The risk of major birth defects was further stratified by

earliest trimester of pregnancy exposure. The registry enrolled 680 evaluable exposed pregnant women, which resulted in 689 infants and fetuses (outcomes). Of these outcomes, 626 were exposed to sumatriptan, 57 were exposed to naratriptan (seven were exposed to both sumatriptan and naratriptan), and six were exposed to the sumatriptan/naproxen sodium combination product. Twenty outcomes with major birth defects were reported among 528 outcomes exposed in the first trimester Kinase Inhibitor Library to sumatriptan. The estimated risk of major birth defects following first-trimester sumatriptan exposure is 4.2% (20/478 [95% confidence interval [CI] 2.6%–6.5%]). Among 52 first-trimester

exposures to naratriptan, major birth defects were reported in one outcome, an infant with exposure to both sumatriptan and naratriptan [birth defect risk of 2.2% (1/46 [95% CI 0.1%–13.0%]). No major defects were reported among the five outcomes with first-trimester exposure to the sumatriptan/naproxen sodium combination products. The Sumatriptan, Naratriptan, and Treximet Pregnancy Registry detected no signal of teratogenicity associated with major birth defects for sumatriptan. This finding is consistent with results from other observational studies using a variety of control groups. CP-690550 mw Enrollment in the registry was insufficient to permit definitive conclusions of the risks associated with naratriptan or sumatriptan/naproxen sodium tablets, or to assess the risk of individual birth defects in any of the products studied. Low enrollment and high rates of loss to follow up within Tau-protein kinase the registry over an extended period of time led the registry’s scientific advisory committee to conclude that continuation of the registry beyond its 16 years would offer little additional power to rule out more moderate increases in the risk of birth defects. Data from the other ongoing surveillance sources constitute an important element of post-marketing surveillance of these medications. The lack of a

signal of major teratogenicity with sumatriptan across these several sources of data is encouraging. “
“No single model of migraine explains all of the known features of the disorder. Migraine has recently been characterized as an abnormality in pain-modulating circuits in the brainstem. The periaqueductal gray appears to have a critical role in migraine genesis and has been labeled the “migraine generator.” The concept of a “pain matrix,” rather than a specific locus of pain, is widely accepted in the pain literature and offers a new dimension to understanding migraine. Recent neuroimaging studies of migraineurs suggest altered functional connectivity between brainstem pain-modulating circuits and cortical (limbic) centers.