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Results for “Neurodevelopmental Disorders”

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PubMed2006

Transient nonketotic hyperglycinemia and defective serotonin metabolism in a child with neonatal seizures.

Neonatal nonketotic hyperglycinemia is usually fatal or, less commonly, severely developmentally disabling, whereas transient nonketotic hyperglycinemia has usually been followed by normal development. We report a boy who had transient neonatal nonketotic hyperglycinemia but a coexistent disorder of serotonin metabolism manifested by initially low cerebrospinal fluid 5-hydroxyindoleacetic acid (which later normalized), low whole blood serotonin, and decreased platelet serotonin uptake. He survived the neonatal period but was neurodevelopmentally delayed and developed an autistic-like disorder. Later, his positron emission tomographic (PET) scans with alpha[(11)C] methyl-l-tryptophan revealed a pattern characteristic of autistic children. Although we know of no link between glycine and serotonin metabolism, and our patient had low, rather than high, central and peripheral serotonin, this case might represent a novel infantile disorder that affects both the glycine and serotonin neurotransmitter systems.

Brain Diseases, Metabolic↗

PubMed2006

Cannabis and neurodevelopment: implications for psychiatric disorders.

The developing brain is susceptible to the effects of exogenous cannabinoids both during the perinatal period through maternal cannabis use and in young adolescent users. Emerging data from human and animal perinatal exposure studies demonstrate a subtle rather than gross effect of cannabis upon later functioning including; specific cognitive deficits especially in visuospatial function; impulsivity, inattention and hyperactivity; depressive symptoms; and substance use disorders. From animal studies motor control systems, neuroendocrine function and nociception may additionally be affected. Fetal studies indicate that these outcomes may be through cannabinoid mediated influences on the ontogeny of, especially dopamine and opioid, neurotransmitter systems. The effect of cannabinoids in the adolescent suggest long-term deleterious outcomes in cognition, depressive symptoms, schizophrenia and substance use disorders. Much of these data support a neurodevelopmental effect, however, predisposing genetic and/or environmental factors cannot be excluded from human studies. Gender specific differences have been observed in both human and animal studies implying sex hormone and related factors may interact with cannabinoids in neurodevelopment. Further understanding how cannabinoids influence neurodevelopment will inform public debate about the health effects of cannabis but also open avenues in discerning how modulation of the endocannabinoid system may assist in the development of therapeutic tools for a variety of neuropsychiatric disorders.

Affect↗

PubMed2001

Reelin gene alleles and haplotypes as a factor predisposing to autistic disorder.

Autistic disorder (MIM 209850) is currently viewed as a neurodevelopmental disease. Reelin plays a pivotal role in the development of laminar structures including the cerebral cortex, hippocampus, cerebellum and of several brainstem nuclei. Neuroanatomical evidence is consistent with Reelin involvement in autistic disorder. In this study, we describe several polymorphisms identified using RNA-SSCP and DNA sequencing. Association and linkage were assessed comparing 95 Italian patients to 186 ethnically-matched controls, and using the transmission/disequilibrium test and haplotype-based haplotype relative risk in 172 complete trios from 165 families collected in Italy and in the USA. Both case-control and family-based analyses yield a significant association between autistic disorder and a polymorphic GGC repeat located immediately 5' of the reelin gene (RELN) ATG initiator codon, as well as with specific haplotypes formed by this polymorphism with two single-base substitutions located in a splice junction in exon 6 and within exon 50. Triplet repeats located in 5' untranslated regions (5'UTRs) are indicative of strong transcriptional regulation. Our findings suggest that longer triplet repeats in the 5'UTR of the RELN gene confer vulnerability to autistic disorder.

Adult↗

PubMed2003

Congenital malformations of the human brainstem.

Congenital disorders of the brainstem often result in multiple severe neurodevelopmental problems. With the advent of magnetic resonance imaging and discovery of genes directing brainstem formation, a more coherent clinical picture of these disorders is emerging. Proper evaluation, management, and counseling for these disorders rests on the clinician having a framework through which to approach them.

