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Biomedical subjects

C A Chiriboga

Publications and source records attributed to C A Chiriboga.

11 recordsLinked to original sources
PubMed2000

Intracerebral aneurysms in human immunodeficiency virus infection: case report and literature review.

We describe a child with human immunodeficiency virus infection who presented with a large subarachnoid hemorrhage. She had multiple saccular and fusiform aneurysms in the proximal cerebral arterial circulation and no evidence of bacterial or fungal infection. The arteriopathy coincided with a high human immunodeficiency virus RNA load. Human immunodeficiency virus may cause cerebral arteriopathy with potentially life-threatening complications.

AIDS Dementia Complex↗
PubMed2000

Dose-response effect of cocaine on newborn head circumference.

OBJECTIVE: To evaluate the relationship between head circumference, birth weight, and cocaine dose in healthy term and near-term newborns exposed to cocaine in utero. METHODS: We used radioimmune assay (RIAH) of cocaine metabolite in maternal hair to quantify third trimester cocaine exposure in 240 healthy newborn infants (gestational age: >36 weeks). Cocaine exposure was categorized into 3 levels: no exposure (n = 136), low cocaine exposure (n = 52; RIAH: 2-66 ng/10 mg hair), and high cocaine exposure (n = 52; RIAH: 81-4457 ng/10 mg hair). We collected information on maternal demographic characteristics, the pregnancy, and the use of substances through a structured interview and from the medical record. RESULTS: Means of birth weight, length, and head circumference of infants with high cocaine exposure differed significantly from those with low exposure and no exposure, but were similar between low exposure and no exposure. We used a multiple linear regression model to assess the association between newborn head circumference and cocaine level, adjusting for the effects of birth weight; gestational age; infant sex; and several maternal factors, including height, weight gain during pregnancy, syphilis during pregnancy, and the use of alcohol, cigarettes, marijuana, and opiates during pregnancy. Only birth weight, sex, and high cocaine exposure were significantly associated with newborn head circumference. The predicted head circumference deficit associated with high cocaine exposure (.44 cm) represents 34% of the unadjusted difference (1.28 cm) between mean head circumferences of infants in the high cocaine exposure and no exposure groups. CONCLUSION: Newborns exposed to a high level of cocaine in utero (RIAH: >81 ng/10 mg hair) exhibit asymmetric intrauterine growth retardation in which the head circumference is disproportionately smaller than would be predicted from the birth weight (head wasting). The deficit in head size associated with cocaine exposure may reflect the effects of a specific central nervous system insult that interferes with prenatal brain growth.

Anthropometry↗
PubMed1999

Dose-response effect of fetal cocaine exposure on newborn neurologic function.

BACKGROUND: Studies of fetal cocaine exposure and newborn neurologic function have obtained conflicting results. Although some studies identify abnormalities, others find no differences between cocaine-exposed and cocaine-unexposed infants. To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function in infants, we prospectively evaluated 253 infants shortly after birth. METHODS: Women who delivered a live singleton >36 weeks by dates were eligible for enrollment. Maternal exclusionary criteria were known parenteral drug use, alcoholism, and acquired immunodeficiency syndrome; infant exclusionary criteria were Apgar scores </=4 at 5 minutes, obvious congenital malformations, seizures, or strokes. A total of 98% of infants were evaluated between 1 to 7 days of age. Newborns were assessed with the Neurological Examination for Children (NEC) by a pediatric neurologist (C.A.C.) who was blinded to exposure status. Gestational age was determined by Ballard's examination. Cocaine exposure was determined for the last trimester by radioimmunoassay of maternal hair (RIAH). Exposure values ranged from 2 to 4457 ng/10 mg hair. Infants were excluded if a maternal hair sample was missing (N = 13). The sample comprises 240 woman and infant pairs-104 cocaine-exposed and 136 cocaine-unexposed. RESULTS: Compared with unexposed controls, cocaine-exposed infants exhibited higher rates of intrauterine growth retardation (24% vs 8%), small head circumference ([HC] <10th% percentile) (20% vs 5%) and neurologic abnormalities: global hypertonia (32% vs 11%), coarse tremor (40% vs 15%), and extensor leg posture (20% vs 4%). We found increasing odds (odds ratio) of growth and neurologic impairment with increasing level of cocaine exposure in stratified analyses. The odds ratio associated with three levels of cocaine exposure (no exposure, low exposure = RIAH 2-66 ng/mg; and high exposure = RIAH 81-4457 ng/mg) respectively are: 1.0, 3.3, and 6.1 for small head size (chi2 for trend); 1.0, 3. 3, and 4.3 for global hypertonia (chi2 for trend); 1.0, 3.4, and 7.4 for extensor leg posturing (chi2 for trend); and 1.0, 3.8, and 3.8 for coarse tremor (chi2 for trend). Significant associations between cocaine exposure and neurologic signs were found in logistic regression equations that controlled for 20 or more variables. CONCLUSION: We conclude that adverse neonatal effects associated with fetal cocaine exposure follow a dose-response relationship: newborns with higher levels of prenatal cocaine exposure show higher rates of impairments in fetal head growth and abnormalities of muscle tone, movements, and posture. Significant relationships between cocaine exposure and these outcomes remain in controlled analyses.

