Cerebellar syndrome in heat stroke (literary review)

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.