Evaluation of Gait

Evaluation of the gait of the horse should include examination of postural reactions and may include evaluation of spinal reflexes in young or small horses. Although they may appear weak and ataxic, foals are ambulatory within hours after birth, making it possible to evaluate gait. Because postural reactions are sometimes difficult to interpret in horses, using gait abnormalities to help localize a lesion is essential. The author nearly always places the feet and limbs in an unusual position to observe the response of the horse. Gait abnormalities that are observed commonly in horses with neurologic disease include ataxia, spasticity, and weakness or paresis.^{1–3,4,15,16}

Evaluation of gait is critical because subtle neurologic gait deficits often go unrecognized or sometimes, incorrectly, may be considered insignificant. One should conduct the examination to observe the horse at a walk and trot in a straight line and while turning. In some horses, observing the horse negotiate over small obstacles such as a curb is helpful. When possible, the examiner should observe the horse turned free and walking up and down an incline. Elevation of the head and walking on a slope may exaggerate a subtle deficit and make it more noticeable.

One should include in the examination observation of the horse at rest to observe its posture while standing, walking, trotting when possible, and sometimes while the horse is being ridden. The examiner should pay attention to which limbs show abnormal posture or abnormal movements and must be able to determine whether the horse has a painful or mechanical musculoskeletal problem or a neurologic gait deficit. The examiner must identify the presence of weakness, ataxia, and spasticity in each limb.

The important centers for posture and coordination in the brainstem and spinal cord are located in the regions of the sixth cervical to second thoracic (T2) and fourth lumbar to second sacral (S2) vertebrae in the spinal cord, along with coordination centers in the brainstem. Horses that demonstrate a wide base stance at rest often have a lesion of the cerebellum or vestibular system or may have conscious proprioceptive abnormalities.

To evaluate the gait of an animal, one begins by observing the horse at a walk and trot. At a walk the examiner can walk alongside, in step with first the pelvic limbs and then the thoracic limbs. This allows the examiner to more easily determine the stride length and foot placement. A weak limb often has a low arc and longer stride length.

One also should observe the horse walking in a circle, on a slope, and with its head elevated. These procedures provide a degree of “challenge” to the horse and may help to demonstrate if the horse is showing persistent irregular movements with its limbs. Horses with a musculoskeletal problem have been described as being a regularly irregular gait, whereas a horse with neurologic gait deficits shows less consistency placing its limbs (an irregularly irregular gait). Although observing the horse running free in a paddock or round pen and while being ridden can sometimes be helpful, this is not always possible. One must consider safety for the horse and rider, as well as certain legal ramifications before asking a person to ride a horse during the examination.

Additional tests that may be helpful during a neurologic examination include blindfolding the horse, walking it over a curb or other obstacle, and walking it with its head and neck extended. One can evaluate the strength and ability of the horse to correct body positions by performing a sway test by applying lateral pressure at the shoulder, hip, and tail while the horse is standing and walking. One should apply pressure several times while the horse is walking to catch the limb in various stages of weight bearing. Observing a horse during the backing process is important. When a normal horse is backing, it should lift each leg and place it in a coordinated and appropriate location. Horses with neurologic abnormalities often place the limbs in wide-based positions or lean back and are reluctant or refuse to move. The horse also may step on the feet of a pelvic limb with the front feet.

The horse should be observed closely while being turned in a tight circle to identify abnormal wide outward excursions of the pelvic limb (circumduction). Additional tests to assess proprioceptive function include a standing sway test in which one applies pressure to the shoulder. The horse initially should press into the examiner and then lean away, and finally it should step away with the offside limb. The author also crosses the limbs over the opposite thoracic or pelvic limb to determine if the horse recognizes and tolerates these unusual limb positions. After this, the examiner might lift one thoracic limb and force the horse to hop on the opposite limb in a modified postural reaction.