Brain Diseases↗

PubMed1984

[Prognostic value of the neurodevelopmental status in the first year of life in children with increased perinatal risk].

Among 503 high-risk newborns followed-up systematically in a prospective study up to 5 years of age, abnormalities of the development of posture, of maturation of tone and of psychomotor development were diagnosed at the age of 6 months in 70 children (13.9%) who form the study group. Among the other 433 high-risk newborns who presented a normal psychomotor development at the age of 6 months, 73 were selected at random and form the control group. In the study group, 59% of the children had a development which became normal during the second year of life (transitory disorders), 21% had persistent minor neurological abnormalities at the age of 5 years, and 20% evolved towards cerebral palsy and/or mental retardation. In the control group, 97.3% of the children remained normal and 2.7% presented minor neurological abnormalities at 5 years. Three parameters are important to estimate the prognosis of the children in the study group. These are: the presence of neurological disorders during the neonatal period, the type of neurodevelopmental abnormalities diagnosed at the age of 6 months, and the evolution of these abnormalities during the second semester of life. Among the 14 major handicaps, 13 were found in children who presented neurological neonatal disorders and 12 appeared in children who had an abnormality of muscular tonus associated with cognitive and social retardation at the age of 6 months. 52% of the children, whose status had not been "normalized" at 12 months, had a major handicap at 5 years. However, a hypertonia predominating in the lower limbs and observed at 6 months has a good prognosis; it disappears during the second year of life in 81.2% of cases (transitory disorders) and is associated with persistent minor neurological abnormalities in 18.8% of cases.--This study gives useful information for the establishment of an early prognosis and a rational management of the high-risk newborn children who present neurodevelopmental abnormalities during their first year of life.

Cerebral Palsy↗

PubMed2006

Structural brain abnormalities in early onset first-episode psychosis.

BACKGROUND: Brain morphometry in children and adolescents with first-episode psychosis offer a unique opportunity for pathogenetic investigations. METHODS: We compared high-resolution 3D T1-weighted magnetic resonance images of the brain in 29 patients (schizophrenia, schizotypal disorder, delusional disorder or other non-organic psychosis), aged 10-18 to those of 29 matched controls, using optimized voxel-based morphometry. RESULTS: Psychotic patients had frontal white matter abnormalities, but expected (regional) gray matter reductions were not observed. Post hoc analyses revealed that schizophrenia patients (n = 15) had significantly larger lateral ventricles as compared to controls. Duration and dose of antipsychotics correlated negatively with global gray matter volume in minimally medicated patients (n = 18). CONCLUSION: Findings of white matter changes and enlarged lateral ventricles already at illness onset in young schizophrenia spectrum patients, suggests aberrant neurodevelopmental processes in the pathogenesis of these disorders. Gray matter volume changes, however, appear not to be a key feature in early onset first-episode psychosis.

Adolescent↗

PubMed1999

Neurodevelopmental processes and psychological functioning in autism.

Autism is a developmental disorder with variable severity, occurring at all levels of cognitive ability and having a number of slightly different clinical presentations. It is associated with neuropsychological deficits that occur in other conditions also, but its pattern may be specific to autism. Genetic and environmental early insults to brain development are etiological determinants of the disorder. Brain circuitries important for social, communicative, and integrational purposes have been suggested to be dysfunctional in autism. There could be at least two different pathways to autism, one connected with primary temporofrontal dysfunction (and late prenatal-early postnatal origins) and another linked to primary brain-stem dysfunction (and early prenatal origins). Further study of neurodevelopmental and neuropsychological processes in autism will help elucidate not only the pathological mechanisms involved in the specific syndromes but also the underpinnings of normal brain development.

Aging↗

PubMed2004

Autism spectrum disorder: screening, diagnosis, and medical evaluation.

Autism spectrum disorder (ASD) are a group of behaviorally defined neurodevelopmental disabilities with core deficits in socialization, communication, and behavior, although the presentation can be extremely variable. This article describes the core deficits in ASD, as well as the differential diagnosis and the more commonly associated comorbid disorders. The importance of early diagnosis is emphasized, and screening and assessment tools are reviewed. Finally, the role of the pediatric neurologist is discussed with regard to specific components of the evaluation, including history, physical examination, and ancillary testing.

