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DOI 10.1016/j.clinph.2013.02.115

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2013

Myopathic EMG findings and type II muscle fiber atrophy in patients with Lambert-Eaton myasthenic syndrome.

Crone Clarissa, Christiansen Ingelise, Vissing John

Клинический случайСтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVE

Lambert-Eaton myasthenic syndrome (LEMS) is a rare condition, which may mimic myopathy. A few reports have described that EMG in LEMS may show changes compatible with myopathy, and muscle biopsies have been described with type II as well as type I atrophy. The EMG results were, however, based on qualitative EMG examination and the histopathological methods were not always clear. The objective of this study was to investigate if the previous EMG findings could be confirmed with quantitative EMG (QEMG) and to describe muscle histology in LEMS.

METHODS

QEMG, nerve conduction studies and muscle biopsy were performed in four consecutive LEMS patients.

RESULTS

QEMG showed significantly decreased mean MUP duration and muscle biopsy showed marked type II fiber atrophy.

CONCLUSION

EMG and biopsy abnormalities mimicking myopathy may often be found in patients with LEMS.

SIGNIFICANCE: LEMS is a debilitating, but treatable disease, which often precedes detection of a malignancy and it is therefore of obvious importance to diagnose these patients with speed and certainty. Hence it is important that neurophysiologists and neurologists are aware that EMG and histological abnormalities mimicking myopathy may be found in LEMS patients so that these findings do not prolong or misdirect the diagnostic process in these patients.

Для цитирования: Crone Clarissa, Christiansen Ingelise, Vissing John. Myopathic EMG findings and type II muscle fiber atrophy in patients with Lambert-Eaton myasthenic syndrome.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2013. DOI: 10.1016/j.clinph.2013.02.115.

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