Clinical Examination

The clinician should observe whether the horse displays cranial nerve dysfunction; muscle hypertrophy, atrophy, or asymmetry; muscle trembling; abnormal hoof wear; or abnormal posture. Muscle atrophy may be caused by disease of the ventral horn cells of the gray matter of the spinal cord, peripheral nerve, or the muscle itself; it also can occur with disuse. Palpation can reveal abnormalities such as altered skin temperature, sweating, muscle fasciculations, abnormal sensitivity, or soreness. The horse should be observed on a flat surface, at a walk and trot, and in straight and curving lines. The horse should be evaluated on a surface that allows detection of abnormal hoof flight and placement, toe dragging, or excessive force when landing. The sound of the feet landing should be noted for consistency and loudness. Hard surfaces also may enhance abnormal hyperflexion in horses with stringhalt. Evaluation on a soft surface may be necessary if the horse is unstable or if the clinician is trying to determine whether the horse could have sore feet. Any abnormal head or neck movement associated with limb movement should be noted. It is important to permit normal neck and head movement when the horse is being led. The person leading the horse should hold the horse as loosely as is safely possible. Collapsing or sinking on a limb, knuckling, hyperflexion, spasticity, hesitance in any part of the stride, dragging of a toe, landing excessively hard, leaning to one side, or failing to track straight can indicate a neurological deficit. Various manipulations are used to diagnose whether proprioceptive or motor deficits exist and to localize the lesion. While being led, the horse should be evaluated while stopping and starting from a walk and trot, backing up, circling tightly in both directions, walking while sideways traction is applied and released on the tail, being pushed sideways from a standstill, and walking with its head elevated. Some clinicians also evaluate repositioning of the foot after placing the horse’s hoof in an abnormal position. We do not find this particularly helpful because a horse’s disposition, age, training, and distractions can affect its response. A horse with a normal gait may stand with its feet placed in an abnormal position for what seems an abnormally long time. Some clinicians also use wheelbarrowing and hopping reactions.¹ We do not use these tests in mature horses because we believe responses may be inconsistent and difficult to evaluate accurately and safely. Observation of the horse walking or trotting up and down inclines can be helpful in revealing whether the horse “knows where its limbs are” (proprioception) and can adjust limb movement appropriately. It may be helpful to observe the horse while it is being ridden or lunged, and in some horses while it is loose in an enclosure. Watching the horse stop and start, turn, back up, and maintain its balance during many postural maneuvers allows detection of neurological deficits that may not be obvious when the horse is being led. Consider the following:

In some horses it is necessary to observe the horse performing its usual activity, providing it is capable. However, gait deficits may be much less apparent at speed than when the horse is walking or trotting slowly. Basically, the clinician is trying to determine whether the horse moves symmetrically and smoothly with normal stride length and height of foot flight appropriate to the breed and use, whether it appears strong and consistently places its feet in the appropriate positions, and whether it moves in balanced harmonious fashion. It is sometimes difficult to determine whether certain postural or gait changes are a result of pain or weakness or are associated with motor or proprioceptive deficits. Is the horse flexing its hindlimbs excessively and holding its croup more ventrally and flexed because of pain or weakness? If the horse is shifting weight between the hind feet, is it because of weakness, as seen, for example, in lower motor neuron disease, or because of pain? When both limbs are affected, manipulation of a limb to try to localize pain may not be possible. Gaited horses can be extremely difficult to evaluate, especially if one is unfamiliar with the specific gaits. Conformation also can confound interpretation of clinical signs. It may be necessary to observe the horse on many occasions and compare its gait before and after exercise. Is the deficit consistent, or does it vary? If it worsens with exercise, is it because of pain or inability to compensate for a neurological deficit as the horse tires? Perineural analgesia may be helpful. Is there palpable evidence of muscle cramping with exercise or an increase in creatine kinase (CK) level, indicating rhabdomyolysis? A variable gait deficit and inconsistent alterations in foot flight or placement are more likely to represent a neurological deficit than lameness; single limb lameness may vary in intensity but usually remains similar in character. Painful and neurological conditions could coexist but may be difficult to differentiate even with use of commonly used analgesics such as phenylbutazone.

