Sclerosis

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Sclerosis

  • ammon horn sclerosis
  • amyotrophic lateral sclerosis
  • benign multiple sclerosis
  • cutaneous systemic sclerosis
  • definite multiple sclerosis
  • dermal sclerosis
  • diffuse cutaneous systemic sclerosis
  • familial amyotrophic lateral sclerosis
  • hippocampal sclerosis
  • horn sclerosis
  • human multiple sclerosis
  • lateral sclerosis
  • mesial temporal sclerosis
  • multiple sclerosis
  • primary progressive multiple sclerosis
  • progressive multiple sclerosis
  • relapsing multiple sclerosis
  • relapsing-remitting multiple sclerosis
  • remitting multiple sclerosis
  • skin sclerosis
  • sporadic amyotrophic lateral sclerosis
  • systemic sclerosis
  • temporal sclerosis
  • tuberous sclerosis
  • vascular sclerosis

  • Terms modified by Sclerosis

  • sclerosis case
  • sclerosis complex
  • sclerosis lesion
  • sclerosis patient
  • sclerosis relapse

  • Selected Abstracts


    AN OPEN STUDY OF RILUZOLE VERSUS RILUZOLE PLUS GABAPENTIN IN AMYOTROPHIC LATERAL SCLEROSIS

    JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000
    V Palma
    A randomised open study has been carried out to evaluate the efficacy of riluzole versus riluzole plus gabapentin in 50 patients (23 males, 27 females) affected by amyotrophic lateral sclerosis (ALS), who received the diagnosis according to El Escorial WFN criteria. At baseline, the mean age of the patients was 58.8 ± 11.7 years and the mean disease duration was 11.4 ± 5.9 months. Twenty patients had bulbar and 30 spinal onset. Twenty-eight patients were randomly assigned to riluzole (100 mg/day) and 22 to riluzole plus gabapentin at the initial dose of 300 mg/day, slowly increased to 1800 mg/day. Informed consent was obtained in all cases. Before treatment, each patient underwent neurological examination, Appel rate scale, pulmonary function tests, electromyography, and transcranial magnetic stimulation. Clinical examination and electrophysiologic tests were repeated at three-month intervals. Over the course of the trial, 4 patients (8%) were lost to follow-up and 16 (32%, 9 in the riluzole and 7 in the riluzole plus gabapentin group) died. The mean age at death was 65.0 ± 6.5 years after a mean disease duration of 20.8 ± 7.9 months (range 13,36). There was no significant difference in response to treatment when severity and duration of the disease were compared in the two groups. [source]


    IS SCLERODERMA RENAL CRISIS WITH ANTI-CENTROMERE ANTIBODY-POSITIVE LIMITED CUTANEOUS SYSTEMIC SCLEROSIS OVERLOOKED IN PATIENTS WITH HYPERTENSION AND/OR RENAL DYSFUNCTION?

    NEPHROLOGY, Issue 2 2008
    TOSHIRO SUGIMOTO
    [source]


    Shave and Phenolization of Periungual Fibromas, Koenen's Tumors, in a Patient with Tuberous Sclerosis

    DERMATOLOGIC SURGERY, Issue 1 2008
    MARTA MAZAIRA MD
    No abstract is available for this article. [source]


    Detection of Subclinical Cardiac Involvement in Systemic Sclerosis by Echocardiographic Strain Imaging

    ECHOCARDIOGRAPHY, Issue 2 2008
    Alper Kepez M.D.
    Background: Cardiac involvement is one of the major problems in systemic sclerosis (SSc). Subclinical cardiac involvement has a higher frequency than thought previously. In this study we investigated whether subclinical cardiac involvement can be detected by using echocardiographic strain imaging in SSc patients without pulmonary hypertension. Methods: Echocardiographic examinations were performed to 27 SSc patients and 26 healthy controls. Left ventricular strain parameters were obtained from apical views and average strain value was calculated from these measurements. Results: There were no significant differences between patients and controls regarding two-dimensional (2D), conventional Doppler and tissue Doppler velocity measurements. Strain was reduced in 6 of 12 segments of the left ventricle (LV) and in 1 of 2 segments of the right ventricle (RV). Strain rate (SR) was reduced in 2 of 12 segments of the LV and 1 of 2 segments of the RV in SSc patients as compared to controls (P < 0.05 for all). These involvements did not match any particular coronary artery distribution. More important differences were detected by average strain and SR values of the LV between patients and controls (19.78 ± 3.00% vs 23.41 ± 2.73%, P < 0.001; 2.01 ± 0.41 vs 2.23 ± 0.27/sec, P = 0.026, respectively). Furthermore, carbon monoxide diffusion capacity (DLCO) in scleroderma patients significantly correlated with LV average strain (r = 0.59; P = 0.001). Conclusion: Evaluation of ventricular function by using echocardiographic strain imaging appears to be useful to detect subclinical cardiac involvement in SSc patients with normal standard echocardiographic and tissue Doppler velocity findings. [source]


    Aortic Valve Sclerosis: Is It a Cardiovascular Risk Factor or a Cardiac Disease Marker?

