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Decreased cerebral blood volume (CBV) in contralateral cerebellar gray matter (cGM) in conjunction with cerebellar white matter (cWM) damage, consistent with crossed cerebro-cerebellar diaschisis (cCCD) develop following supratentorial hemispheric stroke. In this study, we investigated the longitudinal evolution of diaschisis-related cerebellar perfusion and diffusion tensor-imaging (DTI) changes in patients after surgery for supratentorial brain tumors. Eight patients (M:F 5:3, age 8–22 years) who received surgery for supratentorial high-grade gliomas were evaluated. Initial MRI studies were performed 19–54 days postoperatively, with follow-ups at 2- to 3-month intervals. For each study, parametric maps of the cerebellum were generated and coregistered to T1-weighted images that had been previously segmented for cGM and cWM. Aggregate mean values of CBV, cerebral blood flow (CBF), and fractional anisotropy (FA) were obtained separately for cGM and cWM, and asymmetry indices (AIs) were calculated. Hemodynamic changes were more robust in cGM than in cWM. Seven patients showed decreased perfusion within cGM contralateral to the supratentorial lesion on the first postoperative study, and asymmetry was significant for both CBV (p?=?0.008) and CBF (p?p?p?=?0.0003), without evidence of subsequent recovery. Diaschisis-related hemodynamic alterations within cGM appear on early postoperative studies, but CBV recovers over time. Conversely, cWM DTI changes are delayed and progressive. Although the clinical correlates of cCCD are yet to be elucidated, better understanding of longitudinal structural and hemodynamic changes within brain remote from the area of primary insult could have implications in research and clinical rehabilitative strategies.  相似文献   
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The cellular prion protein, encoded by Prnp gene, is involved in neuroprotection, neuroplasticity and neurodevelopment. The variant allele Valine at codon 129 of the Prnp was associated with decreased brain volume in healthy volunteers and schizophrenic patients. We investigate the association between the cerebellum volume and the presence of variant allele Valine at codon 129 of the Prnp gene in patients with mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS). The Prnp coding sequence was determined in 41 refractory MTLE-HS patients. The cerebellum volume corrected by the intracranial volume of patients with the normal Prnp genotypes was compared with that of patients presenting the variant alleles at codon 129. Twenty patients showed the Met129Met genotype, 16 showed Met129Val, and 5 had Val129Val. There were no association among clinical, demographic, electrophysiological, antiepileptic drugs used, and the presence of the Prnp variant alleles. The presence of Prnp variant allele at codon 129 was not associated with the analyzed cerebellum volume. Prnp variant alleles at codon 129 are not associated with cerebellum volume in patients with refractory MTLE-HS.  相似文献   
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Fibromyalgia (FM) syndrome is a disabling clinical condition of unknown cause, and only symptomatic treatment with limited benefit is available. Gluten sensitivity that does not fulfill the diagnostic criteria for celiac disease (CD) is increasingly recognized as a frequent and treatable condition with a wide spectrum of manifestations that overlap with the manifestations of FM, including chronic musculoskeletal pain, asthenia, and irritable bowel syndrome. The aim of this report was to describe 20 selected patients with FM without CD who improved when placed on a gluten-free diet. An anti-transglutaminase assay, duodenal biopsy, and HLA typing were performed in all cases. CD was ruled out by negative anti-transglutaminase assay results and absence of villous atrophy in the duodenal biopsy. All patients had intraepithelial lymphocytosis without villous atrophy. Clinical response was defined as achieving at least one of the following scenarios: remission of FM pain criteria, return to work, return to normal life, or the discontinuation of opioids. The mean follow-up period was 16 months (range 5–31). This observation supports the hypothesis that non-celiac gluten sensitivity may be an underlying cause of FM syndrome.  相似文献   
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