title: Evidence of thalamic disinhibition in patients with hemichorea: semiquantitative analysis using SPECT.
abstract: OBJECTIVE
  Hemichorea sometimes occurs after lesions that selectively involve the caudate nucleus, putamen, and globus pallidus. Some reports have hypothesised that the loss of subthalamic nucleus control on the internal segment of the globus pallidus, followed by the disinhibition of the thalamus may contribute to chorea. However, the pathophysiology is poorly understood. Therefore, clinicoradiological localisation was evaluated and a comparison of the haemodynamic status of the basal ganglia and thalamus was made.
  
  
  METHODS
  Six patients presenting with acute onset of hemichorea were assessed. Neuroimaging studies, including MRI and SPECT examinations in addition to detailed biochemical tests, were performed. A semiquantitative analysis was performed by comparing the ratio of blood flow between patients and normal controls. In addition, the ratio of perfusion asymmetry was calculated as the ratio between each area contralateral to the chorea and that homolateral to the chorea. The comparison was made with a two sample t test.
  
  
  RESULTS
  The causes of hemichorea found consisted of four cases of acute stroke, one non-ketotic hyperglycaemia, and one systemic lupus erythematosus. Brain MRI indicated lesion sites in the contralateral putamen, globus pallidus, caudate nucleus, and subthalamic nucleus. A significant decrease in the ratio of blood flow in the basal ganglia contralateral to the chorea and a significant increase in the thalamus was found when comparing the perfusion asymmetries, which were calculated as the ratio of cerebral blood flow (CBF) for each region to that in the homolateral occipital area (p<0.05).
  
  
  CONCLUSIONS
  An alteration in CBF in both the contralateral thalamus and basal ganglia reflect the loss of pallidal inhibitory input from the pallidum to the thalamus. This change in CBF may be one of epiphenomena, which implicates an occurrence of hemichorea in humans.
authors.affiliation: Department of Neurology, College of Medicine, The Catholic University of Korea.
authors.forename: J S
authors.initials: JS
authors.lastname: Kim
authors.forename: K S
authors.initials: KS
authors.lastname: Lee
authors.forename: K H
authors.initials: KH
authors.lastname: Lee
authors.forename: Y I
authors.initials: YI
authors.lastname: Kim
authors.forename: B S
authors.initials: BS
authors.lastname: Kim
authors.forename: Y A
authors.initials: YA
authors.lastname: Chung
authors.forename: S K
authors.initials: SK
authors.lastname: Chung
mesh_terms: D000328:Adult; D000368:Aged; D001479:Basal Ganglia / Q000000981:diagnostic imaging / Q000503:physiopathology; D001783:Blood Flow Velocity / Q000502:physiology; D002819:Chorea / Q000000981:diagnostic imaging* / Q000503:physiopathology; D004292:Dominance, Cerebral / Q000502:physiology*; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009433:Neural Inhibition / Q000502:physiology*; D009778:Occipital Lobe / Q000000981:diagnostic imaging / Q000502:physiology; D012016:Reference Values; D012039:Regional Blood Flow / Q000502:physiology; D020531:Subthalamic Nucleus / Q000000981:diagnostic imaging / Q000503:physiopathology; D013788:Thalamus / Q000000981:diagnostic imaging* / Q000503:physiopathology; D015899:Tomography, Emission-Computed, Single-Photon