Clinical Signs of EPM

The clinical signs of EPM result from the effects of inflammation, swelling and nerve cell death associated with merozoites and meronts of the protozoan Sarcocystis neurona/falcatula in the central nervous system. The most common presenting complaint for EPM is ataxia (incoordination), but can be any neurologic dysfunction, or even lameness. The disease is often insidious in onset, misdiagnosed until late in disease, and may culminate in death if untreated. Horses with EPM may exhibit a wide array of clinical signs, including primary and secondary problems.

Three "A's"

Profound gluteal muscle atrophy The classic presentation for EPM is progressive asymmetric ataxia and focal muscle atrophy (the three "A's"). The photograph shown above is end stage gluteal muscle atrophy. This horse had little or no use of the affected leg and had to be euthanatized.

Neurologic signs are referable to the site or sites of infection. The actual neurologic abnormalities are the result of both direct damage to neurons from protozoal proliferation within the neuronal cell bodies, and indirect damage to neural elements from edema and inflammation in response to the parasites. The photogr Spinal Cord Lesion aph (thanks to Neil Williams at the University of Kentucky) above depicts the spinal cord of an affected EPM horse. Hemorrhage is evident by the scattered red regions, and edema is evident by the bulging of the tissue on cross section.

Primary Signs

Primary signs from EPM are neurologic abnormalities that result directly from damage to the nervous tissue from the parasitic infection. Most commonly, clinical signs result from infection of the spinal cord and brain stem. Clinical signs associated with infection of the spinal cord include ataxia, and weakness that is usually worse in the rear limbs than in the front limbs. Placing reactions of affected limbs are abnormal, and the horse may appear weak, and be easily pulled over to one side. Focal muscle atrophy may be evident anywhere, but the gluteal muscles appear to be over represented. This is probably because muscle atrophy of the gluteal muscles is much easier to detect than atrophy of other muscle groups. Generalized muscle atrophy or loss of condition may also occur without obvious asymmetry. Apparent lameness, particularly atypical lameness or slight gait asymmetry of the rear limbs are commonly caused by EPM. Occasionally, the only evidence of neurologic deficits in a horse with EPM may be a lameness that fails to block out in a comprehensive lameness examination.

Cranial Nerve Dysfunction

Facial nerve paralysis.

Signs of cranial nerve dysfunction are seen in at least 10% of EPM cases. Cranial nerves are the nerves that supply the head, and are responsible for many of the specialized senses and functions in the head, throat and face. Airway abnormalities, such as laryngeal hemiplegia (roaring), or dorsal displacement of the soft palate (snoring) may result from protozoa infecting the nuclei of the respective cranial nerves. Most horses that are affected by airway abnormalities do not have EPM, and therefore, EPM may be overlooked early in disease. Atrophy of the temporalis (forehead) or masseter (cheek) muscles may be observed. This may or may not be accompanied by difficulty chewing. Evidence of quidding (dropping chewed feed), or chewed material in the nostrils may result from cranial nerve dysfunction.

Secondary Signs

Other signs may occur secondary to the neurologic disease. These signs may include damage to muscles, tendons or ligaments that have their nerve supply damaged, injury that results from ataxia, or behavioral problems resulting from discomfort from the neurologic disease. For example, upward fixation of the patella is a common early finding among horses with neurologic disease. This probably results from quadriceps weakness, which permits laxity of the medial patellar ligament. Another common side effect of EPM is back soreness, which may be severe. Back soreness commonly results from an asymmetric use of the hind limbs, most commonly seen with rear limb lameness, but may also result from asymmetric ataxia. Exertional rhabdomyolysis (tying up) may occur in some affected horses because a limited number of muscle fibers are contracting during performance, and therefore suffer from greater exertion. Some horses develop bad attitudes towards training in general. This may be a direct result of protozoa in the region of the brain which controls emotions (amygdala), but is most likely the result of a lack of confidence, or pain associated with other secondary problems.

