Turkish journal of medical sciences · 2020
Peripheral axonal excitability in hemiplegia related to subacute stroke.
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Turan Zeynep, Zinnuroğlu Murat
Аннотация
BACKGROUND/AIM: This study aims to investigate peripheral nerve excitability in patients with subacute stroke.
MATERIALS AND METHODS: Thestudy was performed in 29 stroke patients within the subacute period and 29 healthy controls using QTRAC software and TRONDNF protocol. The threshold electrotonus, recovery cycle, stimulus-response, strength-duration, and current-threshold relationships were recorded.
RESULTS: The membrane was more hyperpolarized, and excitability was decreased in the hemiplegic side. The impairment of inward rectifying channel function, degree of hyperpolarization, and decrease of excitability were directly related to the Brunnstrom stages, which were more pronounced in lower stages.
CONCLUSION: The lower motor neurons were affected at the level of axonal channels as a result of upper motor neuron lesions. It can be due to dying back neuropathy, homeostasis, and neurovascular regulation changes in the axonal environment, activity-dependent plastic changes, loss of drive coming from the central nervous system, or a combination of these factors.
MATERIALS AND METHODS: Thestudy was performed in 29 stroke patients within the subacute period and 29 healthy controls using QTRAC software and TRONDNF protocol. The threshold electrotonus, recovery cycle, stimulus-response, strength-duration, and current-threshold relationships were recorded.
RESULTS: The membrane was more hyperpolarized, and excitability was decreased in the hemiplegic side. The impairment of inward rectifying channel function, degree of hyperpolarization, and decrease of excitability were directly related to the Brunnstrom stages, which were more pronounced in lower stages.
CONCLUSION: The lower motor neurons were affected at the level of axonal channels as a result of upper motor neuron lesions. It can be due to dying back neuropathy, homeostasis, and neurovascular regulation changes in the axonal environment, activity-dependent plastic changes, loss of drive coming from the central nervous system, or a combination of these factors.