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PubMed2002

Advances in postnatal neuroimaging: relevance to pathogenesis and treatment of brain injury.

The human brain is susceptible to a wide variety of insults. The permanent residua of these abnormalities are represented in dysfunction of one or more areas of neurodevelopment. A full understanding of normal brain development, mechanisms of brain injury, and consequences for subsequent brain development is required to determine which infants are at risk for neurodevelopmental handicap, and to monitor the effects of new treatments and management regimens designed to prevent these disabilities. Advanced magnetic resonance techniques, such as quantitative morphometric magnetic resonance techniques, diffusion-weighted magnetic resonance techniques, and magnetic resonance spectroscopy applied to the study of early human brain development have given us a better understanding of the pathophysiologic mechanisms of brain injury and its effects on subsequent brain development. Magnetic resonance imaging has provided an invaluable tool for the study of the fetal and newborn brain in vivo.

Asphyxia Neonatorum↗

PubMed2000

Behavior, pain perception, and the extremely low-birth weight survivor.

This article explores the literature concerning responses to pain of both premature and term-born newborn infants, the evidence for short-term and long-term effects of pain, and behavioral sequelae in individuals who have experienced repeated early pain in neonatal life as they mature. There is no doubt that pain causes stress in babies and this in turn may adversely affect long-term neurodevelopmental outcome. Although there are methods for assessing dimensions of acute reactivity to pain in an experimental setting, there are no very good measures available at the present time that can be used clinically. In the clinical setting repeated or chronic pain is more likely the norm rather than infrequent discrete noxious stimuli of the sort that can be readily studied. The wind-up phenomenon suggests that, exposed to a cascade of procedures as happens with clustering of care in the clinical setting in an attempt to provide periods of rest for stressed babies, an infant may in fact perceive procedures that are not normally viewed as noxious, as pain. Pain exposure during lifesaving intensive medical care of ELBW neonates may also affect subsequent reactivity to pain in the neonatal period, but behavioral differences are probably not likely to be clinically significant in the long term. Prolonged and repeated untreated pain in the newborn period, however, may produce a relatively permanent shift in basal autonomic arousal related to prior NICU pain experience, which may have long-term sequelae. In the long run, the most significant clinical effects of early pain exposure may be on neurodevelopment, contributing to later attention, learning, and behavior problems in these vulnerable children. Although there is considerable evidence to support a variety of adverse effects of early pain, there is less information about the long-term effects of opiates and benzodiazepines on the developing central nervous system. Current evidence reviewed suggests that judicious use of morphine for adjustment to mechanical ventilation may ameliorate the altered autonomic response. It may be very important, however, to distinguish stress from pain. Animal evidence suggests that the neonatal brain is affected differently when exposed to morphine administered in the absence of pain than in the presence of pain. Pain control may be important for many reasons but overuse of morphine or benzodiazepines may have undesirable long-term effects. This is a rapidly evolving area of knowledge of clear relevance to clinical management likely to affect long-term outcomes of high-risk children.

Animals↗

PubMed2000

Nonerythropoietic roles of erythropoietin in the fetus and neonate.

Epo was once regarded as a cytokine with only hematopoietic effects. It is now clear that the distributions of Epo and Epo-R are more widespread in the developing human. Epo-R is widely distributed during early fetal development, leading to speculation that Epo acts in concert with other growth factors to optimize growth and development. Areas in which Epo has important recognized effects are on endothelial cells, and in the developing heart, gastrointestinal tract, and brain. It may also be important in the regulation of vascular growth during the menstrual cycle, and in the stimulation of testosterone production in men. Epo and Epo-R are prominent in the brain during fetal development, leading to speculation that they play an important role in neurodevelopment. There are also promising data regarding rEpo as a possible neuroprotective agent in such conditions as hypoxia, because it decreases programmed cell death induced during such adverse conditions. It is unlikely, however, that rEpo crosses the blood-brain barrier in normal premature infants, and it is not clear whether the CNS effects of rEpo, should it cross the blood-brain barrier, are harmful or beneficial in the setting of a developing brain.

Animals↗

PubMed2003

Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study.

