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Jose G. Romano, MD
Department of Neurology University of Miami/Jackson Memorial Hospital Suite 701 1150 NW 14th St Miami, FL 33136

Arch Neurol. 1996;53(8):716.

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

Glutamate-mediated excitotoxicity is one of the mechanisms responsible for motor neuron damage in amyotrophic lateral sclerosis. Decreased glutamate transport may result in elevated extracellular glutamate levels,¹ and both riluzole and gabapentin block presynaptic release of glutamine.² Riluzole prevents neuronal degeneration in vitro³ and delays progression of disease in patients with amyotrophic lateral sclerosis.⁴ Fasciculations, a hallmark of amyotrophic lateral sclerosis, are a manifestation of "sick" motor neurons. They typically decrease with progression of the disease.

While waiting for riluzole to be made available, we have been using gabapentin for our patients with amyotrophic lateral sclerosis with the expectation that it will act like riluzole in preventing progression of disease. Of 31 patients who were prescribed gabapentin, 10 reported a decrease in fasciculations within 2 weeks of reaching the dose of 300 mg 3 times a day. In 5 of these patients, the reduction was described as . . . [Full Text PDF of this Article]

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