck extended, and running free in a paddock.
Signs associated with subtle cerebellar or vestibular disease are often exaggerated by the use of a blindfold.
Often seen as dragging of the toes and stumbling, trembling weight shifting or lack of support at rest.
Signs of weakness may be seen with brainstem and spinal cord lesions, as well as with peripheral nerve, neuromuscular and muscular lesions.
With a brainstem or spinal cord lesion, weakness may be present in all limbs caudal to the lesion
Dynamic tail pull:
Test for upper motor neuron paresis.
Pull tail firmly and steadily to one side as horse walked away.
A weak horse is easily pulled but will maintain foot fall rhythm.
A severely neurologically affected horse may fall.
Static tail pull:
Test for lower motor neuron paresis.
Pull the tail firmly when the horse is standing still and evenly weight bearing.
Denotes a proprioceptive abnormality and is characterized by poor co-ordination of movements.
Truncal ataxia is easily recognized, but abnormalities may be noted in each limb, and include:
Abnormal foot placement.
Crossing of the limbs.
Circumduction of limb while circling.
Stepping on other feet.
Spinal ataxia will present differently, depending on the localization of the lesion:
C1-C5: all limbs are affected but the hindlimbs are more severely affected than forelimbs.
C6-T2: all limbs may be affected but the forelimbs are more severely affected than hindlimbs.
T3-L3: only the hindlimbs are affected.
S3-S5: cauda equina syndrome with a normal gait.
Severely ataxic horses will occasionally pace at walking speed.
Appears as if the animal has little joint flexion during protraction.
Often most evident when walking on a slope or backing.
The inability to regulate the rate and direction of movement.
Motions often appear exaggerated.
If hypermetria appears to be the major feature of a gait abnormality, examine horse closely for signs of cerebellar disease.
A horse recumbent after strenuous exercise will be autonomically driven, this will over-ride normal sensory perception and even reflex activity so that a routine neurologic examination may be worthless if conducted at the time. It may take 30-120 min for this phase of epinephrine domination to pass.
When assessing acute brain and spinal cord trauma cases, it is sensible to delay final decisions as to euthanasia Euthanasia for up to 24 h.
Mitchell C W et al (2012) The use of magnetic resonance imaging in evaluating horses with spinal ataxia. Vet Radiol & Ultrasound 53 (6), 613-620 PubMed.
Licka T F (2011) Differentiation of ataxic and orthopedic gait abnormalities in the horse. Vet Clin North Am Equine Pract 27 (3), 411-416 PubMed.
Knottenbelt D C (1996) Equine neurologic disease and dysfunction - a diagnostic challenge for the practitioner. Part 2 - The clinical neurologic examination. Equine Vet Educ 8 (5), 260-270 WileyOnline.
Lunn D P & Mayhew I G (1989) The neurologic examination of horses. Equine Vet Educ 1 (2), 94-101 WileyOnline.
Reed et al Ataxia and paresis in horses - differential diagnosis. The Compendium 3 (3).
Other sources of information
Mayhew I G (1989) Large Animal Neurology - A Handbook for Veterinary Clinicians. Lea & Febiger, USA.