Reply to “Nodal conduction block and reversible conduction failure are not electrophysiological markers for axonal loss”

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

Clinical Neurophysiology ◽

10.1016/j.clinph.2015.07.026 ◽

2016 ◽

Vol 127 (2) ◽

pp. 1739-1741

Author(s):

Giovanna Squintani ◽

Giuseppe Moretto ◽

Sergio Zimatore ◽

Alberto Morini

Keyword(s):

Upper Limb ◽

Conduction Block ◽

Immunomodulatory Treatment ◽

Conduction Failure ◽

Activity Dependent

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CIDP mimics: a case series

BMC Neurology ◽

10.1186/s12883-021-02118-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Orly Moshe-Lilie ◽

Erik Ensrud ◽

Thomas Ragole ◽

Chahin Nizar ◽

Diana Dimitrova ◽

...

Keyword(s):

Weight Loss ◽

Neuropathic Pain ◽

Conduction Block ◽

Case Series ◽

Initial Response ◽

Axonal Loss ◽

Significant Weight Loss ◽

Monoclonal Protein ◽

Electrophysiological Findings ◽

Systemic Symptoms

Abstract Background To report our experience with a group of patients referred for refractory CIDP who fulfilled “definite” electrodiagnostic EFNS criteria for CIDP but were found to have an alternate diagnosis. Methods Patients who were seen between 2017 and 2019 for refractory CIDP that fulfilled “definite” electrodiagnostic ENFS criteria for CIDP, but had an alternate diagnosis, were included. Patients who correctly had CIDP, anti MAG neuropathy, or MMN with conduction block, were excluded from the study. Demographics, clinical and electrophysiological characteristics, pertinent workup, final alternate diagnoses, and outcomes were collected. Results Seven patients were included: POEMS (n = 5), CANOMAD (n = 1), and neurolymphomatosis (n = 1). Most patients reported neuropathic pain and leg swelling (n = 6) or significant weight loss (n = 4). All patients had a monoclonal protein, and most patients who were tested had an elevated VEGF and CSF cyto-albuminologic dissociation. Electrophysiology showed pronounced intermediate more than distal demyelination, and axonal loss in the lower extremities. Response to steroids or IVIG varied, but some patients did respond to these treatments, especially early in the disease. Conclusion Pain, systemic symptoms, suggestive electrophysiological findings, and/or a serum monoclonal protein should raise suspicion for CIDP mimics. Initial response to steroids or IVIG, over reliance on CSF, and electrophysiology findings can all be misleading.

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Temporary Axonal Conduction Block and Axonal Loss in Inflammatory Neurological Disease: A Potential Role for Nitric Oxide?

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1999.tb07843.x ◽

1999 ◽

Vol 893 (1 OXIDATIVE/ENE) ◽

pp. 304-308 ◽

Cited By ~ 32

Author(s):

R. KAPOOR ◽

M. DAVIES ◽

K. J. SMITH

Keyword(s):

Nitric Oxide ◽

Neurological Disease ◽

Potential Role ◽

Conduction Block ◽

Axonal Loss ◽

Axonal Conduction

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Conditions affecting rate of development of anoxic block in C fibers

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.1.39 ◽

1961 ◽

Vol 200 (1) ◽

pp. 39-45

Author(s):

W. J. Crowley ◽

M. A. Thomson

Keyword(s):

Initial Period ◽

Conduction Block ◽

Irreversible Damage ◽

Rate Of Development ◽

C Fibers ◽

Conduction Failure ◽

Second Period

The isolated splenic nerve of sheep conducted impulses for an average of 10 minutes in the complete absence of oxygen at 37.5°C. If, immediately following conduction failure, the nerve was allowed to recuperate for 2 hours in oxygen it became able to conduct impulses as long during a repeated period of anoxia as it had initially. If the initial period of anoxia was prolonged beyond 28 minutes the nerve sustained irreversible damage and its ability to conduct impulses during subsequent periods of anoxia was shortened proportionally. For recuperation periods shorter than 2 hours the conduction block during the course of the second period of anoxia appeared earlier. Temperatures below 37.5°C or CO2 concentrations above 10% prolonged the time to conduction block during anoxia; temperatures above 37.5°C or frequencies of stimulation greater than 1/sec. shortened the time to conduction block during anoxia.

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Entrapment Neuropathies: Electrodiagnostic Criteria

Guides Newsletter ◽

10.1001/amaguidesnewsletters.2019.novdec02 ◽

2019 ◽

Vol 24 (6) ◽

pp. 12-15

Author(s):

Jay Blaisdell ◽

James B. Talmage

Keyword(s):

Nerve Conduction ◽

Task Force ◽

Conduction Block ◽

Cubital Tunnel Syndrome ◽

Conduction Delay ◽

Test Results ◽

Sixth Edition ◽

Entrapment Neuropathies ◽

Axon Loss ◽

Tunnel Syndrome

Abstract Like the diagnosis-based impairment (DBI) method and the range-of-motion (ROM) method for rating permanent impairment, the approach for rating compression or entrapment neuropathy in the upper extremity (eg, carpal tunnel syndrome [CTS]) is a separate and distinct methodology in the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), Sixth Edition. Rating entrapment neuropathies is similar to the DBI method because the evaluator uses three grade modifiers (ie, test findings, functional history, and physical evaluation findings), but the way these modifiers are applied is different from that in the DBI method. Notably, the evaluator must have valid nerve conduction test results and cannot diagnose or rate nerve entrapment or compression without them; postoperative nerve conduction studies are not necessary for impairment rating purposes. The AMA Guides, Sixth Edition, uses criteria that match those established by the Normative Data Task Force and endorsed by the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM); evaluators should be aware of updated definitions of normal from AANEM. It is possible that some patients may be diagnosed with carpal or cubital tunnel syndrome for treatment but will not qualify for that diagnosis for impairment rating; evaluating physicians must be familiar with electrodiagnostic test results to interpret them and determine if they confirm to the criteria for conduction delay, conduction block, or axon loss; if this is not the case, the evaluator may use the DBI method with the diagnosis of nonspecific pain.

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