Parkinsonian rigidity, dopa-induced dyskinesia and chorea--dynamic studies on the basal ganglia-thalamocortical motor circuit using PET scan and depth microrecording.
Regional cerebral glucose metabolism (rCMRGlu-18FDG) was measured in 6 cases with rigid type Parkinson's disease (PD) (2 cases with dopa-induced dyskinesia = DID), 6 cases with chorea (Ch), 5 cases with essential tremor (EssT) and 2 cases with normal subjects (N). The effects of L-Dopa on rCMRGlu was studied in 3 cases with PD. With the aid of depth microrecording study, stereotactic pallidotomy was performed in all cases with PD. Thalamotomy was performed in 3 cases with Ch. In the EssT and N group, the metabolic pattern was high in the frontal cortex (FCx) but low in the lenticular nucleus (LN). In contrast, all cases with a rigid type PD showed lower rCMRGlu in FCx (premotor, prefrontal area). However, 4 out of 6 cases were higher in LN than the control group. Administration of L-Dopa shifted rCMRGlu toward the normal pattern in this group. Five out of 6 cases with Ch represented higher rCMRGlu in FCx (3 focal, 2 diffuse) but lower in LN. Moreover, when DID occurred, it showed almost the same pattern as in Ch. Electrophysiological studies showed high background neuronal activity (BNA) in the medial segment of the globus pallidus (GP) but low BNA in the lateral segment of the GP in the rigid type of PD. In cases with Ch, irregular burst discharges were often encountered in ventro-oral thalamus. From these results, the on-going changes of basal ganglia-thalamocortical motor circuit in cases with a rigid type PD, DID and Ch are discussed. The underlying mechanisms of Parkinsonian rigidity was considered to contrast with those of DID and Ch within the same motor circuit.
Hirato
M
M
Department of Neurosurgery, Gunma University School of Medicine, Japan.
Ishihara
J
J
Horikoshi
S
S
Shibazaki
T
T
Ohye
C
C
D000978:Antiparkinson Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001479:Basal Ganglia / Q000187:drug effects / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000187:drug effects* / Q000503:physiopathology; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D002819:Chorea / Q000139:chemically induced* / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives / Q000378:metabolism; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology*; D004567:Electrodes, Implanted; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D019788:Fluorodeoxyglucose F18; D005917:Globus Pallidus / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D007980:Levodopa / Q000009:adverse effects* / Q000627:therapeutic use; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000503:physiopathology; D009460:Neurologic Examination / Q000187:drug effects; D010300:Parkinson Disease / Q000188:drug therapy* / Q000503:physiopathology; D013238:Stereotaxic Techniques; D013787:Thalamic Nuclei / Q000187:drug effects / Q000503:physiopathology; D014055:Tomography, Emission-Computed; D014202:Tremor / Q000503:physiopathology
D000978:Antiparkinson Agents; D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D007980:Levodopa; D003847:Deoxyglucose