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efficacy of triptans in migraine menstrual

menstrual migraine affects approximately 50-60% of women who suffer from migraines, but knowledge about the role of hormones, particularly estrogen, is yet to be defined in a comprehensive manner. Researchers at Vanderbilt University School of Medicine in Nashville (USA) conducted a systematic review aimed to determine the role of hormones menstrual migraine. From the literature, we selected 643 articoli.L 'influence of estrogen in migraine is evident by the fact that women have an incidence of migraines three times more than men, and significant changes in the incidence of migraine in female reproductive function of the state. The menstrual migraine is generally more resistant to treatment, usually not associated with aura, is long lasting and, in general, involves a greater functional disability compared with attacks occurring at other times of the month. The genetic and biochemical evidence indicates a central and peripheral role of estrogen in the pathophysiology of menstrual migraine, with potential interactions with excitatory circuits, including serotonergic components. Although there is no evidence regarding the use of estrogen as a preventative treatment of menstrual migraine, serotonin receptor agonists (triptans) have a deep relief and may also have a preventive role. In conclusion: the epidemiological evidence, clinical and pathophysiological correlates estrogen migraine. Triptans appear to significantly alleviate the pain and can also be used as a preventive measure.

Brandes JL, JAMA 2006, 295: 1824-1830

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Encouraging results for creatine and minocycline in Parkinson's disease in early

A study by NINDS NET-PD Investigators evaluated whether minocycline creatine el'antibiotico were able to alter the course of Parkinson's disease at an early stage. Participants had been diagnosed with Parkinson's disease for less than 5 years and do not require treatment for the symptoms. The primary endpoint was the change to the scale UPDRS (Unified Parkinson's Disease Rating Scale) from baseline at the time was found sufficient to establish disability symptomatic therapy for Parkinson's disease, or 12 months. A total of 200 patients were randomized in 1:1:1 ratio to receive creatine 10g/die, Minocycline 200 mg or placebo. The futility threshold was defined as a 30% reduction in the progression of the UPDRS scale compared to the placebo arm / DATATOP tocopherol in the study (Deprenyl And Tocopherol Antioxidative Therapy of Parkinsonism). A p value less than or equal to 0.1 index was futility. E 'was observed that neither creatine nor minocycline may be considered futile therapy based on the threshold of futility DATATOP. Tolerability was 91% in the creatine group and 77% in the minocycline group. The most common side effects were: respiratory symptoms (26%), joint pain (19%), nausea (17%). According to the authors, is that the creatine minocycline should be assessed in phase III clinical trials to determine if they are able to change the long-term progression of Parkinson's disease.

NINDS NET-PD Investigators, Neurology 2006; Published online before print

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Indiplon in the treatment of insomnia

Indiplon is a non-benzodiazepine sedative-hypnotic in the short duration of action. It 's a high-affinity allosteric enhancer of GABA-A receptor. E 'Indiplon has been shown that it binds to specific binding sites for BZ1 or GABA-A receptor alpha 1, differing from the classic benzodiazepines. A phase III To evaluate the efficacy and safety of Indiplon, immediate-release formulation, in 200 adult patients with chronic primary insomnia over a period of 35 days. Indiplon showed a statistically significant improvement nell'end primary endpoint of Latency to Persistent Sleep (LPS), a measure obtained by polysomnography. Treatment with LPS Indiplon 10mg reduced to 28 minutes (p <> Q). Rebound insomnia was not observed. A second phase III clinical trial with immediate-release Indiplon showed the achievement of primary and secondary end points in 593 subjects with transient insomnia. The primary end point was represented by Latency to Persistent Sleep (LPS), while the end secondary endpoint was to Latency to Sleep Onset (LSO). The improvements mean nell'end primary endpoint were 36% and 50% for the 10mg dose and 20mg, respectively. Patients also presented an improvement of Sleep Quality for both doses.

Source: Neurocrine Biosciences, 2006