INTRODUCTION: Exposure to methylmercury (MeHg) before birth can adversely affect children's neurodevelopment. The most common form of prenatal exposure is maternal fish consumption, but whether such exposure harms the fetus is unknown. We aimed to identify adverse neurodevelopmental effects in a fish-consuming population. METHODS: We investigated 779 mother-infant pairs residing in the Republic of Seychelles. Mothers reported consuming fish on average 12 meals per week. Fish in Seychelles contain much the same concentrations of MeHg as commercial ocean fish elsewhere. Prenatal MeHg exposure was determined from maternal hair growing during pregnancy. We assessed neurocognitive, language, memory, motor, perceptual-motor, and behavioural functions in children at age 9 years. The association between prenatal MeHg exposure and the primary endpoints was investigated with multiple linear regression with adjustment for covariates that affect child development. FINDINGS: Mean prenatal MeHg exposure was 6.9 parts per million (SD 4.5 ppm). Only two endpoints were associated with prenatal MeHg exposure. Increased exposure was associated with decreased performance in the grooved pegboard using the non-dominant hand in males and improved scores in the hyperactivity index of the Conner's teacher rating scale. Covariates affecting child development were appropriately associated with endpoints. INTERPRETATION: These data do not support the hypothesis that there is a neurodevelopmental risk from prenatal MeHg exposure resulting solely from ocean fish consumption.

Animals↗

PubMed2006

Effect of routine prophylactic supplementation with iron and folic acid on preschool child mortality in southern Nepal: community-based, cluster-randomised, placebo-controlled trial.

INTRODUCTION: Iron deficiency is widespread in the developing world and is especially common in young children who live on the Indian subcontinent. Supplementation with iron and folic acid alleviates severe anaemia and enhances neurodevelopment in deficient populations, but little is known about the risks of mortality and morbidity associated with supplementation. METHODS: We did a community-based, cluster-randomised, double-masked, placebo-controlled, 2x2 factorial trial in children aged 1-36 months and residing in southern Nepal. We randomly assigned children daily oral supplementation to age 36 months with: iron (12.5 mg) and folic acid (50 microg; n=8337), zinc alone (10 mg), iron, folic acid, and zinc (n=9230), or placebo (n=8683); children aged 1-11 months received half the dose. Our primary outcome measure was all-cause mortality, and our secondary outcome measures included cause-specific mortality and incidence and severity of diarrhoea, dysentery, and acute respiratory illness. Analyses were by intention to treat. This study is registered at , number NCT00109551. FINDINGS: The iron and folic acid-containing groups of the study were stopped early in November, 2003, on the recommendation of the data and safety monitoring board; mortality in these groups did not differ from placebo and there was low power to detect positive or negative effects by the time enrollment was completed. We continued to enroll children to the placebo and zinc alone groups. 25,490 children participated and analyses are based on 29,097.3 person-years of follow-up. There was no difference in mortality between the groups who took iron and folic acid without or with zinc when compared with placebo (HR 1.03, 95% CI 0.78-1.37, and 1.00, 0.74-1.34, respectively). There were no significant differences in the attack rates for diarrhoea, dysentery, or respiratory infections between groups, although all the relative risks except one indicated modest, non-significant protective effects. INTERPRETATION: Daily supplementation of young children in southern Nepal with iron and folic acid with or without zinc has no effect on their risk of death, but might protect against diarrhoea, dysentery, and acute respiratory illness.

Anemia, Iron-Deficiency↗

PubMed1987

Prediction of cerebral palsy in very low birthweight infants: prospective ultrasound study.

The value of regular cerebral ultrasound scanning in predicting cerebral palsy (CP) was assessed in very low birthweight infants. The infants were scanned before discharge, and their vision and hearing were assessed at age 9 months and neurodevelopment was assessed at 18 months. Ultrasound abnormalities, defined before the study, were periventricular haemorrhage (PVH), "prolonged flare" (echodensity persisting in the periventricular white-matter for more than 2 weeks without cavitating), and cystic periventricular leukomalacia (PVL). The incidence of these three conditions in surviving infants was 49%, 15%, and 8%, respectively. 158 infants survived to be discharged from hospital and 156 had neurodevelopmental assessment at 18 months of corrected age. All infants with PVH alone and confined to the lateral ventricles were normal at follow-up. The presence of cysts accurately predicted abnormal outcome (94%) and was highly specific (96%). Prolonged flare predicted adverse outcome but the accuracy (79%) was less good than for cystic PVL. 12 infants had CP, and 10 of these had ultrasound evidence of PVL. 8 of the 13 infants with cysts had spastic CP. 4 of these were walking independently and had mild CP. No infant with ultrasound evidence of a single cyst or with cysts confined to the frontal region or centrum semiovale had severe CP. Cysts involving the periventricular white-matter in the occipital region were associated with a poor prognosis. Echolucent cystic lesions detected by ultrasound in the neonatal period accurately predict adverse outcome, and if multiple and present in the occipital region, confer a very high risk of severe CP.