If the horse buckles in a limb, especially on turns, is easily pulled sideways by the tail when standing or walking, or trembles its limb, weakness of the extensor muscle groups should be suspected. When the flexor muscles are weak, the horse is unable to lift its limb normally, and the toe may be worn from dragging. Pushing the horse sideways or trying to pull on the halter and tail simultaneously can reveal weakness. If the horse is weak or has pain in one limb, it is not able to bear weight normally when the contralateral hoof is lifted from the ground. Neck flexion sideways and vertically should be evaluated for ease and range of movement. Skin sensation and the cutaneous trunci reflex and cervical reflexes should be evaluated. Tapping the trunk should elicit contraction of the cutaneous trunci muscle. Abnormalities can delineate a thoracic spinal cord lesion, because afferent input is through the dorsal thoracic nerves and cranially through the spinal cord white matter, and the efferent pathway involves the cranial thoracic motor neurons in the first thoracic and eighth cervical segments and the lateral thoracic nerve. Hypalgesia of the cutaneous trunci as assessed by response to a two-pinch test with a hemostat is rare and occurs only with severe thoracic spinal cord disease.¹ Lack of a cervicofacial reflex (failure of the facial muscles to twitch when the ipsilateral side of the cranial aspect of the neck is tapped) can suggest a lesion in the cervical cord or a branch of cranial nerve VII. If tapping the side of the neck fails to elicit contraction of the cutaneous coli muscle, a cervical cord lesion could exist. If any abnormal response to skin stimulation is detected, the test should be repeated because the horse’s disposition can influence its responses. Limb reflexes usually are not used, although patellar reflexes can be elicited in horses. We do not consider the thoracolaryngeal reflex (slap test) to be helpful. Response is inconsistent in horses with cervical spinal cord lesions and may be absent in normal horses. Blindfolding the horse usually is not part of our routine neurological examination unless vestibular disease is suspected. A complete physical examination should always be conducted. In some horses with hindlimb gait deficits, palpation per rectum of the pelvic bones, lumbar region, caudal aspect of the aorta, and iliac vessels may be necessary. Simple observation may not differentiate hindlimb weakness caused by spinal cord disease from that caused by partial aortoiliac thrombosis. Horses that do not “feel right” to the rider yet show no obvious deficits to the observer whether observed saddled or in hand are problematic. It may be necessary to observe a horse from a jog cart or carriage if the gait deficit about which a driver complains is not visible to the bystander. In attempting to differentiate between a musculoskeletal and neurological condition causing a gait deficit in a limb, diagnostic analgesia may be necessary. Obviously, this does not help differentiate pain from lameness emanating from a lesion proximal to the coxofemoral or scapulohumeral joints. A course of nonsteroidal antiinflammatory drugs (such as moderate doses of phenylbutazone for days or even several weeks) may be helpful in determining whether a gait deficit is caused by pain.

Hematology and Serology

In most horses serum chemistry screens and hematological tests are not particularly helpful; however, in horses with a gait deficit caused by an underlying muscle disease, evaluation of aspartate transaminase (AST) and CK levels may be helpful. Stage of training, exercise pattern, and whether the blood specimen was obtained after exercise preceded by a day of rest must be considered in evaluation of enzyme levels. If a horse consistently has abnormally elevated enzyme levels, then the horse has rhabdomyolysis, and the clinician must decide whether the condition is causing or contributing to the horse’s abnormal gait. Plasma CK and AST levels do not increase simply because of muscle atrophy; rhabdomyolysis must occur to increase the enzyme levels in the blood (see Chapter 83). Elevated plasma concentrations of CK and AST in horses that are not being exercised suggest a primary muscle disorder, such as (but not limited to) polysaccharide storage myopathy (see Chapter 83). An elevation in white blood cell count and fibrinogen level indicates inflammation. In our experience, elevation in fibrinogen level is a more consistent indicator of inflammation in the adult horse than is elevation in white blood cell count.

If clinical signs suggest equine lower motor neuron disease, serum levels of vitamin E (α-tocopherol) should be measured; levels of vitamin E have consistently been low in horses with confirmed equine motor neuron disease, unless the horse has been given supplements.² Thus low vitamin E levels may be suggestive of, but are not specific for, equine lower motor neuron disease. Tocopherol concentrations can decrease during winter when horses lack access to green pasture.³ Daily variations in plasma levels may occur.⁴ Low levels also have been reported in clinically normal horses^5-7 and in one horse with chronic gastrointestinal disease.⁸ The laboratory that performs the test should be contacted for any specific requirements for submission of samples and to ensure they have an established normal range for vitamin E levels.

