A complete neurologic examination is warranted anytime a horse displays signs consistent with neurologicdisease or in any circumstance when establishing thatthe horse is neurologically normal is important (e.g.,pre-purchase examination). Horses can be challeng-ing to examine because of their large size, which pre-vents practitioners from using many of the tests usedfor small animals. Several authors have describedmethods for performing neurologic examinations onhorses; each description varies slightly, and a few ex-amples are provided as references.1–3 Each clinicianhas his or her own method of performing a neurologicexam; the most important aspect is to develop a sys-tem and use it consistently to avoid overlooking abnor-malities. In this paper, a complete yet conciseneurologic examination is described with special at-tention to safety of both the practitioner and the pa-tient. Videos and pictures will be used to highlightnormal and abnormal findings.
2. Methods
The neurologic examination can be divided into foursections: evaluation of mental status, cranial
nerve examination, spinal reflexes and muscle eval-uation (performed standing), and gait and posturalexamination (performed moving). In the author’sopinion, a complete examination can and should beperformed in hand, without any need for assessmentunder saddle. It is not advisable to encourage own-ers to ride potentially ataxic horses to show theneurologic disease. Minimal equipment is re-quired; however, a strong light source (trans-illumi-nator, ophthalmoscope, or even a small flashlight)and a tool to assess pain sensation and induce spinalreflexes (hemostats, pen, or car key) are helpful.
Step 1: Evaluation of Mental StatusObserve the horse in its stall or pasture before en-tering the enclosure. Encephalopathic behavior,such as compulsive circling, head-pressing (Fig. 1),cortical/central blindness, seizures, or significantchange in mentation, is generally obvious. Ifpresent, encephalopathic behavior should trigger anincreased level of caution and in all likelihood, leadto modification of the examination because of safetyconcerns. Any evidence of encephalopathic signs orany horse with neurologic signs and an unknownrabies vaccination history should prompt the prac-
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titioner to wear gloves and limit exposure to thepatient. Subtle behavior changes are often firstnoted by the owner and may or may not be indicativeof neurologic disease. Appropriate descriptions ofthe patient’s mental attitude include hyperesthetic,alert and responsive, depressed or lethargic, ob-tunded, stuporous, and comatose. Normal horsesare alert and responsive, although the spectrum en-compasses very calm, placid horses to overly alert,anxious individuals. Hyperesthestic horses are hy-per-responsive to stimuli and often jerk or tremorwhen stimulated. Depressed or lethargic horsesmay have either mild intracranial disease, systemicdisease, or pain. A thorough physical examinationis necessary to tell the difference. Obtunded horsesdo not respond to normal stimuli (such as a strangerwalking to their stall door or entering the stall) andonly respond to increased stimuli (such as loudnoises, sudden movements, or firm pressure). Stu-porous horses only respond to painful stimuli (suchas skin being squeezed with a hemostat). Coma-tose horses do not respond to any stimuli.
Step 2: Cranial Nerve ExaminationTable 1 summarizes the 12 cranial nerves and teststo assess their function. There are many differentways to perform a cranial nerve (CN) examination;the following description uses a regional approach.1
Start with the eyes: perform a menace response,evaluate pupil size (Fig. 2), perform pupillary lightreflexes, assess eye position, look for normal physi-ologic nystagmus, and ensure that there is no abnor-
mal nystagmus. Assess the palpebral fissure forsize and symmetry and evaluate the palpebral re-flex. Look at the prominence of the third eyelid(sympathetic nerves). Evaluate the horse for nor-mal facial expression and ability to move ears, blink,and wiggle muzzle/lips. Assess the size of the mus-cles of mastication through palpation and observa-tion of the horse eating as well as facial sensation bytouching all regions of the head. Open the horse’smouth to assess jaw tone and remove the tongue toassess the horse’s tongue strength (ability to retract)and symmetry of tongue muscle (Fig. 3). Observethe horse eating and drinking to assess ability toswallow. Endoscopy allows direct visualization ofthe pharynx, larynx, and swallowing ability andmay be useful if dysfunction is suspected in CNs 9and 10 (Fig. 4). CN 1 (olfaction) is rarely specifi-cally tested, but most horses with interest in foodhave normal olfaction. CN 11, which innervatescervical muscles, is also not usually specificallytested.
