Vol.64

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.63

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.62

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.61

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.60

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.59

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.58

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.57

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.56

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.55

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.54

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.53

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.52

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.51

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.50

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.49

• No.1
• No.2/3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.48

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

• Vol.47 to 1
  (Members Only)

• HOME
• Vol.51 No.5
• CLINICA NEUROL, 51: 338−344, 2011
• Vol.51 No.5 contents

Case Report

Convulsive syncope associated with transient hemodynamic ischemia in the basal ganglia

Takashi Murahara, M.D.¹⁾⁴⁾, Shigetoshi Takaya, M.D.²⁾³⁾, Daisuke Yamaguchi, M.D.¹⁾, Tomohiro Tanaka, M.D.¹⁾, Hidenao Fukuyama, M.D.²⁾, Akio Ikeda, M.D.¹⁾ and Ryosuke Takahashi, M.D.¹⁾

¹⁾Department of Neurology, Graduate School of Medicine, Kyoto University
²⁾Human Brain Research Center, Graduate School of Medicine, Kyoto University
³⁾Radioisotope Research Center, Kyoto University
⁴⁾Department of System Neuroscience, School of Medicine, Sapporo Medical University

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.
Full Text of this Article in Japanese PDF (1261K)

(CLINICA NEUROL, 51: 338−344, 2011)
key words: convulsive syncope, electroencephalography, SPECT, orthostatic hypotension

(Received: 6-Nov-10)