Serological testing for antibodies to various infectious agents may be indicated. In EHV-1 infection, detection of an increase in antibody titer is considered diagnostic of the disease. A horse that shows signs of neurological disease secondary to EHV-1 should have an elevated serum antibody titer, and single high titers have been the basis for initial diagnosis in individual horses. Recent vaccination confounds interpretation. Rarely, high titers may be measured in horses with no history of recent vaccination and no obvious clinical signs of EHV-1 infection.

Antibody titers for Borrelia burgdorferi, the cause of Lyme disease, sometimes are measured in serum from horses with ill-defined gait deficits. High titers, or rising titers, have been used as a basis for treatment of the disease. A positive titer, however, does not mean the horse has active disease. Because of the geographical variation in exposure to B. burgdorferi, titers may vary greatly. Serological surveys in the United States have demonstrated positive test results in 1% of samples from nonendemic areas and up to 68% in endemic areas.^9-11 Reports of horses “responding” to treatment exist,^12,13 but to date we are unaware of any horses with Lyme disease in which neurological deficits mimic primary lameness. Currently the importance of Lyme disease as a cause of equine gait deficits is unclear.

A Western blot test for the evaluation of equine protozoal myelitis (EPM) was first made commercially available at the University of Kentucky by Dr. David Granstrom.¹⁴ Serological testing for the presence of antibodies to Sarcocystis neurona can be used only to indicate exposure to the organism. Through exposure to S. neurona, many horses develop antibodies in the absence of clinical disease Serological surveys in certain areas of the United States have shown that a high percentage of horses have positive antibody titers. A positive test result does not mean the horse has EPM. A negative test result could theoretically occur in horses with peracute disease or perhaps in severely immunocompromised animals. However, a negative test result usually indicates that disease caused by S. neurona is highly unlikely. The test result also could be negative in a horse with signs of EPM if another protozoan, such as Neospora, causes the spinal cord lesions. In a U.S. study of several hundred horses with neurological disease, test sensitivity was 89%, but specificity was only 71%, because 30% of horses with other neurological diseases also had antibodies to S. neurona. Although the positive predictive value was only 72% in horses with neurological diseases, the negative predictive value was almost 90%, indicating that a negative test result is useful in this population.¹⁴ In one study of 44 horses on a farm sampled for more than 1 year, all horses were seropositive for at least 50 weeks yet showed no neurological signs (see following discussion).¹⁵

Cerebrospinal Fluid Aspiration and Analysis

Cerebrospinal fluid (CSF) can be obtained from either the atlantooccipital or the lumbosacral space. The advantage of lumbosacral centesis is that it can be performed in the standing sedated horse, whereas atlantooccipital centesis requires general anesthesia. Fluid from the atlantooccipital site is considered easier to obtain and not as likely to be contaminated with blood. The atlantooccipital site is identified by palpating the cranial edge of the wings of the atlas. The hair is clipped and the site prepared aseptically. Atlantooccipital centesis is performed at the intersection of the median plane and a line drawn across the cranial edge of the wings of the atlas. In an adult horse, a 9-cm (-inch), 18- or 20-gauge spinal needle is directed toward the horse’s lower lip with the head held in a flexed position. It is important that the needle remain on the midline as it is advanced, because otherwise it will be too far lateral to enter the subarachnoid space. The needle is initially inserted to a depth of approximately 2.5 cm (1 inch) and then gradually advanced. While the needle is gradually advanced to the subarachnoid space, it should be held carefully to prevent penetrating the spinal cord when advancing through the atlantooccipital membrane and the dura mater. Usually a “pop” is felt as the needle advances through the dura; however, this finding is not consistent and the stylette should be frequently removed to observe for flow of CSF. CSF usually flows from the needle once the subarachnoid space is entered; however, once a substantial depth has been reached (about 5 to 8 cm [2 to 3 inches] in an average-size horse), some clinicians advise gentle and frequent aspiration with a small syringe.

