Disorders of the peripheral nerves include degenerative diseases, inflammatory diseases, metabolic disorders, cancers, nutritional disorders, toxic disorders, disorders caused by injury, and vascular diseases.

Inflammatory Disorders

Acquired myasthenia gravis is a disease of the connections between the muscles and nerves. It is uncommon in cats (see Brain, Spinal Cord, and Nerve Disorders of Dogs: Inflammatory Disorders).

Acute idiopathic polyradiculoneuritis causes inflammation of peripheral nerves. It is uncommon in cats (see Brain, Spinal Cord, and Nerve Disorders of Dogs: Inflammatory Disorders).

Chronic inflammatory demyelinating polyneuropathy is seen in adult cats. The cause is unknown. Partial paralysis slowly spreads to all 4 legs with weakened reflexes. Sometimes, the cranial nerves are also affected. Signs usually improve after treatment with corticosteroids, but relapse may occur when therapy is stopped.

Trigeminal neuritis is common in dogs, but uncommon in cats (see Brain, Spinal Cord, and Nerve Disorders of Dogs: Inflammatory Disorders).

Metabolic Disorders

Diabetic neuropathy is an uncommon complication of diabetes seen more often in cats than in dogs. Signs include weakness, loss of motor control, and muscle wasting. Affected animals often have nerve dysfunction in their lower legs, which results in a flat-footed stance. High blood sugar is the likely underlying cause. Diagnosis requires evidence of diabetes and a nerve biopsy. In some cases, insulin therapy can lead to partial or complete recovery.

Tumors

Several different types of nerve sheath tumors can be found in animals, but are most common in dogs and cattle (see Brain, Spinal Cord, and Nerve Disorders of Dogs: Tumors).

Toxic Disorders

Intermediate organophosphate poisoning is especially common in cats, due to exposure to pesticides that contain chlorpyrifos. Often, signs are not obvious initially, but instead cats develop weakness in all 4 legs and abnormal neck position several days after exposure. Cats usually recover after several weeks of drug treatment (see Poisoning: Organophosphates).

Tick paralysis (see Brain, Spinal Cord, and Nerve Disorders of Cats: Tick Paralysis in Cats) is caused by the bite of several species of ticks that results in rapidly progressing paralysis. In Australia, the tick Ixodes holocyclus causes an especially severe form of tick paralysis. Signs begin with partial paralysis in the hind legs that worsens within 24 to 72 hours to total paralysis in all 4 legs. Sensory perception and consciousness remain normal. Difficulty swallowing, facial paralysis, jaw muscle weakness, and respiratory paralysis may develop in severe cases. Treatment consists of removing the tick and applying a skin ointment to kill any hidden ticks. For all except Ixodes holocyclus cases in Australia, recovery usually occurs in 1 to 2 days. A serum is available for treatment of Ixodes holocyclus paralysis, but death from respiratory paralysis can occur despite treatment.

Injury and Trauma

Brachial plexus avulsion occurs in cats due to injury to the spinal nerve roots in the neck and shoulder area that extend nerves into the front legs. In a severe injury, the nerve roots may stretch or tear from their attachment to the spinal cord. Signs vary depending on the severity. If the nerves are completely torn, paralysis of the leg and a loss of sensation and reflexes below the elbow result. The animal puts little or no weight on the leg and drags the paw on the ground. The leg may need to be amputated because of damage from dragging or self-mutilation. Recovery is possible in mild cases in which the nerve roots are bruised but not completely torn.

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. The paw and toes cannot flex or extend. There may be loss of sensation below the knee. Injury to the branches of the sciatic nerve in the lower leg, such as the tibial nerve or the -peroneal nerve, can result in an inability to extend the paw or flex the toes and reduced sensation over the surface of the foot.

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. Anti-inflammatory drugs have been used to treat traumatic nerve injuries, but 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 limb.

Blood Vessel (Vascular) Diseases

Ischemic neuromyopathy is most common in cats with arterial thromboembolism, a condition that develops secondary to disease of the heart muscle (see Heart and Blood Vessel Disorders of Cats: Blood Clots and Aneurysms in Cats). Emboli lodge in the arteries, blocking blood flow to the area. Blockage occurs most commonly at the aorta, resulting in damage to the muscles and nerves in the hind legs. Partial paralysis develops, and the cat may be unable to flex or extend the leg, lose the knee reflexes, and lose sensation in the lower leg. Diagnosis is based on the history and signs, as well as ultrasound scanning to analyze blood flow to the legs. Underlying heart disease must be treated. Neurologic signs can improve within 2 to 3 weeks, but 6 months may be needed for complete recovery. Permanent damage is possible. Health risks persist for many animals because of the underlying disease and high possibility of recurrence.

Last full review/revision July 2011 by William B. Thomas, DVM, MS, DACVIM (Neurology); 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; Karen R. Munana, DVM, MS, DACVIM (Neurology); T. Mark Neer, DVM, DACVIM; Charles E. Rupprecht, VMD, MS, PhD; Robert Wylie, BVSc, QDA