Autistic Disorder↗

PubMed2004

Cavum septi pellucidi in first-episode schizophrenia and first-episode affective psychosis: an MRI study.

A high prevalence of abnormal cavum septi pellucidi (CSP) in schizophrenia may reflect neurodevelopmental abnormalities in midline structures of the brain. The relationship, however, between abnormal CSP and clinical symptoms, and with abnormalities in other limbic structures remains unclear, as does the question of whether a similar abnormality is present in affective psychosis. Seventy-four patients at their first hospitalization, 33 with schizophrenia and 41 with affective (mainly manic) psychosis, and 56 healthy control subjects underwent high-spatial-resolution magnetic resonance imaging (MRI). CSP on six slices or more on 0.9375-mm resampled coronal images was categorized as abnormal. The prevalence of abnormal CSP in both schizophrenic patients (26.1%) and affective psychosis patients (18.2%) was significantly higher than was observed in control subjects (8.2%). In schizophrenic patients only, larger CSP was significantly associated with more severe thinking disturbance and smaller left parahippocampal gyrus gray matter volumes. While the relationships between CSP ratings and clinical symptoms did not significantly differ between the two psychosis groups as assessed by the comparison of regression slopes, the association with limbic volumes appeared to be specific to schizophrenic patients. These results suggest that psychosis associated with schizophrenia and affective disorder share, at least to some extent, neurodevelopmental abnormalities involving midline structures and associated psychopathological consequences. However, the association between abnormal CSP and limbic systems may be more specific to schizophrenia.

Adolescent↗

PubMed2004

Antenatal risk factors associated with unfavorable neurologic status in newborns and at 2 years of age.

The aim of this prospective cohort study was to evaluate the influence of different antenatal factors on neurologic signs in the first days of life and neurodevelopmental outcome at 2 years of age. The study group consisted of 390 children drawn from a cohort of 828 consecutive live births. The data about potential antenatal risk factors, birth complications, and neonatal course were abstracted from pregnancy and delivery records and the hospital register. Odds ratio estimates with 95% confidence intervals were used to measure the associations between antenatal factors and neurologic status in newborns and at 2 years of age. Significance level was set at P < .05. At the mean age of 2 years, 49 of 390 children exhibited adverse neurodevelopmental outcome (cerebral palsy and other developmental disorders). The development of 341 children was normal. Comparative analysis of risk factors was conducted. The strongest correlation with development of hypoxic-ischemic encephalopathy during the first days of life was found in trichomoniasis during pregnancy (odds ratio 4.34; 95% confidence interval 1.32-14.23) and acute respiratory disease (temperature > or = 38 degrees C) in the second half of pregnancy (odds ratio 2.86; 95% confidence interval 1.08-7.58). Of various antenatal factors, bacterial vaginosis combined with impending abortion in the first half of pregnancy (odds ratio 4.96; 95% confidence interval 1.35-18.26) had a significant association with adverse outcome at 2 years of age. The presence of at least one complication at delivery placed the child at risk of adverse neurologic outcome (odds ratio 2.44; 95% confidence interval 1.32-4.54). The study provides supportive evidence that antenatal factors associated with maternal infections can influence the development of hypoxic-ischemic encephalopathy and later neurodevelopmental outcome. These children should be assigned to risk groups for early intervention.

Adult↗

PubMed1999

Defining the phenotype of schizophrenia: cognitive dysmetria and its neural mechanisms.

All research on schizophrenia depends on selecting the correct phenotype to define the sample to be studied. Definition of the phenotype is complicated by the fact that there are no objective markers for the disorder. Further, the symptoms are diverse, leading some to propose that the disorder is heterogeneous and not a single disorder or syndrome. This article explores an alternative possibility. It proposes that schizophrenia may be a single disorder linked by a common pathophysiology (a neurodevelopmental mechanism), which leads to a misconnection syndrome of neural circuitry. Evidence for disruption in a specific circuit is explored: the cortical-thalamic-cerebellar-cortical circuit (CCTCC). It is suggested that a disruption in this circuit leads to an impairment in synchrony, or the smooth coordination of mental processes. When synchrony is impaired, the patient suffers from a cognitive dysmetria, and the impairment in this basic cognitive process defines the phenotype of schizophrenia and produces its diversity of symptoms.

