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DOI 10.5692/clinicalneurol.51.338

Медицинская библиотека · Rinsho shinkeigaku = Clinical neurology · 2011

[Convulsive syncope associated with transient hemodynamic ischemia in the basal ganglia].

Murahara Takashi, Takaya Shigetoshi, Yamaguchi Daisuke, Tanaka Tomohiro, Fukuyama Hidenao, Ikeda Akio, Takahashi Ryosuke

Клинический случайАннотация на английскомСтатьяПеревод пока не подготовлен

Аннотация

The pathophysiology of convulsive movements in patients with convulsive syncope remains unclear. Here, we report a patient with convulsive syncope whose convulsive movements seemed to be associated with transient hemodynamic ischemia in the basal ganglia. A 74-year-old man had 1-year history of orthostatic hypotension and transient clonic jerks in the limbs and trunk, predominantly in the right upper limb. His convulsive movements were evoked approximately 1 minute after sitting up or standing up from the supine position and lasted for several tens of seconds. He felt mild faint while the convulsive movements lasted, but he was oriented and could follow simple commands. He was diagnosed as pure autonomic failure. Video-electroencephalogram (EEG) recorded generalized slows without any epileptiform discharges when the symptoms appeared. Single-photon emission computed tomography (SPECT) was performed using split-dose method to evaluate the change in blood flow when the convulsive movements appeared. During symptoms, a significant decrease in blood flow was revealed in the anterior part of the left basal ganglia, bilateral frontal areas, and right cerebellar hemisphere. An alteration in the functional balance between the basal ganglia and the cerebral cortices may play a role in the generation of convulsive movements in patients with convulsive syncope.

Для цитирования: Murahara Takashi, Takaya Shigetoshi, Yamaguchi Daisuke, Tanaka Tomohiro, Fukuyama Hidenao, Ikeda Akio, Takahashi Ryosuke. [Convulsive syncope associated with transient hemodynamic ischemia in the basal ganglia].. Rinsho shinkeigaku = Clinical neurology. 2011. DOI: 10.5692/clinicalneurol.51.338.

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