Kuwabara S, Kai M R, Nagase H, Hattori T
Department of Neurology, Chiba University School of Medicine, Chiba, Japan.
Eur Neurol. 1999;41(3):163-7. doi: 10.1159/000008042.
To assess the clinical and electrophysiological features of n-hexane neuropathy caused by addictive inhalation, 4 patients were studied in the progressive phase. The neurological manifestations were characterized by subacute predominantly motor polyneuropathy and disease progression despite discontinuance of the chemicals, which were similar to those reported in industrial exposure, although with a severer degree associated with anorexia and body weight loss. Electrophysiological studies showed that all showed multifocal conduction block and profound conduction slowing, as well as features of axonal degeneration. Sural nerve biopsy showed axonal loss, axonal swelling, and thin myelin probably due to retraction by axonal swelling. n-Hexane abuse causes severe subacute polyneuropathy. The mixed axonal and demyelinating electrophysiological features were consistent with peculiar pathological findings. Conduction block, probably due to paranodal myelin retraction or ongoing wallerian degeneration, is very frequent and could be responsible for the clinical deficits, especially in the early phase of illness.
为评估成瘾性吸入所致正己烷神经病的临床和电生理特征，对4例处于疾病进展期的患者进行了研究。神经学表现以亚急性为主的运动性多发性神经病为特征，尽管停止接触化学物质，但疾病仍在进展，这与工业接触中报道的情况相似，不过程度更严重，伴有厌食和体重减轻。电生理研究显示，所有患者均表现为多灶性传导阻滞和严重的传导减慢，以及轴索性变性的特征。腓肠神经活检显示轴突丢失、轴突肿胀以及可能因轴突肿胀回缩所致的薄髓鞘。正己烷滥用会导致严重的亚急性多发性神经病。轴索性和脱髓鞘性混合的电生理特征与特殊的病理表现一致。传导阻滞可能由于结旁髓鞘回缩或正在进行的华勒氏变性，非常常见，可能是临床缺陷的原因，尤其是在疾病早期。
