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John M. Hoffman, MD; John C. Mazziotta, MD, PhD; Thomas C. Hawk; Ron Sumida

Arch Neurol. 1992;49(8):849-854.

Abstract
• Positron emission tomography with fludeoxyglucose F 18 (¹⁸F-fluorodeoxyglucose) was used to examine regional cerebral glucose metabolism in individuals with motor neuron disease. Motor neuron disease involves selective loss of motor neurons, large pyramidal cells in the motor cortex, and corticospinal tract degeneration. We postulated that the local cerebral metabolic rate of glucose should correlate with this regional neuronal cell loss. Glucose metabolism values in patients with motor neuron disease were reduced compared with those of controls in several regions; however, when corrected for multiple comparisons, no significant difference was observed between patients with motor neuron disease and age-matched controls. No correlation was noted between the local cerebral metabolic rate of glucose and duration or severity of illness. Correlation between metabolic changes with objective findings on neurologic examination, including motor weakness and tendon reflexes, provided interesting results, including a decline in glucose metabolism with progressive weakness and upper motor neuron dysfunction. Moreover, in supplementary motor areas, there appears to be an increase in regional glucose metabolism as the neurologic condition deteriorates, possibly representing increased metabolic activity of the motor association cortex in response to primary loss of pyramidal cells.

Author Affiliations
From the Division of Nuclear Medicine and Biophysics (Drs Hoffman and Mazziotta and Messrs Hawk and Sumida) and the Department of Neurology (Drs Hoffman and Mazziotta), UCLA School of Medicine. Dr Hoffman and Mr Hawk are now with the Division of Nuclear Medicine, Department of Radiology, Duke University Medical Center, Durham, NC.

Footnotes
Accepted for publication March 23, 1992.

Reprint requests to the Division of Nuclear Medicine, Box 3949, Duke University Medical Center, Durham, NC 27710 (Dr Hoffman).

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