Intracerebral hemorrhage associated with drug abuse

Intracerebral hemorrhage associated with drug abuse
Drugs implicated in precipitating cerebral hemorrhage are three main groups: - Stimulant and hallucinogenic drugs (amphetamines) - Stimulant drugs and other agents, including methylphenidate, pentazocine, tripelenamine, administered per os (oral), and intravenous (iv) - Opiates group - from which heroin is the most common
Pathophysiology 
 Etiopathogenic mechanisms by which these drugs cause intracranial bleeding are: - Changes in blood flow and blood pressure; anfetaminele, cocaine, mescaline pressor effects. Cocaine sensitizes the vessels to the effects of adrenaline and noradrenaline. Sudden changes in blood pressure (BP) and blood flow of arterioles and capillaries cause rupture. - Endocarditis - occur when administering IV Embolization with bacterial vegetation may occur in arterial walls with the development of fungal aneurysms that rupture leading to bleeding. Vascular necrosis may also occur through infected material, with the same result of vessel rupture with hemorrhage generation. - Vascular lesion with secondary bleeding. Vascular lesion may result from foreign material embolization, bacterial endocarditis through invasion or by vascular mediated immune deficiency. - Blood clotting - known to abuse drugs cause liver and kidney damage, resulting in coagulopathy.
Amphetamines cause hemorrhagic strokes, especially. Hemorrhage by amphetamines often starts within minutes after drug administration. Pressure increases rapidly, focal neurological signs appear variable intensity. Amphetamines produce and besides microinfarcte intracerebral hemorrhage or subarachnoid. 
 There have been reports of intracranial bleeding after amphetamine-like and hallucinogenic substances. Among these ephedrine norefedrina, like other phencyclidine anorexines and sympathomimetic stimulants have capabilities and can cause intracerebral hemorrhage. The risk increases at higher doses in the presence of hypertension, while the consumption of alcohol and coffee.
Intracerebral hemorrhage in cocaine consumption
 Cocaine is currently the most used and most dangerous drug, especially the segment of the population of interest for up to 40 years. Cocaine use is closely correlated with the incidence of neurological complications and death in patients.
Intracerebral haemorrhages cocaine have a high mortality rate. In addition to cerebral hemorrhage, cocaine also produces ischemia in the heart, kidneys, intestines. These effects are both beginners, as well as chronic users, without regard to quality or cocaine, or mode of administration (effects are the same in all cases). It was observed that in the case of cocaine hiroclorice bleeding stroke are twice more frequent than ischemic.
If an accident occurs on the background of intracerebral hemorrhage cocaine, it occurs within minutes or hours after dosing.
The mechanism of bleeding events is the increase in blood pressure caused by stimulation of sympathetic activity. Angiographic images ranging from normal matter arteries ocluzionate or stenosed arteries, vasospasm or vasculitis type changes. Approximately half of patients are seen pre-existing brain vascular lesions, lobar hemorrhage or hematoma in the subcortical white matter. Over 50% of intracranial hemorrhages are intracerebral, the rest being subarahnoid. In the latter case one can identify the aneurysm which usually gives the sacular made hypertensive.
Although heroin is also commonly used, have not been reported rarely cerebral hemorrhage than in direct relationship with the drug.
Alcohol toxicity is felt both CNS and peripheral. Increased risk for brain hemorrhage is twice the big drinkers than those who consume small amounts of alcohol. Among the mechanisms that contribute to the onset of cerebral hemorrhage, induced hypertension would be most important.