Clinical neurophysiology of demyelinating polyneuropathy.

Demyelinating neuropathies are remarkably varied in their clinical characteristics: In etiology they may be inherited or acquired, in their time course, acute or chronic, and in their distribution, multifocal or generalized. They present with phenotypes that range from an indolent disorder that begins in childhood and progresses slowly over decades (as might be seen in an inherited form) and leads to weakness but preserved ambulation, to a neuropathy with fulminant onset and rapid progression culminating in tetraparesis and respiratory failure (as seen in the Guillain-Barre syndrome). Often demyelinating neuropathies are amenable to treatment that greatly reduces the burden of disease and extent of disability.

Developing multidisciplinary clinics for neuromuscular care and research.

Multidisciplinary care is considered the standard of care for both adult and pediatric neuromuscular disorders and has been associated with improved quality of life, resource utilization, and health outcomes. Multidisciplinary care is delivered in multidisciplinary clinics that coordinate care across multiple specialties by reducing travel burden and streamlining care. In addition, the multidisciplinary care setting facilitates the integration of clinical research, patient advocacy, and care innovation (e.

A standardized clinical evaluation of phenotypic diversity in diabetic polyneuropathy.

Diabetic polyneuropathy (DPN) is a major cause of neuropathic pain and a frequent target condition in analgesic treatment trials. Differences in the clinical symptoms and signs associated with DPN suggest distinct pathophysiological mechanisms underlying nerve damage and dysfunction that are likely to have therapeutic relevance. The aim of this study was to develop a tool for the bedside assessment of painful neuropathies such as DPN that captures the diversity of phenotypes.

Case Records of the Massachusetts General Hospital. Case 30-2015: A 50-Year-Old Man with Cardiogenic Shock.

A 50-year-old man with a history of cardiomyopathy and progressive muscle weakness was admitted with cardiogenic shock. Electroencephalography showed total suppression of cerebral activity; ventilator support was withdrawn, and he died. An autopsy was performed.