A case of upper limb chronic motor axonopathy with reversal of conduction failure and activity-dependent conduction block after immunomodulatory treatment

We examined the effect of ischemia on nerve conduction in experimental diabetic neuropathy (EDN) and related electrophysiological changes to nerve adenosine triphosphate (ATP), creatine phosphate (CP), and lactate under anoxic conditions. Rats rendered diabetic with streptozotocin had a resistance to ischemic conduction block (RICB). Caudal nerve action potential (NAP) was well maintained for 10 min in controls and for 15 min in EDN, after which time NAP declined in both groups but more rapidly in normal rats. Time to 50% reduction in nerve ATP and CP was 10 and 3 min, respectively, in controls and delayed to 20 and 8 min in EDN. Rate of utilization of high-energy phosphate (approximately P) was linear for 5 min in controls to be followed by a progressive decline. In EDN rate of utilization of approximately P was linear to 15 min to be followed by a more gradual decline than in normal nerves. These findings suggest that the maintenance of nerve transmission in anoxic-ischemic states depends on anaerobic metabolism and that RICB in EDN is due in part to the ability of diabetic nerves to maintain a higher level of anaerobic glycolysis and for a longer time than normal nerves.

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Microstructural integrity of corticospinal and medial lemniscus tracts: insights from diffusion tensor tractography of right-hand amputees

Journal of Neurophysiology ◽

10.1152/jn.00316.2018 ◽

2019 ◽

Vol 122 (1) ◽

pp. 316-324 ◽

Cited By ~ 2

Author(s):

Huiling Peng ◽

Carmen M. Cirstea ◽

Christina L. Kaufman ◽

Scott H. Frey

Keyword(s):

White Matter ◽

Upper Limb ◽

Structural Integrity ◽

Diffusion Tensor ◽

Medial Lemniscus ◽

Residual Limb ◽

Healthy Control ◽

Continued Use ◽

Microstructural Integrity ◽

Activity Dependent

Reductions in sensory and motor activity following unilateral upper limb amputation during adulthood are associated with widespread, activity-dependent reorganization of the gray matter and white matter through the central nervous system. Likewise, in cases of congenital limb absence there is evidence that limited afferent or efferent activity affects the structural integrity of white matter pathways serving the affected side. Evidence that the structural integrity of mature sensory and motor tracts controlling the lost upper limb exhibits similar activity dependence is, however, sparse and inconsistent. Here we used diffusion tensor tractography to test whether amputation of the dominant right hand during adulthood ( n = 16) alters the microstructural integrity of the major sensory (medial lemniscus, ML) and motor (corticospinal tract, CST) pathways controlling missing hand function. Consistent with prior findings, healthy control subjects ( n = 27) exhibited higher fractional anisotropy (FA), an index of white matter microstructural integrity, within dominant left CST and nondominant right ML. Critically, in contrast to what might be expected if the microstructural organization of these tracts is activity dependent, these asymmetries persisted in amputees. Moreover, we failed to detect any differences in dominant left ML or CST between healthy control subjects and amputees. Our results are consistent with these white matter tracts being robust to changes in activity once mature or that continued use of the residual limb (in a compensatory fashion or with prosthesis) provides stimulation sufficient to maintain tract integrity. NEW & NOTEWORTHY We report that unilateral hand amputation in adults has no significant effects on the structure of major sensory or motor pathways contralateral to the amputation. Our results are consistent with the organization of these white matter tracts being robust to changes in activity once mature or that continued use of the residual limb (with or without a prosthesis) provides stimulation sufficient to maintain tract integrity.

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Role of Activity-Dependent Conduction Block in the Diagnosis of Primary Demyelinating Polyneuropathy

Journal of Clinical Neuromuscular Disease ◽

10.1097/cnd.0b013e3182596166 ◽

2012 ◽

Vol 14 (1) ◽

pp. 40-44 ◽

Cited By ~ 1

Author(s):

Johnny S. Salameh ◽

Nizar Souayah ◽

Peter S. T. Chong

Keyword(s):

Conduction Block ◽

Demyelinating Polyneuropathy ◽

Activity Dependent

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Loss of Potassium Homeostasis Underlies Hyperthermic Conduction Failure in Control and Preconditioned Locusts

Journal of Neurophysiology ◽

10.1152/jn.91174.2008 ◽

2009 ◽

Vol 102 (1) ◽

pp. 285-293 ◽

Cited By ~ 20

Author(s):

Tomas G. A. Money ◽

Corinne I. Rodgers ◽

Stuart M. K. McGregor ◽

R. Meldrum Robertson

Keyword(s):

Action Potential ◽

Conduction Block ◽

Extreme Temperature ◽

Membrane Properties ◽

Extracellular Potassium ◽

Movement Detector ◽

Ion Distribution ◽

Extracellular Potassium Concentration ◽

Failure Event ◽

Conduction Failure

At extreme temperature, neurons cease to function appropriately. Prior exposure to a heat stress (heat shock [HS]) can extend the temperature range for action potential conduction in the axon, but how this occurs is not well understood. Here we use electrophysiological recordings from the axon of a locust visual interneuron, the descending contralateral movement detector (DCMD), to examine what physiological changes result in conduction failure and what modifications allow for the observed plasticity following HS. We show that at high temperature, conduction failure in the DCMD occurred preferentially where the axon passes through the thoracic ganglia rather than in the connective. Although the membrane potential hyperpolarized with increasing temperature, we observed a modest depolarization (3–6 mV) in the period preceding the failure. Prior to the conduction block, action potential amplitude decreased and half-width increased. Both of these failure-associated effects were attenuated following HS. Extracellular potassium concentration ([K+]o) increased sharply at failure and the failure event could be mimicked by the application of high [K+]o. Surges in [K+]o were muted following HS, suggesting that HS may act to stabilize ion distribution. Indeed, experimentally increased [K+]o lowered failure temperature significantly more in control animals than in HS animals and experimentally maintained [K+]o was found to be protective. We suggest that the more attenuated effects of failure on the membrane properties of the DCMD axon in HS animals is consistent with a decrease in the disruptive nature of the [K+]o-dependent failure event following HS and thus represents an adaptive mechanism to cope with thermal stress.

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