Crack‐associated stroke

Levine, Steven R.; Washington, Jacqueline M.; Moen, M; Kieran, Stuart N.; Junger, Sly; Welch, K. M. A.

doi:10.1212/wnl.37.6.1092-b

“…Subarachnoid and intracerebral hemorrhages as well as CNS infarcts and ischemic strokes are associated with use of cocaine (Altes-Capella et al 1987;Brody et al, 1990;Brust and Richter, 1977;Golbe and Merkin, 1986;Jacobs et al, 1989;Johanson and Fischman, 1989;Levine et al, 1987;Lichtenfeld et al, 1984;Lowenstein, et al, 1987;Mangiardi et al, 1988;Nolte and Gelman, 1989;Schwartz and Cohen, 1984;Tuchman et al, 1987, Wojack andFlamm, 1987). Such patients seek medical assistance initially because of serious neurological symptoms.…”

Section: Introductionmentioning

confidence: 99%

Long‐Term frontal brain metabolic changes in cocaine abusers

Volkow

¹

,

Hitzemann

²

,

Wang

³

et al. 1992

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Neurological complications from cocaine use are well recognized. We propose that chronic cocaine use can also cause clinically silent brain dysfunction. We investigated brain glucose metabolism with positron emission tomography (PET) and 2-deoxy-2[18F] fluoro-D-glucose (FDG) in 21 neurologically intact chronic cocaine abusers (C) and 18 normal controls (N). The cocaine abusers were tested 1-6 weeks after the last use of cocaine and seven were retested after a 3 month drug-free period. Global cerebral glucose metabolism was not significantly different between controls and cocaine abusers (N = 38.4 +/- 3, C = 36.5 +/- 5 mumol/100 g of tissue, min). However, cocaine abusers had significantly (P less than 0.05) lower metabolic activity in 16 of the 21 left frontal regions and 8 of the 21 right frontal regions. These decreases persisted after 3-4 months of detoxification and were correlated with the dose (P less than or equal to 0.01) and the years of cocaine use (P less than or equal to 0.05). This study shows reduced rates of frontal metabolism in neurologically intact cocaine abusers that persist even after 3-4 months of detoxification.

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“…The understanding of pathophysiologic mechanisms causing vascular toxicity in cocaine abusers is essential for the correct diagnoses, treatment and prevention of potentially lethal outcomes. Myocardial Infarction [36,37] Ischemic stroke [38][39][40] Mesenteric Ischemia [41] Renal infarction [42] Pulmonary Infarction [48] Vasoconstriction Platelet activation Thrombus formation Atherosclerosis Plaque disruption…”

Section: Discussionmentioning

confidence: 99%

“…The demonstration of platelet rich thrombi in coronary arteries of patients undergoing fatal myocardial infarction gives credence to this theory [47]. Besides the coronary arteries, cocaine-mediated thrombosis has also been observed in the pulmonary [48], skin [49], peripheral [50] renal [42] and cerebral circulation [38][39][40]. Fig.…”

Section: Effects On Platelets and Thrombus Formationmentioning

confidence: 95%

Vascular Toxicity of Cocaine

Bansal¹,

Morgan²

2009

VDP

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Cocaine acts on the vascular system by a number of mechanisms including monoamine re-uptake inhibition, local anesthesia, anti-cholinergic activity, alpha-adrenergic stimulation, regulation of various vasoconstrictor and vasodilator agents and promotion of prothrombotic state. These effects lead to a number of clinical syndromes via vasoconstriction, platelet activation, thrombus formation and early atherosclerosis in almost every organ of the body. Many of these effects may be under appreciated. Furthermore, cocaine is commonly associated with the use of tobacco and alcohol which can lead to superadditive effects and/or prolonged toxicity.

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“…The demonstration of platelet rich thrombi in coronary arteries of patients undergoing fatal myocardial infarction gives credence to this theory [47]. Besides the coronary arteries, cocaine-mediated thrombosis has also been observed in the pulmonary [48], skin [49], peripheral [50] renal [42] and cerebral circulation [38][39][40]. Fig.…”

Section: Effects On Platelets and Thrombus Formationmentioning

confidence: 95%

“…The clinico-pathologic effects mediated by cocaine induced vasoconstriction include myocardial infarction [36,37], stroke [38][39][40], mesenteric ischemia [41], renal infarction [42], gastric and duodenal ulceration and perforation [43].…”

Section: Effect On Vascular Resistancementioning

confidence: 99%

Vascular Toxicity of Cocaine

Bansal¹,

Morgan²

2009

VDP

2

0

View full text Add to dashboard Cite

Cocaine acts on the vascular system by a number of mechanisms including monoamine re-uptake inhibition, local anesthesia, anti-cholinergic activity, alpha-adrenergic stimulation, regulation of various vasoconstrictor and vasodilator agents and promotion of prothrombotic state. These effects lead to a number of clinical syndromes via vasoconstriction, platelet activation, thrombus formation and early atherosclerosis in almost every organ of the body. Many of these effects may be under appreciated. Furthermore, cocaine is commonly associated with the use of tobacco and alcohol which can lead to superadditive effects and/or prolonged toxicity.

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Crack‐associated stroke

Cited by 15 publications

References 0 publications

Long‐Term frontal brain metabolic changes in cocaine abusers

Long‐Term frontal brain metabolic changes in cocaine abusers

Vascular Toxicity of Cocaine

Vascular Toxicity of Cocaine

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