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MRI Evidence (mri + evidence)
Selected AbstractsNeuropathic pain and diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2003Dilip Kapur Abstract Neuropathic pain is a common phenomenon resulting from injury to the central or peripheral nervous system. The means by which diabetes results in nerve injury is unclear but the effect is to cause injury at all levels of the nervous system from the level of the peripheral nerves to the brain. Nerve injury causes pain through a cascade of mechanisms resulting in altered processing of sensory input into the nervous system. This alteration occurs through chemical and anatomical changes in the nervous system that are similar to some of the processes seen in central sensitisation following acute pain. Following nerve injury, neuropathic pain occurs not only when these mechanisms are activated but also when sensitisation is maintained. Other processes occurring in neuropathic pain appear to be a loss of normal inhibitory controls as seen by a reduction in local GABA-ergic and descending monoaminergic influences. There are also important changes mediated via glial cells that can maintain neuropathic pain. Diabetes affects all areas of the nervous system and the contribution of higher levels of the nervous system is often overlooked. Neurophysiological and MRI evidence strongly suggest that these may contribute to the pain of diabetic neuropathy. Psychological dysfunction in diabetic patients is an important factor in increasing the suffering associated with all aspects of the disease, but treatment and control of pain can greatly improve the quality of life. Copyright © 2003 John Wiley & Sons, Ltd. [source] Voxel-based T2 Relaxation Rate Measurements in Temporal Lobe Epilepsy (TLE) with and without Mesial Temporal SclerosisEPILEPSIA, Issue 2 2007Susanne G. Mueller Summary:,Introduction: Quantitative measurements of T2 relaxation in the hippocampus for focus lateralization in mesial temporal lobe epilepsy (mTLE) are well established. Less is known to what degree such relaxation abnormalities also affect regions beyond the ipsilateral hippocampus. Therefore, the aim of this study was to characterize extent and distribution pattern of extrahippocampal relaxation abnormalities in TLE with (TLE-MTS) and without MRI evidence of mesial-temporal sclerosis (TLE-no). Methods: Double spin echo images (TE1/2: 20/80 ms) acquired in 24 TLE-MTS and 18 TLE-no were used to calculate relaxation rate maps. These maps were analyzed by SPM2 and by selecting regions of interest (ROI) in the hippocampus and several extrahippocampal brain regions. Results: In TLE-MTS, the results of the SPM and ROI analysis were in good agreement and showed the most severe relaxation rate decreases in the ipsilateral hippocampus but also in other ipsilateral temporal regions, orbitofrontal, and parietal regions and to a lesser degree in contralateral frontal regions. The relaxation rate decreases in TLE-no were confined to small regions in the ipsilateral anterior inferior and medial temporal lobe in the SPM analysis while ROI analysis showed additional regions in the ipsilateral hippocampus, amygdala, and anterior cingulate. Conclusion: TLE-MTS showed extensive, widespread but predominantly ipsilateral temporal and also extratemporal T2 relaxation rate decreases. In contrast, the findings of the SPM and ROI analyses in TLE-no suggested that if relaxation rate decreases are present, they are less uniform and generally milder than in TLE-MTS. This further supports the hypothesis that TLE-no is a distinct clinicopathological entity from TLE-MTS and probably heterogeneous in itself. [source] Quantitative EEG Asymmetry Correlates with Clinical Severity in Unilateral Sturge-Weber SyndromeEPILEPSIA, Issue 1 2007Laura A. Hatfield Summary:,Purpose: Sturge-Weber syndrome (SWS) is a neurocutaneous disorder with vascular malformations of the skin, brain, and eye. SWS results in ischemic brain injury, seizures, and neurologic deficits. We hypothesized that a decrease in quantitative EEG (qEEG) power, on the affected side, correlates with clinical severity in subjects with SWS. Methods: Fourteen subjects had 16-channel scalp EEG recordings. Data were analyzed using fast Fourier transform and calculation of power asymmetry. Blinded investigators assigned scores for clinical neurological status and qualitative assessment of MRI and EEG asymmetry. Results: The majority of subjects demonstrated lower total power on the affected side, usually involving all four frequency bands (delta, theta, alpha, and beta). qEEG asymmetry correlated strongly with neurologic clinical severity scores and MRI asymmetry scores. qEEG data generally agreed with the MRI evidence of regional brain involvement. In MRI-qEEG comparisons that did not agree, decreased power on qEEG in a brain region not affected on MRI was more likely to occur in subjects with more severe neurologic deficits. Conclusions: qEEG provides an objective measure of EEG asymmetry that correlates with clinical status and brain asymmetry seen on MRI. These findings support the conclusion that qEEG reflects the degree and extent of brain involvement and dysfunction in SWS. qEEG may potentially be a useful tool for early diagnosis and monitoring of disease progression in SWS. qEEG may prove useful, in severely affected individuals with SWS, for determining regions of brain dysfunction. [source] MRI evidence of bilateral hippocampal sclerosis in amnestic mild cognitive impairmentEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2006M. Sepe-Monti We present the case of a man affected by amnestic mild cognitive impairment (aMCI) who showed bilateral hippocampal sclerosis at magnetic resonance imaging (MRI). We argue the concept that aMCI is heterogeneous syndrome and suggested the utility of coronal T2-weighted MRI images in the routine dementia workup. [source] The prevalence, clinical features and association of HLA-B27 in sacroiliitis associated with established Crohn's diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2009T. R. ORCHARD Summary Background Sacroiliitis is a recognized complication of Crohn's disease and may occur distinct from progressive ankylosing