Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stroke is the third most common cause of death in developed countries. In England and Wales, 1000 people under the age of 30 have a stroke each year. Cocaine is the most commonly used class A drug, and the first report of cocaine-induced stroke was in 1977. Since the development of alkaloidal "crack" cocaine in the 1980s, there has been a significant rise in the number of case reports describing both ischaemic and haemorrhagic stroke associated with cocaine use. Cocaine is a potent central nervous system stimulant, and acts by binding to specific receptors at pre-synaptic sites preventing the reuptake of neurotransmitters. The exact mechanism of cocaine-induced stroke remains unclear and there are likely to be a number of factors involved including vasospasm, cerebral vasculitis, enhanced platelet aggregation, cardioembolism, and hypertensive surges associated with altered cerebral autoregulation. The evidence surrounding each of these factors will be considered here.
 ...
PMID:Cocaine use and stroke. 1755 Oct 70

It has been postulated that ischemic stroke due to acute cocaine usage involves constriction of the cerebral vasculature. However, the mechanism underlying the constriction remains unclear. This study tested whether cocaine constriction was mediated via endothelin-1. Cocaine suffusion induced maintained constriction in the rabbit basilar artery in situ. The constriction was relaxed by PD145065, an endothelin A and B receptor antagonist. These results support the hypothesis that constriction of the cerebral vasculature due to acute cocaine exposure is via endothelin-1 release. Endothelin receptor antagonists may be of therapeutic benefit in cerebrovascular pathophysiologies involving cocaine constriction.
 ...
PMID:Acute cocaine induces endothelin-1-dependent constriction of rabbit basilar artery. 1757 7

Cocaine and amphetamine-regulated transcript (CART) is a neuropeptide that protects brains against ischemic injury in vivo and in vitro. By using small interference RNA against CART(CARTi), this study shows that CART knockdown by CARTi downregulated exogenous and endogenous CART mRNA and protein expression in vivo and in vitro. Consequently, CART knockdown exacerbated neuronal cell death induced by oxygen and glucose deprivation (OGD). It also showed that CART knockdown increased infarct size in a mouse middle cerebral artery occlusion model. CART's protective effects are most likely mediated through the ERK 1/2 pathway, since ERK 1/2 phosphorylation, not that of p38 or JNK is activated in CART-treated neurons after OGD. Furthermore, neuroprotection of CART is abolished by CART knockdown and by pretreatment with ERK antagonist PD98059 and U0126, but not with p38 or JNK antagonists SB203580 or SP600125. These results provide further evidence that CART is an endogenous neuroprotective peptide against cerebral ischemia and it does so through the MAPK/ERK signaling pathway. Therefore, CART may be developed into a therapeutic agent for stroke-related brain injury.
 ...
PMID:CART protects brain from damage through ERK activation in ischemic stroke. 1864 22

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.
 ...
PMID:Cardiovascular complications of cocaine: imaging findings. 1877 29

Stroke, which is unusual in young adults, has been linked to recreational drug use and the antiphospholipid syndrome (aPS). Cocaine use has been related to stroke in this population, and aPS is a known cause of thrombotic neurologic events. We report a patient with positive lupus anticoagulant and anticardiolipin antibodies as well as a history of cocaine use immediately preceding the acute onset of multiple neurologic deficits. The findings in this case suggest a relationship between the use of cocaine, the aPS, and stroke in young adults.
 ...
PMID:Antiphospholipid antibodies, cocaine use, and stroke in a young woman. 1907 91

Cocaine is a risk factor for both ischemic and haemorrhagic stroke. We present the case of a 31-year-old man with bilateral ischemia of the globus pallidus after excessive alcohol and intranasal cocaine use. Drug-related globus pallidus infarctions are most often associated with heroin. Bilateral basal ganglia infarcts after the use of cocaine, without concurrent heroin use, have never been reported. In our patient, transient cardiac arrhythmia or respiratory dysfunction related to cocaine and/or ethanol use were the most likely causes of cerebral hypoperfusion.
 ...
PMID:Bilateral haemorrhagic infarction of the globus pallidus after cocaine and alcohol intoxication. 1968 52