Signs in Training

Early signs of EPM can be detected by observing horses being trained. Many early signs can also be caused by problems other than EPM, but identifying horses with these problems will help to single out horses which should be evaluated more closely. Because the prognosis of EPM is probably related to the duration of signs in many cases, this can be a valuable screening method, especially at facilities where EPM has been diagnosed in more than one horse. Horses with EPM commonly exhibit evidence of discomfort, and weakness of the rear limbs while training. This includes frequent bucking during training, constant head tossing, or excessively high head carriage. Weakness of the rear limbs is manifested during training as traveling heavy on the forehand, with minimal forward extension during galloping. This gait may result in multiple minor injuries of the front limbs, including bucked shins, splints and bowed tendons. Horses may have difficulty maintaining a specific lead while galloping, and may cross-canter or frequently switch leads. The front limbs also reflect abnormalities of gait during training. They may be observed to "float" in the forward phase of the stride at the trot. Horses with EPM may also take short, choppy strides, or drag one or all of their feet while walking or trotting. Other signs may be observed, depending upon what type of athletic endeavor a horse is expected to perform. Thoroughbred racehorses may have a history of difficulty breaking from the starting gate, or maintaining position around the turns of the race track. Standardbred racehorses commonly lean on one or the other shaft of the sulky, and also may have difficulty negotiating turns. Dressage horses may have a history of a gait abnormality that is evident only when the horse is permitted to travel on a loose rein, and is much improved when the horse is "in a frame." Any gait abnormality that occurs while training and cannot be attributed to a musculoskeletal abnormality may result from EPM. Horses exhibiting any of these signs while training should be evaluated more closely for the presence of neurologic abnormalities by a veterinarian.

Rehabilitation of EPM horses

No specific research efforts have been directed at rehabilitation of horses with EPM. However, some ideas can be extrapolated from the rehabilitation of people that have been affected with polio, spinal cord injury, or other central nervous system damage. The central nervous system has an amazing ability to recover, reinnervate, regrow and compensate. Unlike other organ systems, once a nerve cell dies, it cannot grow back. Skin, liver, kidneys and even lungs have greater ability to regenerate than the central nervous system. Nonetheless, injured nerves that are not permanently damaged can regrow their axons, and neighboring neurons can take on the function of the neurons that are missing. Rehabilitation of EPM horses involves taking advantage of these natural occuring phenomena.

Almost all horses with neurologic deficits benefit and actually improve in neurologic signs with exercise. The amount and type of exercise that an EPM horse can perform depends upon the severity and symmetry of the neurologic signs observed.

Severe ataxia (incoordination), severe debilitation (weight loss), marked asymmetry (much worse on one side than the other), or cranial nerve deficits (facial paralysis, respiratory noise, inability to chew or swallow):

These horses are dangerous to themselves and/or to any people that may work around them. Therefore, stall rest or turnout in a small paddock without other horses is recommended. If these horses do not begin to improve within 10 days of initiation of treatment, it is STRONGLY recommended that aggressive anti-inflammatory treatment be initiated, and the prognosis for survival is poor.

Horses that are moderately ataxic, moderately asymmetric and in good condition (good flesh):

These horses are too dangerous to themselves and/or to a potential rider, so an exercise program should NOT include work under tack. However, some enforced exercise may be beneficial to improve these horse to the point that they may be able to be ridden.

Jogging, or trotting is a symmetric gait that may gradually strengthen the horses muscles enabling it to move on to more complicated gaits. I begin by working a horse for 5 minutes at the trot both directions in a round pen, or on a longe line. Fatigue should be avoided, because fatigue can be accompanied by injury as the horse loses the ability to compensate. Gradually work up to 20 minutes both directions before moving on to the canter (or lope).
If the horse is safe to ride at the walk (consult your veterinarian before riding any EPM horse) and well controlled at this gait, you may "power-walk" over flat terrain at first and then move on to slightly uneven terrain. Once the horse can handle short distances without fatigue, you can move on to hill work in order to strengthen muscles more quickly. If at any time, the horse becomes fatigued, immediately dismount and handwalk directly back to the barn.
Once a horse is started in a forced exercise program, it is important to monitor for lameness, back soreness or pain. Too much exercise may result in muscle strain which manifests in one of these types of pain. If this occurs, use anti-inflammatory medication (under the supervision of your veterinarian) and let the problem resolve completely before returning to forced exercise.

Horses that are mildly ataxic and symmetric in clinical signs:

Jogging or trotting over even ground, gradually working up to 10-20 minutes both directions will strengthen muscles. Always avoid fatigue, and monitor for pain as above.
Once the horse has regained strength and stamina, most horses in this category of ataxia are likely to be normal or very close to normal. If determined by your veterinarian to be normal, you may go on to normal work. However, do not get frustrated if it seems that the horse has "forgotten" how to perform to the previous level of work. Retraining of nerves and muscles may require relearning things that were previously simple. Just persevere.

Additional rehabilitation ideas:

Any horse with EPM may benefit from physical therapy. In particular, horses that are spastic, or walk stiffly (tin soldier-like gait), may benefit from passive flexion exercises. These exercises "remind" the muscles and tendons how to function properly. Try alternating from left rear to right rear and flex the limbs fully (so that the hoof is next to the belly), then extend fully (pull the limb out behind the horse, similar to a farrier).
If the horse is safe to ride, trot him/her over poles on the ground, and do flexibility exercises, such as bending, circling and figures of eight. If the horse is not safe to ride, try these exercises in hand or on a longe line.

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