Neurologic complications of cocaine abuse

Spivey, William H; Euerle, Brian D.

doi:10.1016/s0196-0644(05)82612-5

Cited by 71 publications

(25 citation statements)

References 52 publications

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“…However, ion channels associated with these sites may be associated with the cascade of events leading to convulsions following initial binding of cocaine at 5-HT transporters. Indeed, drugs acting at BZ, GABA and NMDA receptors have been shown to be effective for treating cocainerelated convulsions in clinical settings (Spivey and Euerle 1990) as well as for inhibiting acute observable convulsions (Derlet and Albertson 1990b;Derlet et al 1990). …”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors

Ritz¹,

George²

1997

Psychopharmacology

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The concurrent influence of multiple neurotransmitter systems in mediating cocaine-induced convulsions is predicted by the results of previous receptor binding studies. The present results demonstrate that pharmacological manipulations of these predicted neurotransmitter systems alters the occurrence of cocaine-induced convulsions. The 5-HT reuptake inhibitor fluoxetine enhanced the occurrence and severity of convulsions produced by 100 mg/kg (-) cocaine, while the 5-HT2 receptor antagonists cinanserin, ketanserin and pirenperone antagonized cocaine-induced convulsions in a dose-dependent manner. Further, the M1 receptor antagonist pirenzepine antagonized cocaine-induced convulsions, but atropine did not. In addition, both the (+) and (-) stereoisomers of the sigma ligand SKF 10047 significantly attenuated cocaine-induced convulsions. (+)SKF 10047 was more potent than (-)SKF 10047 in this effect, suggesting a stereoselective effect at sigma receptor sites. In constrast, DA and NE neurotransmission do not appear to modulate the proconvulsant effects of cocaine in a specific, dose-dependent manner. Thus, of the CNS binding sites with which cocaine is known to interact, the results are consistent with the conclusion that 5-HT transporters and 5-HT2 receptor sites appear to be direct and primary sites related to cocaine-induced convulsions, while M1 and sigma binding sites appear to play important but secondary and modulatory roles in this response.

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Section: Discussionmentioning

confidence: 99%

Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors

Ritz¹,

George²

1997

Psychopharmacology

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“…It is well recognized that cocaine abuse is associated with neurological deficits that can be mild and transient such as facial paralysis to severe and irreversible such as permanent tetraplegia (Spivey and Euerle, 1990). In as much as increases in [Ca 2ϩ ] i are associated with cell death (Schanne et al, 1979), cocaine-induced increases in [Ca 2ϩ ] i are likely to be clinically relevant, particularly when considering that they occur in parallel to cocaineinduced decreases in MABP, blood volume, tissue oxygenation, and CBF.…”

Section: Clinical Significancementioning

confidence: 99%

Cocaine Increases the Intracellular Calcium Concentration in Brain Independently of Its Cerebrovascular Effects

Du¹,

Yu²,

Volkow³

et al. 2006

J. Neurosci.

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Cocaine abuse increases the risk of life-threatening neurological complications such as strokes and seizures. Although the vasoconstricting properties of cocaine underlie its cerebrovascular effects, the mechanisms underlying its neurotoxicity remain incompletely understood. ] i in the brain. The effects of cocaine were compared with those of methylphenidate, which has similar catecholaminergic effects as cocaine (except for serotonin increases) but no local anesthetic properties, and of lidocaine, which has similar local anesthetic effects as cocaine but is devoid of catecholaminergic actions. To control for the hemodynamic effects of cocaine, we assessed the effects of cocaine in animals in which normal blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of transient hypotension (mimicking that induced by cocaine). We show that cocaine induced significant increases (ϳ10 -15%) in [Ca 2ϩ ] i that were independent of its hemodynamic effects and of the anesthetic used (isofluorance or ␣-chloralose).

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“…Cocaine use can elicit life-threatening seizures, which play a major role in cocaine-associated mortality [42]. Prompt seizure treatment can thus impact outcome with administration of benzodiazepines the initial therapy recommended.…”

Section: Seizuresmentioning

confidence: 99%

Perioperative care of the cocaine-dependent neurosurgical patient

Dwarakanath¹,

Cook²,

Fahy³

2013

J Anesthesiol Clin Sci

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Purpose: Cocaine, a commonly abused drug, can cause life-threatening complications, significantly impacting patient management. Cocaine is associated with an increased risk of stroke including subarachnoid hemorrhage (SAH) that may require expectant surgical management. Patients presenting for anesthesia with acute cocaine toxicity pose additional concerns. Clinical Features: A 48 year old woman presented with a seizure, acute cocaine intoxication, and was diagnosed with a SAH. Further diagnostic evaluation revealed a bleeding cerebral aneurysm requiring urgent surgical aneurysm clipping. Her perioperative course was complicated by hypertension requiring treatment to minimize further aneurysm bleeding before clipping. Cocaine-associated cardiac complications impacting management included a non-ST elevation myocardial infarction and severe anteroseptal hypokinesis on echocardiogram. Conclusion: Hemodynamic management with a recent SAH and acute cocaine intoxication required special considerations. Perioperative SAH management initially focused to prevent additional bleeding before clipping and then after clipping to minimize cerebral ischemia. Benzodiazepines were used early in this case to treat seizures and cocaine-associated hemodynamic effects. Specific treatments for life-threatening ventricular arrhythmias are discussed including sodium bicarbonate as a first line treatment and potential benefits of magnesium administration. With prolongation of a QT interval secondary to cocaine and/ or SAH, medications that often are utilized during the perioperative period may further prolong the QT interval and should be avoided.

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Neurologic complications of cocaine abuse

Cited by 71 publications

References 52 publications

Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors

Cocaine-induced convulsions: pharmacological antagonism at serotonergic, muscarinic and sigma receptors

Cocaine Increases the Intracellular Calcium Concentration in Brain Independently of Its Cerebrovascular Effects

Perioperative care of the cocaine-dependent neurosurgical patient

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