3 Peripheral Nerve Disease
Injury to a single or group of peripheral nerves (i.e., brachial plexus) causes weakness or paralysis of the muscles innervated by those nerves, loss of spinal reflexes, and rapid muscle atrophy. If the injury occurred before muscle atrophy is noticeable, the muscles will feel flaccid when palpated.
Animals with generalized peripheral nerve disease appear weak and poorly muscled, and have diminished or absent spinal reflexes. With the exception of the optic nerve, cranial nerves are peripheral nerves and are susceptible to the same diseases as spinal nerves. Therefore laryngeal paralysis, weak gag responses, facial paralysis, atrophy of the muscles of mastication, and abnormal pupillary light reflexes may be seen as well.
The clinical signs of generalized peripheral nerve disease and muscle disease overlap considerably. It often requires laboratory testing to distinguish between these. With most, but not all muscle diseases, there will be increased serum concentrations of creatine kinase. Electrophysiologically, both neuropathies and myopathies cause abnormal electromyographic spontaneous activity. However, nerve conduction velocities are normal in myopathies. If electrophysiologic tests are not available, muscle biopsy histology will distinguish the two. With peripheral nerve injury, there will be angular atrophy of both type I and type II myofibers. With primary muscle disease, pathology specific to the type of myopathy will be seen.
It is best to break these down into acute or chronic in onset. With acute monoparesis, trauma is the most common cause. This can be due to specific nerve injury or to avulsion of the brachial plexus during extreme abduction of the limb. Avulsion of the pelvic plexus is much less common.
In cases of chronic, progressive monoparesis, neoplastic infiltration by nerve sheath tumors or entrapment of the peripheral nerves by surrounding neoplastic growths is common.
Yes and no. Certainly peripheral axons are capable of regeneration. However, they do so slowly, at the rate of about 1 to 2 mm per day. Therefore functional regeneration is more likely with distal injuries. Injuries in which the nerve is not completely severed (e.g., crush injury or stretch injury) have a much better prognosis than complete transections mainly because the conduits through which regenerating axons can regrow are still intact. If the nerve has been completely transected, it is very difficult for regenerating axons to find appropriate channels to enable functional regrowth.
For a limb to be functional, the radial nerve must be intact. Unfortunately, this nerve is usually injured with cranial plexus avulsions (injuring nerve roots C6-C8) or caudal plexus avulsions (injuring nerve roots C8-T2) and complete avulsions. In all cases of closed peripheral nerve trauma, there are some fibers that are stretched, but not transected. It is therefore important to wait for a minimum of 4 to 6 weeks to see how much functional return will occur. If the animal is unable to fix the elbow in extension, then salvage procedures for the limb are of little use. Limb amputation should be considered if self-mutilation or trauma occurs in areas without sensation.
In the early stages, nerve sheath tumors can easily be confused with orthopedic problems. Presence of a Horner’s syndrome or loss of panniculus response on the side of the lameness generally indicates nerve damage. Denervation muscle atrophy can be distinguished from disuse muscle atrophy electromyographically.
Computed tomography has been helpful in identifying tumors of peripheral nerves. Occasionally, enlarged nerve roots can be identified with ultrasonography. However, a definitive diagnosis requires surgical exploration and biopsy of the nerves involved. Wide surgical excision has resulted in complete cures in isolated cases. However, tumors usually recur because not all neoplastic cells can be removed. Radiation therapy has been proposed to decrease the incidence of recurrence. However, the efficacy of this therapy is not known.
