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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drug abuse is associated with a variety of neurological complications. The use of certain recreational drugs shows a marked temporal association with the onset of both haemorrhagic and ischaemic strokes, the majority of which develop within minutes to 1 h after the administration of the index drug. Delayed onset of stroke has also been observed. Acute, severe elevation of blood pressure, cardiac dysrhythmias, cerebral vasospasm, vasculitis, embolization due to infective endocarditis or dilated cardiomyopathy, embolization due to foreign material injected with the diluents under non-sterile conditions and 'street drug' contaminants with cardiovascular effects have been suggested as possible underlying mechanisms. Rupture of aneurysms and arteriovenous malformations have been detected in up to half of the patients with haemorrhagic stroke due to cocaine abuse. The less common findings reported have included a mycotic cerebrovascular aneurysm in a patient with infective endocarditis and haemorrhagic stroke. In addition to stroke, cocaine seems to provoke vascular headache. Seizures precipitated by recreational drug abuse are usually caused by acute intoxication in contrast to the withdrawal seizures encountered in subjects with alcohol abuse. Movement disorders and cerebral atrophy correlating with the duration of abuse have been described. Snorting of organic solvents may cause encephalopathy. Cases of spongiform leukoencephalopathy in heroin addicts have also been reported. Peripheral neuropathy is occasionally precipitated by drug poisoning after intravenous administration. Impurities of the drug, risky administration techniques, and the use of mixtures of various drugs, frequently with simultaneous alcohol drinking, should be taken into account when assessing the background of the adverse event as well as the overall lifestyle of the addicted subjects.
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PMID:Neurological complications of drug abuse: pathophysiological mechanisms. 1113 45

Epidemiological evidences indicated that substance abuse disorders are increasingly prevalent among Nigerians. The psychosocial deleterious effects of these drugs appear well recognised, but their medical consequences are less often considered in the region. The potential for these drugs to precipitate life threatening cardiac and brain event needs to be reemphasised. We report the clinical and laboratory findings in 4 Nigerians in whom non-intravenous use (recreational and ritualistic) of cocaine was temporally related to acute myocardial ischaemia, cardiac dysarrhythmias, convulsion and cerebrovascular accident. These findings suggest that the observations--that underlying heart disorders were not sinequanon for the cardiotoxic effects of cocaine; the brain and cardiac consequences were not restricted to parenteral use of the drug; the development of seizures were not prerequisite for cerebrovascular accident and vice versa; and that massive doses of the drug needed not be ingested to produce toxic effects on the heart and brain--may also apply in these Nigerian patients. Perhaps with the increase in user population, it is timely to embark on public enlightenment on the medical dangers of cocaine abuse, as these are no less important than the psychosocial consequences.
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PMID:Brain cardiac events in Nigerian patients with cocaine abuse. 1150 92

Cocaine abuse represents a worldwide significant forensic issue as it is becoming widely recognized as one of the most dangerous illicit drugs in common use today. Besides cardiovascular complications, psychiatric and neurologic symptoms are the most common manifestations of cocaine toxicity. The latter include seizures, movement disorders and cerebrovascular complications. In chronic cocaine abusers morphological, physiological, and neurochemical abnormalities have been demonstrated by using neuroradiological techniques such as computed tomography, magnetic resonance imaging, positron emission tomography or single photon emission computed tomography. The spectrum of neuropathologic changes encountered in the brains of cocaine abusers is broad, but the major findings consist of ischemic and hemorrhagic stroke, subarachnoid and intracerebral hemorrhages and cerebral ischemia. Especially persons with underlying arteriovenous malformation or aneurysm are at risk for such events. Except for a few instances of vasculitis, the etiology of cocaine-related cerebrovascular accidents is still unclear. Besides pharmacologically-induced vasospasm, impaired hemostasis and platelet function and decreased cerebral blood flow have been proposed. At the cellular level, abnormalities in the expression of transcription factors and changes of brain neurotransmitter systems have been reported.
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PMID:The neuropathology of cocaine abuse. 1293

Cocaine abuse is known to induce different types of brain-microvascular damage and many adverse cerebrovascular effects, including cerebral vasculitis, intracranial hemorrhage, cerebral infarction and stroke. A major physiological event leading to these pathophysiological actions of cocaine could be apoptosis. Whether cocaine can cause brain-microvascular pathology and vascular toxicity by inducing apoptosis of cerebral vascular smooth muscle cells is not known. This study, using several different methods to discern apoptosis, was designed to investigate if primary cultured canine cerebral vascular smooth muscle cells can undergo apoptosis when treated with cocaine. After treatment with cocaine (10(-6)-10(-3) M) for 12-24 h, the death rates of cerebral vascular smooth muscle cells increased in a concentration-dependent manner compared with controls. Morphological analysis of cerebral vascular smooth muscle cells using confocal fluoresence microscopy showed that the percentage of apoptotic cerebral vascular smooth muscle cells increased after cocaine (10(-6)-10(-3) M) treatment in a concentration-dependent manner. TUNEL assays also showed positive results for cerebral vascular smooth muscle cells treated with cocaine. These results clearly demonstrate that cerebral vascular smooth muscle cells can undergo rapid apoptosis in response to cocaine in a concentration-dependent manner. Cocaine-induced apoptosis may thus play a major role in brain-microvascular damage, cerebral vascular toxicity and strokes.
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PMID:Cocaine induces apoptosis in cerebral vascular muscle cells: potential roles in strokes and brain damage. 1466 5

