Cerebellar syndrome in heat stroke (literary review)

O. Kravets, V.V. Yekhalov, V. Sedinkin, Y. Ploshchenko
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Abstract

The central nervous system is very sensitive to hyperthermia, which causes neurological complications through alteration of the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Cerebellar damage is associated with generalized atrophy and signs of Purkinje cell involvement. Heat shock (stroke) is a critical condition caused by hyperthermia, typified by symmetrical damage to the cerebellum. The critical core temperature for the brain is 40–41 °C, but damage to the cerebellum can occur at lower temperatures. In the central nervous system, cerebellar Purkinje cells are most susceptible to hyperpyrexia-induced dysfunction. The degree of their loss correlates with the severity and duration of hyperthermia. Heat hyperpyrexia-induced cerebellar atrophy usually involves both the vermis and the cerebellar hemispheres. Heat stroke can also cause neurological dysfunction, most commonly due to cerebellar damage. During the acute stage, typical neurological disorders are cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. The convalescent period is characterized by transient cerebellar dysfunction; diffuse cerebellar atrophy has been described, and cerebellar degeneration is a well-known consequence of heat stroke. In permanent cerebellar dysfunction after heat stroke, permanent neurological deficit is relatively rare, and the most common manifestation is cerebellar syndrome. The most common X-ray finding in heat stroke is diffuse cerebellar atrophy with preserved brain volume, which is caused by diffuse loss of Purkinje cells and, according to computed tomography and magnetic resonance imaging, mostly affects the vermis or the cerebellar hemispheres, with the hemispheres of the brain mostly remain intact. Cerebellar disorders caused by heat stroke is a complex neurological problem. To rule out an alternative diagnosis, a thorough special examination with neuroimaging is necessary.
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中暑的小脑综合征(文学评论)
中枢神经系统对高热非常敏感,它会通过改变小脑、基底节、前角细胞和周围神经而引起神经系统并发症。小脑损伤伴有全身萎缩和浦肯野细胞受累的迹象。热休克(中风)是一种由高热引起的危重病症,以小脑的对称性损伤为典型特征。大脑的临界核心温度为 40-41 °C,但在较低温度下也会对小脑造成损害。在中枢神经系统中,小脑浦肯野细胞最容易受到高热引起的功能障碍的影响。其损失程度与高热的严重程度和持续时间有关。高热引起的小脑萎缩通常涉及蚓部和小脑半球。中暑也会导致神经功能障碍,最常见的是小脑损伤。在急性期,典型的神经系统疾病是小脑共济失调、认知障碍、吞咽困难和失语。恢复期的特点是一过性小脑功能障碍;弥漫性小脑萎缩已被描述,小脑变性是中暑的一个众所周知的后果。在中暑后出现的永久性小脑功能障碍中,永久性神经功能缺损相对少见,最常见的表现是小脑综合征。中暑时最常见的 X 射线检查结果是弥漫性小脑萎缩,脑容量保留,这是由于普肯耶细胞弥漫性缺失造成的,根据计算机断层扫描和磁共振成像,主要影响蚓部或小脑半球,大脑半球大多保持完好。中暑引起的小脑功能紊乱是一个复杂的神经系统问题。为了排除其他诊断,有必要通过神经影像学进行全面的特殊检查。
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