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DOI 10.1016/j.clinph.2018.03.044

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2018

Altered motor axonal excitability in patients with cervical spondylotic amyotrophy.

Zheng Chaojun, Zhu Yu, Nie Cong, Lu Feizhou, Zhu Dongqing, Weber Robert, Jiang Jianyuan

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVE

To investigate the changes in motor axonal excitability properties in cervical spondylotic amyotrophy (CSA).

METHODS

Threshold tracking was used to measure the median motor axons in 21 patients with CSA, 10 patients with cervical spondylotic radiculopathy (CSR) and 16 normal controls.

RESULTS

Compared with normal controls, patients with distal-type CSA showed increased threshold electrotonus hyperpolarization (TEh [90-100]) and increased superexcitability on the symptomatic side (P < 0.05), which are suggestive of distal motor axonal hyperpolarization, presumably due to motor axonal regeneration. More importantly, compared with normal controls and CSR cases, both distal- and proximal-type CSA cases showed lower accommodation during depolarising currents (reduced S2 accommodation, decreased TEd [undershoot] and/or lower subexcitability) (P < 0.05), indicating that slow K+ conductance may be less active in motor axons in patients with CSA.

CONCLUSIONS

The present study demonstrated changes in motor axonal excitability in patients with CSA compared with both normal controls and patients with CSR.

SIGNIFICANCE: Less expression of slow K+ conductance may confer greater instability in membrane potential in CSA, thereby presumably contributing to the increased vulnerability of motor axons in patients with CSA.

Для цитирования: Zheng Chaojun, Zhu Yu, Nie Cong, Lu Feizhou, Zhu Dongqing, Weber Robert, Jiang Jianyuan. Altered motor axonal excitability in patients with cervical spondylotic amyotrophy.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2018. DOI: 10.1016/j.clinph.2018.03.044.

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