Diseases of the peripheral nerves include degenerative diseases, inflammatory diseases, metabolic disorders, cancers, nutritional disorders, toxic disorders, disorders caused by injury, and vascular diseases.
Stringhalt in horses is characterized by brisk, involuntary flexing of one or both hind legs during the lengthening phase of the gait. Severity ranges from a mild jerk in the leg to contractions so severe that the horse can hardly walk. Muscle wasting may occur in the lowest parts of the affected leg(s).
Stringhalt is seen in 2 forms. Ordinary or classic stringhalt is seen sporadically throughout the world and usually affects individual horses. The cause is unknown. Some cases resolve spontaneously, while removal of the affected portion of lateral digital extensor tendon is done in others. Australian stringhalt occurs in outbreaks, affecting multiple horses in a region and often affecting both hind legs. Horses in Australia, New Zealand, and the United States have contracted the disorder, usually in late summer or autumn. Australian stringhalt may be caused by eating Australian dandelion, European dandelion, or mallow, and it is possibly caused by toxic molds in these plants. Horses with Australian stringhalt usually recover spontaneously when removed from pastures with these plant varieties.
Polyneuritis equi (neuritis of the cauda equina) causes inflammation of the nerves around the sacral vertebrae at the rear of the spine, near the pelvis. It can occasionally affect other nerves, including cranial nerves. The cause is unknown, although it may be an immune response to a viral infection. The disorder is seen in adult horses of all breeds in Europe and North America. Signs include urinary and fecal incontinence, tail paralysis, loss of sensation in the perineum, and mild loss of coordination in the hind legs. Affected horses may rub the tail. A rectal examination and x-rays are done to check for a fracture of the vertebrae in the tail, which can cause similar signs. If a diagnosis of polyneuritis equi is determined, there is no treatment, and the outlook is poor.
Botulism (see Disorders Affecting Multiple Body Systems of Horses: Botulism in Horses) is an intoxication with a neurotoxin that is produced by a microorganism called Clostridium botulinum. The toxin is often found in rotting carcasses or vegetation. Multiple animals can be affected from a single source. Less commonly, botulism can develop from wound infection in which the spores germinate in the wound. Partial paralysis develops rapidly, and reflexes are lost in all 4 legs. Cranial nerves can also be affected, leading to a loss of motor control in the head and face. Definitive diagnosis requires identifying the toxin in the food, blood, or feces. Treatment is generally limited to supportive therapy while the body clears out the toxin. The outlook is poor for large animals that are recumbent. To help prevent botulism, feed should be kept dry and free from contamination by rodent carcasses. A vaccine is available for horses in areas where botulism is common.
Occasionally Clostridium botulinum has been found to grow in the gastrointestinal tract and produce toxins there. When the toxins are released, they cause typical botulism. This occurs in foals up to about 8 months of age and results in the shaker foal syndrome. Most often, foals show signs of paralysis that slowly progresses. Stilted gait, muscle tremors, and the inability to stand for more than 4 to 5 minutes are common signs. Other signs include difficulty swallowing, constipation, dilated pupils, and frequent urination. As the disease progresses, labored breathing with extension of the head and neck, rapid heart rate, and respiratory arrest occur. Death occurs most often 1 to 3 days after signs are first noted.
Ionophores are antiprotozoal drugs used in the poultry industry but also included in some animal feeds as growth promotants. The ionophores include monensin and lasalocid. Ionophore toxicity occurs when horses accidentally ingest these feeds. It is often fatal in horses. Signs include lethargy, depression, degeneration of heart muscle, and death. There is no antidote. It is critical to provide only feeds and mineral supplements that are formulated for horses to avoid this toxicity.
Organophosphate poisoning can result from exposure to pesticides, herbicides, or other industrial chemicals. The signs depend on the severity of exposure. The acute form, or suddenly form, prevents the body's acetylcholinesterase from working properly. Acetylcholinesterase is an enzyme that is essential for the proper function of connections between neurons, and between nerve and muscle. Signs of severe poisoning can include vomiting, diarrhea, salivation, shortness of breath, muscle tremors and twitching, seizure, or coma.
The intermediate form can cause generalized muscle weakness. Affected animals may not show obvious signs at first, but partial paralysis of the legs and stiffness of the neck can develop several days after exposure. The pupils may appear to be dilated. Treatment of acute or intermediate toxicity includes the drug atropine, which blocks the effects of the organophosphate. Other medications are used to relieve the tremors and muscle weakness. Treatment for several weeks may be necessary.
In the delayed form of toxicity, the nerves slowly degenerate. This form is unrelated to the effects on acetylcholinesterase. Signs develop several weeks after exposure and typically involve weakness and loss of motor control in the hind legs. There is no specific treatment (see Poisoning: Organophosphates).
Injury and Trauma
Peripheral nerve injuries are common in traumatic injuries. The sciatic nerve, which runs from the lower back to the hind legs, may be injured by hip fractures or during surgery to correct a broken leg. Irritants injected in or near the nerve can also cause nerve damage. The leg may be partially paralyzed, or the animal may not be able to bend the knee. There may be loss of sensation below the knee. The femoral nerve may be injured in foals during a difficult birth. The foal is unable to bear weight on the leg because of an inability to extend the stifle. The patellar reflex is weak or lost. The suprascapular nerve is most commonly damaged in large animals in an injury to the shoulder region. Damage to the suprascapular nerve causes muscle wasting and difficulty moving the shoulder joint. In horses, the nerve may be damaged by the growth of connective tissue in the shoulder after an injury.
Facial nerve injuries are most common in large animals that lie down for long periods of time with pressure on the side of the face. It can be caused by pressure from a halter in horses after general anesthesia. Signs include lip paralysis on the same side of the face as the injury, the muzzle twisted away from the injury, and weak or lost facial reflexes. A drooping ear can also result from injuries to the nerve.
For function to return after nerve connections are lost, the nerve must regenerate from the point of injury all the way to where it ends in the muscle. Nerve tissue regenerates or heals very slowly. Recovery is unlikely if the severed ends of the nerve are widely separated or if scar tissue interferes with healing. Although anti-inflammatory drugs have been used to treat traumatic nerve injuries, there is little evidence of any benefit. Surgery should be performed promptly in cases in which the nerve has been cut. In cases of injury from a fall or a blunt object, surgical exploration and removal of scar tissue may help. Longterm care consists of physical therapy to minimize muscle wasting and to keep the joints moving. Bandages or splints may be necessary to help protect a damaged leg.
Last full review/revision July 2011 by William B. Thomas, DVM, MS, DACVIM (Neurology); Daniela Bedenice, DVM, DACVIM, DACVECC; Kyle G. Braund, BVSc, MVSc, PhD, FRCVS, DACVIM (Neurology); Cheryl L. Chrisman, DVM, MS, EDS, DACVIM (Neurology); Caroline N. Hahn, DVM, MSc, PhD, DECEIM, DECVN, MRCVS; Charles M. Hendrix, DVM, PhD; Maureen T. Long, DVM, PhD, DACVIM; Robert J. Mackay, BVSc, PhD; Karen R. Munana, DVM, MS, DACVIM (Neurology); Charles E. Rupprecht, VMD, MS, PhD; Josie L. Traub-Dargatz, DVM, MS, DACVIM; Susan L. White, DVM, MS, DACVIM