Cerebral Hemorrhage↗

PubMed2001

L1 cell adhesion molecule signal cascades: targets for ethanol developmental neurotoxicity.

A major mechanism guiding neural development is through cell-cell and cell-matrix adhesions and signaling mediated by cell adhesion molecules (CAMs). The majority of CAMs have been grouped into three families: the cadherins, the integrins and the members of the immunoglobulin superfamily including L1. While the elucidation of new receptors and matrix components has become a frequent occurrence, the elucidation of the mechanisms by which they operate, and the function of those mechanisms in complex developmental events remains rudimentary. Members of all three families participate in differential adhesion, signal transduction and physical/mechanical effects. Each of these modes of action is a potential target for developmental neurotoxicants. In this brief review, the role of L1 in normal and abnormal neurodevelopment will be summarized. L1 is a cell surface transmembrane glycoprotein with a single copy gene on the X chromosome. There are two alternatively spliced exons, with the RSLE containing form found only on axons and growth cones of post-mitotic neurons. L1 mediates the following functions: adhesion, neurite extension, neuronal migration, and axon fasciculation. L1 is critical for normal neural development; humans with genetic defects in L1, termed corpus callosum hypoplasia, mental retardation, adducted thumbs, spasticity and hydrocephalus (CRASH) syndrome, and mice lacking expression of L1 have extensive neuropathologic and aberrant behaviors. The observation that patients with fetal alcohol syndrome share similar features to patients with CRASH has lead to the investigation of the effects of ethanol on L1. Physiologic concentrations of ethanol have been shown to inhibit L1 mediated neurite outgrowth in cerebellar granule neurons. Such inhibition may result from decreased expression, altered cell surface distribution, impaired signal transduction, or impaired interaction with the cytoskeleton. These data indicate that L1 and its associated signaling pathways are potentially targets for developmental neurotoxicants.

Animals↗

PubMed2004

Minor physical anomalies in non-familial unipolar recurrent major depression.

BACKGROUND: The prevalence of minor physical anomalies (MPAs) was evaluated in patients with unipolar recurrent major depression to get indirect data on the possible role of aberrant neurodevelopment in the aetiology of major depression. One published study [Lohr et al., Am. J. Geriatr. Psychiatry 5 (1997) 318] on the MPA prevalence in unipolar depression, evaluated by the recently widely criticized Waldrop-scale, reports on a significantly higher MPA rate among patients. METHODS: A scale developed by Méhes [Prog. Clin. Biol. Res. 163 (1985) 45] was used to detect the presence or absence of 57 MPAs in 30 patients with major depression and in 30 matched controls. RESULTS: The depressive sample did not differ significantly from the control group (P=0.200). By comparing each MPA individually we could not find any significant differences between the depressive and the control sample. LIMITATIONS: Patients and control subjects had a negative family history in connection with affective disorders; a high-risk population should give significant positive results. CONCLUSIONS: The results do not support the role of an 'early neurodevelopmental origin' in unipolar depression.

Adult↗

PubMed1997

Neurotrophin-3 levels in the cerebrospinal fluid of patients with schizophrenia or medical illness.

Neurotrophin-3 (NT-3) may have a potential role in the pathogenesis of schizophrenia, given evidence of abnormal neurodevelopment in schizophrenia, as well as a potential association of an NT-3 gene polymorphism with schizophrenia. Cerebrospinal fluid NT-3 protein was assayed using an enzyme-linked immunosorbent assay in five patients with schizophrenia and 49 patients with medical illness. None of the patients with schizophrenia had detectable levels of NT-3 (above 4.7 pg/ml). Eleven samples from 10 different patients with medical or neurological illness had detectable levels of NT-3, associated with surgery for hydrocephalus or central nervous system infection.

Adolescent↗

PubMed2000

Whole brain spheroid cultures as a model to study the development of nitric oxide synthase-guanylate cyclase signal transduction.

