Archive for the ‘Peripheral Neuropathies’
Bell’s palsy is an idiopathic facial paresis of lower motor neuron type that has been attributed to an inflammatory reaction involving the facial nerve near the stylomastoid foramen or in the bony facial canal. A relationship of Bell’s palsy to reactivation of herpes simplex virus has recently been suggested, but there is little evidence to support this.
The clinical features of Bell’s palsy are characteristic. The facial paresis generally comes on abruptly, but it may worsen over the following day or so. Pain about the ear precedes or accompanies the weakness in many cases but usually lasts for only a few days. The face itself feels stiff and pulled to one side. There may be ipsilateral restriction of eye closure and difficulty with eating and fine facial movements. A disturbance of taste is common, owing to involvement of chorda tympani fibers, and hyperacusis due to involvement of fibers to the stapedius occurs occasionally.
The management of Bell’s palsy is controversial. Approximately 60% of cases recover completely without treatment, presumably because the lesion is so mild that it leads merely to conduction block. Considerable improvement occurs in most other cases, and only about 10% of all patients are seriously dissatisfied with the final outcome because of permanent disfigurement or other long-term sequelae. Treatment is unnecessary in most cases but is indicated for patients in whom an unsatisfactory outcome can be predicted. The best clinical guide to progress is the severity of the palsy during the first few days after presentation. Patients with clinically complete palsy when first seen are less likely to make a full recovery than those with an incomplete one. A poor prognosis for recovery is also associated with advanced age, hyperacusis, and severe initial pain. Electromyography and nerve excitability or conduction studies provide a guide to prognosis but not early enough to aid in the selection of patients for treatment.
The only medical treatment that may influence the outcome is administration of corticosteroids, but studies supporting this concept have been criticized. Many physicians nevertheless routinely prescribe corticosteroids for patients with Bell’s palsy seen within 5 days of onset. The author prescribes them only when the palsy is clinically complete or there is severe pain. Treatment with prednisone, 60 or 80 mg daily in divided doses for 4 or 5 days, followed by tapering of the dose over the next 7–10 days, is a satisfactory regimen. It is helpful to protect the eye with lubricating drops (or lubricating ointment at night) and a patch if eye closure is not possible. There is no evidence that surgical procedures to decompress the facial nerve are of benefit.
An individual nerve may be injured along its course or may be compressed, angulated, or stretched by neighboring anatomic structures, especially at a point where it passes through a narrow space (entrapment neuropathy). The relative contributions of mechanical factors and ischemia to the local damage are not clear. With involvement of a sensory or mixed nerve, pain is commonly felt distal to the lesion. Symptoms never develop with some entrapment neuropathies, resolve rapidly and spontaneously in others, and become progressively more disabling and distressing in yet other cases. The precise neurologic deficit depends on the nerve involved. Percussion of the nerve at the site of the lesion may lead to paresthesias in its distal distribution.
Entrapment neuropathy may be the sole manifestation of subclinical polyneuropathy, and this must be borne in mind and excluded by nerve conduction studies. Such studies are also indispensable for the accurate localization of the focal lesion.
In patients with acute compression neuropathy such as Saturday night palsy, no treatment is necessary. Complete recovery generally occurs, usually within 2 months, presumably because the underlying pathology is demyelination. However, axonal degeneration can occur in severe cases, and recovery then takes longer and may never be complete. In chronic compressive or entrapment neuropathies, avoidance of aggravating factors and correction of any underlying systemic conditions are important. Local infiltration of the region about the nerve with corticosteroids may be of value; in addition, surgical decompression may help if there is a progressively increasing neurologic deficit or if electrodiagnostic studies show evidence of partial denervation in weak muscles. Generic Drugs Online
Peripheral nerve tumors are uncommon, except in Recklinghausen’s disease, but also give rise to mononeuropathy. This may be distinguishable from entrapment neuropathy only by noting the presence of a mass along the course of the nerve and by demonstrating the precise site of the lesion with appropriate electrophysiologic studies. Treatment of symptomatic lesions is by surgical removal if possible. Read the rest of this entry »
Neuropathies Associated With Systemic & Metabolic Disorders
A. Diabetes Mellitus: In this disorder, involvement of the peripheral nervous system may lead to symmetric sensory or mixed polyneuropathy, asymmetric motor neuropathy (diabetic amyotrophy), thoracoabdominal radiculopathy, utonomic neuropathy, or isolated lesions of individual nerves. These may occur singly or in any combination.