    ECHOCARDIOGRAPHY, Issue 3 2007
    F.I.S.C.U., Pasquale Palmiero M.D.
    Background: Aortic valve sclerosis, without stenosis, has been associated with an increased cardiovascular mortality and morbidity due to myocardial infarction. However, it is unclear whether it is a cardiovascular risk factor or a cardiac disease marker. The goal of our study is to evaluate the difference in the prevalence of cardiovascular disease and risk factors among patients with or without aortic sclerosis. Methods: This observational study compared a group of 142 consecutive subjects with aortic valve sclerosis, assigned as group S, with a group of 101 subjects without aortic sclerosis, assigned as group C. Patients with bicuspid aortic valves and those with antegrade Doppler velocity across aortic valve leaflets exceeding 2.0 m/sec were excluded. Results: Mean ages of groups S and C were 71 ± 8, and 68.8 ± 6 years, respectively (P value = not significant). The prevalence of smoking, diabetes, hypercholesterolemia, hypertension, pulse pressure, left ventricular diastolic dysfunction, atrial fibrillation, and stroke was not significantly different between the two groups. However, there was a significantly higher prevalence of left ventricular hypertrophy (P = 0.05), ventricular arrhythmias (P = 0.02), myocardial infarction (P = 0.04), and systolic heart failure (P = 0.04) in aortic sclerosis group. Conclusions: Aortic sclerosis is associated with a higher prevalence of left ventricular hypertrophy, ventricular arrhythmias, myocardial infarction, and systolic heart failure, while the prevalence of cardiovascular risk factors is not different between aortic sclerosis patients and controls. Hence, aortic sclerosis represents a cardiac disease marker useful for early identification of high-risk patients beyond cardiovascular risk factors rate. [source]


    Voxel-based T2 Relaxation Rate Measurements in Temporal Lobe Epilepsy (TLE) with and without Mesial Temporal Sclerosis

    EPILEPSIA, Issue 2 2007
    Susanne 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]


    Facial Emotion Recognition after Curative Nondominant Temporal Lobectomy in Patients with Mesial Temporal Sclerosis

    EPILEPSIA, Issue 8 2006
    Shearwood McClelland III
    Summary:,Purpose: The right (nondominant) amygdala is crucial for processing facial emotion recognition (FER). Patients with temporal lobe epilepsy (TLE) associated with mesial temporal sclerosis (MTS) often incur right amygdalar damage, resulting in impaired FER if TLE onset occurred before age 6 years. Consequently, early right mesiotemporal insult has been hypothesized to impair plasticity, resulting in FER deficits, whereas damage after age 5 years results in no deficit. The authors performed this study to test this hypothesis in a uniformly seizure-free postsurgical population. Methods: Controls (n = 10), early-onset patients (n = 7), and late-onset patients (n = 5) were recruited. All patients had nondominant anteromedial temporal lobectomy (AMTL), Wada-confirmed left-hemisphere language dominance and memory support, MTS on both preoperative MRI and biopsy, and were Engel class I 5 years postoperatively. By using a standardized (Ekman and Friesen) human face series, subjects were asked to match the affect of one of two faces to that of a simultaneously presented target face. Target faces expressed fear, anger, or happiness. Results: Statistical analysis revealed that the early-onset group had significantly impaired FER (measured by percentage of faces correct) for fear (p = 0.036), whereas the FER of the late-onset group for fear was comparable to that of controls. FER for anger and happiness was comparable across all three groups. Conclusions: Despite seizure control/freedom after AMTL, early TLE onset continues to impair FER for frightened expressions (but not for angry or happy expression), whereas late TLE onset does not impair FER, with no indication that AMTL resulted in FER impairment. These results indicate that proper development of the right amygdala is necessary for optimal fear recognition, with other neural processes unable to compensate for early amygdalar damage. [source]


    Hippocampal Malformations Do Not Necessarily Evolve into Hippocampal Sclerosis

    EPILEPSIA, Issue 6 2005
    Arjune Sen
    Summary:,Purpose: Hippocampal malformations have been proposed to underlie or evolve into hippocampal sclerosis, a common cause of refractory partial epilepsy. We report two patients with chronic epilepsy and developmental abnormalities of the hippocampus and cortex. We seek to address, in patients with recurrent convulsive seizures over many decades, whether hippocampal malformations necessarily progress to hippocampal sclerosis. Methods: The first patient died at age 76 years and had experienced convulsive seizures for 43 years. The second patient, aged 64 years at death, had experienced convulsive seizures for 49 years. The brains were processed routinely. Immunohistochemistry for dynorphin and neuropeptide Y was performed. Results: The first case exhibited bilateral perisylvian polymicrogyria. Both hippocampi demonstrated abnormal convolution in the CA1 subfield and subiculum. In the second case, periventricular heterotopia was found in the wall of the right lateral ventricle. The right hippocampus was abnormally oriented with excessive convolutions of the pyramidal cell layer between CA1 and the subiculum. In neither patient did the hippocampi exhibit neuronal loss. Furthermore, dynorphin immunohistochemistry revealed no reactivity in the molecular layers, and staining with neuropeptide Y confirmed normal numbers of hilar interneurons. Conclusions: These two cases demonstrate histologically that, even in long-standing epilepsy, malformations of the hippocampus do not necessarily develop into hippocampal sclerosis. [source]


