The most common entrapment neuropathies are discussed below. For the most part, the nerve damage is reversible, and referral to the appropriate specialist for relief on entrapment is necessary.
Carpal tunnel syndrome (CTS) is the most commonly seen entrapment neuropathy. Patients describe intermittent pain and/or numbness in the thumb and first two fingers, prominently at night. Symptoms frequently awaken the patient from sleep, occur in both hands independently, and may be poorly localized (i.e., numbness is often described going up to the elbow). The symptoms usually can be reproduced by compression of the nerve over the carpal tunnel or by tapping on the nerve, although these signs are neither sensitive nor specific. Occasionally, these symptoms are mistaken for cerebrovascular disease until a history of bilateral, repeated, and stereotypical nocturnal occurrence is obtained. When symptoms become long-standing and severe, weakness of the thenar musculature develops. Wrist splints worn at night are useful in the conservative management of CTS. Patients should be referred to a hand surgeon as an outpatient for further diagnostics and management. A carpal tunnel release may be performed in patients who fail to respond to conservative management.
Ulnar nerve entrapment, usually occurring at the elbow, produces numbness in the fifth digit and medial half of the fourth finger, but symptoms are frequently poorly localized. Weakness and wasting of the hypothenar muscles occur very late in the course. The patient should be referred to a specialist for electrodiagnostic confirmation because occasionally C8 radiculopathy can mimic this common condition. Severe cases are treated surgically with ulnar nerve transposition.
Entrapment of the deep peroneal nerve at the fibular head can cause footdrop and numbness of the web between the great and second toes. This condition occurs in the setting of injury to the leg, rapid weight loss, or habitual crossing of the legs. Peroneal entrapment should be confirmed by EMG to be differentiated from lumbar root disease or motor neuron disease. Almost all cases are treated conservatively and improve without specific therapy.
Meralgia paresthetica is entrapment of the lateral cutaneous nerve of the thigh. The diagnosis is often overlooked in the ED, being mistaken for a hip-related orthopedic disorder. Patients describe numbness and dysesthesias of the lateral aspect of the upper leg. This occurs after weight loss and notably following pelvic surgery or obstetric procedures where the legs are abducted and flexed for a prolonged period of time. Tricyclic antidepressants (TCA) are useful in the management of the dysesthesias associated with meralgia paresthetica. The condition resolves without sequelae and requires no specific therapy.
Mononeuritis multiplex is a syndrome of multiple nerve dysfunctions caused by a vasculitis. Patients experience multiple deficits in a stepwise fashion, usually involving both sides of the body. For example, a patient may experience wristdrop on the right, followed by footdrop on the left, and then footdrop on the opposite side a few weeks later. This condition requires urgent referral to a neurologist to determine the etiology and initiate treatment, usually in collaboration with a rheumatologist. Frequently this disorder is caused by a systemic vasculitis, and a thorough serologic examination and nerve biopsy are required to establish specific treatment plans. The condition must be differentiated from multiple compression neuropathies and from multifocal motor neuropathy.
Bell's palsy should be viewed as a diagnosis of exclusion. It is the most common cause of acute facial paralysis but is similar to other processes that are important to recognize. Patients with Bell's palsy complain of sudden facial weakness, difficulty with articulation, problems keeping an eye closed, or inability to keep food in the mouth on one side. Because the seventh cranial nerve also serves other functions, the patient may have variable degrees of dry eye, metallic taste of the mouth, and facial pain, commonly around the ear. The examination is notable for one-sided weakness of the face involving the forehead. There may be decreased sensation along the external acoustic meatus (Hitselberger's sign). Other cranial nerves are normal. Diminished reflexes suggest a different diagnosis.
Several alternative diagnoses should be considered. Stroke can lead to sudden facial weakness that involves only the lower face but also leads to neurologic involvement below the neck or other cranial neuropathies. Lyme disease and GBS can cause facial paralysis, as discussed elsewhere in this chapter. In patients with cancer, facial weakness may herald the metastatic spread of malignancy. The ear should be inspected carefully to rule out ulcerations caused by cranial herpes-zoster activation (Ramsay Hunt syndrome), which should be treated with oral acyclovir. Facial paralysis also can be seen in sarcoidosis, collagen vascular disease, and polio. All patients with facial weakness should be screened for HIV risk factors, since seventh nerve palsy can occur at the time of seroconversion.
The treatment of Bell's palsy with steroids is controversial. While some believe that they have no role, most neurologists argue in favor of a short course of prednisone in individuals with low risk for complications from corticosteroids. The recommended dose is 50 mg per day for 7 days. More recent studies 3 have suggested that steroids in combination with acyclovir (200 mg five times a day for 10 days) leads to better outcomes. If the patient is seen more than a week after paresis began, steroids generally are not given.
Eye care must be meticulous to avoid corneal abrasions. Patients are instructed to tape the affected eye so that the palpebral fissure is narrowed to prevent drying of the cornea. Patients should apply Lacrilube and patch the eye before sleeping.
Lyme disease affects individuals exposed to the tick-born pathogen Borrelia burgdorferi. Although its neurologic manifestations are multiple, one of the most common sites of involvement is the peripheral nervous system.4 Patients often, but not always, report prior tick exposure and have spent time in areas known to have deer ticks. Initial manifestations of Lyme disease include arthralgias and fatigue. Neurologic complications ensue in the following weeks. A common neurologic sign of Lyme infection is seventh nerve palsy, which should not be confused with Bell's palsy. Lyme disease affects the peripheral nerves and the nerve roots. The patient may describe the acute or subacute progression of weakness and sensory loss, sometimes associated with radicular pain. On examination, the patient will have one of several signs. Unless there is encephalitis (a rare complication of Lyme disease), mental status will be normal. Apart from seventh nerve involvement, there may be weakness in the limbs, and if there is localized radicular inflammation, there will be a patchy myotomal pattern. Similarly, depending on the regional involvement of the disease, selected deep tendon reflexes will be diminished. Laboratory features suggestive of Lyme disease include serum and CSF Lyme antibodies. A CSF pleocytosis and increased protein with a normal glucose is the most common abnormality. When the diagnosis is made with confidence and other entities such as syphilis, carcinomatous meningitis, and sarcoidosis excluded, a 3-week course of intravenous antibiotics, either ceftriaxone or doxycycline, is given. Further discussion and treatment of Lyme disease are found in Chap 145.
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