Neonatal neurologic and electroencephalographic effects of intrauterine cocaine exposure

doi:10.1016/S0022-3476(88)80283-X

The Journal of Pediatrics

Volume 113, Issue 2, August 1988, Pages 354-358

https://doi.org/10.1016/S0022-3476(88)80283-X Get rights and content

Thirty-nine infants with intrauterine exposure to cocaine were examined for neurologic and electroencephalographic (EEG) abnormalities. Of the 39 infants, 34 displayed central nervous system irritability, but only two of the infants required sedation. The EEGs were abnormal in 17 of 38 infants during the first week of life; abnormalities were characterized as showing central nervous system irritability. The EEG abnormalities could not be predicted on the basis of clinical neurologic dysfunction or perinatal variables. On follow-up, 9 of the 17 abnormal EEGs remained abnormal during the second week of life. One infant had an abnormal first EEG at 13 days of age. By 3 to 12 months of age, however, 9 of the 10 previously abnormal tracings had normalized and one is pending. These transient clinical and EEG abnormalities may be the result of changes in neurotransmitter availability and function.

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Drugs can exert major effects on the developing central nervous system (CNS). In the broadest sense, drugs may disturb specific developmental events in the brain and, in turn, produce teratogenic effects. In addition, maternal ingestion of certain drugs can result in passive addiction of the fetus and postnatally lead to a neonatal withdrawal or abstinence syndrome. Although some effects may be transient, most are likely to persist in some form into childhood and adolescence with multiple systems affected spanning cognition, motor function, language, and behavior. This chapter provides a comprehensive overview of the neurological effects of a range of licit and illicit drugs on the infant and growing child. Drugs reviewed include fetal exposure to alcohol, antiepileptic drugs, stimulants, opioids, selective serotonin reuptake inhibitors (SSRIs), sedatives, anesthetics, and marijuana. Clinical considerations in the evaluation and care of the drug-exposed neonate are also discussed.
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Citation Excerpt :
As there are no studies examining effects of prenatal MA on epileptiform EEG, our results may be compared only to the studies examining the effect of prenatal exposure to other psychostimulant drugs. There is clinical evidence showing changes in EEG activity in children of mothers exposed to cocaine during pregnancy; such as significant excess of relative power in the alpha frequency band, and deficits of absolute and relative power in the delta and theta bands (Doberczak et al., 1988; Legido et al., 1992; Prichep et al., 1995). There is also an experimental work that monitored EEG activity in rats exposed prenatally to cocaine (Baraban et al., 1997), which demonstrated reduced latency to the first EEG seizure phenomenon after prenatal cocaine.
Administration of psychostimulants is often associated with increased seizure susceptibility. In our previous studies prenatal methamphetamine (MA) exposure increased seizure susceptibility of adult rats in models of primarily or secondarily generalized seizures induced by convulsant drugs. The effect of a single MA challenge dose in adulthood on chemically induced generalized seizures however, depends on the prenatal MA exposure history. Thus, the present study used a model of focal electrical stimulation to determine whether prenatal MA exposure with or without the adult challenge MA dose has the same outcome in a focal seizure model. Total of six groups of adult male rats were tested (prenatally MA-exposed, prenatally saline-exposed and rats without prenatal injections), each of these groups was either postnatally challenged with MA or with vehicle injection (MA-MA, MA-S; S-MA, S-S; C-MA, C-S). Seizures were induced by repetitive electrical stimulation (15 s/8 Hz) of sensorimotor cortex. Stimulation threshold, duration of afterdischarges (ADs), and presence and duration of spontaneous ADs (SAD) were evaluated. Additionally, behaviors associated with stimulation and ADs, and occurrence of wet-dog shakes (WDS) were analyzed. Our data demonstrate that daily injection of MA (5 mg/kg) within prenatal period decreased the occurrence of WDS and SADs, and shortened the duration of ADs and SADs suggesting anticonvulsant effects. Moreover, the challenge dose of MA (1 mg/kg) increased seizure threshold in all groups of rats, shortened duration of ADs in controls and prenatally saline-exposed animals, shortened duration of SADs in prenatally saline-exposed rats and totally eliminated WDS in all groups. Thus, the present study demonstrates that both chronic prenatal MA exposure and a single dose of MA in adulthood decrease focally induced epileptiform activity in adult male rats.
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Neonatal neurologic and electroencephalographic effects of intrauterine cocaine exposure

J Pediatr

J Pediatr

Electroencephalogr Clin Neurophysiol

Electroencephalogr Clin Neurophysiol

Am J Med

J Pediatr

Toxicol Appl Pharmacol

Am J Obstet Gynecol

Am J Obstet Gynecol

Current research on the consequences of maternal drug abuse

Cocaine use in pregnancy

N Engl J Med

Effects of intrauterine exposure to alkaloidal cocaine (“crack”)

Am J Dis Child

Cocaine smoking

J Psychoactive Drugs

Cocaine: acute medical and psychiatric complications

Psychiatr Ann