The examiner should observe the movements of each limb carefully to determine if a deficit is present and should assign a grade to the deficit. The author uses a system modified from the grades described by deLahunta³ and Mayhew.¹ The severity is graded between 0 and 5. Grade 0 means no gait deficits. A grade 1 deficit requires careful observation to be certain the gait abnormality is caused by a neurologic dysfunction. Grade 2 deficits are mild to moderate but obvious to most observers as soon as the horse begins to move. Grade 3 deficits are obvious and are exaggerated during the negotiation of a slope or with head elevation. Grade 4 gait deficits may cause a horse to fall or nearly fall. When attempting to walk, an animal with these severe deficits often displays abnormal positioning while standing in its stall. Grade 5 horses are recumbent.

Weakness or paresis is a deficiency of voluntary movement as a result of loss of muscle power because of either damage to upper motor neurons, lower motor neurons, or the muscle. It can be described as knuckling, stumbling, or buckling and sometimes can be characterized by toe-dragging while walking. Weakness may be associated with an upper motor neuron or lower motor neuron lesion. In the case of a lower motor neuron or peripheral nerve injury or illness, the horse shows muscle atrophy and sensory loss. A spastic movement of the limbs often accompanies the weakness that results from loss of upper motor neurons. Ataxia is typified by abnormal foot placement and wide swaying of the foot and limb, especially while turning. Ataxia appears as a lack of coordination of motor movements. It can arise from damage to the vestibular, cerebellar, or sensory portions of the nervous system. Ataxia in horses is most often a result of loss of sensory input through injury, damage, or disease in the spinal cord blocking normal input to the cerebellum. Cerebellar ataxia is seen most often in young horses, typically Arabians with a condition known as cerebellar abiotrophy. Vestibular ataxia is often accompanied by a head tilt and other cranial nerve deficits.

Horses may also demonstrate dysmetria, which is characterized as exaggerated hypermetric or hypometric movements of the limbs. Horses with hypometric gaits often appear to have a straight leg or “tin soldier” way of moving (sometimes referred to as spasticity). A spastic gait is the result of increased muscle tone and is generally associated with upper motor neuron disease resulting from reduced inhibition of extensor motor neurons.

The gait abnormalities, along with the findings from other parts of the neurologic examination, allow the examiner to determine the neuroanatomic site of the problem. The severity of the clinical signs also helps one evaluate the extent or severity of the problem.

One should reexamine horses with an obscure or unusual gait that might be the result of lameners after the use of local anesthetics (to block selected peripheral nerves) or intra-articular medications. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) for a period of 1 to 2 days also may alleviate pain and help one distinguish between lameness and a neurologic gait deficit.

One must realize that many horses that have minimal (grade 1 or mild grade 2) deficits often can race or perform other athletic activities.¹³ The examining veterinarian has the responsibility of separating a neurologic from a musculoskeletal gait deficit and helping the owner determine the usefulness of the horse. For example, a horse with gait deficits up to grade 3 may be useful as a broodmare or breeding stallion (if the horse is handled by careful, knowledgeable persons who understand the risks and have the facilities to accommodate a horse in need of special management). Stallions with this degree of impairment may require assistance when mounting and dismounting mares. If the breed association allows artificial insemination, then the stallion may be easier to manage.

ce:small-caps>Localization of the Lesion

At the conclusion of the examination, the veterinarian needs to determine if a neurologic abnormality exists and where it is located. If the horse showed no evidence of abnormal behavior, seizures, or abnormal mental status and showed no cranial nerve deficits, then the lesion is most likely caudal to the foramen magnum.

The most difficult lesions to localize are in the brainstem, unless the signs include cranial nerve deficits or depression. Horses with brainstem lesions often show signs of weakness and ataxia similar to horses with a lesion in the cervical spinal cord. Two of the most common brainstem lesions in horses involve the seventh and eighth cranial nerves. Vestibular disease or injury may be a sequela of head trauma or an inner ear infection. Facial nerve paralysis may result from trauma to the nerve root origin in the brainstem or where the nerves course along the neck and face to the ears, eyelids, and nares.

