第49回日本神経学会総会
＜シンポジウム11-3＞末梢神経障害の研究―最新の進歩―
代謝・栄養性ニューロパチー
服部 直樹, 小池 春樹, 祖父江 元
名古屋大学大学院医学系研究科神経内科〔〒466-8550 名古屋市昭和区鶴舞町65〕
We assessed whether postgastrectomy polyneuropathy associated with thiamine deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of thiamine status. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Thiamine-deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that thiamine deficiency can be a major cause of postgastrectomy polyneuropathy. Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine-deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without and with coexisting thiamine deficiency. Thirty-two patients with nonalcoholic thiamine-deficiency neuropathy also were investigated for comparison. We concluded that pure-form of alcoholic neuropathy was distinct from pure-form of thiamine-deficiency neuropathy, supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant thiamine-deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.
Full Text of this Article in Japanese PDF (170K)
(臨床神経, 48：1026−1027, 2008)
key words：ビタミンB1欠乏, アルコール, ニューロパチー
（受付日：2008年5月17日）