Adult↗
PubMed1998

Neurological correlates of fetal cocaine exposure.

Cocaine is a highly psychoactive substance with numerous effects that readily crosses the placenta, achieving variables levels in the fetus. Determining whether prenatal exposure to cocaine and its metabolites damages the developing human nervous system is hindered by the multiple intervening factors (confounders) that plague clinical settings, which warrant consideration in controlled studies. Prenatal cocaine exposure has been linked to numerous adverse neonatal outcomes, affecting fetal growth (i.e., low birth weight, intrauterine growth retardation, and small head size) and neurobehavior. These neurobehavior effects span the gamut from no abnormalities to impairments in arousal, neurological function, neurophysiological function, and state regulation. Strokes and possibly seizures are also noted. Dose-response effects of fetal cocaine exposure on fetal growth and neonatal neurobehavior are reported using quantitative methods of ascertainment. In early infancy, irritability and hypertonia are also described. Most cocaine associations are transient and resolve in infancy and early childhood. Whether such transient abnormalities place infants at increased risk for later neurodevelopmental impairments is not known. Controlled studies have found no cognitive differences related to prenatal cocaine exposure among toddlers or school age children, except as mediated through effects on head growth. Anecdotally, cocaine-exposed children seem to suffer from neurobehavioral abnormalities, but to date controlled studies have not established an association between cocaine and behavioral disorders, except for inattentiveness. Despite encouraging reports, the question of whether cocaine exerts long-term adverse effects on the developing human nervous system has not yet been resolved, largely because of the limitations of existing studies that rely on inadequate, mostly qualitative ascertainment of cocaine exposure as well as the dearth of studies in older children. Such methodological limitations may have compromised our ability to identify cocaine-exposed children at most risk.

Cocaine↗
PubMed1997

Massive intracranial arachnoid cyst in a developmentally normal infant: case report and literature review.

Intracranial arachnoid cysts are developmental anomalies that are generally asymptomatic. We describe a 6-month-old boy with macrocephaly but normal neurological development who was found to have a rare, massive basal arachnoid cyst occupying most of the cranium and extending superiorly, causing significant shift due to mass effect. A cystoperitoneal shunt was placed, producing both a decrease in the arachnoid cyst dimensions and a concomitant reexpansion of parenchyma. After consideration of various management options, such a shunt system appears to offer a low risk of complications and a high likelihood of success.

Arachnoid Cysts↗
PubMed1995

Neurological correlates of fetal cocaine exposure: transient hypertonia of infancy and early childhood.

