Relation of Cocaine Use to Seizures and Epilepsy

Koppel, Barbara S.; Samkoff, Lawrence; Daras, Michael

doi:10.1111/j.1528-1157.1996.tb00041.x

Cited by 93 publications

(41 citation statements)

References 24 publications

(8 reference statements)

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“…Cocaine abusers may suffer from seizures (Koppel et al, 1996), cerebral ischaemia, cerebral hemorrhages, infarction, optic neuropathy, cerebral atrophy, cognitive impairment, and mood and movement disorders (Majewska, 1996). Brain lesions and cerebral atrophy are mainly observed in the prefrontal cortex and basal ganglia of human cocaine abusers (Bartzokis et al, 1996;Langendorf et al, 1996).…”

Section: Neurological Impairmentsmentioning

confidence: 99%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

194

136

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Section: Neurological Impairmentsmentioning

confidence: 99%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

194

136

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“…Cocaine-induced seizures are a manifestation of the toxicity associated with the drug, and estimates are that 8-12% of patients admitted to emergency departments with cocaine intoxication have seizures (Derlet and Albertson, 1989;Dhuna et al, 1991;Koppel et al, 1996). These seizures can be resistant to common anticonvulsant drugs, such as benzodiazepines and barbiturates, and constitute a major fraction of cocaine-related deaths (Dhuna et al, 1991;Benowitz et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Effects of disulfiram and dopamine beta-hydroxylase knockout on cocaine-induced seizures

Gaval-Cruz

Schroeder

Liles

et al. 2008

Pharmacology Biochemistry and Behavior

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The antialcoholism drug disulfiram has shown recent promise as a pharmacotherapy for treating cocaine dependence, probably via inhibition of dopamine β-hydroxylase (DBH), the enzyme that catalyzes the conversion of dopamine (DA) to norepinephrine (NE). We previously showed that DBH knockout (Dbh -/-) mice, which lack NE, are susceptible to seizures and are hypersensitive to the psychomotor, rewarding, and aversive effects of cocaine, suggesting that disulfiram might exacerbate cocaine-induced seizures (CIS) by inhibiting DBH. To test this, we examined CIS in wild-type and Dbh -/-mice following administration of disulfiram or the selective DBH inhibitor nepicastat. We found that Dbh genotype had no effect on CIS probability or frequency, whereas disulfiram, but not nepicastat, increased the probability of having CIS in both wild-type and Dbh -/-mice. Both disulfiram and nepicastat increased CIS frequency in wild-type but not Dbh -/-mice. There were no genotype or treatment effects on serum cocaine levels, except for an increase in disulfiram-treated Dbh -/-mice at the highest dose of cocaine. These results suggest that disulfiram enhances CIS via two distinct mechanisms: it both increases CIS frequency by inhibiting DBH and increases CIS frequency in a DBH-independent manner.

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“…Cocaine abuse is associated with life-threatening medical complications (Marzuk et al 1995), including increased risk of neurological complications including strokes, seizures, transient ischemic attacks, and headaches (Mody and Miller 1988;Qureshi et al 1995;Koppel et al 1996). With cocaine-related stroke as a neurological complication, it is reasonable to suggest an increased prevalence of subclinical neurovascular deficits in this population.…”

mentioning

confidence: 99%