Fealey Robert D
Department of Neurology, Mayo Clinic, Rochester, MN, United States.
Handb Clin Neurol. 2018;157:777-787. doi: 10.1016/B978-0-444-64074-1.00048-3.
Peripheral neuropathy affecting autonomic and small sensory fibers can cause abnormalities of both autonomic and behavioral thermoregulation. Quantitative autonomic and sensory neurophysiologic tests and quantification of the linear density of intraepidermal nerve fibers potentially can stratify those at risk of impaired thermoregulation during cold and heat challenges. New data relating to thermoregulatory sweating impairment in neuropathy are presented in this chapter. Of 516 neuropathy patients analyzed, 345 were found to have thermoregulatory sweat test (TST) abnormalities with a mean percentage of anterior body surface anhidrosis (TST%) of 12% and a significant reduction in total body sweat rate, although the rate of core temperature rise with heating (slope) was not significantly different from that of patients with a normal TST. However a subset of abnormal TST patients having 25% or greater TST% showed a significantly more rapid rise in core temperature (lower slope) than age- and sex-matched neuropathy patients with a normal TST. Etiologies of neuropathy in this more severe group included diabetes, erythromelalgia, immune-mediated autonomic neuropathy, primary systemic amyloidosis, and neuropathy associated with postganglionic-autonomic degenerative disorders.
影响自主神经和小感觉纤维的周围神经病变可导致自主神经和行为性体温调节异常。定量自主神经和感觉神经生理学测试以及表皮内神经纤维线性密度的量化，有可能对在寒冷和炎热刺激期间体温调节受损风险的人群进行分层。本章介绍了与神经病变中体温调节性出汗障碍相关的新数据。在分析的516例神经病变患者中，345例被发现有体温调节汗液测试（TST）异常，前体表无汗的平均百分比（TST%）为12%，全身出汗率显著降低，尽管加热时核心体温上升速率（斜率）与TST正常的患者无显著差异。然而，TST%为25%或更高的异常TST患者亚组，其核心体温上升明显更快（斜率更低），比年龄和性别匹配的TST正常的神经病变患者更快。这个更严重组的神经病变病因包括糖尿病、红斑性肢痛症、免疫介导的自主神经病变、原发性系统性淀粉样变性以及与节后自主神经退行性疾病相关的神经病变。