Whole brain spheroids provide a suitable model to study neurodevelopment. In the literature a role for the nitric oxide (NO)-cyclic guanosine 3',5'-monophosphate (cGMP) signalling pathway during development has frequently been suggested. In this study we investigated whether functional cGMP pathways were present in differentiated spheroids. In 3-week-old spheroids soluble guanylate cyclase was stimulated with N-methyl D-aspartic acid or sodium nitroprusside (NO donor). The results showed that the NO synthase-cGMP pathway is present in the culture system. Soluble guanylate cyclase-dependent cGMP formation was found in NO synthase containing neurons, in neurons of the GABAergic, glutamatergic and cholinergic system, and in astroglia and oligodendroglia. Activation of particulate guanylate cyclase by atrial natriuretic peptide also triggered an increase in cGMP production. Particulate guanylate cyclase was found in astroglia and in microglia as well as in glutamic acid decarboxylase and calbindin containing structures and neuronal NO synthase containing neurons. Chronic inhibition of NO synthase during culture development had no effect on soluble or particulate guanylate cyclase functioning. Similarly, inhibition of soluble guanylate cyclase during culture development did not have any effect on NO synthase and particulate guanylate cyclase functioning. It is concluded that NO synthase and both soluble and particulate guanylate cyclase are present in whole brain spheroid cultures and that their activity can be influenced by several stimuli. The spheroid culture system constitutes a suitable model to study the NO-cGMP pathway during brain development in mammals.

1-Methyl-3-isobutylxanthine↗

PubMed2002

Apoptosis in the preterm and near term ovine fetal brain and the effect of intermittent umbilical cord occlusion.

Programmed cell death or apoptosis plays a central role during the development of the brain, but can also be activated by hypoxic/ischemic insult. The purpose of the present study was to determine the regional distribution of apoptotic cells in the preterm and near term ovine fetal brain and thus in relation to the maturation of neurobehavioural activity, and the effect of intermittent umbilical cord occlusion (UCO), which might then contribute to adverse neurodevelopment. Fetal sheep (control and experimental groups at 0.75 and 0.90 of gestation) were studied over 4 days with UCOs performed in the experimental group animals by complete inflation of an occluder cuff for 90 s every 30 min for 3 to 5 h each day. Animals were then euthanized and the fetal brain perfusion-fixed and prepared for subsequent histology and apoptosis staining using the TUNEL assay method. The number of TUNEL positive cells for both the preterm and near term control group animals was low but with a significant regional hierarchy whereby values were higher in the cerebellar peduncle and cortex and lower in the cortical grey and white matter, hippocampus, and pons. While the apoptotic indices (expressed as TUNEL positive cells/1000 cells or high powered field) for most brain regions were not significantly changed between the preterm and near term control group animals, that for the hippocampus and pons were increased approximately 5- and 4-fold, respectively, (both P<0.05), in the near term animals. Intermittent UCO with severe but limited hypoxemia and no cumulative acidosis to ensure longer term survival, had no significant effect on apoptotic indices in the brains of either the preterm or near term animals, although hippocampal values for both occlusion groups were increased approximately 2-3-fold. Levels of apoptosis noted for the ovine fetal brain at 0.75 to 0.90 of gestation are thus low and likely approaching the basal levels of later life, but there are regional differences and changes over this period although little change in response to intermittent cord occlusion as studied, with implications for behavioural state activity and antenatal hypoxic insults in the brain's development.

Animals↗

PubMed2002

Early expression of thyroid hormone deiodinases and receptors in human fetal cerebral cortex.