OBJECTIVE: To assess whether prenatal cocaine exposure has any long-term effects on neurodevelopment. DESIGN: A prospective cohort study with examiners blind to drug exposure and human immunodeficiency virus (HIV) status. SUBJECTS: Of 144 high-risk infants enrolled in a perinatal HIV neurodevelopmental study, 119 (83%) infants with both neurological and urine toxicology measures were followed up to age 24 months. METHODS: Neurological and developmental assessments were analyzed at 6-month intervals grouped according to the presence of cocaine in urine toxicology: 51 infants were cocaine-positive. Adjusted odds ratios (ORs) and 95% confidence interval (CI) were obtained by logistic regression equations that adjusted for perinatal variables, including measures of fetal growth, gestation, HIV status, and infant toxicology results. SETTING: Harlem Hospital Center from 1988 to 1992. RESULTS: At age 6 months, 21 of 51 (41%) cocaine-positive children exhibited hypertonia of any type (hypertonic tetraparesis, hypertonic diparesis, and hypertonic hemiparesis) compared with 17 of 68 (25%) cocaine-negative infants (OR = 2.1, CI = 1.0-4.6). Cocaine-positive infants were four times more likely to show hypertonic tetraparesis (HTP) than cocaine-negative infants (OR = 4.0; CI = 1.5-10.8). The association remained significant in multivariate analyses. Hypertonia, consistent with cerebral palsy, diminished over time in both groups. In 97% of affected infants hypertonia resolved by 24 months. Arm hypertonia abated first; leg hypertonia remained in some children up to age 18 months. No differences in development scores between cocaine-positive and cocaine-negative were noted at any age interval. However, among cocaine-positive infants those with early HTP showed significantly lower mean developmental scores at 6 and 12 month compared to infants without HTP. CONCLUSION: Cocaine positivity urine toxicology at birth is associated with hypertonia during infancy. Such cocaine-induced effects are usually symmetrical, transient, and the majority of exposed children outgrow hypertonia by 24 months of life. Among cocaine-positive infants, HTP may be a marker for later developmental impairments.

Adult↗
PubMed1993

Fetal effects.

The adverse effects of fetal drug exposures are well documented. Evidence for FAS, impaired intrauterine growth, birth defects, and mental retardation related to alcohol is compelling; evidence for alcohol-induced adverse behaviors and impaired speech is tenuous. Teratogenic, cognitive, or behavioral effects associated with prenatal exposure to marijuana, cigarettes, cocaine, or opiates have not been well established. The most convincing finding related to prenatal exposure to such substances is IUGR. Impaired fetal growth, especially of brain, may indirectly mediate drug effects on cognition. The abnormal neonatal neuro-behaviors described herein have no apparent impact on subsequent development. The development of opiate-exposed children, particularly those with withdrawal symptoms, however, appears to be more vulnerable to the adverse effects of an impoverished environment.

Central Nervous System Agents↗
PubMed1989

Chronic ACTH treatment increases striatal dopamine D-2 receptor binding in developing rat brain.

ACTH has been reported to decrease elevated levels of dopamine metabolites in the CSF of patients with infantile spasms who respond clinically to ACTH therapy. To study the possible role of dopamine receptors in the effect of ACTH, we treated rat pups for thirty days with 40 IU/kg subcutaneously of porcine ACTH or with normal saline. Using 10 nM 3H-spiperone and sulpiride to determine nonspecific binding, specific binding of D-2 receptors increased significantly (46%) in the striata of ACTH-treated rats when compared to controls. No significant difference in specific binding was found in the nucleus accumbens. Protein concentration was significantly decreased by ACTH treatment. Saturation studies will be necessary to determine if the increase in dopamine receptor binding induced by a high dose of ACTH represents a change in receptor density or affinity. The effect of lower clinical doses of ACTH on dopamine receptors warrants study.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Neurologic findings in neonates with intrauterine cocaine exposure.

To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function, 30 term infants were evaluated prospectively: 14 cocaine-exposed and 16 unexposed. Cocaine-exposed infants had significantly lower mean birth weights, birth lengths, and head circumferences than urine-negative controls. Neurologic abnormalities among cocaine-exposed newborns included hypertonia of any type (86% vs 33%), axial hypertonia (79% vs 19%), plantar extension (46% vs 19%), and coarse tremor (57% vs 12%). The degree of hypertonia was sufficiently severe to warrant a diagnosis of "hypertonic tetraparesis" in 64% of cocaine-exposed and 12% of unexposed infants (P = .007). This diagnosis was highly correlated to small head size (r = 0.48; P = .01). Persistent tonic downward gaze was evident in two neurologically abnormal cocaine-exposed newborns. Gaze abnormalities improved slightly over the next 3 weeks of observation. One such infant re-evaluated at 6 months of age revealed resolution of tonic downward gaze and neurologic findings. We conclude that prenatal cocaine exposure is associated with tone and movement abnormalities in newborn infants.

Cephalometry↗