The differential diagnosis for cranial and peripheral nerve disorders includes trauma, inflammatory (or infectious), idiopathic (immunologic) and neoplastic diseases. The facial nerve is susceptible to trauma at the angle of the jaw. The radial nerve can be damaged by trauma as it passes laterally along the humerus in the musculospiral groove. The sciatic nerve can be damaged secondary to pelvic fractures. All cranial and peripheral nerves can be affected by neoplasia including neurofibromas, neurofibrosarcomas, schwannomas and lymphosarcoma. Immune attack against the neural-specific proteins in cranial and peripheral nerves is not infrequent and leads to either specific cranial neuropathies or polyradiculopathy.
Trigeminal neuritis (an immune disorder affecting the myelinated pathways in the trigeminal nerve) is usually transient, but can present as a significant problem. The cardinal signs of trigeminal neuritis if a dropped jaw with the inability to close the mouth. It affects adult dogs and cats with no breed or sex predilection. It must be differentiated from fracture or subluxation of the temporomandibular joint (evaluated by skull radiographs). On pathologic examination, there is bilateral nonsuppurative neuritis of the trigeminal nerve. As an idiopathic immune-related disorder, the condition will usually improve over 1-3 weeks. On the other hand, methylprednisolone therapy may help reduce the severity of an attack. Additional measures includes the use of antioxidant medications such as vitamin E and C, n-acetylcysteine and ginkgo biloba. These latter measures may help prevent reoccurrence of episodes, which are occasionally seen. Other measures including feeding liquified food and/or introduction of a PEG tubes to support nutrition while the neuritis slowly responds. Some have supported the patients nutrition by placing a wide rubber band around the mouth (which helps close the mouth) while the patient is allowed to eat.
Masseter and temporalis myositis is a chronic progressive disease which presents with acute exacerbations and remissions. It is an auto-immune disease directed at the unique antigenic markers of the muscles innervated by the trigeminal nerve. The cardinal signs of this myositis is the inability to open the jaw, which differentiates it from primary diseases of the trigeminal nerve. In the acute phase, there is elevation of serum muscle enzymes (CPK, AST, LDH and aldolase). On the CBC, there is often an elevation of eosinophils (giving the condition its name, eosinophilic myositis). On the other hand, in the chronic phase, the amount of remaining muscle and, therefore, the amount of inflammation are reduced. The diagnosis can be confirmed on muscle biopsy and determination of serum antibody titers to the 2M antigen. The treatment of acute masseter-temporalis myositis is with immunosuppressive medication. We use oral prednisolone at 1 mg/kg/day divided into 2 or 3 doses for 1-2 weeks, followed by 0.5 mg/kg/day for 1-3 weeks. There is no evidence to suggest that keeping patients on alternate day steroid therapy between attacks will reduce the chances for progression. Here is another area where using dietary supplements might be useful. In the chronic phase, the jaw may be locked shut. In these cases, it may be necessary to manually open the mouth under anesthesia. This may lead to fracture of the jaw. The hope is that, once the fibrosis is broken, the remaining muscle mass will allow enough function for the patient to be able to feed itself. The jaw must open about 1-1.5 inches for this to happen.
Acute unilateral or bilateral facial nerve paralysis may be seen in adult dogs, particularly in the cocker spaniel. There are no other signs of neurologic disease. There is no evidence of otitis on physical, neurologic or radiographic examination. EMG changes (fibrillation potentials and positive sharp waves) are usually present in the muscle innervated by the facial nerve, only. There is no therapy; but, if attention is given to supporting tear production, the animal does not appear to have difficulty living with its deficits. It is felt that this represents an autoimmune disease and immune therapy may be indicated.
This disorder can affect any age, breed or sex of dog or cat, although the condition is rare before the age of 6 months. The onset of signs begins as rear leg weakness which rapidly ascends over 24-48 hours until the animal is quadriplegic. Occasionally, the condition can start in the fore legs and then progress to quadriplegia. Physical examination is usually within normal limits (an old raccoon bite might be apparent in hounds). Usually, there are no cranial nerve signs; however, in severe cases, the bark may be altered, swallowing impaired and facial nerve signs be evident. In some cases, respiration is impaired necessitating respiratory support.
The diagnosis is supported by finding mild elevation of CSF protein, particularly from lumbar spinal tap. The EMG reveals denervation potentials (fibrillation potentials and positive sharp waves). The motor conduction velocity is usually slower (< 50 M/sec), particularly later in the course of the disease.
There is no specific treatment for polyradiculopathy. Corticosteroid therapy may reduce the recovery time, but have not been shown to reduce the time to reach maximal severity nor the eventual severity of the disease. Recent evidence, support a role of antioxidant steroids (methylprednisolone) in reducing clinical signs. When respiratory depression is evident, this may be helpful in treating the patient. The clinical course is variable and may last from a few days to several weeks. In some cases, there are permanent neurologic deficits. Recovered animals may have the condition reoccur. Recurrences are often more severe than the initial incident. Some cases become chronic in nature, requiring more aggressive medication in hopes of controlling the problem. I have found that many of these patients respond better to antioxidant therapy with drugs like acetylcysteine or ginkgo biloba than to steroid medication alone.
The diagnosis may be confirmed by EMG examination in 5-7 days. The evidence of denervation will be evident. If there is no nerve conduction 72 hours after the injury, then avulsion is most likely.
Treatment is with time, physical therapy and protection from injury.
If there is no problem with the leg, then amputation is not warranted until,
at least, 6 months of time has past. On the other hand, if the leg gets
infected or troubles the patient, amputation may help the patient. Serial
neurologic assessments and EMG examinations may help determine the ultimate
prognosis. Some patients experience "tingling" of the foot as healing occurs.
These patients can attack the foot causing considerable self-mutilation,
even months after the initial injury.
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Last updated 27 August 2002