spondylitis (AS). Aim To estimate prospectively the prevalence of sacroiliitis in patients with established Crohn's disease, to characterize the clinical features and to correlate these with the presence of HLA-B27. Methods All Crohn's disease patients under active follow-up of between 5 and 12 years duration were invited to participate. Patients underwent a clinical evaluation including symptom questionnaire, rheumatological examination and underwent HLA genotyping. Patients then underwent magnetic resonance imaging (MRI) of the sacroiliac joints. The clinical and radiological factors were correlated with HLA-B27 status. Results 56 patients underwent initial assessment and 44 had MRI scans. Seventeen of 44 (39%) patients had MRI evidence of sacroiliitis, of whom 5 fulfilled the criteria for AS. Symptoms of low back pain were elicited in a majority of these patients , 11/17 (65%) compared to 3 of 27 (11%) patients with normal scans (P = 0.003). There were no differences in functional indices with the exception of patients with AS. HLA-B27 was present in seven patients, and all seven had MRI evidence of sacroiliitis, five had AS. Conclusions Sacroiliitis is common in patients with established Crohn's disease and in the majority of cases, patients have symptoms of inflammatory low back pain if questioned carefully. HLA-B27 is not associated with isolated sacroiliitis, but is associated with AS. However, possession of HLA-B27 appears to convey a very high risk of developing axial inflammation in Crohn's disease. [source] CSF cytology has limited value in the evaluation of patients with ependymoma who have MRI evidence of metastasis,PEDIATRIC BLOOD & CANCER, Issue 2 2006Igor M. Poltinnikov MD Abstract Purpose To investigate the usefulness of cerebrospinal fluid (CSF) cytology in pediatric patients with ependymoma who relapsed after focal irradiation. Methods Eighty-eight patients with ependymoma received conformal radiotherapy (CRT) from July 1997 through January 2003 on an IRB approved prospective treatment protocol. CSF cytology results from evaluations performed prior to CRT and at the time of failure were reviewed for patients who progressed after CRT as documented by magnetic resonance imaging (MRI). Results Twenty-two patients had MRI documented evidence of progression after CRT. Ten patients developed distant failure without local failure, four had combined local and distant failure and eight had local failure without distant failure. The median time from the start of CRT to progression was 19 months (range: 6,73). CSF cytology at diagnosis was negative for the presence of malignant cells in all patients. At the time of progression, CSF cytology was performed in 16 of 22 patients including all 10 patients with distant failure without local recurrence. Malignant cells were not found in any of the evaluated CSF specimens including those with distant failure documented by MRI. Conclusions CSF cytology does not add valuable information when evaluating patients with ependymoma who have evidence of distant failure documented by MRI. The usefulness of CSF cytology in the general follow-up evaluation of pediatric patients with ependymoma remains uncertain. © 2005 Wiley-Liss, Inc. [source] Patterns of intraneural ganglion cyst descentCLINICAL ANATOMY, Issue 3 2008Robert J. Spinner Abstract On the basis of the principles of the unifying articular theory, predictable patterns of proximal ascent have been described for fibular (peroneal) and tibial intraneural ganglion cysts in the knee region. The mechanism underlying distal descent into the terminal braches of the fibular and tibial nerves has not been previously elucidated. The purpose of this study was to demonstrate if and when cyst descent distal to the articular branch-joint connection occurs in intraneural ganglion cysts to understand directionality of intraneural cyst propagation. In Part I, the clinical records and MRIs of 20 consecutive patients treated at our institution for intraneural ganglion cysts (18 fibular and two tibial) arising from the superior tibiofibular joint were retrospectively analyzed. These patients underwent cyst decompression and disconnection of the articular branch. Five of these patients developed symptomatic cyst recurrence after cyst decompression without articular branch disconnection which was done elsewhere prior to our intervention. In Part II, five additional patients with intraneural ganglion cysts (three fibular and two tibial) treated at other institutions without disconnection of the articular branch were compared. These patients in Parts I and II demonstrated ascent of intraneural cyst to differing degrees (12 had evidence of sciatic nerve cross-over). In addition, all of these patients demonstrated previously unrecognized MRI evidence of intraneural cyst extending distally below the level of the articular branch to the joint of origin: cyst within the proximal most portions of the deep fibular and superficial fibular branches in fibular intraneural ganglion cysts and descending tibial branches in tibial intraneural ganglion cysts. The patients in Part I had complete resolution of their cysts at follow-up MRI examination 1 year postoperatively. The patients in Part II had intraneural recurrences postoperatively within the articular branch, the parent nerve, and the terminal branches, although in three cases they were subclinical. The authors demonstrate that cyst descent distal to the take-off of the articular branch to the joint of origin occurs regularly in patients with fibular and tibial intraneural ganglion cysts. The authors believe that parent terminal branch descent follows ascent up the articular branch from an affected joint of origin. This mechanism for bidirectional flow explains cyst within terminal branches of the fibular and tibial nerves and is dependent on pressure fluxes and resistances. This new pattern is consistent with principles previously described in a unified (articular) theory, is generalizable to other intraneural ganglion cysts arising from joints, and has important implications for pathogenesis and treatment of these intraneural cysts. Clin. Anat. 21:233,245, 2008. © 2008 Wiley-Liss, Inc. 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