    Leptomeningeal Enhancement and Enlarged Choroid Plexus Simulating the Appearance of Sturge,Weber Disease in a Child with Tuberous Sclerosis

    EPILEPSIA, Issue 4 2005
    Stephane Kremer
    No abstract is available for this article. [source]


    Correlation between 1H MRS and Memory before and after Surgery in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

    EPILEPSIA, Issue 6 2004
    Lütfü Hano
    Summary: Purpose: Proton magnetic resonance spectroscopy (1H MRS), which can demonstrate neuronal loss and gliosis, may be used as a sensitive tool for lateralization of temporal lobe epilepsy (TLE). Although the correlation between the memory functions and 1H MRS has been investigated, its predictive value after surgery has not been studied previously. This study evaluated memory and 1H MRS values of medically intractable patients with mesial TLE and hippocampal sclerosis (MTLE-HS) before and after selective amygdalohippocampectomy (SAH). Methods: Twenty-two patients underwent memory tests and 1H MRS investigation before and 6 months after SAH and were compared with nine control subjects. Results: The 1H MRS scores were found to be significantly low on the pathological side of the patients. Both right-sided 1H MRS of right TLE and left-sided 1H MRS values of left TLE patients were correlated only with verbal memory scores. Statistical analysis did not reveal any significance for nonverbal memory scores for both TLE groups on either side, which showed no significant correlation between material specificity and 1H MRS findings. Conversely, regression analyses demonstrated that high right- and low left-sided 1H MRS values obtained before surgery may predict a decline in verbal learning scores after surgery. Conclusions:1H MRS can be considered as a useful tool to determine the lateralization in patients with MTLE-HS before the surgery. Although only a weak relation exists between the MRS values and memory scores, presurgical MRS scores may be predictive for a possible deterioration in verbal memory after surgery. However, further studies with higher numbers of cases are needed for confirmation of the results. [source]


    Neuronal Death in Mesial Temporal Sclerosis: Separating Morphology from Mechanism

    EPILEPSIA, Issue 12 2003
    Denson G. Fujikawa
    No abstract is available for this article. [source]


    Neocortical Temporal FDG-PET Hypometabolism Correlates with Temporal Lobe Atrophy in Hippocampal Sclerosis Associated with Microscopic Cortical Dysplasia

    EPILEPSIA, Issue 4 2003
    Beate Diehl
    Summary: ,Purpose: Medically intractable temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS), with or without cortical dysplasia (CD), is associated with atrophy of the hippocampal formation and regional fluorodeoxyglucose positron-emission tomography (FDG-PET) hypometabolism. The relation between areas of functional and structural abnormalities is not well understood. We investigate the relation between FDG-PET metabolism and temporal lobe (TL) and hippocampal atrophy in patients with histologically proven isolated HS and HS associated with CD. Methods: Twenty-three patients underwent en bloc resection of the mesial and anterolateral neocortical structures. Ten patients were diagnosed with isolated HS; 13 patients had associated microscopic CD. Temporal lobe volumes (TLVs) and hippocampal volumes were measured. Magnetic resonance imaging (MRI) and PET were co-registered, and regions of interest (ROIs) determined as gray matter of the mesial, lateral, and anterior temporal lobe. Results: All patients (HS with or without CD) had significant ipsilateral PET hypometabolism in all three regions studied (p < 0.0001). In patients with isolated HS, the most prominent hypometabolism was in the anterior and mesial temporal lobe, whereas in dual pathology, it was in the lateral temporal lobe. TLVs and hippocampal volumes were significantly smaller on the epileptogenic side (p < 0.05). The PET asymmetries ipsilateral/contralateral to the epileptogenic zone and TLV asymmetries correlated significantly for the anterior and lateral temporal lobes (p < 0.05) in the HS+CD group, but not in the isolated HS group. Mesial temporal hypometabolism was not significantly different between the two groups. Conclusions: Temporal neocortical microscopic CD with concurrent HS is associated with more prominent lateral temporal metabolic dysfunction compared with isolated HS in TL atrophy. Further studies are needed to confirm these findings and correlate the PET hypometabolic patterns with outcome data in patients operated on for HS with or without CD. [source]