Specific cranial nerve involvement, such as head tilt, facial nerve paralysis, or loss of facial sensation, can result from trauma, guttural pouch infection, THO, or equine protozoal encephalomyelitis. In addition, cranial nerve deficits may occur with polyneuritis equi and equine motor neuron disease (EMND).

Cerebellar lesions are characterized by a failure to blink to bright light, lack of a menace response, and a head tremor that worsens with intentional movements. The most common form of cerebellar disease in horses is abiotrophy, which occurs most frequently in Arabian horses.

Cervical spinal cord disease includes gait and proprioceptive deficits in all four limbs with no signs of brain, brainstem, or cranial nerve deficits. One should note that horses with cervical vertebral stenotic myelopathy might have mild pelvic limb deficits with minimal or barely detectable signs in the thoracic limbs.¹⁶

Horses with signs of neurologic gait deficits confined to the pelvic limbs have a neuroanatomic localization caudal to T2. When examining a horse with a lesion caudal to T2, carefully checking the tail and anus for involvement of the peripheral nerves or spinal cord segments in this region is important.

Horses that have peripheral nerve injury (Table 12-1), EMND, or polyneuritis equi show evidence of weakness, muscle atrophy, and in some cases selected areas of sensory loss. Primary muscle diseases such as exertional rhabdomyolysis, myotonia (congenita or dystrophica), and hyperkalemic periodic paralysis are covered elsewhere in this book (see Chapter 11). These conditions sometimes can mimic a neurologic problem.

Description of Normal Gaits

A walk is a natural four-beat gait in the horse. At this gait the normal horse has three feet on the ground at all times. Therefore the walk is a stable gait. Overtracking and interference may occur if the conformation of the horse is abnormal (e.g., with long limbs and a short body) and not as a result of neurologic disease.¹¹ The trot is a two-beat symmetrical gait in which the diagonal limbs are in contact with the ground at the same time. If one examines the horse on hard pavement, then the trot is the most helpful gait to distinguish lameness from a neurologic gait deficit. The pace is a two-beat symmetrical gait in which the legs on the same side of the body strike the ground simultaneously, resulting in significant truncal sway. In horses that have neurologic disease, identifying ataxia with truncal sway, which is often accompanied by pacing, is common. In horses with subtle ataxia, one observes pacing when horses walk with the head held in an extended position. Whenever one observes a horse pacing, the pacing may indicate an underlying neurologic disorder.

The gallop is a high-speed four-beat gait that often seems to be easier to perform than walking in a tight circle or moving at a slow trot. Therefore some horses with a neurologic gait deficit may perform better at high speed. As the horse accelerates or slows down, one may detect abnormalities, and one must observe the horse carefully at this time when an ataxic horse is most unsafe.

Abnormal gaits associated with stringhalt, upward fixation of the patella, and fibrotic myopathy deserve careful attention. Horses that show these gait abnormalities have a mechanical lameness, although the exact cause is unknown and may sometimes be associated with underlying neurologic disease.

Stringhalt often begins as an abrupt onset of excessive flexion of one or both rear limbs. In some horses the condition may worsen and result in frequent episodes of the foot hitting the abdomen. The condition has been reported for a long time and in some areas of the world may occur as an outbreak.¹⁷ The clinical syndrome is similar to the movement of a horse with a tibial neurectomy with unopposed flexion of the hock and extension of the digit. In the case of Australian stringhalt, the forelimbs and neck muscles may be involved. Stringhalt deserves mention in this chapter because when the examiner observes this gait, the examiner should be certain no other signs of neurologic gait deficits exist. The primary condition usually can be corrected by a tenectomy of the lateral digital extensor tendon, including a portion of the muscle belly. The underlying cause of the disease may be a sensory neuropathy, a myopathy, or primary spinal cord disease. The defect likely affects the neuromuscular spindle, as well as the efferent and afferent pathways controlling muscle tone.¹⁰

Fibrotic myopathy results from scar tissue formation after injury to the semitendinosus and semimembranosus muscles. One may confuse the characteristic foot placement coupled with the abrupt rearward movement of the affected limb with a spastic gait caused by spinal cord injury (SCI) or disease. With careful examination, a horse suffering from fibrotic myopathy likely will not go undiagnosed.

