Evidence for motor axon depolarization in Fabry disease
| Autor: | Hugh Bostock, Philip J. Lee, Stella V. Tan, Atul Mehta, Richard J. Walters |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Adult
Male medicine.medical_specialty Hyperkalemia Physiology Ischemia Action Potentials Motor nerve Severity of Illness Index Membrane Potentials Cellular and Molecular Neuroscience Physiology (medical) Internal medicine medicine Humans Axon business.industry Depolarization Middle Aged medicine.disease Fabry disease Axons Electric Stimulation Median nerve Pathophysiology Median Nerve Electrophysiology medicine.anatomical_structure Sensory Thresholds Cardiology Fabry Disease Female Neurology (clinical) medicine.symptom business Neuroscience |
| Zdroj: | Muscle & Nerve. 32:548-551 |
| ISSN: | 1097-4598 0148-639X |
| DOI: | 10.1002/mus.20390 |
| Popis: | To investigate the pathophysiology of neuropathy in Fabry disease, multiple nerve excitability properties of median motor axons in 20 patients with this disorder but without hyperkalemia were compared with 35 age-matched normal controls. In the patients, depolarizing threshold electrotonus was reduced (P < 0.0001) and superexcitability was reduced (P < 0.001), but late subexcitability was normal. These findings indicate that the axons were mildly depolarized, probably due to ischemia, and are consistent with the hypothesis that poor nerve perfusion in Fabry disease contributes to axonal damage. |
| Databáze: | OpenAIRE |
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