Sensory polyneuropathy, the most common manifestation, may lead to no more than depressed tendon reflexes and impaired appreciation of vibration in the legs. When symptomatic, there may be pain, paresthesias, or numbness in the legs, but in severe cases distal sensory loss occurs in all limbs. Diabetic amyotrophy is characterized by asymmetric weakness and wasting involving predominantly the proximal muscles of the legs, accompanied by local pain.
Online Canada Drugs Thoracoabdominal radiculopathy leads to pain over the trunk. In patients with autonomic neuropathy, postural hypotension, impaired thermoregulatory sweating, postgustatory hyperhidrosis, constipation, flatulence, diarrhea, impotence, urinary retention, and incontinence may occur, and there may be abnormal pupillary responses. Isolated lesions of individual peripheral nerves are common and in the limbs tend to occur at sites of compression or entrapment. Treatment is symptomatic. Entrapment neuropathies may be helped by surgical decompression.
Treatment of neuropathic pain is discussed above.
B. Uremia: Uremia may lead to a symmetric sensorimotor polyneuropathy that tends to affect the lower limbs more than the upper limbs and is more marked distally than proximally. The diagnosis can be confirmed electrophysiologically, for motor and sensory conduction velocity is moderately reduced. The neuropathy improves both clinically and electrophysiologically with renal transplantation and to a lesser extent with chronic dialysis. Buy Online Generic Viagra Read the rest of this entry »
Peripheral neuropathies are classified on the basis of the structure that is primarily affected. The predominant pathologic feature may be axonal degeneration (axonal or neuronal neuropathies) or paranodal or segmental demyelination. The distinction may be possible on the basis of neurophysiologic findings. Motor and sensory conduction velocity can be measured in accessible segments of peripheral nerves. In axonal neuropathies, conduction velocity is normal or reduced only mildly and needle electromyography provides evidence of denervation in affected muscles. In demyelinating neuropathies, conduction may be slowed considerably in affected fibers, and in more severe cases, conduction is blocked completely, without accompanying electromyographic signs of denervation.
Peripheral neuropathies may also occur as a result of disorders affecting the connective tissues of the nerves or the blood vessels supplying the nerves, but these are much less common than the preceding varieties. Buy Celexa
Nerves may be injured or compressed by neighboring anatomic structures at any point along their course. Common mononeuropathies of this sort are considered below. They lead to a sensory, motor, or mixed deficit that is restricted to the territory of the affected nerve. A similar clinical disturbance is produced by peripheral nerve tumors, but these are rare except in patients with Recklinghausen’s disease. Multiple mononeuropathies suggest a patchy multifocal disease process such as vasculopathy (eg, diabetes, arteritis), an infiltrative process (eg, leprosy, sarcoidosis), radiation damage, or an immunologic disorder (eg, brachial plexopathy). Diffuse polyneuropathies lead to a symmetric sensory, motor, or mixed deficit, often most marked distally. They include the hereditary, metabolic, and toxic disorders; idiopathic inflammatory polyneuropathy (Guillain-Barre Guillain-Barré syndrome); and the peripheral neuropathies that may occur as a nonmetastatic complication of malignant diseases. Involvement of motor fibers leads to flaccid weakness that is most marked distally; dysfunction of sensory fibers causes impaired sensory perception. Tendon reflexes are depressed or absent. Paresthesias, pain, and muscle tenderness may also occur. Read the rest of this entry »