    Lamotrigine Therapy of Epilepsy in Tuberous Sclerosis

    EPILEPSIA, Issue 7 2001
    David Neal Franz
    Summary: ,Purpose: Lamotrigine (LTG), a newer antiepileptic drug (AED), has activity against both partial-onset and generalized seizures. Its reported benefits for behavior, and its effectiveness in Lennox,Gastaut syndrome and other forms of refractory epilepsy, make it a logical choice for treatment of epilepsy in tuberous sclerosis complex (TSC). We present our experience with LTG therapy of epilepsy in 57 patients with TSC. Methods: Patients fulfilled the diagnostic criteria for clinically definite TSC. LTG was initiated and increased until improvement in seizure frequency was noted, intolerable side effects occurred, or maximal doses were reached. Seizure frequency and behavioral changes were recorded during LTG therapy and compared with those prior to the introduction of LTG. Results: Twenty-four (42%) were seizure free, and 21 (37%) had a >50% reduction in seizure frequency. Eighteen (32%) had subjectively improved behavior and/or alertness with daily activities. Thirty-eight (67%) had no change in this regard, whereas one (2%) became worse. Responders were more likely to not have a history of infantile spasms, and to have experienced only partial seizures (p < 0.05). Otherwise no phenotypic correlations with response were apparent. Conclusions: Among patients with TSC and epilepsy, LTG was effective and well tolerated, including as initial monotherapy. Improved alertness and behavior were apparent in many patients. The incidence of side effects is similar to that reported for other pediatric populations with symptomatic partial epilepsy. The usefulness of LTG in TSC may relate to an underlying defect of glutamatergic neurotransmission in partial epilepsy. [source]


    Frontal-lobe mediated behavioral dysfunction in amyotrophic lateral sclerosis

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2010
    M. Witgert
    Background:, Cognitive impairment secondary to frontal lobe atrophy exists in 40,60% of Amyotrophic Lateral Sclerosis (ALS) cases. We aimed to determine the prevalence of frontal-lobe mediated behavioral impairment in (ALS) and to ascertain its relationship to cognitive impairment. Methods:, Two-hundred and twenty five patients diagnosed with sporadic ALS were evaluated for behavioral dysfunction using the Frontal Systems Behavior Scale (FrSBe), a validated measure used to examine frontal-lobe mediated behaviors, specifically apathy, executive dysfunction and disinhibition; a total behavior score is also provided. Additionally, a subset of patients also underwent a comprehensive neuropsychological evaluation. Results:, Changes in the total FrSBe scores were observed in 24.4% of the patients and 39.6% of the patients had impairment in at least one behavioral domain with symptoms of Apathy being the most common (31.1%). Cognitively impaired ALS patients had worse total (P = 0.05) and apathy scores (P < 0.01); however, behavioral dysfunction was also present in 16% of the cognitively intact patients. Half of the behaviorally intact patients exhibited cognitive impairment. Significant correlations were observed for performance on certain neuropsychological tests (Animal fluency, Block Design, Logical Memory I and Verbal Series Attention Test) and severity of behavioral dysfunction on certain FrSBe sub scores. Conclusions:, Frontal-lobe mediated behavioral dysfunction appears to be common in ALS. Cognitively impaired ALS patients had greater behavioral dysfunction. Recognition of behavioral and cognitive dysfunction may assist health-care providers and care-givers recognize changes in decision-making capacity and treatment compliance of patients with ALS. [source]


    A Case of Hemodialysis Patients with Encapsulating Peritoneal Sclerosis (EPS)-like Finding

    HEMODIALYSIS INTERNATIONAL, Issue 1 2003
    H Kawanishi
    Encapsulating peritoneal sclerosis (EPS) is recognized as a serious complication of peritoneal dialysis (PD). Involvement of the inflammation is indispensable as the EPS emission factor. We experienced the surgery of the EPS-like case that emits it to the hemodialysis (HD) patient without the PD. Patient: In November 1996 the patients, a 47-year old male developed end-stage renal failure due to chronic nephritis and started HD. Before and during HD, he complicated alcohol liver cirrhosis with ascites. In September 2001 he had intestinal obstructive symptoms and recovered with repeated puncture and drainage of ascites. Abdominal CT examination revealed the intestine oppression by the ascites with thick tunic formation. At May 2002, he underwent a laparotomy. Thick capsules formed surroundings to the ascites. This capsules covered parietal peritoneum and intestine surface and oppressed the intestine. The total ablation of small intestine was succeeded. Ascites examinations IL-6 20,350 pg/mL FDP 80 micro-g/mL TAT 1090 micro-g/L, was suspected to conjecture the involvement of inflammation and coagulate-fibrinolysis. Histology of peritoneum showed absence of mesothelium but not fibrosis and sclerosis. Discussion: EPS is caused by the inflammation on the deteriorated peritoneum, resulting in encapsulation after the accumulation of inflammatory products such as fibrin. Even if there is not the peritoneum deterioration, chronic inflammation and stimulation that continues for long-time causing EPS-like findings with encapsulation. The encapsulating ileus findings irrespective of the peritoneum deterioration should call with encapsulated peritonitis (EP). [source]


