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Corticomotor threshold is reduced in early sporadic amyotrophic lateral sclerosis
Author(s) -
Mills Kerry R.,
Nithi Kannan A.
Publication year - 1997
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199709)20:9<1137::aid-mus7>3.0.co;2-9
Subject(s) - amyotrophic lateral sclerosis , upper motor neuron , motor neuron , neuroscience , lower motor neuron , transcranial magnetic stimulation , motor cortex , medicine , lesion , spinal cord , stimulation , psychology , pathology , disease
The pathogenesis of idiopathic amyotrophic lateral sclerosis (ALS) remains unknown, but accumulating evidence suggests a neu roexcitotoxic mechanism may have some credence. Glutamate‐induced hyperexcitability of cortical or spinal motoneurons may be expected to manifest itself as a reduced threshold for activation of these structures. We have measured corticomotor threshold to the first dorsal interosseous (FDI) muscles of 48 patients with sporadic ALS using magnetic brain stimulation and have correlated the findings with physical signs of upper and/or lower motor neuron degeneration. We find that if FDI in patients with ALS shows no weakness, wasting, or signs of an upper motor neuron lesion, mean corticomotor threshold is significantly lower than in 102 healthy control FDI muscles ( P = 0.02). In contrast, FDI muscles showing signs of lower motor neuron degeneration only or mixed upper and lower motor neuron signs are associated with a raised corticomotor threshold ( P = 0.008, P < 0.001, respectively). We conclude that early in ALS, at a time when hand muscle function is normal, corticomotor threshold is reduced and suggest that this may be a manifestation of abnormal excitability of cortical or spinal motoneurons to neurotransmitters, whose action will ultimately lead to cell death. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 1137–1141, 1997