Upward fixation of the patella in horses with neurologic disease may result from weakness in the quadriceps muscle group. This weakness is thought to occur because of a lack of use of these muscles or may be caused by abnormal transmission of proprioceptive information to and from the muscles and joint capsule because of damage to the spinal cord.

Horses with profound ataxia may pace when they walk, which often is accompanied by circumduction of the outside rear limb while turning. These signs suggest general proprioceptive deficits. If the horse has these deficits while walking, then the examiner should observe the horse walking with its head elevated and on a slope (these maneuvers often exaggerate a subtle problem).

If the horse shows signs only in the trunk and pelvic limbs, the neuroanatomic localization of the lesion is between T2 and S2 or involves the nerves and muscles of the pelvic limbs. However, horses with cervical spinal cord lesions often demonstrate signs in the pelvic limbs that are one grade worse than those observed in the thoracic limbs. Therefore a mild cervical spinal cord or brainstem lesion could show minimal or no thoracic limb signs with grade 1 or subtle signs in the pelvic limbs.

Palpating the horse over its back, rump, and muscles of the rear limbs while being careful to detect any muscle atrophy is helpful. The author routinely stimulates the horse over the side of its body and observes for any twitching of the cutaneous trunci muscles. Such twitching usually is accompanied by a cerebral response and requires a fairly severe lesion to detect areas of analgesia.

A sway reaction performed while the horse is standing and walking is also necessary to assess the pelvic limb strength and proprioceptive functions. In addition, one may evaluate strength by slow but deliberate and forceful pressure along the back and sacral muscles. A normal horse should reflexively arch its back upward, whereas a horse with rear limb weakness may be unable to withstand this pressure and its rear limbs may even buckle.

To complete the neurologic examination, one must examine the tail and anus to determine whether damage has occurred to the sacrococcygeal nerve and muscle segments. A normal perineal reflex results in contraction of the anus and clamping of the tail in response to light stimulation of the skin in this region. Cauda equina neuritis or polyneuritis equi, trauma, and iatrogenic injury resulting from an alcohol tail block are some disorders that may affect this area.

The evaluation of the major peripheral nerves in the horse is also an important part of the neurologic examination (Table 12-1). The important points to remember are that damage to a peripheral nerve can result in sensory and motor deficits in the area supplied by the nerve and that focal muscle atrophy follows within a short time after damage to one of these nerves. The examiner is referred to other portions of this book for a more detailed anatomic description of these nerves in the horse; however, a dropped elbow joint with radial nerve paralysis, inability to fix the stifle with femoral nerve paralysis, and atrophy of the supraspinatus and infraspinatus muscles (sweeney) with damage to the suprascapular nerve are classic examples of what to expect with peripheral nerve injuries.^1–3

Pressure

One can measure opening CSF pressure before withdrawal of CSF by attaching a manometer tube with a three-way stopcock to a properly placed spinal needle, allowing the CSF to rise within it.¹² Because the cranial and vertebral cavities are enclosed in a rigid bony compartment, changes in blood pressure or volume can cause a concomitant increase in CSF pressure. Thus increased CSF pressure may occur from venous compression or jugular occlusion. Venous compression causes increased blood volume in the cranial cavity and compression of the CSF space, leading to increased CSF pressure. One can use jugular occlusion clinically to increase CSF pressure and facilitate collection of CSF fluid.¹³ The jugular compression maneuver, or Queckenstedt’s phenomenon, can help one diagnose compressive lesions, neoplastic lesions, or an abscess along the spinal cord. With compression and obliteration of the subarachnoid space by a compressive lesion in the cervical or thoracic spinal cord, jugular vein compression does not cause a CSF pressure increase in the lumbosacral site.¹

