Volume 21, Issue 12 pp. 1692-1700
Main Article

Ischemic resistance of cutaneous afferents and motor axons in patients with amyotrophic lateral sclerosis

Ilona Mogyoros MD, PhD

Corresponding Author

Ilona Mogyoros MD, PhD

Department of Neurology, Prince of Wales Hospital, University of New South Wales and Prince of Wales Medical Research Institute, High Street, Randwick, N.S.W. 2031, Australia

Department of Neurology, Prince of Wales Hospital, University of New South Wales and Prince of Wales Medical Research Institute, High Street, Randwick, N.S.W. 2031, AustraliaSearch for more papers by this author
Matthew C. Kiernan PhD, FRACP

Matthew C. Kiernan PhD, FRACP

Department of Neurology, Prince of Wales Hospital, University of New South Wales and Prince of Wales Medical Research Institute, High Street, Randwick, N.S.W. 2031, Australia

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David Burke MD, DSc

David Burke MD, DSc

Department of Neurology, Prince of Wales Hospital, University of New South Wales and Prince of Wales Medical Research Institute, High Street, Randwick, N.S.W. 2031, Australia

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Hugh Bostock PhD

Hugh Bostock PhD

Department of Neurology, Prince of Wales Hospital, University of New South Wales and Prince of Wales Medical Research Institute, High Street, Randwick, N.S.W. 2031, Australia

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Abstract

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

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