Jacob Hansen-Schwartz

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OBJECTIVE Delayed cerebral vasospasm has long been recognized as an important cause of poor outcome after an otherwise successful treatment of a ruptured intracranial aneurysm, but it remains a pathophysiological enigma despite intensive research for more than half a century. METHOD Summarized in this review are highlights of research from North America,(More)
Eleven pregnant women on lamotrigine (LTG) monotherapy were retrospectively reviewed. A significant decrease in the ratio of plasma LTG concentration-to-dose by 65.1% was observed during the second trimester (TM2) (p=0.0058) and by 65.8% during TM3 (p=0.0045) compared to pre-pregnancy values. Five patients experienced seizure deterioration during pregnancy.(More)
OBJECT The authors investigated early changes in the cerebral arteries of rats that occur after subarachnoid hemorrhage (SAH). METHODS Messenger RNA was investigated by performing microarray and quantitative real-time polymerase chain reaction (PCR) analyses, and protein expression was shown by performing immunohistochemical studies. The array data(More)
Thirteen pregnancies in ten women on oxcarbazepine (OXC) monotherapy and one pregnancy in a woman on OXC and topiramate therapy were retrospectively analyzed. A significant decrease of ratio plasma concentration of 10-monohydroxy derivate (MHD) of oxcarbazepine to dosage was found by 26.2% during first trimester, by 36.5% during second trimester and by(More)
OBJECT Cerebral vasospasm following subarachnoid hemorrhage (SAH) leads to reduced blood flow in the brain. Inspired by organ culture-induced changes in the receptor phenotype of cerebral arteries, the authors investigated possible changes in the 5-hydroxytryptamine (HT) receptor phenotype after experimental SAH. METHODS Experimental SAH was induced in(More)
OBJECTIVE Inspired by organ culture-induced changes in the vascular endothelin (ET) receptor population, we investigated whether such changes occur in cerebral arteries in a rat subarachnoid hemorrhage (SAH) model. METHODS SAH was induced with injection of 250 microl of blood into the prechiasmatic cistern. After 2 days, the middle cerebral artery,(More)
BACKGROUND Aneurysmal rebleeding poses a serious risk in patients with subarachnoid hemorrhage (SAH). Studies have shown that antifibrinolytic therapy with tranexamic acid has a dramatic effect on the rate of rebleeding. Therefore, changes in the fibrinolytic system could be hypothesized. METHODS We have used an experimental SAH rat model to demonstrate(More)
OBJECTIVES Given that reliable markers for early ischemic brain damage are lacking, we set out to test whether pimonidazole can be used as a reliable tool in the quantification of hypoxic insults, at early time points following experimental stroke. METHODS We have used semi-quantitative Western blotting detection of pimonidazole adducts in a rat model of(More)
The cellular mechanisms responsible for cerebral vasospasm (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed(More)
The inflammatory response plays a pivotal role in propagating injury of intracerebral hemorrhage (ICH). Glucagon-like-peptide-1 (GLP-1) is a hormone with antidiabetic effect and may also have antiinflammatory properties. Despite consensus that the glucoregulatory action is mediated by the GLP-1 receptor (GLP-1R), mechanisms in the brain remain unclear. We(More)