Increased CSF pressure may occur after injury, after systemic changes in blood pressure, and in the presence of an intracranial space-occupying mass such as a tumor, abscess, hemorrhage, or edema. One must provide an adequate airway after injury and during surgery to prevent hypoxia-mediated cytotoxic cerebral edema and vasogenic cerebral edema.¹⁴ Cytotoxic edema is caused by inadequate cerebral oxygenation and leads to neuronal, glial, and endothelial cell swelling. Such reactions are especially important during long surgical procedures or recumbency in which respiratory hypoxia and poor alveolar ventilation (hypercapnia) may occur. Hypercapnia increases cerebral blood flow in the cranial cavity and CSF pressure and may worsen existing cerebral edema.¹

Increased CSF volume may occur in hydrocephalus, which is defined as an increased volume of CSF and can be classified as compensatory or obstructive.¹⁵ Compensatory hydrocephalus is an accumulation of CSF in areas in which brain tissue has been destroyed and may occur from brain injury or inflammation. Hydranencephaly is destruction of brain tissue from a viral or other infectious agent and results in severe accumulation of CSF.¹⁵ CSF pressure in compensatory hydrocephalus usually does not increase.¹

Obstructive hydrocephalus is an accumulation of CSF in the ventricles from an obstruction to CSF outflow or absorption. Cerebral aqueduct malformation may lead to obstruction of ventricular CSF outflow. Inflammatory lesions, especially of the arachnoid villi, result in decreased absorption of CSF and increased CSF pressure. The white matter is affected more severely than the gray matter in obstructive hydrocephalus, but the cerebral cortex usually is spared.¹ CSF pressure in obstructive hydrocephalus usually increases. The presence of an abnormally high opening pressure that drops by 25% to 50% after removing 1 to 2 ml of fluid suggests a space-occupying intracranial mass or spinal cord compression cranial to the site of collection. The removal of more fluid would risk causing tentorial herniation.¹²

Appearance

One can evaluate the appearance of CSF immediately after collection. Normal CSF is clear and colorless and does not clot, and newsprint is visible through it.¹⁶ CSF may be red tinged from blood contamination after a traumatic tap or from preexisting trauma to the CNS. In the case of a traumatic tap, the CSF usually will clear if allowed to flow for several seconds (about 0.5 to 1.0 ml). With preexisting trauma and secondary hemorrhage, the supernatant of CSF after centrifugation is xanthochromic.

Other causes of CSF xanthochromia include increased protein concentration (150 mg/dl)¹⁶ and direct bilirubin leakage from serum in horses with high serum bilirubin concentration. In addition, indirect bilirubin may leak across a damaged blood-brain barrier. Clots in the CSF are abnormal and may be caused by increased amounts of fibrinogen resulting from inflammation.¹

Turbid CSF may indicate an increased number of white blood cells (>200/μl), an increased number of red blood cells (RBCs) (>400/μl), epidural fat, bacteria, fungal elements, or amebic organisms.¹ Cytologic evaluation and cultures can help differentiate causes of turbidity.

Cytologic Evaluation

One can use a standard hemocytometer to obtain a complete blood count (CBC). In addition, a sedimentation chamber requiring 0.5 to 1.0 ml of CSF is a rapid method for cytologic evaluation.¹⁷ One must perform cell counts and cytologic evaluation within 30 minutes to avoid degeneration. If cell counts or cytologic evaluation cannot be performed immediately, then one can mix a portion of the sample with an equal volume of 50% ethanol to preserve cellular characteristics.¹² CSF from normal horses and foals usually contains fewer than 10 white blood cells per microliter. However, much variation occurs in CSF white blood cell counts in horses.^9,10

Most studies show no differences in white blood cell counts in normal CSF samples obtained from the atlantooccipital space as compared with samples obtained from the lumbosacral space.¹⁰ However, one study did show a slightly higher total white blood cell count in CSF obtained from the lumbosacral site, but white blood cell counts in all of those horses were less than 10 per microliter.⁶