    Interleukin-12 P40 induces the expression of TNF-, in microglia and macrophages

    JOURNAL OF NEUROCHEMISTRY, Issue 2002
    M. Jana
    Recently, it has been found that overproduction of IL-12 can be dangerous to the host as it is involved in the pathogenesis of a number of autoimmune inflammatory diseases such as multiple sclerosis. It is composed of two different subunits , p40 and p35. Expression of p40 mRNA but not that of p35 mRNA in excessive amount in the CNS of patients with Multiple Sclerosis (MS) suggests that IL-12 p40 may have a role in the pathogenesis of the disease. The present study was undertaken to explore the role of p40 in the expression of TNF-, in microglia. Interestingly, we have found that IL-12 p70, p402 (the p40 homodimer) and p40 (the p40 monomer) dose-dependently induced the production of TNF-, in BV-2 microglial cells. This induction of TNF-, production was accompanied by an induction of TNF-, mRNA. In addition to BV-2 glial cells, p70, p402 and p40 also induced the production of TNF-, in mouse primary microglia and peritoneal macrophages. Since the activation of both NF-,B and C/EBPb is important for the expression of TNF-, in microglial cells, we investigated the effect of p40 on the activation of NF-,B as well as C/EBPb. Activation of NF-,B as well as C/EBPb by p40 and inhibition of p40-induced expression of TNF-, by Dp65, a dominant-negative mutant of p65, and DC/EBPb, a dominant-negative mutant of C/EBPb, suggests that p40 induces the expression of TNF-, through the activation of NF-,B and C/EBPb. This study delineates a novel role of IL-12 p40 in inducing the expression of TNF-, in microglial cells which may participate in the pathogenesis of neuroinflammatory diseases. Acknowledgements:, This study was supported by NIH grants (NS39940 and AG19487). [source]


    Closing the Clinical-Imaging Gap in Multiple Sclerosis?

    JOURNAL OF NEUROIMAGING, Issue 1 2009
    Imaging Iron Deposition in Deep Gray Matter
    No abstract is available for this article. [source]


    Diffusion Tensor Tractography-based Analysis of the Pyramidal Tract in Patients with Amyotrophic Lateral Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 3 2008
    Yoon-Ho Hong MD
    ABSTRACT BACKGROUND AND PURPOSE We attempted to measure DTI parameters of the brainstem pyramidal tract using two approaches, ie, simple ROI and tract-specific analyses. Results obtained for healthy subjects and ALS patients were compared. METHODS DTI was performed using a single shot SE-EPI with 25 noncollinear diffusion gradient directions (b= 1000 second/mm2) and with no diffusion gradient on a 3.0-T MR system in 10 ALS patients and in 8 age- and sex-matched normal controls. To delineate the brainstem pyramidal tract, tractography was performed using two ROIs, ie, a seed ROI at the cerebral peduncle (ROI-1) and a target ROI at the lower pons (ROI-2). ROI-1 was subsequently restricted to voxels that contained streamlines in the tract reconstruction, thus creating a sub-ROI. RESULTS Mean fractional anisotropy (FA) and mean diffusivity values were highly reproducible by tract specific analysis, whereas simple ROI analysis yielded larger variabilities between operators. FA values were significantly lower in ALS patients than in normal controls in the tractography-derived sub-ROI (P= .01), but not in the seed or target ROIs. CONCLUSIONS These results suggest, compared with simple ROI analysis, that tract-specific analysis using DTI fiber-tracking is more reliable and sensitive for detecting upper motor neuron pathology in ALS. [source]


    Conventional MRI in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2007
    Massimo Filippi MD
    ABSTRACT During the past 10 years, conventional magnetic resonance imaging (cMRI) has become an established tool for the assessment of patients with multiple sclerosis (MS) and to monitor treatment trials. This is mainly due to the sensitivity and reproducibility of cMRI in the detection of MS-related damage. A large effort has also been devoted to develop imaging strategies capable of providing accurate estimates of the extent of disease-related damage not only in the brain, but also in the spinal cord and optic nerve. Guidelines have been defined to integrate MR findings in the diagnostic evaluation of patients at presentation with clinically isolated syndromes suggestive of MS, and specific acquisition protocols have been offered for monitoring longitudinal changes in patients with established disease. Despite the fact that the role of cMRI in MS has been profoundly obviated by the advent of modern and quantitative MR techniques, several issues are still unresolved. Technical development in acquisition and postprocessing, as well as the introduction of high-field magnets in the clinical arena, are likely to increase our understanding of disease pathobiology, mainly through an increased ability to quantify the extent of gray matter damage. [source]


    Measuring Brain Atrophy in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2007
    Nicola De Stefano MD
    ABSTRACT The last decade has seen the development of methods that use conventional magnetic resonance imaging (MRI) to provide sensitive and reproducible assessments of brain volumes. This has increased the interest in brain atrophy measurement as a reliable indicator of disease progression in many neurological disorders, including multiple sclerosis (MS). After a brief introduction in which we discuss the most commonly used methods for assessing brain atrophy, we will review the most relevant MS studies that have used MRI-based quantitative measures of brain atrophy, the clinical importance of these results, and the potential for future application of these measures to understand MS pathology and progression. Despite the number of issues that still need to be solved, the measurement of brain atrophy by MRI is sufficiently precise and accurate. It represents one of most promising in vivo measures of neuroaxonal degeneration in MS, and it should be used extensively in the future to assess and monitor pathological evolution and treatment efficacy in this disease. [source]