Thyroid hormones are known to be important for optimal development of the human central nervous system. Classically, maternal thyroid hormones have not been thought to have a major role in defining central nervous system development. However, recent epidemiological evidence has indicated that subtle deficiencies in circulating maternal thyroid hormones in the first trimester of pregnancy are associated with adverse neurodevelopment. We have used real time PCR to quantitate the expression of mRNAs encoding the thyroid receptor isoforms (TR alpha1, alpha2, beta1 and beta2) and thyronine deiodinase subtypes (5'-DI, 5'-DII and 5-DIII) in human fetal cerebral cortex from the first and second trimesters of pregnancy. Deiodinase subtype activities have also been determined in these tissues and compared to 'normal' adult human cerebral cortex. Iodothyronine deiodinase mRNAs were expressed in human fetal cerebral cortex from 7 to 8 weeks of gestation. The expression of 5'-DI mRNA was variable in fetal life but increased relative to adult cortex (P<0.05), whereas the activity of this enzyme was below the level of assay detection. 5'-DII mRNA and activity in fetal cerebral cortex was detectable from as early as 7-8 weeks but not significantly different from that in adult life except at 15-16 weeks when mRNA expression increased (P<0.05). Fetal cortex 5-DIII mRNA expression was present from the early first trimester but less abundant than in adult tissue (P<0.01) and 5-DIII activity appeared greater in fetal cortex (P<0.01) as compared to adults. Only TR alpha1 mRNA was more abundantly expressed in fetal cortex than adult tissues (P<0.01). In contrast, the TR isoforms (alpha2 and beta1) were expressed significantly less than in adult tissues (P<0.05). Only 26% of fetal cerebral cortex samples expressed TR beta 1. There is evidence that the developing fetal brain, as early as the first trimester, expresses TRs and exhibits the mechanisms of pre-receptor control of thyroid hormone supply.

Adult↗

PubMed2003

Activity-dependent neuroprotective protein: a novel gene essential for brain formation.

We have recently cloned the novel homeobox-containing activity-dependent neuroprotective protein (ADNP). In the current study, mouse ADNP was shown to be expressed at the time of neural tube closure, detected at E7.5 and increased on E9.5. Expression was augmented in the brain (E12.5), sustained throughout embryogenesis and regulated by VIP. To assess the function of ADNP, knockout mice were established. Detailed analysis revealed cranial neural tube closure failure and death on E8.5-9.0 of the ADNP-knockout embryos. The expression of Oct4, a gene associated with germ-line maintenance was markedly augmented in the knockout embryos. In contrast, the expression of Pax6, a gene crucial for cerebral cortex formation, was abolished in the brain primordial tissue of the knockout embryos. Thus, Pax6 and Oct4 constitute a part of the mechanism of action of ADNP on brain formation, inhibiting germ-line division while activating morphogenesis. In conclusion, ADNP is identified here as a new key gene essential for organogenesis in the developing embryo and may be implicated as a clinical target associated with proper neurodevelopment.

Animals↗

PubMed2000

Developmental expression of Bcl-2 protein in human cortex.

Apoptosis is essential for normal human neurodevelopment and is increasingly recognized for its role in various neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. Bcl-2 is a 26 kDa membrane-associated protein known to protect neurons against apoptosis. Interestingly, Bcl-2 protein levels are altered in certain neurodegenerative disorders that reveal increased apoptosis. However, little is known about the normal expression of Bcl-2 protein in human brain. Bcl-2 protein levels were determined by ELISA and semiquantitative Western Blotting in the frontal cortex of 20 human post-mortem brains, separated into three groups: six infants (age: 0.83+/-1.0 years, mean+/-S.D.), five adolescents (age: 17.4+/-1.7 years), and nine adults (age: 41.0+/-9.6 years). All subjects died of non-CNS related illness and had no history of psychiatric illness. Bcl-2 increased significantly across the age groups in the ELISA (p=0.0058) and the Western Blot (p=0.002) experiments. The ELISA demonstrated significant differences in Bcl-2 levels between infant and adolescent cortex (p<0.05), and between infant and adult cortex (p<0.01) using a post-hoc Tukey's multiple comparison test. The Western blots demonstrated a similar significant increase in Bcl-2 between infant and adult cortex (p<0. 01). A secondary analysis showed significant correlation between individual ages and Bcl-2 levels (r(2)=0.4933, p=0.0006). This study demonstrates that Bcl-2 protein expression in human cortex is developmentally regulated and supports the hypothesis that Bcl-2 is involved in normal aging.

Adolescent↗

PubMed2002

Behavioral perinatology: biobehavioral processes in human fetal development.