Small mononuclear cells (70% to 90%) and large mononuclear cells (10% to 30%) predominate in equine CSF. Rarely, one may see neutrophils in horse CSF. Increased CSF large mononuclear phagocytes are visible in horse CSF in diseases of axonal degeneration.⁹ One may see increased CSF neutrophil numbers in encephalomyelitis, bacterial meningitis, parasitism, and diseases with extensive inflammation. Occasionally, in severe inflammatory diseases of the neurologic system or parasitism, eosinophils may be visible.^9,17,18 In some cases, cytologic evaluation of CSF may reveal specific agents causing neurologic disease such as fungal organisms,¹⁶ bacteria, or tumor cells. Although CSF cytologic examination may support a diagnosis of neurologic disease, it may not yield a specific causative diagnosis.

Protein Concentration and Composition

Normal total protein values range between 20 to 124 mg/dl, depending on the measuring method used^1,6–10 (Table 12-2). Total protein concentration is higher in lumbosacral CSF compared with atlantooccipital CSF.⁶ A difference of 25 mg/dl of protein between the atlantooccipital and lumbosacral spaces may suggest a lesion closer to the space with greater spinal fluid protein.¹⁰ Proteins in the CSF are derived from the peripheral blood and include albumin, IgG, and possibly other globulins. Increased CSF albumin and IgG concentrations may occur with damage to the blood-brain barrier or increased intrathecal production of IgG. One can determine CSF albumin and IgG concentrations by electrophoresis and radial immunodiffusion, respectively, and can compare these with serum concentrations.⁶ Special low-level radial immunodiffusion plates (VMRD Inc, Pullman, WA) are available to quantify CSF IgG concentration. One can calculate the albumin quotient (AQ) ([Albc]/[Albs] × 100) and IgG index ([IgGc]/[IgGs] × [Albs]/[Albc]) to determine blood-brain barrier permeability and intrathecal IgG production.⁶ Increased intrathecal IgG production (increased IgG index) may occur in inflammatory spinal cord disease such as equine protozoal myeloencephalitis (EPM), bacterial meningitis, some tumors, and EMND. Increased blood-brain barrier permeability (increased AQ) may occur in equine herpesvirus-1 (EHV-1) after necrotizing vasculitis.⁷ Determining blood-brain barrier integrity is also important in planning therapy. If the blood-brain barrier is damaged, then pharmacologic agents such as penicillin that do not normally penetrate the blood-brain barrier will penetrate a disrupted blood-brain barrier and attain bactericidal CSF concentration.

TABLE 12-1 Localization of peripheral nerve injuries in horses

Enzyme Determination

CSF enzyme activity may be increased in neurologic disease. CK and AST activity may be increased in diseases with myelin degeneration and neuronal cell damage such as EPM, polyneuritis equi, equine degenerative myelopathy, and EMND. Increased CK activity also may occur in conditions that alter blood-brain barrier permeability, such as EHV-1. In diseases in which the blood-brain barrier is damaged, serum CK can leak into the CSF and increase CSF CK activity. This increased CK activity is not associated with damaged myelin.

Increased CK activity also may suggest other diseases of the CNS. In one study, CK activity (>1 IU/L) most often was associated with EPM in horses and may be helpful in differentiating compressive spinal cord disease from EPM. Furthermore, persistently increased CSF CK activity may be associated with a poor prognosis in horses with EPM.¹⁹ Lactate dehydrogenase activity may be increased in spinal lymphosarcoma.

Lactic Acid Concentration

CSF lactic acid concentration may be an indicator of neurologic disease (see Table 12-2). CSF lactic acid concentration increases in eastern equine encephalomyelitis (4.10 ± 0.6 mg/dl), head trauma (5.40 ± 0.9 mg/dl), and brain abscess (4.53 mg/dl). Lactic acid concentration may be the only CSF parameter increased in horses with brain abscess.²⁰

TABLE 12-2 Cerebrospinal Fluid Values from Atlantooccipital and Lumbosacral Spaces of Normal Healthy Adult Horses^∗

∗ Total protein concentration next to the mean ± SD in parentheses is the value expected using a total protein standard.