Atherosclerosis increases cardiovascular risk and the possibility of developing acute myocardial infarction (AMI) or stroke. Patients infected with human immunodeficiency virus (HIV) often present morphological and metabolic alterations (hypercholesterolemia, hypertriglyceridemia, insulin resistance, diabetes) that can increase vascular risk. The frequent coexistence of classic risk factors (atherogenic diet, smoking, physical inactivity, cocaine abuse), the progressive increase in mean age of HIV-1 infected patients, and the polymedication they receive make it difficult to estimate the direct effect that new therapies may have on cardiovascular risk. Retrospective clinical studies with diverse designs in large cohorts offer contradictory results for cardiovascular risk in the HIV-infected population. Longer observational periods are needed and the effect of other classic risk factors needs to be controlled, in order to establish the possible detrimental effect the new therapies may have on cardiovascular risk in this population.
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PMID:[Cardiovascular risk in patients with chronic HIV-1 infection: a controversy with therapeutic, clinical and prognostic implications]. 1475 7

Stroke in young adults has been related to mechanisms different to those found in older individuals. Cardiogenic embolism, arteritis, atherosclerosis, fibromuscular dysplasia, pregnancy-related angiopathy, migrainous stroke, anaemia, antiphospholipid syndrome, arterial dissection, the consumption of toxic substances and head trauma have been described. We present a young man with a case history of tobacco and cocaine abuse who suffered a mild head trauma, with normal neurological examination, and a computed tomography scan image of a right anterior cerebral infarction. Serum biochemistry showed no alterations according to the diagnosis protocol for stroke in young patients. Various mechanisms have been involved, such as vasospasm, increasing arterial pressure and embolism. Considering the cocaine abuse and the mild head trauma, in our patient vasospasm was thought to be the mechanism involved in the cerebral infarction, which proved a challenge to diagnose in the emergency room.
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PMID:Stroke in young patients: a diagnostic challenge in the emergency room. 1516 83

Psychostimulant drugs abuse is associated with an increased risk of stroke. Cytochromes P450 (CYP), especially the astrocytic members of the CYP2C subfamily may play an important role in the modulation of cerebrovascular functions, by generating vasodilatator metabolites from arachidonic acid (AA). Our study examined the regulation of CYP2C genes in response to cocaine or amphetamine in the human astrocyte-like U373 MG cells, using reverse transcription-polymerase chain reaction (RT-PCR) and western-blot analysis. A treatment for 48h with increasing concentrations of cocaine caused a significant down-regulation of CYP2C8 and CYP2C9 genes and decreased the protein level. These effects were not observed with amphetamine. One mechanism of the CYP2C mRNA regulation implicates various specific receptors including glucocorticoid receptor (GR) and constitutive androstane receptor (CAR). Effects of cocaine on CYP2C were accompanied by a decrease in the GR and CAR gene expression suggesting that these nuclear receptors could be involved in the CYP2C repression by cocaine in the U373 MG cell line. These findings represent a possible molecular mechanism involved in the cerebrovascular risk associated with cocaine abuse.
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PMID:Down-regulation of astroglial CYP2C, glucocorticoid receptor and constitutive androstane receptor genes in response to cocaine in human U373 MG astrocytoma cells. 1618 4

Arterial ischemic infarction occurring around the time of birth is an increasingly recognized cause of neurological disability in children. The rate of arterial infarction in neonates is as high as the annual incidence of large-vessel ischemic stroke in adults. Factors contributing to this increased risk of stroke among neonates include complications that occur before, during, and after delivery. Maternal conditions that have been associated with perinatal stroke in the fetus include prothrombotic disorders, cocaine abuse, and placental complications such as chorioamnionitis and placental vasculopathy. In many cases, the placenta is suspected to be the underlying embolic source for perinatal stroke, although data on placental pathology is often lacking. During the delivery process, an infant may develop a cervical arterial dissection that leads to stroke. Several conditions in the neonatal period predispose to perinatal stroke including prothrombotic disorders, congenital heart disease, meningitis, and systemic infection. Perinatal stroke may present with neonatal seizures during the first weeks of life or may be asymptomatic until months later when the infant is first noted to have pathological handedness. The outcome of perinatal stroke is variable and depends on severity, anatomic localization, and other factors not yet well characterized. As many as 50% of infants with documented stroke recognized in the newborn period do not develop a hemiparesis. The incidence, clinical presentation, pathogenesis, risk factors, and outcome of this increasingly recognized disorder are reviewed.
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PMID:Perinatal arterial stroke: understanding mechanisms and outcomes. 1634 98

The authors report the case of a 30-year-old woman who was a long-term intranasal cocaine abuser and who presented with transient ischemic attacks and multiple cerebral infarctions that were associated with moyamoya syndrome. The authors suggest that, because of its sympathomimetic effects, chronic cocaine use may promote intracranial arterial stenosis, distal ischemia, and subsequent formation of moyamoya-like vessels. The patient has remained clinically stable with no new episodes of stroke 6 years after undergoing "pial synangiosis" (modified encephaloduroarteriosynangiosis) to revascularize both hemispheres. Cocaine abuse may lead to moyamoya syndrome and may represent a chronic effect on the cerebral vasculature.
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PMID:Moyamoya syndrome associated with cocaine abuse. Case report. 1711 10

Cocaine is the second most commonly abused illicit drug in the US and the most common one involved in emergency department visits, the majority of which are related to the cardiovascular system. Cardiovascular complications related with cocaine abuse include myocardial ischemia and infarction, myocarditis, hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic dissection, thrombosis, stroke and cerebral hemorrhage, and different forms of visceral ischemia, among others. In an era where cocaine use has reached epidemic proportions, it is necessary for the radiologist to understand the pathophysiology, clinical presentation, and imaging characteristics of its cardiovascular complications.
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PMID:Cardiovascular complications of cocaine: imaging findings. 1877 29


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