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Ischemic resistance of cutaneous afferents and motor axons in patients with amyotrophic lateral sclerosis
Author(s) -
Mogyoros Ilona,
Kiernan Matthew C.,
Burke David,
Bostock Hugh
Publication year - 1998
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(199812)21:12<1692::aid-mus11>3.0.co;2-x
Subject(s) - amyotrophic lateral sclerosis , medicine , ischemia , hyperpolarization (physics) , motor nerve , refractory period , depolarization , diabetes mellitus , cardiology , anesthesia , endocrinology , anatomy , disease , chemistry , organic chemistry , nuclear magnetic resonance spectroscopy
Compared with control subjects, patients with amyotrophic lateral sclerosis (ALS) have been reported to experience less or no paresthesias during and after release of ischemic compression of the upper arm for 10 min. This is reminiscent of the resistance to ischemia of diabetic patients, in whom sensory and motor axons undergo less ischemic depolarization and less postischemic hyperpolarization than in control subjects. The present study compared the changes in axonal excitability produced by ischemia for 10 min in 21 patients with ALS and 14 age‐matched control subjects. Fewer patients reported intraischemic or postischemic paresthesias and the intensity of paresthesias was less, but this was significant only for postischemic paresthesias. There were quantitatively similar changes in refractoriness, supernormality, and strength‐duration time constant during ischemic compression, but the increase in excitability of motor axons was less during the second half of ischemia in the patients. After release of ischemia the postischemic hyperpolarization was greater in the ALS patients, the opposite of what occurs in diabetes. These changes could reflect reduced intraneural K + accumulation due to loss of motor axons or an alteration in nerve metabolism or membrane properties. Either way, the present study has failed to confirm previous reports of “ischemic resistance” in ALS, and indicates that the changes in axonal properties in ALS are not analogous to those in diabetes mellitus. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 1692–1700, 1998