Electromyographic Examination

A history and physical and neurologic examination always should precede the EMG examination; these aid in localizing the lesion, shortening the examination time, and minimizing trauma to the horse. Initially, one examines the standing horse that is under mild sedation. One can tranquilize the horse with 0.2 to 0.5 mg/kg xylazine administered intravenously or 0.2 to 0.5 mg/kg xylazine and 2 to 10 mg butorphanol administered intravenously. Examination of the awake horse aids in evaluating individual motor unit action potentials (MUAPs), summated MUAPs, and interference pattern. One can evaluate normal and abnormal MUAPs and measure their amplitudes. Unfortunately, in the awake horse an interference pattern (many MUAPs) sometimes can obscure abnormal low-amplitude EMG potentials. In this case, further examination may require general anesthesia.

In the needle EMG examination, one should thrust the exploring electrode briskly into the muscle and hold it until the animal completely relaxes. To enable relaxation, one can force the animal to bear weight on the opposite limb. Once relaxation has occurred, one can evaluate the resting activity or any postinsertional activity of the muscle. One should evaluate at least four areas and depths of smaller skeletal muscles and six to eight areas and depths of larger skeletal muscles when possible. One should examine the horse systematically so as not to miss a lesion. Needle EMGs can also be performed in many of the major extrinsic muscles of the horse (Table 12-3). In addition, they can be performed on facial, laryngeal, esophageal, pectoral, and external anal sphincter muscles when indicated by neurologic examination. One may perform nerve conduction studies and collect muscle biopsy specimens to define suspected lesions further or confirm a diagnosis.

TABLE 12-3 Muscles, Nerves, and Nerve Roots Evaluated during Routine Electromyographic Examination of Horses

Nerve Conduction Studies

The evaluation of nerve conduction velocities requires knowledge of the topographic anatomy of nerves and muscles, plus a stimulator capable of delivering up to 150 V at durations of 0.1 to 3.0 ms at variable frequencies, up to 100 Hz. Most standard EMGs have built-in stimulators with adequate parameters to do nerve conduction studies. The peripheral nerve to be assessed can be located by palpation or by anatomic landmarks and then can be stimulated. One can palpate or observe the resultant muscle contraction and can view the evoked muscle action potential, which has a thumping sound, on the oscilloscope.

Nerve conduction studies are difficult to do in horses and therefore are not done routinely. However, the technique for radial and median nerve conduction studies in the horse has been reported.^5,6 One must perform nerve conduction studies with the horse under general anesthesia and may use them to evaluate the speed of conduction of large myelinated motor nerves. To do this, the horse should be placed in lateral recumbency, with the affected side up. One stimulates the appropriate motor nerve by monopolar needle electrodes inserted at or near the nerve and records an evoked MUAP from an innervated muscle (Figures 12-4 and 12-5). The examiner may see or palpate the contraction of appropriate muscles and insert needle electrodes until a repeatable response is obtained. The unaffected limb can be used as a control.

FIGURE 12-4 Illustration of anatomy and electrode placement used in median nerve conduction velocities. DDF, Deep digital flexor.

(From Henry RW, Diesem CD, Wiechers MD: Evaluation of equine radial and median nerve conduction velocities, Am J Vet Res 40:1406–1410, 1979.)

FIGURE 12-5 Illustration of anatomy and electrode placement used in radial nerve conduction velocities. ECR, Extensor carpi radialis; CDE, common digital extensor; LDE, long digital extensor; ECO, extensor carpi obliquus.

(From Henry RW, Diesem CD, Wiechers MD: Evaluation of equine radial and median nerve conduction velocities, Am J Vet Res 40:1406–1410, 1979.)

