Background and Purpose-Although functional imaging studies suggest that recruitment of contralesional areas hinders optimal functional reorganization in patients with aphasic stroke, only limited evidence is available on the efficacy of noninvasive brain stimulation such as repetitive transcranial magnetic stimulation aimed at suppression of contralateral overactivation. Methods-In this randomized, controlled, blinded pilot study, the effect of 1-Hz repetitive transcranial magnetic stimulation over right-hemispheric Broca homolog in subjects with poststroke aphasia in the subacute stage was examined. According to their group allocation, patients received, in addition to conventional speech and language therapy, multiple sessions of repetitive transcranial magnetic stimulation either over the right-hemispheric inferior frontal gyrus (intervention group) or over the vertex (control group). The primary outcome parameter was the change in laterality indices as quantified by activation positron emission tomography before and after the 2-week intervention period. The clinical efficacy was evaluated with the Aachen Aphasia Test. Results-At baseline, no group differences were discovered for age, laterality indices, or mean Aachen Aphasia Test scores. Four patients were lost to follow-up, but none due to side effects of the transcranial magnetic stimulation. Positron emission tomography revealed an activation shift toward the right hemisphere in the control group (Pϭ0.0165), which was absent in the intervention group. Furthermore, the latter improved significantly clinically by a mean of 19.8 points in the Aachen Aphasia Test total score (Pϭ0.002), whereas the control group did not. There was however no clear linear relationship between the extent of laterality shift and clinical improvement (rϭ0.193, Pϭnonsignificant). Conclusions-Repetitive

Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using 1H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD). In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction. Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) 1H MRSI to measure CSF lactate; (ii) single-voxel 1H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) 31P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction. We found elevated ventricular lactate and decreased GSH in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD. We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.

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