OBJECTIVE: To determine, using proton magnetic resonance spectroscopy (1H MRS) whether thalamotomy in patients with Parkinson's disease gives rise to significant changes in regional brain metabolism. MATERIALS AND METHODS: Fifteen patients each underwent stereotactic thalamotomy for the control of medically refractory parkinsonian tremor. Single-voxel 1H MRS was performed on a 1.5T unit using a STEAM sequence (TR/TM/TE, 2000/14/20 msec), and spectra were obtained from substantia nigra, thalamus and putamen areas, with volumes of interest of 7-8ml, before and after thalamotomy. NAA/Cho, NAA/Cr and Cho/Cr metabolite ratios were calculated from relative peak area measurements, and any changes were recorded and assessed. RESULTS: In the substantia nigra and thalamus, NAA/Cho ratios were generally low. In the substantia nigra of 80% of patients (12/15) who showed clinical improvement, decreased NAA/Cho ratios were observed in selected voxels after thalamic surgery (p < 0.05). In the thalamus of 67% of such patients (10/15), significant decreases were also noted (p < 0.05). CONCLUSION: Our results suggest that the NAA/Cho ratio may be a valuable criterion for the evaluation of Parkinson's disease patients who show clinical improvement following surgery. By highlighting variations in this ratio, 1H MRS may help lead to a better understanding of the pathophysiologic processes occurring in those with Parkinson's disease.
Adult ; Aged ; Aspartic Acid/*analogs & derivatives/metabolism ; Brain/*metabolism/pathology ; Choline/metabolism ; Female ; Human ; Magnetic Resonance Imaging ; Magnetic Resonance Spectroscopy ; Male ; Middle Age ; Parkinson Disease/*metabolism/pathology/*surgery ; Protons ; Putamen/metabolism/pathology ; Substantia Nigra/metabolism/pathology ; Thalamus/*metabolism/pathology/*surgery

The mechanism of chorea underlying nonketotic hyperglycemia was controversial. Serial follow up of brain MRI, 99mTc-ECD SPECT, and 18F-FDG PET in conjunction with clinical observation was done to clarify the pathologic localization. From the functional neuroimages, according to the clinical improvement, the relevant pathology was localized on the lentiform nucleus, mainly on the putamen. In caudate, the mismatch between glucose metabolism and blood flow was observed during and after choreoballistic movement which suggested an important cue to understand the pathogenesis of chorea.
Basal Ganglia* ; Brain ; Chorea ; Corpus Striatum ; Cues ; Fluorodeoxyglucose F18 ; Follow-Up Studies* ; Glucose ; Humans ; Hyperglycemia* ; Magnetic Resonance Imaging ; Metabolism ; Pathology* ; Putamen ; Tomography, Emission-Computed, Single-Photon

AIMTo explore the protective effect of propyl gallate against neuronal injury in the boundary zone of the infarction area in the rat cerebral ischemia-reperfusion model and its possible mechanism.

METHODSTransient focal ischemia induced by middle cerebral artery occlusion in the rats was established by ligation of the left internal carotid artery for 2 h. Rats were treated by propyl gallate with different doses (23.5, 47 and 94 micromol x kg(-1)) for three days before operation. Coronal brain sections were collected after 1 , 2, 4, 6, 12 and 24 h of reperfusion, neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining. The expression of activated Caspase-3, total SAPK/JNK, p38MAPK and their phosphorylation (Thr183/Tyr185, Thr180/Tyr182) was investigated by immunohistochemistry and Western blotting with corresponding antibodies.

RESULTSAlthough SAPK/JNK immunoreactivity did not increase at each time point in the boundary zone of the infarction area after reperfusion, p-SAPK/JNK immunoreactivity increased significantly at 1 h and then decreased gradually, and p38MAPK immunoreactivity was enhanced at each time point, peaked at 6 h. Expression of p-p38MAPK peaked at 6 h. Activated Caspase-3 immunoreactivity appeared at 6 h in the boundary zone of the infarction area and peaked at 12 h. TUNEL positive neurons were observed at 12 h and became more abundant at 24 h. The number of Nissl positive neurons decreased gradually and apoptosis ratio of neurons peaked at 24 h. Propyl gallate reduced the immunoreactivity of SAPK/JNK, p-SAPK/JNK, p38MAPK and p-p38MAPK markedly at 1 and 6 h. Propyl gallate with doses of 47 and 94 micromol x kg(-1) were more effective.

CONCLUSIONInhibition on the activation of SAPK/JNK and p38MAPK is the possible protective mechanism of propyl gallate against neuronal injury induced by cerebral ischemia-reperfusion.

Animals ; Apoptosis ; drug effects ; Brain Ischemia ; etiology ; Caspase 3 ; metabolism ; Enzyme Activation ; drug effects ; Infarction, Middle Cerebral Artery ; complications ; MAP Kinase Kinase 4 ; metabolism ; Male ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Propyl Gallate ; pharmacology ; Putamen ; pathology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; enzymology ; etiology ; pathology ; p38 Mitogen-Activated Protein Kinases ; metabolism