For practitioners accustomed to performing CNexaminations on small animals, note that the equineexam is similar with a few minor differences.
● Pupillary light reflexes subjectively appearslower, particularly if a penlight is used.
● The eyelids of normal horses audibly snap shutwhen the palpebral reflex is tested—if no snap-ping sound is heard, eyelid weakness should besuspected.
● Mild ptosis can be detected by examining thehorse’s eyelash angles, which should be bilat-erally symmetrical, usually with the eyelashesperpendicular to the globe and parallel withthe ground.
● Mild bilateral ventral strabismus is expectedwhen the head is elevated; as long as thisstrabismus is symmetrical, it is considerednormal.
● The gag reflex is not routinely checked manu-ally—either the horse is observed eating anddrinking or endoscopy is used to evaluate thehorse’s pharynx and larynx.
● Loss of sympathetic innervation will cause pro-fuse sweating (e.g., Horner’s syndrome).
Step 3: Spinal Reflexes and Muscle Evaluation (Tone andSize)Tendon and withdrawal reflexes are not usually per-formed in ambulatory horses. Tendon reflexesshould be performed in recumbent adult horses butmay be difficult to interpret. Withdrawal reflexesshould be assessed in recumbent horses. Reflexesthat the practitioner should assess in the standinghorse include: cervicofacial/auricular and cutane-ous trunci (panniculus), tail tone, perineal reflex,and anal tone. Additionally, the clinician shouldcarefully observe the patient for any loss of skinsensation (hypalgesia or analgesia), increased sen-sitivity (hyperesthesia), or abnormal sweating indic-
Fig. 1. Encephalopathic horse showing abnormal head-pressingbehavior. (Photo courtesy of Dr. Alexandra J. Burton.)
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ative of sympathetic denervation (Fig. 5). Allhorses should be carefully inspected for any signs ofmuscle atrophy.
Step 4: Gait and Posture Examination Plus PosturalReactionsPosture (head, neck, and body position) can be eval-uated in the stall or outside (Figs. 6 and 7). All butthe most ataxic horses should be taken outside forgait evaluation. Again, every clinician develops asystem for gait evaluation. The author’s normalroutine is as follows: walk the horse in a straightline, trot the horse in a straight line, walk the horsein serpentine, walk the horse with head elevated,walk the horse while pulling the tail in each direc-tion, spin the horse in tight circles, walk the horsebackward (Fig. 8), and finally, walk the horse onuneven ground (back and forth over a curb or caval-etti and up and down a hill). This exam is designedto start with relatively easy maneuvers and increase
in complexity to highlight subtle neurologic deficits.Some clinicians will perform foot-placing tests byplacing the hoof on its dorsum, placing one limb infront of the other, or placing one limb laterally toassess rate of replacement. In small animals, theseplacing tests evaluate the patient’s proprioceptionbut are not specific for a lesion in any particularlocation. In the author’s opinion, these foot-placingreactions (commonly known as CPs) are not usefulin detecting abnormalities, because neurologicallynormal horses have quite variable responses andphlegmatic horses may be quite slow to replace theirlimbs. Hopping the horse on one thoracic limb mayshow thoracic limb weakness or hyper/dysmetria.Although some practitioners routinely hop horses,the author does not believe that this test lends anysignificant additional information and can be moredifficult and dangerous for the practitioner and pa-tient. In lieu of these tests, the author instead per-
Table 1. Cranial Nerves
Cranial Nerve Function Assessment
I. Olfactory Smell Not routinely performed.II. Optic Vision Menace response and pupillary light
reflex. Lesion causes blindness and loss ofpupillary light reflex (PLR).
