Belastungen mit chlororganischen Schadstoffen und Metallen bei Patienten mit Multipler Sklerose

Bei der Multiplen Sklerose (MS, Encephalomyelitis disseminata) handelt es sich um eine chronische, multilokuläre demyelinisierende Erkrankung des Zentralen Nervensystems, deren Ursachen bisher nicht exakt geklärt werden konnten. Die im ZNS disseminiert auftretenden Entzündungs- und Entmarkungsherde sind Ursache der sehr unterschiedlich verlaufenden klinischen Symptomatik u.a. mit multifokalen sensiblen Ausfällen, Paresen, Hirnnervenbefall, zerebellären Störungen, Blasenstörungen sowie neuropsychologischen Defiziten (z.B. hirnorganisches Psychosyndrom). Bei einer Prävalenz von etwa 50-100/100.000 und einer Inzidenz von 4-6/100.000 in Deutschland beträgt das Verhältnis von Frauen zu Männern etwa 2:1. Ätiologisch werden u.a. T-Zell-vermittelte Autoimmunmechanismen, Virusinfektionen, genetische Dispositionen und der Einfluß verschiedener Umweltfaktoren diskutiert. Es stellt sich auch die Frage nach erhöhten Belastungen mit chlororganischen Schadstoffen und Metallen

Belastungen mit chlororganischen Schadstoffen und Metallen bei Patienten mit Multipler Sklerose

Bei der Multiplen Sklerose (MS, Encephalomyelitis disseminata) handelt es sich um eine chronische, multilokuläre demyelinisierende Erkrankung des Zentralen Nervensystems, deren Ursachen bisher nicht exakt geklärt werden konnten. Die im ZNS disseminiert auftretenden Entzündungs- und Entmarkungsherde sind Ursache der sehr unterschiedlich verlaufenden klinischen Symptomatik u.a. mit multifokalen sensiblen Ausfällen, Paresen, Hirnnervenbefall, zerebellären Störungen, Blasenstörungen sowie neuropsychologischen Defiziten (z.B. hirnorganisches Psychosyndrom). Bei einer Prävalenz von etwa 50-100/100.000 und einer Inzidenz von 4-6/100.000 in Deutschland beträgt das Verhältnis von Frauen zu Männern etwa 2:1. Ätiologisch werden u.a. T-Zell-vermittelte Autoimmunmechanismen, Virusinfektionen, genetische Dispositionen und der Einfluß verschiedener Umweltfaktoren diskutiert. Es stellt sich auch die Frage nach erhöhten Belastungen mit chlororganischen Schadstoffen und Metallen

Extrapontine myelinolysis presenting as acute parkinsonism

BACKGROUND: Extrapontine myelinolysis presenting with extra pyramidal features suggestive of parkinsonism may be a challenging clinical syndrome. Clinicians should maintain their vigilance while correcting electrolyte imbalances, especially with associated co-morbidity. CASE PRESENTATION: A 41-year-old woman presented with acute parkinsonism like features while on a holiday. This followed slow correction of hyponatraemia after repeated vomiting. MRI changes were suggestive of Extrapontine myelinolysis(EPM). This case is at variance with four previous cases reported in the medical literature in that the patient made a full clinical recovery and the MR changes resolved with symptomatic support alone. CONCLUSION: Extrapontine myelinolysis could make a complete recovery with symptomatic support alone. During hyponatraemia correction, rapid osmotic shifts of fluid that cause hypernatremia, causes myelinolysis rather than absolute serum sodium level. Even gradual correction of hyponatraemia can produce myelinolysis, especially with pre-existing malnourishment, alcoholism, drug misuse, Addison's disease and immuno-suppression. Pallidial sparing is typical of EPM in MRI scans

An extended association screen in multiple sclerosis using 202 microsatellite markers targeting apoptosis-related genes does not reveal new predisposing factors

Apoptosis, the programmed death of cells, plays a distinct role in the etiopathogenesis of Multiple sclerosis (MS), a common disease of the central nervous system with complex genetic background. Yet, it is not clear whether the impact of apoptosis is due to altered apoptotic behaviour caused by variations of apoptosis-related genes. Instead, apoptosis in MS may also represent a secondary response to cellular stress during acute inflammation in the central nervous system. Here, we screened 202 apoptosis-related genes for association by genotyping 202 microsatellite markers in initially 160 MS patients and 160 controls, both divided in 4 sets of pooled DNA samples, respectively. When applying Bonferroni correction, no significant differences in allele frequencies were detected between MS patients and controls. Nevertheless, we chose 7 markers for retyping in individual DNA samples, thereby eliminating 6 markers from the list of candidates. The remaining candidate, the ERBB3 gene microsatellite, was genotyped in additional 245 MS patients and controls. No association of the ERBB3 marker with the disease was detected in these additional cohorts. In consequence, we did not find further evidence for apoptosis-related genes as predisposition factors in MS

BG-12 reduces evolution of new enhancing lesions to T1-hypointense lesions in patients with multiple sclerosis

BG-12, an immunomodulatory agent, reduces frequency of new gadolinium-enhancing (Gd+) lesions in relapsing multiple sclerosis (MS). This study reports the effect of 240 mg BG-12 orally three times daily (tid) for 24 weeks on the evolution of new Gd+ lesions to T1-hypointense lesions. Brain magnetic resonance imaging (MRI) scans from patients in placebo and 240 mg BG-12 tid arms of a phase 2b study were examined retrospectively. Included patients had at least one new Gd+ lesion from weeks 4 to 12. Week 24 scans were analyzed for number and proportion of new Gd+ lesions that evolved to T1-hypointense lesions. Eighteen patients receiving BG-12 and 38 patients receiving placebo were included in the analysis. The analysis tracked 147 new Gd+ lesions in patients from the BG-12 group and 221 Gd+ lesions in patients from the placebo group. The percentage of Gd+ lesions that evolved to T1-hypointense lesions was 34% lower with BG-12 treatment versus placebo (29%, BG-12; 44%, placebo; odds ratio 0.51; 95% confidence interval 0.43, 0.61; p > 0.0001). In addition to reducing frequency of new Gd+ lesions, BG-12 significantly reduced probability of their evolution to T1-hypointense lesions in patients with MS compared with placebo