hereditary sensory and motor neuropathy/fever

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[Limb myokymia with involuntary finger movement caused by peripheral neuropathy due to systemic lupus erythematosus (SLE)--a case report].

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A 24-year-old woman with SLE since the age of 12 developed sensory-motor peripheral neuropathy in 1990. Her sensory neuropathy was symmetrical in all limbs and distally dominant. Electrophysiological study showed marked reduction of motor and sensory conduction velocities. Sural nerve biopsy

Acute disseminated encephalomyelitis in a female with hereditary neuropathy with susceptibility to pressure palsy.

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A 7-year-old female presented with fever, urinary incontinence, mental regression, gait disturbance, and lethargy after diarrhea. Magnetic resonance imaging revealed multifocal T(2)-weighted hypersignal lesions supportive of acute disseminated encephalomyelitis. Her mother had been diagnosed with

Miller-Fisher syndrome associated with chronic lymphocytic leukemia.

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Chronic lymphocytic leukemia (CLL) is a frequent hematological malignancy, with meningeal or peripheral nerve infiltrations being the most commonly encountered neurological complications. In this report, we describe a CLL patient with Miller-Fisher syndrome (MFS) who responded to immune modulation

Anesthetic Management of a Patient With Charcot-Marie-Tooth Disease.

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Charcot-Marie-Tooth disease (CMTD) is a hereditary peripheral neuropathy and is characterized by progressive muscle atrophy and motor-sensory disorders in all 4 limbs. Most reports have indicated that major challenges with general anesthetic administration in CMTD patients are the appropriate use of

Molecular genetics and clinical aspects of inherited disorders of nerve and muscle.

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Rapid progress has been made in elucidating the molecular genetic basis of several neuromuscular disorders in the past year. Candidate genes have been identified or analysed in hereditary motor and sensory neuropathy (HMSN) type I, X-linked bulbospinal neuronopathy and non-dystrophic myotonic

Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.

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BACKGROUND Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and

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