Behavioral perinatology is as an interdisciplinary area of research that involves conceptualization of theoretical models and conduct of empirical studies of the dynamic time-, place-, and context-dependent interplay between biological and behavioral processes in fetal, neonatal, and infant life using an epigenetic framework of development. The biobehavioral processes of particular interest to our research group relate to the effects of maternal pre- and perinatal stress and maternal-placental-fetal stress physiology. We propose that behavioral perinatology research may have important implications for a better understanding of the processes that underlie or contribute to the risk of three sets of outcomes: prematurity, adverse neurodevelopment, and chronic degenerative diseases in adulthood. Based on our understanding of the ontogeny of human fetal development and the physiology of pregnancy and fetal development, we have articulated a neurobiological model of pre- and perinatal stress. Our model proposes that chronic maternal stress may exert a significant influence on fetal developmental outcomes. Maternal stress may act via one or more of three major physiological pathways: neuroendocrine, immune/inflammatory, and vascular. We further suggest that placental corticotropin-releasing hormone (CRH) may play a central role in coordinating the effects of endocrine, immune/inflammatory, and vascular processes on fetal developmental outcomes. Finally, we hypothesize that the effects of maternal stress are modulated by the nature, duration, and timing of occurrence of stress during gestation. In this paper, we elaborate on the conceptual and empirical basis for this model, highlight some relevant issues and questions, and make recommendations for future research in this area.

Behavior↗

PubMed2002

Cloning and characterization of a novel NMDA receptor subunit NR3B: a dominant subunit that reduces calcium permeability.

We report the cloning and characterization of a novel NMDA receptor subunit cDNA, which encodes a predicted polypeptide of 1003 amino acids. Phylogenic analysis indicates that this new subunit is most closely related to NR3A. Therefore, we term it NR3B. Important functional domains of glutamate receptors, such as the ligand-binding domain, the channel pore, and the channel gate, are conserved in NR3B. NR3B mRNA was expressed highly in pons, midbrain, medulla, and the spinal cord, but at low levels in the forebrain and the cerebellum. Although NR3A mRNA expression decreases sharply after the second postnatal weeks, NR3B mRNA expression levels in whole brain were constant during postnatal development and into adult. Coimmunoprecipitation analysis showed that NR3B could form NMDA receptor complex with NR1a and NR2A subunits in heterologous cells. Although expression of NR3B alone did not reconstitute functional NMDA receptors, coexpression of NR3B reduced the Ca(2+) permeability of glutamate-induced currents in cells expressing NR1a and NR2A. These results indicate that NR3B is a dominant modulatory subunit that can modify the function of NMDA receptors. Since high Ca(2+) permeability of NMDA receptors is thought to be a key feature for NMDA receptors to play critical roles in neurodevelopment, synaptic plasticity, and neuronal death, NR3B may contribute to the regulation of these physiological and pathological processes.

Animals↗

PubMed2001

PACAP activates PKA, PKC and Ca(2+) signaling cascades in rat neuroepithelial cells.

Several studies have reported that the PAC(1) receptor (PAC1-R), the specific receptor for PACAP, is expressed at early developmental stages. Here, we describe that the cytosolic Ca(2+) concentration ([Ca(2+)](i)) was increased by PACAP, but not VIP, in a concentration range from 10(-12) to 10(-8) M via the PAC(1)-R in isolated single cells from the rat neural fold. This activation of the cells by PACAP was mimicked by agonists and inhibited by antagonists of the cAMP/PKA and PLC/PKC cascades. These data indicate that PACAP/PAC(1)-R is linked to [Ca(2+)](i) signaling via two G-protein-coupled protein kinase pathways and may thereby play an important role in early neurodevelopment.

Animals↗

PubMed1982

A study of neurodevelopmental findings in early adolescent delinquents.

Subtle deficits or delays in the development of the central nervous system in young children are associated with problems affecting learning, behavior, and social adjustment. Less is known about the impact of such neurodevelopmental dysfunction in adolescents. This study assesses the possible association between neurodevelopmental delays and juvenile delinquency. An adolescent neurodevelopment examination was devised and administered to 54 delinquents and 51 secondary school students. Six areas were assessed. There were no significant differences in the prevalence of minor neurologic signs (P = 0.37) or in gross motor function (P = 0.02) and temporal sequential organization (P = 0.04). The greatest differences were in visual processing (P = 0.0002) and auditory-language function (P = 0.0001). Eighteen percent of delinquents and 4% of the comparison group were deficient in two or more neurodevelopmental areas. Nine percent of the delinquents and none of the comparison group had three or more dysfunctions. A neurodevelopmental examination may be a useful diagnostic tool for identifying endogenous factors in behavior, learning, and adjustment problems of this age group. Such findings have implications for the formulation of individualized management strategies.

Adolescent↗