    Cerebral Atrophy Measurement in Clinically Isolated Syndromes and Relapsing Remitting Multiple Sclerosis: A Comparison of Registration-Based Methods

    JOURNAL OF NEUROIMAGING, Issue 1 2007
    Valerie M. Anderson BSc
    ABSTRACT Background and Purpose. Brain atrophy is a proposed marker of disease progression in multiple sclerosis (MS). Many magnetic resonance imaging-based methods of atrophy quantification exist, but their relative sensitivity and precision is unclear. Our aim was to compare atrophy rates from the brain boundary shift integral (BBSI), structural image evaluation, using normalization of atrophy (SIENA) (both registration-based methods) and segmented brain volume difference, in patients with clinically isolated syndromes (CIS), relapsing remitting MS (RRMS), and controls. Methods. Thirty-seven CIS patients, 30 with early RRMS and 16 controls had T1-weighted volumetric imaging at baseline and 1 year. Brain atrophy rates were determined using segmented brain volume difference, BBSI, and SIENA. Results. BBSI and SIENA were more precise than subtraction of segmented brain volumes and were more sensitive distinguishing RRMS subjects from controls. A strong correlation was observed between BBSI and SIENA. Atrophy rates were greater in CIS and RRMS subjects than controls (RRMS P < .001). With all methods, significantly greater atrophy rates were observed in CIS patients who developed clinically definite MS relative to subjects who did not. Conclusion. Registration-based techniques are more precise and sensitive than segmentation-based methods in measuring brain atrophy, with BBSI and SIENA providing comparable results. [source]


    A Magnetization Transfer MRI Study of Deep Gray Matter Involvement in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 4 2006
    Jitendra Sharma MD
    ABSTRACT Background/Purpose: Gray matter involvement in multiple sclerosis (MS) is of growing interest with respect to disease pathogenesis. Magnetization transfer imaging (MTI), an advanced MRI technique, is sensitive to disease in normal appearing white matter (NAWM) in patients with MS. Design/Methods: We tested if MTI detected subcortical (deep) gray matter abnormalities in patients with MS (n= 60) vs. age-matched normal controls (NL, n= 20). Magnetization transfer ratio (MTR) maps were produced from axial proton density, conventional spin-echo, 5 mm gapless slices covering the whole brain. Region-of-interest,derived MTR histograms for the caudate, putamen, globus pallidus, thalamus, and NAWM were obtained. Whole brain MTR was also measured. Results: Mean whole brain MTR and the peak position of the NAWM MTR histogram were lower in patients with MS than NL (P < .001) and mean whole brain MTR was lower in secondary progressive (SP, n= 10) than relapsing-remitting (RR, n= 50, P < .001) patients. However, none of the subcortical gray matter nuclei showed MTR differences in MS vs. NL, RR vs. SP, or SP vs. NL. Conclusions: The MTI technique used in this cohort was relatively insensitive to disease in the deep gray matter nuclei despite showing sensitivity for whole brain disease in MS. It remains to be determined if other MRI techniques are more sensitive than MTI for detecting pathology in these areas. [source]


    Imaging Spinal Cord Damage in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 4 2005
    M. A. Rocca MD
    ABSTRACT During the past 2 decades, the considerable improvement of magnetic resonance (MR) technology and the development of new MR strategies capable of providing an in vivo overall assessment of multiple sclerosis (MS) pathology have allowed us to obtain important novel pieces of information on disease evolution in the brain. However, despite this, the correlation between brain MR imaging metrics and clinical disability are still suboptimal. A reason for this discrepancy might be the involvement of clinically eloquent structures, such as the spinal cord, which owing to technical challenges have not been extensively studied using MR imaging until very recently. An objective and accurate estimate of the presence and extent of spinal cord damage might indeed contribute to increasing the strength of the correlations between clinical and MRI metrics. This review summarizes the main results obtained from the application of conventional and modern MR-based techniques for the evaluation of spinal cord damage in MS. [source]


    Clinical,Magnetic Resonance Imaging Correlations in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2005
    Robert Zivadinov MD
    ABSTRACT Conventional magnetic resonance imaging (MRI) has routinely been used to improve the accuracy of multiple sclerosis (MS) diagnosis and monitoring, detect the effects of diseasemodifying therapy, and refine the utility of clinical assessments. However, conventional MRI measures, such as the use of lesion volume and count of gadolinium-enhancing and T2 lesions, have insufficient sensitivity and specificity to reveal the true degree of pathological changes occurring in MS. Newer metrics of MRI analysis, including T1-weighted hypointense lesions (black holes) and central nervous system (CNS) atrophy measures, are able to capture a more global picture of the range of tissue alterations caused by inflammation, demyelination, axonal loss, and neurodegeneration. There is mounting evidence that these MRI measures correlate well with existing and developing neurological impairment and disability. In so doing, these MRI techniques can help elucidate the mechanisms underlying the pathophysiology and natural history of MS. The current understanding is that T1 black holes and CNS atrophy more accurately reflect the neurodegenerative and destructive components of the MS disease process. Therefore, the shortand long-term studies that aim to measure the degree and severity of the neurodegenerative MS disease process should incorporate these MRI metrics as part of their standard routine MRI protocols. [source]


