Cerebral glucose utilization in motor neuron disease
J. M. Hoffman, J. C. Mazziotta, T. C. Hawk and R. Sumida
Division of Nuclear Medicine and Biophysics, UCLA School of Medicine.
Positron emission tomography with fluorodeoxyglucose 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.