V. Trigeminal Sensory to head; motor to masticatory muscles Palpebral blink, nociception when head istouched. Lesion causes loss of sensation andpalpebral and corneal reflex. Chewing, jawtone, masticatory muscle size. Lesion causesatrophy and dropped jaw.
VI. Abducent Extraocular muscles (retractor bulbi and lateralrectus)
Globe retraction and lateral movement ofglobe. Lesion causes medial strabismus andloss of corneal reflex.
VII. Facial Motor to muscles of facial expression;parasympathetics to salivary and lacrimalglands
Facial symmetry, palpebral blink, ear andmuzzle/lip movement. Lesion causes facialparalysis, loss of palpebral reflex and blink,and dry eye.
VII. Vestibulocochlear Posture and balance; hearing Head and eye position (strabismus) andphysiologic nystagmus. Lesion causes headtilt, nystagmus, and balance loss. Responseto noise: lesion causes deafness.
IX. Glossopharyngeal Sensory and motor to pharynx Ability to swallow (observation andendoscopy). Lesion causes dysphagia anddisplaced soft palate.
X. Vagus Sensory and motor to pharynx and larynx Ability to swallow, laryngeal movement(observation, palpation, andendoscopy). Lesion causes dysphagia,laryngeal paralysis, and displaced palate.
XI. Spinal accessory Motor to cervical muscles, larynx, esophagus Muscle atrophy; otherwise not routinelyassessed.
XII. Hypoglossal Motor to tongue Tongue strength and symmetry. Lesions causeatrophy and paralysis.
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forms an extensive gait examination to look forataxia, proprioceptive deficits, and paresis. If thehorse has difficulty with easier maneuvers, such aswalking in a straight line, and displays obviousataxia or weakness, it is both acceptable and appro-
priate to curtail the exam and not continue to moredifficult maneuvers to prevent the patient fromfalling.
3. Results
The examination should be recorded. If abnormal-ities are detected, the practitioner should then de-termine the most likely location of the problem(neuroanatomic localization) and appropriate list ofdifferential diagnoses. From this list, an appropri-ate diagnostic and therapeutic plan can be con-structed. Although several forms have beendeveloped for this purpose,1–3 it is also appropriatesimply to describe any abnormalities in the record aswell as the assessment. A sample form is included(Fig. 9).
Fig. 2. Note mydriasis of horse’s right pupil compared with theleft pupil. Also note the mild ptosis (on horse’s right side) withsmaller palpebral fissure. These abnormalities were caused byright-sided oculomotor nerve damage subsequent to polyneuritisequi.
Fig. 3. Unilateral tongue-muscle atrophy in a horse with uni-lateral hypoglossal nerve damage.
Fig. 4. Evidence of dysphagia in a horse: saliva and feed ma-terial dripping from nostrils and mouth.
Fig. 5. Abnormal sweating in a single dermatome, indicative ofsympathetic denervation.
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Although detailed discussion of neurolocalizationis outside the scope of this paper, a few generalitiesshould be kept in mind.
1. If the horse has intracranial disease, abnor-malities are usually detected during the firsttwo steps (evaluation of mental status and CNexamination). Significant changes in thehorse’s mental status usually indicate lesionsin the brainstem or forebrain.
2. Abnormalities in CN function can indicate in-tracranial brainstem disease or peripheraldamage to those nerves, which may occur withdirect trauma or guttural pouch disease.Other neurologic examination findings andancillary diagnostic tests are often required todifferentiate peripheral cranial neuropathiesfrom brainstem disease.
3. Moderate to severe ataxia can result from le-sions in the cerebellum, brainstem, and spinalcord. Distinguishing the type of ataxia thatthe horse is displaying—cerebellar, vestibu-lar, or general proprioceptive (spinal)—willaid in neurolocalization. Determining thenumber of affected limbs and the type of pa-resis shown (i.e., upper motor neuron versuslower motor neuron) will allow regional local-ization of spinal-cord disease. Table 2 sum-marizes the differentiation of types of ataxiain horses.
