Hawley R J, Kurtzke J F, Armbrustmacher V W, Saini N, Manz H
Acta Neurol Scand. 1982 Nov;66(5):582-9. doi: 10.1111/j.1600-0404.1982.tb03146.x.
63 patients with alcoholic-nutritional peripheral neuropathy were given neurologic, electrophysiologic and nutritional examinations. 24 of these patients were reexamined later in the course of their disease, after from 2 to 72 months (mean 33). Alcoholic-nutritional neuropathy appeared and worsened after bouts of heavy alcohol intake and malnutrition. Initially it was sensory and symmetric in character, with prominent involvement of the posterior tibial nerves. With repeated attacks it became more proximal, more motor, and associated with more severe slowing of nerve conduction velocity. 11 of the patients were able to stop drinking alcohol. Initial subjective improvement was seen within the first week or two, but substantial improvement was not seen for 5 to 6 months. Most leg motor nerve velocity improved at a mean rate of increase of 0.12 M/sec per abstinent month. Large motor units and slowed nerve conduction persisted in "cured" patients. The largest motor units detected in the legs grew, despite alcohol intake.
对63例酒精性营养性周围神经病患者进行了神经学、电生理学和营养检查。其中24例患者在病程后期（2至72个月，平均33个月）进行了复查。酒精性营养性神经病在大量饮酒和营养不良发作后出现并加重。最初，它具有感觉性和对称性，胫后神经受累明显。随着反复发作，它变得更靠近近端，更多涉及运动功能，并且伴有更严重的神经传导速度减慢。11例患者能够戒酒。最初在第一周或第二周内可见主观改善，但5至6个月内未见实质性改善。大多数腿部运动神经速度平均每月戒酒增加0.12米/秒。“治愈”患者中仍存在大运动单位和神经传导减慢。尽管饮酒，但腿部检测到的最大运动单位仍在增大。
