MR Imaging and Proton MR Spectroscopy of the Brain in Behçet's Disease

2003 ◽  
Vol 16 (2) ◽  
pp. 267-273 ◽  
Author(s):  
M. Cellerini ◽  
M. Bartolucci ◽  
M. Mortilla ◽  
M. Mascalchi ◽  
F. Li Gobbi ◽  
...  

Cerebral MR imaging (MR) and proton-MR spectroscopy (H-MRS) data are lacking in neurologically asymptomatic patients with Behçet's disease (BD). Aim of the following work was to assess MR and H-MRS characteristics of brain involvement over time in patients with BD without clinical neurological involvement. Forty cerebral MR and 12 H-MRS examinations obtained over a one to nine year follow-up in 17 patients with (group A n=9) or without (group B n=8) neurological involvement were retrospectively reviewed. Four group-B patients had a normal first MR examination whereas all group-A and four group-B patients showed single (n?3) or multiple (n=10) subcortical white matter foci of signal change. Large midbrain, basal ganglia or subcortical white matter lesions were depicted in six group-A patients. Comparison between initial and last MR examinations revealed 28 new small-to-medium size lesions. Over the course of the study, lesion enhancement was seen in five patients all belonging to group A. NAA/Cr and Cho/Cr ratios of supraventricular white matter did not show significant differences between patients and healthy controls or between group-A and group-B patients. Clinically silent cerebral involvement in the form of small-to-medium size subcortical lesions may be present at MR examination in BD patients. Large brainstem and basal ganglia lesions associated with overt neurological symptoms are characteristic of the disease. H-MRS of cerebral normal-appearing white matter does not show any significant metabolic change in BD.

2020 ◽  
Author(s):  
Xiangyun Yin ◽  
Jixiu Zhao ◽  
Jian Jiang ◽  
Hongmin Xi ◽  
Xianghong Li ◽  
...  

Abstract Background:Premature infant is a significant health care burden. White matter damage (WMD) is a leading cause of acute mortality and chronic morbidity in preterm. Xenon (Xe) intervention was given to the 3-day-old neonatal rats with brain white matter injury. By detecting the changes in the expression level of microRNA210 and hypoxia inducible factor 1α (HIF-1α) in brain tissue before and after xenon intervention, we can research the molecular basis and the mechanism of neuroprotective on effect of xenon on brain white matter damage in neonatal rats.Methods:Three-day-old SD rats were randomly divided into sham group(Group A, n=24), lipopolysaccharide(LPS)+hypoxia-ischemia(HI) group (Group B, n=24) and LPS+HI+Xe group ( n=72). The onset of Xe inhalation started at 0,2 and 5 hours in subgroups C,D,and E respectively.We investigated the neurobehavioral deficits by performing TUNEL and hematoxylin and eosin (HE) staining and examining the expression of miR-210and HIF-1α in brain tissues via RT-PCR and western blot. Results: Xe treatment improved the histological alterations and decreased the number of apoptotic cells in group C pups.Compared to group A,Detection of miR-210 level by RT-PCR. the expression level of miR-210 in neonatal rats' periventricular tissue increased significantly at all time points in group B (p<0.05).While the expression level of miR-210 in brain tissues of group B was significantly lower at 48h and 72h than that of group C(p<0.05).Similarly,Detection of HIF-1α protein by Western blot. The level of HIF-1α protein in group B brain tissues was significantly higher than that of group A at each time point (p<0.05), Xe treatment resulted in a marked increase in HIF-1α in C,D, and E subgroups (P < 0.05, compared to group B).Conclusions: These results demonstrate that the expression of HIF-1α and miR-210 increased in periventricular tissues and Xe could relieve the white matter damage by up-regulating the expression of HIF-1α and its target gene miR-210.The Xe therapeutic time window was within 5 hours after intervention, the sooner the better.


