Abstract |
We investigated the mechanism of cramps in 2 patients: a 48-year-old man with bulbospinal neuronopathy, and a 46-year-old man with amyotrophic lateral sclerosis. Cramps were quite easily induced by volitional exertion and high-frequency stimulation of the peripheral nerves. When an ulnar nerve was blocked with lidocaine at the elbow, no cramp was induced despite the application of high-frequency stimulation at the wrist. Diazepam (GABAA agonist) was effective in the first patient and baclofen (GABAB agonist) in the second, with no cramps induced in spite of increasing stimulation intensity. Impairment of interneurons mediated by GABA as the neurotransmitter is thought to be involved in the mechanism of the cramps.
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Authors | T Obi, K Mizoguchi, H Matsuoka, M Takatsu, Y Nishimura |
Journal | Muscle & nerve
(Muscle Nerve)
Vol. 16
Issue 11
Pg. 1228-31
(Nov 1993)
ISSN: 0148-639X [Print] United States |
PMID | 8413375
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- GABA Antagonists
- Levodopa
- gamma-Aminobutyric Acid
- Lidocaine
- Baclofen
- Clomipramine
- Diazepam
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Topics |
- Amyotrophic Lateral Sclerosis
(complications, physiopathology)
- Baclofen
(pharmacology)
- Clomipramine
(pharmacology)
- Diazepam
(pharmacology)
- Electric Stimulation
- Evoked Potentials
(drug effects, physiology)
- GABA Antagonists
- Humans
- Levodopa
(pharmacology)
- Lidocaine
- Male
- Middle Aged
- Motor Neurons
(drug effects, physiology)
- Muscle Cramp
(etiology, physiopathology)
- Muscular Atrophy, Spinal
(complications, physiopathology)
- Nerve Block
- Neural Conduction
(drug effects, physiology)
- Sensory Thresholds
(drug effects, physiology)
- Ulnar Nerve
(drug effects, physiopathology)
- gamma-Aminobutyric Acid
(physiology)
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