Cortical pathology in multiple sclerosis patients with epilepsy: a 3 year longitudinal study.
ABSTRACT The cause of epilepsy in multiple sclerosis (MS) has not yet been elucidated. The relevance of cortical pathology (cortical lesions and thickness) in MS patients with and without epilepsy was evaluated in a longitudinal study.
32 relapsing-remitting MS patients with epilepsy (RRMS/E) and 60 matched RRMS patients without epilepsy were included in a 3 year longitudinal study. The following clinical and MR parameters were analysed: Expanded Disability Status Scale (EDSS), cognitive score (CS), cortical lesion (CL) number and volume, grey matter fraction (GMf), global cortical thickness (CTh), T2 white matter lesion volume (T2WMLV), new CLs and new WM lesions.
At baseline (T0), CLs were observed in 27/32 (84.4%) RRMS/E and in 26/60 (43.3%) RRMS (p<0.001) patients, and the RRMS/E group had a higher number (10.2 ± 8.9 vs 4.5 ± 2.4; p<0.001) and total volume (2.0 ± 1.3 vs 0.7 ± 0.8 cm(3); p<0.001) of CLs compared with the RRMS group. No significant difference in T2WMLV was observed. Global CTh was lower in RRMS/E (2.12 ± 0.19 vs 2.35 ± 0.14 mm; p<0.001), and this group also showed a decline in cognition (CS 10.9 ± 6.3 vs 6.2 ± 3.5; p<0.001). After 3 years (T1), the RRMS/E group had a higher accumulation of new CLs (3.4 ± 3.2 vs 1.2 ± 1.1; p<0.001) and faster reduction of GMf (p=0.022) while the two groups did not differ in the number of new WM and new Gad+ lesions.
RRMS/E had a more severe and rapidly evolving cortical pathology (CLs and atrophy) compared with RRMS without epilepsy. The RRMS/E group was also characterised by more pronounced cognitive decline, higher EDSS and higher prevalence of men.
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ABSTRACT: Cerebral cortex shows a high endogenous propensity for remyelination. Yet, widespread subpial cortical demyelination (SCD) is a common feature in progressive multiple sclerosis (MS) and can already be found in early MS. In the present study, we compared oligodendroglial loss in SCD in early and chronic MS. Furthermore, we addressed in an experimental model whether repeated episodes of inflammatory SCD could alter oligodendroglial repopulation and subsequently lead to persistently demyelinated cortical lesions. NogoA(+) mature oligodendrocytes and Olig2(+) oligodendrocyte precursor cells were examined in SCD in patients with early and chronic MS, normal-appearing MS cortex, and control cortex as well as in the rat model of repeated targeted cortical experimental autoimmune encephalomyelitis (EAE). NogoA(+) and Olig2(+) cells were significantly reduced in SCD in patients with chronic, but not early MS. Repeated induction of SCD in rats resulted only in a transient loss of NogoA(+), but not Olig2(+) cells during the demyelination phase. This phase was followed by complete oligodendroglial repopulation and remyelination, even after four episodes of demyelination. Our data indicate efficient oligodendroglial repopulation in subpial cortical lesions in rats after repeated SCD that was similar to early, but not chronic MS cases. Accordingly, four cycles of experimental de- and remyelination were not sufficient to induce sustained remyelination failure as found in chronic cortical MS lesions. This suggests that alternative mechanisms contribute to oligodendrocyte depletion in chronic cortical demyelination in MS.Acta Neuropathologica 02/2014; · 9.78 Impact Factor
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ABSTRACT: Background Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system with a low incidence in the paediatric population; cortical atrophy is often striking, even in the early stages of the disease. Evidence of cortical thinning in childhood MS is scant. Aims This study aimed to assess cortical thickness in paediatric patients during the initial attack of remitting-relapsing MS. Methods We report two cases of remitting-relapsing MS, with initial attacks at 12 and 16 years of age. We analysed brain cortical thickness (CTh) in these patients and compared these data to the CTh of a control group comprised of six 12-year-old females and six 16-year-old males. Results Both cases exhibited a total brain CTh significantly below that of the control group. This difference was also observed when analysing the CTh of all lobes except the left parietal lobe in one of the cases. Conclusions Cortical atrophy is already present at the time of onset of MS. Studies with larger patient populations that have a more homogenous clinical presentation could identify the time of onset of cortical atrophy and use this parameter as a prognostic and/or treatment marker of MS.European journal of paediatric neurology: EJPN: official journal of the European Paediatric Neurology Society 01/2013; · 2.01 Impact Factor
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ABSTRACT: Objectives The prevalence of multiple sclerosis (MS) is increasing worldwide. Epileptic seizures are more common in MS patients than in the general population. The aim of this study was to investigate changes in the prevalence and incidence of MS in a well-defined population over several decades and estimate the occurrence of epilepsy in the same cohort.Materials and methodsPatients diagnosed with MS in the County of Vestfold, Norway in the period of 1983–2003 were identified. Point prevalence for MS and epilepsy was calculated for January 1, 2003. The average annual incidence rates were calculated in five-year periods from 1983 to 2002. These numbers were compared to previously published figures of prevalence from 1963 and incidence from 1953.ResultsOn prevalence day, we identified 364 patients diagnosed with MS living in Vestfold. Thus, the prevalence increased from 61.6/100,000 in 1963 to 166.8/100,000 in 2003. In the period 1983–2002, the annual incidence fluctuated between 4.2 and 7.3/100,000/year (mean 4.5, 95% CI 3.6 – 5.5). In 2003, the portion of MS patients with epileptic seizures was 7.4%, compared to 2.9% in 1963.Conclusions During the 40 years follow-up of this population, the incidence of MS was stable, while the prevalence of MS and the share of MS patients with epileptic seizures increased. Compared to the general population, the risk of having active epilepsy was increased fourfold. We assume that this is a consequence of an increased survival in MS patients.Acta Neurologica Scandinavica 09/2014; · 2.44 Impact Factor