Brain Mapping↗

PubMed2002

Expression of macrophage colony-stimulating factor and its receptor in microglia activation is linked to teratogen-induced neuronal damage.

Prenatal exposure to teratogen agents is linked to the pathogenesis of neurodevelopment disorders, but the mechanisms leading to the neurodevelopmental disturbance are poorly understood. To elucidate this, an in vitro model of microglial activation induced by neuronal injury has been characterized. In this connection, exposure of primary microglial cells to the conditioned medium from the neuronal damage induced by teratogen, cyclophosphamide, is accompanied by a reactive microgliosis as assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, lectin histochemistry, double labeling immunohistochemistry and in situ hybridization. Our results showed that reactive microglia were capable of releasing various cytokines such as tumor necrosis factor-alpha, interleukin-1, interleukin-6, transforming growth factor-beta and nitric oxide. Also, we have shown that macrophage colony-stimulating factor (M-CSF) was in fact produced by the reactive microglia. Concomitant to this was the increased expression of M-CSF receptor in these cells following the teratogen-induced neuronal injury. The up-regulation of M-CSF receptor suggests that the cells are capable of responding to self-derived M-CSF in an autocrine fashion. Results with antibody neutralization further suggest that microglial proinflammatory response, as manifested by cytokine expression in culture, is mediated by M-CSF, which acts as a molecular signal that initiates a microglial reaction. We therefore suggest that microglial activation following cyclophosphamide treatment is not only a response to the neuronal damage, but is also a cause of the damage during pathogenesis of neurodevelopment disorders. To this end, the increased expression of M-CSF and its receptor on microglia would be directly linked to the active cell proliferation and proinflammatory response in the teratogen-induced injury.

Animals↗

PubMed2000

Developmental brain anomalies in children with attention-deficit hyperactivity disorder.

The pathoetiology of attention-deficit hyperactivity disorder (ADHD) has been considered to be neurodevelopmental, yet the timing and processes involved are not clearly identified. Neurodevelopmental brain anomalies have been associated with a variety of psychiatric conditions. However, they have never been evaluated in a population of patients with ADHD. This study was designed to determine the frequency of specific developmental brain anomalies in a group of children with ADHD (n = 85; mean age, 10.9 years) and healthy control children (n = 95; mean age, 11.7 years) by visually inspecting brain magnetic resonance imaging scans. Compared to controls, the ADHD group showed an increase in frequency of two developmental anomalies: (1) gray-matter heterotopia, a neuronal migration anomaly, in 2 of 85 patients versus 0 of 95 controls; and (2) posterior fossa abnormality (excess cerebrospinal fluid in the posterior fossa) in 8 of 85 patients versus 2 of 95 controls. There were no differences in frequency of enlarged cavum septi pellucidi between the two groups. These findings support and extend the idea that ADHD is of developmental origin, and further suggest that the timing of aberrant brain development could be in early gestation.

Adolescent↗

PubMed1983

High risk appropriate for gestational age (AGA) and small for gestational age (SGA) preterm infants. Neurological handicap and developmental abnormalities at five years of age.

Outcome at five years of age of 110 high risk AGA, 71 high risk SGA preterm infants with similar birth weight and 102 term control infants was studied. Mean IQ in the 3 groups was not statistically different. Major handicaps were found in 16.3% of the AGA and in 8.5% of the SGA preterms. There was no major handicap among the controls. Minor neurodevelopmental abnormalities were present in 25.6% of AGA, 28.2% of SGA and 19.6% of controls. The types of neurodevelopmental handicaps were different in the 3 groups and generally more severe in the AGA group. All the major handicaps among AGA preterms were found in children with severe neonatal complications. In the SGA preterm group, only 1/3 of the major handicaps can be related to perinatal complications. Affective and behavior disorders were probably related in some way to neurodevelopmental achievement. This study showed that preterm infants with GA less than or equal to 32 weeks are more at risk than more mature SGA preterms with similar birth weight.