Cocaine use is reaching epidemic proportions in the UK and the consequences are a number of debilitating effects. Strokes may result from a number of mechanisms related to cocaine use. This report describes a case of cocaine induced stroke in an apparently healthy young man with unusual patterns of radiological findings on his brain MRI.
 ...
PMID:Spastic paraparesis following cocaine inhalation. 1970 79

Cocaine use is associated with ischemic stroke through unique mechanisms, including reversible vasospasm, drug-induced arteritis, enhanced platelet aggregation, cardioembolism, and hypertensive surges. To date, no study has described disability in patients with cocaine-related ischemic stroke. The present study compared risk factors, comorbidities, complications, laboratory findings, medications, and outcomes in patients with cocaine-related (n = 41) and non-cocaine-related (n = 221) ischemic stroke (n = 147) and transient ischemic attack (n = 115) in 3 academic hospitals. The patients with cocaine-related stroke were younger (mean age, 51.9 years vs 59.1 years; P = .0008) and more likely to be smokers (95% vs 62.9%; P < .004). The prevalence of arrhythmias was significantly higher in the patients with cocaine-related stroke, and that of diabetes was significantly higher in those with non-cocaine-related strokes. The prevalence of hypertension and lipid profiles were similar in the 2 groups; however, those with cocaine-related stroke were less likely to receive statins. Antiplatelet use was similar in the 2 groups. Survivors of both groups had similar modified Rankin scores and lengths of hospital stay. In the older urban population, smoking and cocaine use may coexist with other cerebrovascular risk factors, and cocaine-related strokes have similar morbidities and mortality as non-cocaine-related strokes. Moreover, because the patients with cocaine-related stroke is younger, they have an earlier morbidity. New strategies for effective stroke prevention interventions are needed in this subgroup.
J Stroke Cerebrovasc Dis
PMID:Clinical profiles, complications, and disability in cocaine-related ischemic stroke. 2081 50

In arterial dissection, blood may enter the arterial wall through an intimal tear, splitting the arterial wall and activating the coagulation cascade at the site of endothelial damage. Dissection of extracranial and intracranial vessels may lead to ischemic stroke through thromboembolic or hemodynamic mechanisms. Major blunt trauma or rapid acceleration-deceleration may cause dissection, but in patients with inherent arterial wall weakness, dissection can occur spontaneously or as a result of minor neck movement. Cocaine use has been associated with dissection of the aortic arch and coronary and renal arteries through cocaine-mediated hypertension. Recent preclinical studies have suggested, however, that cocaine may cause apoptosis of cells in the vascular wall. In this article, we postulate that cocaine may cause apoptosis of vascular endothelial and/or smooth muscle cells, thus weakening the vascular wall and resulting in a dissection-prone state. We review the literature and propose a biological basis for vasculopathy, vascular dissection, and ischemic stroke in the setting of cocaine use. Further research studies on vascular cells, as well as focused analysis of human pathological material, will be important in providing evidence for or against our hypotheses.
 ...
PMID:Cocaine mediated apoptosis of vascular cells as a mechanism for carotid artery dissection leading to ischemic stroke. 2154 66

Cocaine induced brain damage can be divided into primary neurotoxic effects causing toxic encephalopathy, secondary effects of compromised cerebral blood flow in ischaemic and haemorrhagic stroke, cerebral vasculitis and vasospasm, and tertiary effects due to hypoxia as a result of cardiopulmonary collapse. Toxic leucoencephalopathy mainly affects white matter (WM) tracts serving higher cerebral function, thereby leading to altered personality, attention deficits and memory impairment in mild cases and to dementia, coma and brain death in severe cases. Here we describe the case of a 21-year-old man who committed suicide by injecting cocaine. The cocaine induced a toxic leucoencephalopathy, which was proven at autopsy.
 ...
PMID:Fatal encephalopathy after an isolated overdose of cocaine. 2173 86


<< Previous 1 2 3 4 5 6 7 8 Next >>