4. Discussion
There is nothing inherently difficult about per-forming a neurologic examination, and the exam-ination is easily performed in field settings. The
Fig. 6. Example of abnormal posture: left head tilt in a horsewith left peripheral vestibular disease.
Fig. 7. Example of abnormal posture: abnormal limb positionin a horse with cervical spinal-cord disease.
Fig. 8. Example of a normal horse walking backwards. Thelegs move in diagonal pairs (i.e., right front and left hind movesimultaneously).
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Date: Location: Patient ID, signalment:
History:
Mental status:
Cranial nerves:
II, VII. Menace OD OS V, VII. Palpebral blink OD OS
II, III, Sympathetic nn. III, VII, Sympathetic nn.Pupils – Size OD OS Palpebral fissure OD OS
II, III. Light in OD OD OS VIII. Vestibular
Light in OS OD OS Phys. nystagmus OD OS
III, IV, VI, VIII. (also requires III, VI)Strabismus OD OS Abn. nystagmus
Resting Head tilt
Positional VIII. Cochlear
VI. Globe retraction OD OS IX, X. Swallow
V. Motor (jaw tone) Endoscopy
V, VII. Facial sensation, symmetry, & movement XII. Tongue symmetry & strength
Spinal reflexes and muscle evaluation:
Cervicofacial/auricular R L Cutaneous trunci R L
Tail tone Anal tone Perineal reflex R L
Skin sensation
Muscle atrophy
Gait and posture evaluation (description of stride):
Straight line/serpentine
Head elevated
Tail pull
Circling
Backing
Anatomic diagnosis:
Differential diagnoses:
Diagnostic plan:
Therapeutic plan:
Fig. 9. Neurologic examination sample form.
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challenge is to develop a system and use it consis-tently. Recognizing the horse’s normal responseto the examination is necessary to detect abnor-malities. After abnormalities are confirmed andlocalized, construction of a differential diagnoseslist becomes much easier, and both the diagnosticand therapeutic plans will fall into place.
References1. de Lahunta A, Glass E. Veterinary neuroanatomy and clin-
ical neurology. St. Louis, MO: Saunders, 2009;487–501.2. Mayhew IGJ. Large animal neurology. Ames, IA: Wiley-
Blackwell, 2009;11–46.3. Furr M, Reed S. Neurologic examination. In: Furr M,
Cerebellum Bilateral lesion (all four); unilateral lesion (ipsilateraltwo; front and hind).
Spastic, “bursty,” dysmetric. Loss of control ofrate, range, and force of motion. Strength ismaintained. Head and neck (intention)tremors. Tendency to rear.
Vestibular system Peripheral disease (no proprioceptivedeficits). Central disease (proprioceptive deficitson ipsilateral two �front and hind� because ofinvolvement of adjacent UMN/GP tracts).
Loss of appropriate posture and balance.Drifting, leaning, circling, falling to one side(worsens when blindfolded). Head tilt � headand neck turn. Recumbent horses prefer to lieon the affected side.
C1–C5/6 spinal cord Bilateral lesion (all four); unilateral lesion (ipsilateraltwo; front and hind).
Loss of proprioception causes toescuffing/dragging, delayed protraction,knuckling, crossing-over, stepping on anotherfoot, pivoting or circumduction on circling, oruneven/irregular stride length. Elongatedstride (UMN paresis) in all four limbs.
C6-T2 spinal cord Bilateral lesion (all four); unilateral lesion (ipsilateraltwo; front and hind).
Loss of proprioception (as above), more evident inhindlimbs than forelimbs. Short, choppystride with pronounced weakness in forelimbs(LMN paresis). Elongated stride in hindlimbs(UMN paresis).