    Measurement of Brain and Spinal Cord Atrophy by Magnetic Resonance Imaging as a Tool to Monitor Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2005
    FAAN, Rohit Bakshi MD
    ABSTRACT Evaluation of brain and spinal cord atrophy by magnetic resonance imaging (MRI) has become an increasingly important component of understanding the multiple sclerosis (MS) disease process. These destructive aspects of the disease develop early in the disease course. A growing body of data links brain and spinal cord atrophy to clinical impairment more closely than can be linked with conventional measures of overt lesions. Thus, irreversible tissue damage may be a key factor leading to disease progression. In this review, the authors present the proposed mechanisms leading to central nervous system (CNS) atrophy. They describe the available MRI-based techniques to measure regional and global atrophy of the brain and spinal cord. They compare the rate of atrophy among MS phenotypes and summarize the emerging data linking atrophy to neurological and neuropsychological impairment. Finally, they discuss the effect of disease-modifying immunotherapies on the rate of CNS atrophy in patients with MS. Future research to clarify the etiology and pathophysiology of brain and spinal cord atrophy should provide new targets for therapeutic development. [source]


    Pathogenesis of Brain and Spinal Cord Atrophy in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2004
    Alireza Minagar MD
    ABSTRACT For more than a century, multiple sclerosis was viewed as a disease process characterized by oligodendrocyte and myelin loss, and research into the pathogenesis of multiple sclerosis was mainly focused on the mechanisms of inflammation. However, with development of more sophisticated neuroimaging and molecular biology techniques, attention has shifted to new aspects of pathogenesis of multiple sclerosis: axonal loss and neurodegeneration. Evidence is increasing that tissue destruction, primarily axonal loss and neurodegeneration, is a key element in the pathogenesis of multiple sclerosis. In addition, it is now known that brain and spinal cord atrophy begins early in the disease process of multiple sclerosis and advances relentlessly throughout the course of the disease. Cumulative data suggest that axonal loss is the major determinant of progressive neuro logic disability in patients with multiple sclerosis. Magnetic resonance imaging and magnetic resonance spectroscopy in patients with multiple sclerosis for < 5 years indicate brain atrophy and loss of axonal integrity. Neurodegeneration and axonal loss in patients with multiple sclerosis are initially accompanied by a local response from oligodendrocyte progenitor cells and some remyelination. However, these repair mechanisms eventually fail, and patients typically develop generalized brain atrophy, cognitive decline, and permanent disability. Although the exact mechanisms underlying central nervous system atrophy in patients with multiple sclerosis are largely unknown, evidence exists that atrophy may represent an epiphenomenon related to the effects of dynamic inflammation within the central nervous system, including demyelination, axonal injury, neuronal loss, Wallerian degeneration, and possibly iron deposition. This article summarizes the potential mechanisms involved in central nervous system atrophy in patients with multiple sclerosis. [source]


    Measurement of Whole-Brain Atrophy in Multiple Sclerosis

    JOURNAL OF NEUROIMAGING, Issue 2004
    Daniel Pelletier MD
    ABSTRACT Brain atrophy reflects the net result of irreversible and destructive pathological processes in multiple sclerosis (MS). The gross morphological changes can be accurately quantified using standard magnetic resonance imaging (MRI) acquisitions and various image analysis tools. The current methods used to assess whole-brain atrophy in patients with MS can be classified into 2 groups based on their reliance on segmentation and registration. Segmentation-based methods employed to measure whole-brain atrophy in MS include the brain parenchymal fraction, the index of brain atrophy, the whole-brain ratio, the brain to intracranial capacity ratio, fuzzy connectedness/Udupa's method, 3DVIEWNIX, the Alfano method, and SIENAX. Current registration-based methods used to measure whole-brain atrophy in MS include the brain boundary shift integral, SIENA, statistical parametric mapping, template-driven seg mentation, and voxel-based morphometry. Most of the methods presented here are sensitive to subtle changes in brain structures and have been successfully applied to MS as measures of whole-brain atrophy. Yet comparative studies of these methods are limited and are complicated by the lack of a gold standard for image acquisition, a segmentation algorithm, an image analysis method, or a reproducibility measure. Overall, the measure of whole-brain atrophy from MRI contributes to an appreciation of the dynamics of MS pathology and its relationship to the clinical course of MS. Determination of the relative reproducibility, precision, sensitivity, and validity of these methods will promote the use of whole-brain atrophy measures as components of comprehensive MRI-based outcome assessment in MS clinical trials. [source]


    Is Gadolinium Enhancement Predictive of the Development of Brain Atrophy in Multiple Sclerosis?

