Neonatal Cocaine-Related Seizures

Kramer, Lynn D.; Locke, George E.; Ogunyemi, Abayomi O.; Nelson, Lowell

doi:10.1177/088307389000500115

Cited by 82 publications

(21 citation statements)

References 18 publications

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“…One uncontrolled retrospective study proposed subtle seizures among cocaine-exposed infants based on a correlation between stereotypic movements and "ictal" discharges. 76 Most "seizures" were treated with anticonvulsants without improvement. It is highly likely that such behaviors were not epileptic but rather cocaine-related neurobehaviors.…”

Section: Strokesmentioning

confidence: 99%

Fetal Alcohol and Drug Effects

Chiriboga¹

2003

The Neurologist

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Most adverse effects of prenatal drug exposure are self-limited, with catch-up growth and resolution of withdrawal and of prior neurobehavioral abnormalities noted over time. The exception is alcohol, which is linked to life-long impairments (i.e., mental retardation and microcephaly) and possibly cigarette-related behavioral effects. The absence of tangible evidence of detrimental long-term cocaine effects may reflect limitations in the methodology used to identify children at greatest risk for adverse outcome.

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Section: Strokesmentioning

confidence: 99%

Fetal Alcohol and Drug Effects

Chiriboga¹

2003

The Neurologist

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“…Our findings may explain why generalized seizures are more frequent after acute cocaine intake, whereas after chronic use the less frequent nongeneralized seizures occasionally occur (Merriam et al, 1988;Ogunyemi et al, 1989a,b;Kramer et al, 1990b). The relatively prolonged presence of the BE metabolite as compared with cocaine could also account for the time course of seizures and behavioral disturbances in human neonates exposed to cocaine in utero (Kramer et al, 1990b). Therefore, we predict that the cocaine-type seizure is more likely to occur in the acute period of intoxication, whereas with chronic use BE levels may reach a threshold sufficient to produce partial complex seizures (Merriam et al, 1988;Ogunyemi et al, 1989a).…”

Section: Time After Injection (Minutes)mentioning

confidence: 71%

Seizures Induced by the Cocaine Metabolite Benzoylecgonine in Rats

et al. 1992

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The half-life (t1/2) of cocaine is relatively short, but some of the consequences of its use, such as seizures and strokes, can occur hours after exposure. This led us to hypothesize that a metabolite of cocaine may be responsible for some of those delayed sequelae. We evaluated the potential of the major metabolite of cocaine, benzoylecgonine (BE), to cause seizures. Two separate equimolar doses (0.2 and 0.4 mumol) of either cocaine or BE were injected ventricularly in unanesthetized juvenile rats. Treated rats were then evaluated for incidence, latency, and seizure pattern or for locomotor activity in animals without seizures. BE-Induced seizures occurred more frequently and had significantly longer latencies than those induced by equimolar amounts of cocaine. Whereas cocaine-induced seizures were best characterized as brief, generalized, and tonic and resulted in death, those induced by BE were prolonged, often multiple and mixed in type, and rarely resulted in death. Electrical recordings from the hippocampus showed a rhythmic progression in EEG frequency and voltage with clinical seizure expression. BE-Injected rats that did not have seizures had significantly more locomotor activity than cocaine-injected animals without seizures. The finding that cocaine- and BE-induced seizures differ in several respects suggests more than one mechanism for cocaine-induced seizures and emphasizes the importance of a cocaine metabolite, BE.

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“…30 Other electrophysiological alterations have been noted. These include seizure activity, 31 EEG abnormalities, 32 sleep discordance, 33 and abnormal brainstem conduction time. 34 Serious destructive lesions suggesting prenatally occurring insults were reported in a series of case studies.…”

Section: Human Studiesmentioning

confidence: 99%

Fetal Cocaine Exposure:

Arendt

Minnes

Singer

1996

Physical & Occupational Therapy In Pediatrics

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SUMMARYResearch on animal models demonstrates that fetal cocaine exposure results in neurologic deficits in memory and learning. Although drug effects on human infants are difficult to separate from other environmental influences of a drug-using lifestyle, studies suggest that infants exposed to cocaine in utero have reduced growth, delays in sensory-motor development, attentional deficits, and depressed responsivity to social stimulation. Standard interventions to promote behavioral state regulation in affected infants may be helpful when parents are capable of participating.The history of research on the effects of in utero cocaine exposure has been both short and turbulent. In the 10 years since the "crack baby" was first identified and birth outcomes reported, findings have been controversial and at times contradictory. Perinatal epidemiologic studies in the late 1980s documented the large numbers of infants born after fetal exposure to cocaine. Estimates of the proportion of babies born in urban teaching hospitals who test positive for cocaine range from 5-45%. [1][2][3][4] Early alarming reports about pronounced neurobehavioral abnormalities in neonates exposed to cocaine in utero 5-7 raised subsequent concerns about potential long-term neurodevelopmental effects on fetal and infant outcome. Recent reports, however, indicate that the effects may be subtle and could be masked and/or confounded by environmental factors, such as amount of prenatal care 8 or socioeconomic status. 9 Part of the ambiguity in results might be attributed to the initial lack of information regarding effects of cocaine on human development. With little else to go on, investigators interested in studying the effects of cocaine on the human fetus had two potential bodies of research on which to draw, the known effects of cocaine on adults and on animals. As the volume of literature grew, several issues central to the further study of prenatal exposure to a potentially neurotoxic agent became evident: (a) whether any pre-or perinatal neurologic effect could be attributed to cocaine, (b) whether identified effects could be related to specific neurobehavioral outcomes, and (c) the long-term consequences. An examination, therefore, of the evidence pertaining to the neurologic development of infants exposed to cocaine follows. Additionally, some considerations concerning intervention are offered.

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Neonatal Cocaine-Related Seizures

Cited by 82 publications

References 18 publications

Fetal Alcohol and Drug Effects

Fetal Alcohol and Drug Effects

Seizures Induced by the Cocaine Metabolite Benzoylecgonine in Rats

Fetal Cocaine Exposure:

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