Migraine is a common neurological disease of two main types: migraine with aura and migraine without aura. Familial clustering suggests that genetic factors are involved in the etiology of migraine. Recently, a gene for familial hemiplegic migraine, a rare autosomal dominant subtype of migraine with aura, was mapped to chromosome 19p13. We tested the involvement of this chromosomal region in 28 unrelated families with the common forms of migraine with and without aura, by following the transmission of the highly informative marker D19S394. Sib-pair analysis showed that affected sibs shared the same marker allele more frequently than expected by chance. Our findings thus also suggest the involvement of a gene on 19p13 in the etiology of the common forms of migraine.
This was a phase-IV double-blind equivalence trial designed to assess the efficacy and tolerability of two doses of flunarizine (10 mg o.d.=FLU 10 mg and 5 mg o.d.=FLU 5 mg) in the prophylaxis of migraine, in comparison with slow-release propranolol (160 mg o.d.). A total of 808 subjects were treated in a treatment period of 16 weeks. 142 subjects discontinued the trial prematurely, mainly because of adverse events (n=58). The mean attack frequency in the double-blind period was 2.0 for the FLU 5 mg group, 1.9 for the FLU 10 mg group, and 1.9 for the propranolol group. The mean attack frequency in the last 28 days of the double-blind period was 1.8 for FLU 5 mg, 1.6 for FLU 10 mg, and 1.7 for propranolol. Both flunarizine groups were at least as effective as propranolol (P<0.001 in one-sided test). The percentage of responders (defined as subjects for whom attack frequency decreased by at least 50% compared to run-in) in the last 28 days of the double-blind period was 46% (118/259) for FLU 5 mg, 53% (141/264) for FLU 10 mg, and 48% (125/258) for propranolol. Statistical analysis showed that FLU 10 mg is at least as effective as propranolol (P<0.001) and showed a trend for noninferiority of FLU5 and propranolol (P=0.053). No statistically significant differences between the treatment groups were found for any of the secondary parameters. Overall, 190 subjects reported one or more adverse events during the run-in phase: 54 (20.5%) in the FLU 5 mg group, 76 (27.7%) in the FLU 10 mg group and 60 (22.3%) in the propranolol group. The results of this equivalence trial show that 10 mg flunarizine daily with a drug-free weekend is at least as effective as 160 mg propranolol in the prophylaxis of migraine for all evaluated parameters (one-sided equivalence tests) after 16 weeks of treatment. In addition, 5 mg flunarizine proves to be at least as effective as 160 mg propranolol when looking at the mean attack frequency for both the whole double-blind period and the last 28 days of treatment. However, in the analysis of responders, 160 mg propranolol seems to be slightly better than 5 mg flunarizine. In addition, no significant differences between the three treatments were found with regard to safety: all three treatments were generally well-tolerated and safe.
Die Inzidenz der Migräne beträgt 6-8% für Männer und 12-14% für Frauen. Die Attacken gehen mit pulsierenden, pochenden, halbseitigen Kopfschmerzen und vegetativen Begleiterscheinungen einher. Bei ca. 15% der Patienten kommt es vor den Kopfschmerzen zu einer Aura, meist mit visuellen Symptomen.Leichte und mittelschwere Migräneattacken werden mit der Kombination eines prokinetischen Antiemetikums wie Metoclopramid oder Domperidon und einem ausreichend dosierten Analgetikum (Azetylsalizylsäure, Paracetamol, Ibuprofen, Naproxen, Diclofenac) behandelt. Mittelschwere und schwere Migräneattacken werden mit den modernen 5-HT 1B/D -Rezeptoragonisten ("Triptane") behandelt. Die Kombination eines Antiemetikums und Ergotamintartrat ist weniger wirksam als die "Triptane".Patienten mit häufigen oder schweren Migräneattacken benötigen eine medikamentöse und nicht-medikamentöse Prophylaxe. Medikamente der ersten Wahl sind die Beta-Rezeptorenblocker Metoprolol oder Propranolol und der Kalziumantagonist Flunarizin. Substanzen der zweiten Wahl sind Valproinsäure und nicht-steroidale Antirheumatika. Bei den nichtmedikamentösen Therapien sind multimodale Therapieansätze, die Techniken der progressiven Muskelrelaxation, kognitive Techniken, Stress-und Reizverabreitungstraining und Schmerzbewältigungstechniken verbinden, sowie die Sporttherapie (aerobes Ausdauertraining) wirksam.Die Deutsche Migräne-und Kopfschmerzgesellschaft hat letztmals 1997 Therapieempfehlungen für die Behandlung der Migräne veröffentlicht [16]. Seitdem sind mehrere neue 5-HT 1B/1D -agonisten ("Triptane") zugelassen und zahlreiche Studien zur Akuttherapie und Prophylaxe der Migräne publiziert worden. Die Therapieempfehlungen orientieren sich formal an den ᭤ Kriterien der evidence-based medicine. Die Kategorien der Evidenz wurden von der Arzneimittelkommission der Deutschen Ärzteschaft übernommen. Sie sind wie folgt definiert: ›› Aussage zur Wirksamkeit wird gestützt durch mehrere adäquate, valide klinische Studien (z.B. randomisierte klinische Studien) bzw. durch eine oder mehrere valide Metaanalysen oder systematische Reviews. Positive Aussage gut belegt. › Aussage zur Wirksamkeit wird gestützt durch zumindest eine adäqute, valide klinische Studie (z.B. randomisierte klinische Studie). Positive Aussage belegt. 269 ᭤ Kriterien der evidence-based medicine Schmerz 2000 · 14:269-283
Background: The long-term follow-up system for Guillain-Barré syndrome (GBS) is not well established worldwide. In our study, the preliminary data of the long-term prognosis of GBS are collected to explore the prognosis of GBS and the effect of intravenous immunoglobulin (IVIg) treatment. Methods: The follow-up data of 186 patients with GBS admitted from 2003 to 2013 were collected in 2015 via phone interview. The GBS disability scale score was ranked by clinician to evaluate the long-term prognosis. The clinical data during the acute phase were also collected. Results: The mortality rates were 2.15%, 5.45% and 7.89% at discharge, 2-5 years and 6-10 years after disease, respectively. The GBS disability scale score improved dramatically from discharge to 2-12 years after the acute phase. The self-limitation, the spontaneous recovery of disease, occurred both at acute phase and 2-5 years after discharge. Comparisons between IVIg-treated patients and GBS patients who only received supportive care revealed no significant difference of long-term prognosis. Conclusion: The long-term prognosis of GBS appears not to be influenced by treatment options. The long-term improvement of IVIg treated-patients might be due to the self-limitation of GBS per se instead of the IVIg treatment.
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