在炎性脱髓鞘性神经病中，由于运动神经元或近端轴突的兴奋性受损，F波消失。
The F wave disappears due to impaired excitability of motor neurons or proximal axons in inflammatory demyelinating neuropathies.
作者信息
Yokota T, Inaba A, Yuki N, Ichikawa T, Tanaka H, Saito Y, Kanouchi T
机构信息
Department of Neurology, Tokyo Medical and Dental University, Japan.
出版信息
J Neurol Neurosurg Psychiatry. 1996 Jun;60(6):650-4. doi: 10.1136/jnnp.60.6.650.
OBJECTIVES
Investigation of pathophysiology of F wave disappearance in demyelinating neuropathies.
METHODS
The peripheral motor nerve conduction was studied by motor evoked potential (MEP) on transcranial magnetic stimulation as well as conventional nerve conduction studies before and after the treatment in 26 patients with inflammatory demyelinating neuropathies. In addition, serum antiganglioside antibodies in the acute or active stage were examined.
RESULTS
The F wave was abolished in 10 patients. Seven of the 10 patients showed motor evoked potentials (MEPs) on transcranial magnetic stimulation that ranged from 1-4 mV. In six of them the F wave reappeared in the recovery stage, but the MEP size did not change. This may be caused by humoral factors, because the F wave reappeared immediately after plasma exchange or intravenous immunoglobulin treatment. A correlation of F wave disappearance with the presence of serum antiganglioside antibodies was found.
CONCLUSIONS
The major pathophysiology of F wave disappearance in demyelinating neuropathies is impairment of motor neuron excitability or prolonged refractoriness of the most proximal axon for backfiring. The conventional interpretation that absent F waves suggest a conduction block at the proximal site is often inadequate.
目的
研究脱髓鞘性神经病中F波消失的病理生理学机制。
方法
对26例炎性脱髓鞘性神经病患者在治疗前后采用经颅磁刺激运动诱发电位（MEP）及传统神经传导研究检测周围运动神经传导。此外，检测急性期或活动期血清抗神经节苷脂抗体。
结果
10例患者F波消失。其中7例患者经颅磁刺激运动诱发电位（MEP）为1 - 4 mV。其中6例患者在恢复阶段F波重新出现，但MEP波幅未改变。这可能是由体液因素引起的，因为血浆置换或静脉注射免疫球蛋白治疗后F波立即重新出现。发现F波消失与血清抗神经节苷脂抗体的存在相关。
结论
脱髓鞘性神经病中F波消失的主要病理生理学机制是运动神经元兴奋性受损或最近端轴突回传的不应期延长。F波消失提示近端部位传导阻滞的传统解释往往不充分。
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