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November 1992

Mitochondrial Myopathy or Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)?

Author Affiliations

The Emory Clinic Section of Neurology 1365 Clifton Rd NE Atlanta, GA 30322

Arch Neurol. 1992;49(11):1111. doi:10.1001/archneur.1992.00530350021008

To the Editor.  —Bernsen and coworkers1 recently described a patient in whom they found a defect in mitochondrial complex 1 and carnitine deficiency in skeletal muscle. However, the clinical features of their patient suggest CIDP. These features include the course (progression over 3 months from normal to severely disabled); areflexia; slowing of motor nerve conduction to a degree that suggested primary demyelination (presuming compound muscle action potential amplitudes were not significantly decreased—information not provided in the article)2; and the elevated level of the cerebrospinal fluid protein. Proximal weakness is not uncommon in CIDP. Normal sensory conduction does not exclude the diagnosis, and, although normal histologic appearance of the sural nerve is unusual, it should not be incompatible with CIDP since the lesions are commonly multifocal and may preferentially involve motor fibers. The targetoid fibers and small angular fibers in the soleus muscle suggest denervation.Convincing evidence of myopathy

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