In preparation for aspiration from the lumbosacral space the type and degree of restraint is guided by the horse’s behavior, the horse’s stability, and the clinician’s personal preference. A nose twitch, stocks, sedation, or a combination of physical and chemical restraint are options. We prefer to use light sedation with xylazine, sometimes combined with butorphanol. However, lumbosacral CSF pressure can be transiently decreased up to 15 minutes after administration of a high dose of xylazine (1.1 mg/kg intravenously).¹⁶ The puncture site for lumbosacral centesis is identified by combining several landmarks, realizing that individual variation exists. A line drawn between the caudal edge of the tubera coxae and the intersection with the midline can be used to locate the lumbosacral space. The lumbosacral space is bordered cranially by the caudal edge of the sixth lumbar vertebra, caudally by the cranial edge of the sacrum, and laterally by the medial rim of the tubera sacrale. The dorsal spinous process of the last lumber vertebra is lower than the dorsal spinous process of the fifth lumbar vertebra. The V formed by the medial rim of the tubera sacrale is one of the more useful landmarks, and the appropriate site for puncture is within this V. The site should be prepared aseptically, and local anesthetic solution is placed subcutaneously. A small skin stab incision is usually made. The needle is inserted on the midline, at the depression palpated just caudal to the last lumbar vertebra, in the middle of the V formed by the tubera sacrale. A 15-cm, 18-gauge spinal needle is generally adequate for a horse that is 16 hands or less. A 20-cm needle may be necessary in a horse greater than 16 to 17 hands. While the clinician advances the needle, it is critical to remain on the midline. The needle can be advanced until a pop indicates it is advancing through the dura or until the horse responds as the needle stimulates nervous tissue. These responses can be unreliable and occasionally dangerous for the horse, the handler, and the individual performing the centesis. Because horses can react unpredictably (including rearing, bolting, collapsing, or kicking), it is safer to advance the needle gradually until it is near the spinal canal, approximately 12.5 cm (5 inches) in a 15- to 16-hand horse. Once the needle is near the canal, it should be advanced slowly with repeated frequent removal of the stylette and aspiration with a small syringe. The horse may move its tail when the dura is penetrated, but usually minimal reaction occurs. If fluid is obtained but the amount is small, the needle can be rotated 180 degrees. Jugular vein compression for at least 10 seconds (Queckenstedt’s test) is thought to elevate intracranial CSF pressure and aid fluid collection, provided flow is not obstructed. If a hemorrhagic sample is thought to be from iatrogenic causes, the syringe can be changed frequently until subsequent aliquots are clear. If fluid is not obtained on the first attempt, the needle is withdrawn and the procedure is repeated slightly cranial or caudal to the original location. CSF samples should be placed in sterile tubes and rapidly processed after collection.

Normal CSF is clear and colorless, and red discoloration indicates hemorrhage. However, normal fluid can sometimes appear mildly hazy when grossly examined, especially in a tube with ethylenediamine tetraacetic acid. Hemorrhage can be iatrogenic or caused by underlying disease. Fluid may appear clear even with red blood cell contamination, and studies indicate that subjective evaluation of spinal fluid is sensitive in detecting blood only when the red blood cells number more than 1200/mcL.^17,18 Centrifugation of a bloody sample should produce a clear fluid with a pellet of red blood cells on the bottom of the sample tube. If hemorrhage occurred before collection and lysis of cells occurred, the supernatant may be slightly pink or xanthochromic (orange/yellow or yellow). Lysis of red blood cells reportedly can occur within 1 to 4 hours.¹⁹ Xanthochromic CSF results from red blood cell breakdown products (bilirubin) and suggests hemorrhage or vasculitis. A centrifuged xanthochromic sample does not become clear. Turbid CSF may appear with hypercellularity or epidural fat contamination. The latter is not uncommon with lumbosacral aspirates. Formulas used to differentiate between white cell or protein elevations caused by iatrogenic blood contamination of CSF versus pathological increases have been shown to be unreliable. Contamination with a few thousand red blood cells results in minimal increase in white blood cell count or protein content.¹⁸

The normal reported range for leukocyte counts has been variable; usually a range of 0 to 6/mcL is cited,²⁰ but higher values have been reported.^21,22 Diversity in techniques can account for different values in normal CSF. Undiluted fluid can be assayed in a hemocytometer, or acidified crystal violet can be added to accentuate the cells.²⁰ It is important that equine reference values be determined in the laboratory the practitioner uses. As previously stated, the cell quality rapidly deteriorates in CSF, and samples for cytological testing should be processed rapidly or a portion fixed in 40% ethanol if processing must be delayed. For morphological and differential evaluation, cytocentrifugation or filtration through a glass fiber membrane filter is the preferred method of processing spinal fluid. In our experience, cell and differential counts are often normal in horses with spinal cord disease. Small lymphocytes and monocytes are normally seen. Neutrophils may be seen with blood contamination or inflammation. Eosinophilia is rarely seen in equine CSF but could occur secondary to parasite migration. Rarely, eosinophils have been seen in samples from horses with protozoal encephalomyelitis,²¹ but frequently spinal fluid from horses with EPM is normal. A relative neutrophilia, with or without an increase in cell count, indicates inflammation, and intracellular bacteria may be seen in horses with bacterial meningitis.

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