1985). Most cases of ICH involve brain regions commonly affected in hypertensive ICH (Ho et al. 2009). Histopathological evidence support that repeated amphetamine abuse can result in blood vessel injury, leading to vessel wall necrosis, microinfarcts in small vessels, and atherosclerosis (McGee et al. 2004; Ho et al. 2009). Amphetamine-related SAHs mostly frequently Inhibitors,research,lifescience,medical report underlying aneurysms (Ho et al. 2009; Kaku and Lowenstein 1990). Ecstasy Ecstasy is a nonspecific name for a variety of

“designer drugs” used mainly by young adults. They are derivatives of amphetamine. The majority of Ecstasy in use is 3,4-methylenedioxymeth-amphetamine, or MDMA, N-ethyl-3,4-methylenedioxyamphetamine or MDEA (sometimes called “Eve”), or 3.4-methylenedioxyamphetamine (MDA). Recent epidemiological Inhibitors,research,lifescience,medical data indicate that Ecstasy use is increasing among college students (Strote et al. 2002). Pathophysiology Though Ecstasy is derivative of amphetamine, the drug more closely resembles the hallucinogen mescaline, rendering it to be a blend of hallucinogenic and catecholaminergic effects. Ecstasy increases the release of, and inhibits Inhibitors,research,lifescience,medical the reuptake of, serotonin

and norephinephrine, with lesser effects on dopamine. The toxicity, time course, and intensity of reaction can differ significantly between preparations. The drug is usually ingested in pill form, metabolized by the liver, and generally achieves peak concentration in the blood approximately two hours after ingestion. Ecstasy and CHIR-258 in vitro stroke There are no epidemiological studies specifically studying the incidence

of Ecstasy-related strokes. There are a small number of case studies of both ischemic and hemorrhagic strokes occurring within hours of ingestion of Ecstasy Inhibitors,research,lifescience,medical (Hughes et Inhibitors,research,lifescience,medical al. 1993; Harries and De Silva 1992; Gledhill et al. 1993; Manchanda and Connolly 1993; Hanyu et al. 1995; Kalant 2001; Auer et al. 2002). Mechanisms of stroke The vascular distribution of AISs related to Ecstasy use is variable. The possible etiologies of MDMA-induced stroke are similar to those of cocaine- and amphetamine-related strokes. Cardiac arrhythmias, have been implicated in Ecstasy-related cardiac death, and are potential causes of Ecstasy-related stroke via cardioembolism (Hughes et al. 1993). Cardiomyopathy has also been described in Ecstasy users and is associated with congestive heart failure, arrhythmia, Sitaxentan and stroke. After exposure to Ecstasy, vasospasm and necrosis have been observed in the vasculature of the globus pallidus and occipital cortex, making damage from AIS most likely in these areas (Reneman et al. 2000; Rojas et al. 2005; Hagan and Burney 2007). Damage to the vessel walls over time from chronic vasospasm and necrosis may also lead to both thrombosis and aneurysmal dilatation of cerebral vessels. This can then lead to AIS, ICH, or SAH (Kalant 2001; Auer et al. 2002).