    JOURNAL OF NEUROIMAGING, Issue 4 2002
    A Review of the Literature
    ABSTRACT Background and Purpose. Several studies have demonstrated that brain atrophy can be detected over relatively short intervals from the earliest stages of multiple sclerosis (MS). Reviewing the published data, the authors highlight some hypothetical pathological mechanisms proposed as determinants of brain atrophy. Methods. Using the terms multiple sclerosis, MRI (magnetic resonance imaging), and brain atrophy, 181 citations were identified. The authors considered only studies with prospective designs with natural-course MS patients and/or placebo-treated patients of therapeutic trials, in which patients under-went baseline and follow-up scans with a T1-weighted gadolinium diethylenetriamine penta-acetic acid sequence (0.1 mmol/kg body weight), and correlation analyses between Gd enhancement activity and brain atrophy progression. Results. Five hundred thirty-two patients of 5 natural history studies and 5 therapeutic trial studies participated in the review process. The main observation was that in patients with a relapsing-remitting (RR) disease course, there was a correlation between Gd enhancement activity and brain atrophy progression. This correlation was not influenced by any other demographic and clinical additional data considered in the review process. Conclusions. Examination of the pathological mechanisms pro-posed in the reviewed studies led the authors to believe that inflammation is only in part responsible for the development of brain atrophy. This conclusion may have an implication for the strategies of tissue protection advocated in the early stages of the RR course and strengthen recent evidence indicating that anti-inflammatory immunomodulatory agents and immunosuppressive treatments, which predominantly act against the inflammatory component of disease activity, may not have similar effects on progressive tissue loss, either in RR or progressive MS. [source]


    Dental Amalgam and Multiple Sclerosis: A Systematic Review and Meta-Analysis

    JOURNAL OF PUBLIC HEALTH DENTISTRY, Issue 1 2007
    Kevin K. Aminzadeh Bsc Pharm
    Abstract Objectives: Amalgam restorations have long been controversial due to their mercury content. Allegations that the mercury may be linked to nervous disorders such as Alzheimer's, chronic fatigue syndrome, and multiple sclerosis (MS) have fueled the calls for the removal of amalgam restorations from dentists' armamentarium. To explore and quantify the association between amalgam restorations and MS we have conducted a systematic review and meta-analysis of the literature. Methods: A systematic search in Medline (from 1966 to April 2006), EMBASE (2006, Week 16), and the Cochrane library (Issue 2, 2006) for English-language articles meeting specific definitions of MS and amalgam exposure was conducted. Studies were also identified using the references of retrieved articles. Studies were independently reviewed by two authors and disagreements were resolved by consensus. Studies were selected based on an a priori of defined criteria. Odds ratios (ORs) or relative risks were pooled using the random effects model. Heterogeneity was assessed using Q statistics. Results: The pooled OR for the risk of MS among amalgam users was consistent, with a slight, nonstatistically significant increase between amalgam use and risk of MS. Conclusion: Future studies that take into consideration the amalgam restoration size and surface area along with the duration of exposure are needed in order to definitively rule out any link between amalgam and MS. [source]


    14-3-3 protein in the CSF of inflammatory peripheral neuropathies

    JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004
    A Bersano
    14-3-3 proteins are a highly conserved protein family of unknown function, although some authors suggested a role in cellular proliferation and differentiation, neurotransmitters biosynthesis and apoptosis. The expression of these proteins increases during development, in particular, in large projection neurons such as spinal motor neurons. Recently the protein was described in cerebrospinal fluid (CSF) of patients with spongiform encephalopathies, in particular Creutzfeld-Jacob disease, where the protein is considered a highly sensitive and specific marker. 14-3-3 protein has been also detected in CSF of other prion-unrelated dementias and other neurodegenerative (Parkinson disease, stroke and paraneoplastic syndromes) and inflammatory diseases like Multiple Sclerosis. The aim of our study was to evaluate whether the 14-3-3 protein is also present in the CSF of peripheral nervous system diseases. We studied by Western Blot the CSF of 120 patients including 38 with Guillain-Barré syndrome (GBS), 23 with chronic inflammatory demyelinating polyneuropathy (CIDP), 12 with multifocal motor neuropathies (MMN), 20 motor neuron disease (MND), 8 paraneoplastic syndrome, 14 other neuropathies or radiculopathies (OPN), and 5 normal subjects (NC). We found the 14-3-3 protein in the CSF of 21 (55%) patients with GBS, 13 (56%) with CIDP, 1 (5%) with MND, 3 (21%) with OPN and none with paraneoplastic syndrome, MMN or NC. Our results reveal that 14-3-3 protein can be detected not only in central but also in peripheral nervous system diseases where it is significantly associated (p < 0.0001) with GBS and CIDP. [source]