Treatment of peripheral neuropathies.

Hallett, Mark; Tandon, Deepak S.; Berardelli, Alfredo

doi:10.1136/jnnp.48.12.1193

Cited by 18 publications

(6 citation statements)

References 226 publications

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“…these patients often become addicted to narcotics. 19 Antidepressants, continued being relatively nontoxic, should be considered for these patients. Neuroleptics such as carbamazepine (Tegretol)l 5 or phenytoin (Dilantln, Diphenylan Sodium) 20 are possible alternative treatments for chronic pain syndrome, since neither is habitforming or hJghly sedative.…”

Section: Treatment Of Thiamine Deftclencymentioning

confidence: 99%

Thiamine deficiency neuropathy

Skelton¹,

Skelton²

1989

Postgraduate Medicine

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Despite the fact that thiamine deficiency neuropathy is increasing in incidence in our society, it remains an underdiagnosed disorder. The typical complaints of weakness and burning feet are often regarded as trivial by the attending physician. Electrophysiologic studies are sensitive and often provide supportive evidence to aid in the diagnosis. Since chronic pain therapy is often ineffective, a high index of suspicion should be maintained to help ensure early diagnosis and successful intervention.

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Section: Treatment Of Thiamine Deftclencymentioning

confidence: 99%

Thiamine deficiency neuropathy

Skelton¹,

Skelton²

1989

Postgraduate Medicine

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“…In many cases, however, treatment directed toward the cause is not possible or effective, and management consists of treating complications, providing symptomatic treatment, and helping the patient adapt to his disability. 35 Where there is sensory loss, special care needs to be taken to avoid burns, other trauma, and pressure sores, all of which may turn into chronic ulcers. Physiotherapy can help prevent contractures in weak muscles, and judicious use of exercise, heat, and massage can help pain and aid function.…”

Section: Treatmentmentioning

confidence: 99%

The Aging Neuromuscular System

Baker¹

1989

Semin Neurol

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Symptoms and signs suggestive of neuromuscular dysfunction are very common in old age but do not necessarily indicate definable neurologic disease. The frail, wasted hands seen in an 80-year-old person may, as in a younger patient, indicate a diabetic neuropathy or amyotrophic lateral sclerosis (ALS), but after investigation the clinician is often left with the conclusion that this finding is simply due to "old age." Frequently, the cause is multifactorial, and neuromuscular function may be influenced by disorders affecting various levels of the neuraxis, as well as by disease and age-related factors outside the nervous system, such as changes in cardiopulmonary function, nutrition, and the endocrine system. Often the distinction between age changes and disease is blurred and consequently a different approach is required in assessing abnormal neurologic findings.Common symtoms reported by the elderly are muscle weakness, slowness of movement, fatigue, impaired fine coordination, muscle pain and cramps, loss of or disordered sensation, and pain. On examination, frequent findings are muscle wasting and weakness, loss of sensation, hypersensitivity, areflexia, and orthostatic hypotension. CHANGES IN THE NEUROMUSCULAR SYSTEM IN NORMAL AGING THE SENSORY UNITClinical studies have shown an increase with age in touch-pressure thresholds in the index fingeri and impairment of cutaneous thermal discriminati~n.~ Vibration sense diminishes after the age of 50 years, especially in the feet,3 and there is commonly a decline in proprioceptive f e e d b a~k .~ Special senses, including smell, taste, and hearing, also deteriorate with age, but discussion of these is beyond the scope of this review. Pathologic changes at various levels of the peripheral or central nervous system could account for the abnormalities in sensation and, for example, impaired vibration sense in the feet could be due to loss of pacinian corpuscles, demyelination of peripheral nerves, nerve root disease, spondylosis, impaired blood supply to the spinal cord, or dysfunction in central sensory systems. It is likely, however, that the primary sensory neuron or the peripheral receptors, or both, are principally involved (see Spencer and 0choa5 for review). The neuronal cell bodies in dorsal root ganglia and cranial ganglia show structural changes or drop-out with age and consequently there is loss of their nerve fibers in peripheral nerves, sensory roots, and posterior columns. Lumbosacral roots are more affected than cervical roots. Morphologic studies of peripheral nerves reveal increased evidence in old age of demyelination and, more particularly, remyelination, and also degeneration of unmyelinated and myelinated fibers and "empty" Schwann cell columns.' These changes in peripheral nerves are reflected by abnormalities on nerve conduction tests. The amplitude of sensory action potentials decreases from the third decade, and there is a lesser decline in conduction velocities, this being more pronounced across segments subject to chronic entrapment. Measure...

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“…Pain resulting from peripheral nerve damage is particularly difficult to treat. In this condition, called deafferentation pain, the pain-conduction pathways are interrupted, making the usual methods of pain control U~S U C C~S S~U~.~~~ 54 The mechanism by which antidepressants act in this syndrome is unknown.…”

Section: Neurologic Painmentioning

confidence: 99%

Antidepressants in the Management of Chronic Pain Syndromes

Egbunike,

Chaffee

1990

Pharmacotherapy

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Conditions in which antidepressants have been used include diabetic neuropathy, postherpetic neuralgia, headaches, arthritis, chronic back pain, cancer, thalamic pain, facial pain, and phantom limb pain. Although much of the available information is derived from inadequately controlled trials, it seems that antidepressants provide analgesia in many of these disorders. The analgesic effects tend to be independent of antidepressant effects, and doses of heterocyclic antidepressants used for analgesia seem to be lower than those considered effective in the treatment of depression. Doses should be started low and gradually increased until the patient reaches the highest tolerable dose. Onset of analgesia is variable, ranging from 1 day to 10 weeks. Common side effects include dry mouth, drowsiness, urinary retention, orthostatic hypotension, and constipation. Optimum dosages and schedules have not been established.

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Treatment of peripheral neuropathies.

Cited by 18 publications

References 226 publications

Thiamine deficiency neuropathy

Thiamine deficiency neuropathy

The Aging Neuromuscular System

Antidepressants in the Management of Chronic Pain Syndromes

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