This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

David A. Krendel, MD
The Emory Clinic Section of Neurology 1365 Clifton Rd NE Atlanta, GA 30322

Arch Neurol. 1992;49(11):1111.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?