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Kinuko Suzuki, MD; Isabelle Rapin, MD

Arch Neurol. 1969;20(1):62-72.

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

THE application of electron microscopic techniques to the investigation of various neurological diseases has yielded significant contributions for understanding several classical diseases.^1,2 Furthermore, altered submicroscopic structures such as abnormal synapses and mitochondria were reported as the sole significant abnormality and presumably causal in some disorders. Gonatas and co-workers^3,4 found abnormal, enlarged presynaptic terminals in the cerebral cortex of two patients who had mental retardation and seizure disorders. Luft and co-workers⁵ demonstrated morphologically abnormal mitochondria in the skeletal muscle of a patient who had a hypermetabolic state of unknown etiology and they found a three to fourfold increase in total mitochondrial protein together with an increased cytochrome activity per unit of mitochondrial protein. Their conclusion was that this was a primary hypermetabolic state, caused by an abnormal quality and type of mitochondria. Following the report of Luft and co-workers, several further cases of myopathy with abnormal mitochondria . . . [Full Text PDF of this Article]

Author Affiliations
Bronx, NY

From the Department of Pathology (Neuropathology) and The Saul Korey Department of Neurology, Albert Einstein College of Medicine, and the Pediatric Neurology Service, Bronx Municipal Hospital Center, Bronx, NY.

Footnotes
Submitted for publication Aug 14, 1968; accepted Aug 29.

Read in part before the 43rd Annual Meeting of the American Association of Neuropathologists, Atlantic City, NJ, June 1967.

Reprint requests to Department of Pathology (Neuropathology), Hospital of the University of Pennsylvania, Philadelphia 19104 (Dr. Suzuki).

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