Neurology: examination - adult in Horses (Equis) | Vetlexicon
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Neurology: examination – adult

ISSN 2398-2977


  • The neurologic examination is the most important diagnostic tool in the evaluation of neurologic disease.
  • The objective is to localize the site of the lesion in the nervous system and decide upon possible etiologies.
  • An understanding of the function and anatomy of the central nervous system (CNS) is essential.


  • Suspected lesion(s) involving the CNS.
  • Recumbency following trauma.
  • To determine the site(s) of lesions and therefore, their possible etiologies, treatment and prognosis for recovery.
  • Possible hepatic encephalopathy.


  • Diagnostically very informative.
  • Within the scope of all veterinarians and no specialist equipment required, although subtle lesions can be difficult to assess if facilities and expertise are not good enough.


  • Neurological status can change rapidly.
  • Multi-lesion diseases can be difficult to interpret.
  • Must be analyzed with adjunctive diagnostics including blood work and advanced imaging.

Technical problems

  • A sound knowledge of the functioning and anatomy of the CNS is essential.
  • Suitable facilities are essential; this should include a trot up, different surfaces, poles and light and dark rooms.


  • 15-30 min.

Decision taking

Criteria for choosing test

  • General physical examination may lead to suspicion of neurologic disease.
  • History of tripping, stumbling, changes in behavior, circling or any other clinical signs associated with neurological diseases.

Risk assessment

  • Horses with neurological disease can be dangerous to handle and care should be taken.
  • Ensure the handler and examiner are always on the same side of the horse.
  • Wear appropriate personal protective equipment.
  • If in the stable with the horse, then ensure there is a safe exit route.



Veterinarian expertise

  • Suitable training should be undertaken to be able to interpret findings appropriately.
  • Knowledge of local/national diseases will be essential for diagnosis and management of the case.
  • If considering CSF collection, then only those with experience and training should undertake this part of the examination.

Materials required

Minimum equipment

  • Blunt instruments, eg artery forceps to test skin sensation and reflexes and large plexor, eg twitch handle to test spinal reflexes in recumbent horse.
  • Light (transilluminator or penlight).
  • Blindfold.

Minimum consumables

  • If CSF analysis is to be considered then you will require a spinal need 8-12 inches, sterile preparation equipment, multiple syringes and stocks.




Step 1 - Complete history

  • Breed, age and sex predilections are known for certain neurologic diseases.

Step 2 - Thorough physical examination

  • To detect concurrent and related problems.
  • Neurologic signs may be secondary to diseases of other systems, eg hepatoencephalopathy, so blood sampling at this stage is imperative.

Step 3 - Neurologic examination

  • Be systematic - work from head backwards along neck, thoracic limbs, trunk and pelvic limbs to the tail.
  • Follow with an analysis of the horse's gait Musculoskeletal: gait evaluation.
  • Record all observations at the time of the examination.
  • Repeat the examination at regular intervals using a consistent technique.

Core procedure

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, eg aggression Behavior: aggression - hormone related, mania, headpressing, circling, wandering and seizures may be observed.
  • 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 Head: tilt 01Head: tilt 02 - blindfoldmost 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 Head: tilt 03 - cranial trauma.
  • 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.
Olfactory nerve
  • Olfaction is very difficult to assess in the horse.
Optic nerve II
  • Vision.
  • Menace response Neurology: 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)
  • Pupillary light response (PLR) Neurology: vision testing - pupillary light reflex (with oculomotor III). This does not assess vision therefore you would expect to see a dazzle response as well if visual.
  • With central blindness, the PLR is normal.
  • Peripheral optic nerve lesions result in ipsilateral blindness and abnormal PLRs.
  • Fundoscopic examination should be undertaken before a diagnosis of neurologic disease is made.
Oculomotor nerve III
  • Pupillary light response Neurology: vision testing - pupillary light reflex tests the parasympathetic component of this nerve.
  • 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.
  • 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.
Trigeminal V
  • 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 Head: facial paralysis 02.
Vestibulocochlear VIII
  • 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.
  • Rare.
Hypoglossal nerve XII
  • Motor to tongue and epiglottis.
  • Dysphagia.
  • Grasp tongue and pull out side of mouth (test both sides) - most horses will normally retract tongue Tongue: protruding - botulismBotulism.

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.
  • Thoracolaryngeal (slap) response Larynx: slap test.
Spinal reflexes
  • 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.
  • Patellar reflex:
    • 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 Neurology: reflex - scratch itch.

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:
    • Paresis (weakness).
    • Ataxia (incoordination).
    • Hypometria or spasticity.
    • Hypermetria.
  • Grading ataxia:
    1. Deficits are just detectable at walk but are worsened by pertuberations.
    2. Deficits easily detected at walk and exaggerated by pertuberations - backing, circling, neck extension.
    3. Deficits prominent at walk with a tendency to buckle or fall.
    4. Spontaneous stumbling, tripping or falling.
    5. Recumbent.
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.
  • Paresis:
    • 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.
  • Ataxia:
    • 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.
  • Spasticity:
    • Appears as if the animal has little joint flexion during protraction.
    • Often most evident when walking on a slope or backing.
  • Dysmetria:
    • 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.

Step 6 - Peripheral nerves

  • See Peripheral nerve: trauma.
  • Usually manifest as localized areas of cutaneous hypoalgesia or unilateral muscle atrophy and loss of function.
  • Clinical signs depend upon nerve affected.
Ancillary tests


Immediate Aftercare

Special precautions

  • 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.


Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • 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 (5), 260-270 WileyOnline.
  • Lunn D P & Mayhew I G (1989) The neurologic examination of horses. Equine Vet Educ (2), 94-101 WileyOnline.
  • Reed et al Ataxia and paresis in horses - differential diagnosis. The Compendium (3).

Other sources of information

  • Mayhew I G (1989) Large Animal Neurology - A Handbook for Veterinary Clinicians. Lea & Febiger, USA.