In horses, one can obtain radial nerve recordings from the extensor carpi radialis and abductor digiti longus (extensor carpi obliquus) muscles (see Figure 12-4) and can obtain median nerve recordings from the humeral and radial heads of the deep digital flexor tendon^5,6 (see Figure 12-5). Facial nerve recordings can be obtained from the levator nasolabialis muscle by stimulating the buccal branch of the facial nerve just ventral to the facial crest.⁷ Often a supramaximal stimulus can be obtained at 70 to 90 V for 0.1-ms duration. Nerve conduction studies are helpful in diagnosing radial nerve, median nerve, and possibly facial nerve injury.

Insertional Activity

Insertional activity consists of short bursts of high-amplitude, moderate- to high-frequency (<200 Hz) electric activity after insertion or movement of the exploring electrode in the muscle (Figures 12-6 and 12-7). In normal skeletal muscle this activity stops a few milliseconds after cessation of needle movement. Insertional activity may be caused by mechanical stimulation, muscle fiber injury,^3,8,9 or depolarization of muscle fibers directly adjacent to the EMG needle.¹ Positive sharp waves and fibrillation potentials observed during (or associated with) needle insertion that stop after cessation of needle movement are considered normal. Damage to muscle fibers by needle insertion is probably the source of these potentials. However, positive sharp waves and fibrillation potentials persisting after needle insertion are considered abnormal and may suggest early muscle denervation.³

FIGURE 12-6 Normal insertional activity in the infraspinatus muscle. Gain: 0.500 mV/division; time: 10 ms/division.

FIGURE 12-7 Electromyograph of the middle gluteal muscle showing normal resting activity (arrowheads), fasciculation potentials (A, E, G), fibrillation potentials (C), positive sharp waves (B, F), and a small motor and action potential (D).

Resting Activity (Postinsertional Baseline)

Resting activity is observed in relaxed muscle and is characterized by electric silence. A flat line appears on the oscilloscope. When the needle comes to rest near a nerve twig or end plate, the needle may irritate small intramuscular nerve terminals, which results in the production of two characteristic potentials: (1) end plate noise and (2) end plate spikes. End plate noise produces a rippling of the baseline and a low-pitched continuous noise (Figure 12-8). End plate spikes, on the other hand, are high-amplitude intermittent spikes and make a popping sound. End plate noise and spikes can occur alone or together. The origin of end plate noise is thought to be extracellularly recorded miniature end plate potentials,^10,11 whereas end plate spikes are thought to be single muscle fiber contractions after needle electrode irritation of the nerve terminals.¹¹ In human beings, these potentials are associated with dull pain³; repositioning the needle often eliminates their activity.

FIGURE 12-8 Electromyograph from triceps brachii muscle showing end plate spikes (large arrowheads) and end plate noise (small arrowheads). Gain: 0.500 mV/stair step; time: 10 ms/division.

Motor Unit Action Potentials

Motor unit action potentials (MUAPs) are voluntary or reflex muscle contractions observed after insertion of the needle electrode. They represent the sum of a number of single muscle fiber potentials belonging to the same motor unit. MUAPs are usually monophasic, biphasic, and triphasic. Because individual muscle fibers fire nearly synchronously, the prefixes refer to the number of phases above and below the baseline (see Figure 12-7). A few polyphasic potentials (greater than four phases) may occur in normal muscle but usually do not exceed 5% to 15% of the population of MUAPs observed.³ MUAPs have an amplitude ranging between 500 to 3000 μV and a duration ranging between 1 to 15 ms. Examination of the conscious horse enhances the evaluation of the amplitude and number of phases of MUAPs in the muscle.

One may see these MUAPs when one forces the animal to bear weight on or retract a limb, resulting in contraction of that explored muscle. In lightly stimulated muscle, one may see single MUAPs, because single motor units are recruited (see Figure 12-7). As muscle contraction becomes more intense, more motor units are recruited and the greater frequency of MUAPs appears on the oscilloscope. Once MUAPs fill the screen, one observes an interference pattern. Clinically, the number of phases and the duration of MUAPs are of greater importance than amplitude, because amplitude may be influenced by species, the muscle explored, the age of the horse, and electrode position.⁹ Furthermore, MUAP duration has been shown to increase with age in human beings.¹²