2010 ◽  
Vol 113 (3) ◽  
pp. 511-515 ◽  
Author(s):  
Andrew C. Zacest ◽  
Stephen T. Magill ◽  
Jonathan Miller ◽  
Kim J. Burchiel

Object Trigeminal neuralgia (TN) is a neuropathic pain syndrome that is often associated with neurovascular compression of the trigeminal nerve and may be effectively treated with microvascular decompression (MVD). The authors used high-resolution MR imaging with 3D reconstruction in patients with constant facial pain (Type 2 TN) to determine the presence/absence of neurovascular compression and thus a potential MVD benefit. They retrospectively contacted patients to evaluate outcome. Methods All patients who reported spontaneous onset of constant facial pain (Type 2 TN), which occurred at least 50% of the time, who had undergone high-resolution 3-T MR imaging with 3D reconstruction were retrospectively selected for this study. Clinical history, facial pain questionnaire data, physical examination findings, and results from 3-T 3D MR imaging reconstruction were recorded for all patients. Intraoperative findings and clinical pain outcome were recorded for all patients who underwent MVD. Results Data obtained in 27 patients were assessed. On the basis of history and 3D MR imaging reconstruction findings, 13 patients were selected for MVD (Group A) and 14 underwent conservative treatment (Group B). Typical or suspected artery- or vein-induced neurovascular compression was predicted preoperatively in 100% of Group A patients and in 0% of Group B patients. At the time of MVD, definitive neurovascular compression was confirmed in 11 (84.6%) of 13 Group A patients. Following MVD, facial pain was completely relieved in 3 (23%), improved in 7 (53.8%), and no better in 3 (23%) of 13 Group A patients. A history of episodic (Type 1 TN) pain at any time was reported in 100 and 50% of Group A and Group B patients, respectively. A Type 1 TN pain component was reportedly improved/relieved in all Group A patients, but the Type 2 TN pain component was improved in only 7 (53.8%) of 13 patients. The mean postoperative follow-up duration was 13 months. Conclusions High-resolution 3D MR imaging reconstruction in patients with constant facial pain (Type 2 TN) can help determine the presence/absence of neurovascular compression. Surgical selection based on both clinical and radiological criteria has the potential to improve surgical outcome in patients with Type 2 TN who may potentially benefit from MVD. However, even in such selected patients, pain relief is likely to be incomplete.


Stroke ◽  
1999 ◽  
Vol 30 (2) ◽  
pp. 378-382 ◽  
Author(s):  
Toshiyuki Uehara ◽  
Masayasu Tabuchi ◽  
Etsuro Mori

2020 ◽  
Vol 21 (3) ◽  
pp. 1020 ◽  
Author(s):  
Mario Mascalchi ◽  
Alessandra Vella

A variety of Magnetic Resonance (MR) and nuclear medicine (NM) techniques have been used in symptomatic and presymptomatic SCA2 gene carriers to explore, in vivo, the physiopathological biomarkers of the neurological dysfunctions characterizing the associated progressive disease that presents with a cerebellar syndrome, or less frequently, with a levodopa-responsive parkinsonian syndrome. Morphometry performed on T1-weighted images and diffusion MR imaging enable structural and microstructural evaluation of the brain in presymptomatic and symptomatic SCA2 gene carriers, in whom they show the typical pattern of olivopontocerebellar atrophy observed at neuropathological examination. Proton MR spectroscopy reveals, in the pons and cerebellum of SCA2 gene carriers, a more pronounced degree of abnormal neurochemical profile compared to other spinocerebellar ataxias with decreased NAA/Cr and Cho/Cr, increased mi/Cr ratios, and decreased NAA and increased mI concentrations. These neurochemical abnormalities are detectable also in presymtomatic gene carriers. Resting state functional MRI (rsfMRI) demonstrates decreased functional connectivity within the cerebellum and of the cerebellum with fronto-parietal cortices and basal ganglia in symptomatic SCA2 subjects. 18F-fluorodeoxyglucose Positron Emission Tomography (PET) shows a symmetric decrease of the glucose uptake in the cerebellar cortex, the dentate nucleus, the brainstem and the parahippocampal cortex. Single photon emission tomography and PET using several radiotracers have revealed almost symmetric nigrostriatal dopaminergic dysfunction irrespective of clinical signs of parkinsonism which are already present in presymtomatic gene carriers. Longitudinal small size studies have proven that morphometry and diffusion MR imaging can track neurodegeneration in SCA2, and hence serve as progression biomarkers. So far, such a capability has not been reported for proton MR spectroscopy, rsfMRI and NM techniques. A search for the best surrogate marker for future clinical trials represents the current challenge for the neuroimaging community.


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