Child, Preschool↗

PubMed1998

[Current trends in clinical psychiatric research].

SCHIZOPHRENIA: The long-standing dopaminergic hypothesis is based on well-established findings, mainly related to a dysfunction of the mesolimbic C2 and D3 receptors, negative signs of prefrontal hypodopaminergia concerning the D2 and D4 receptors. Immune disorders are also involved as well as a possible neurodevelopmental component. Finally genetic factors play an important role. DEPRESSIVE STATES: Three monoaminergic systems appear to be implicated: the catecholaminergic, serotaminergic and homovanilic systems. It is not known whether the disorder of the serotaminergic system results from pre-existing fragilization or a symptom-related modification. HYPOTHESES CONCERNING DEPRESSION: According to the chronobiology hypothesis, certain biological rhythms (cortisol, temperature, perhaps melatonin) are desynchronized, a disequilibrium which disappears after cure. The fragilization hypothesis is based on the progressive development of a stress-related pathological organization in the hippocampo-hypothalamo-adrenal axis. PERSPECTIVES: The development of new psychotropes remains a challenge to meet the unsatisfied demands in psychiatrics. Drugs with rapid action and minimal side effects are needed.

Brain Chemistry↗

PubMed2004

Role of melatonin in carbon monoxide-induced hypoxemia.

Melatonin (MEL) works in tandem with serotonin (5HT), where an equilibrium exists in perfect health. Under stress or in crisis, it may be that the production of MEL predominates in conjunction with ever increasing production of reactive oxygen species (ROS), may lead to hypoxemia and consequently, to metabolic disruption. The Melatonin Hypothesis could offer an explanation towards certain clinical observation and may support the Catacholamine Hypothesis in the development of depression but it is the role played by carbon monoxide (CO) in inducing hypoxemia which may result in the Cascade Effect that could in turn explain the development of neurodegenerative, neurodevelopmental as well as immune dysfunctional type disorders, prevalent today. CO-induced hypoxemia is an important aspect in any discussion of cell integrity as CO is formed endogenously from the degradation of erythrocytic heme, any hemolytic disturbance or lipid peroxidation, may increase the level in blood. CO, in inducing hypoxemia, causes the generation of large quantities of hydroxyl (-OH) which could damage specific amino acid and disorder protein metabolism that may result in the creation of toxic metabolites. Hydroxyl damage is emerging as the precursor to low-grade inflammation in the presence of C Reactive Protein (CRP) that is currently speculated in the etiology of many known disorders. As disordered protein metabolism may play a crucial role in the formation of the cascade, the hypothesis aims to address the issues of cell viability and the process of cell replication in the event where cell integrity is severely compromised in the face of apoptotic and/or necrotic damage, as the intra-cellular and extra-cellular environments are becoming increasingly hostile. Where -OH damage to specific amino acid in protein may contribute to the Cascade Effect, the hypothesis goes further to explain the importance of the Circardian Cycle and the role of paradoxical sleep, by taking into consideration the need for repair and for regeneration in order to maintain morphology as any cellular event that depends on a redox state is likely to be compromised in an event of hypoxemia. As MEL enters a cell readily because of its high lipid solubility, the role of MEL becomes clear as in its diversity, MEL is a potent oxygen radical scavenger that operates throughout the cell.

Carbon Monoxide↗

PubMed1993

Cerebral palsy.

Over the last century, our understanding of cerebral palsy has broadened. For example, we now know that it results more commonly from prenatal abnormalities than from perinatal difficulties. Yet, in most cases we are still no closer to understanding the operant mechanism of injury or how the injury results in the expressed motor disorder. Hopefully, the strides being made in neurodevelopmental physiology and neurotransmitter communication will help elucidate the mechanism of injury in cerebral palsy and thereby lead to methods of prevention. Meanwhile, comprehensive clinical evaluation and treatment and periodic reassessment will help tailor strategies to the individual needs of the child. This should enable the child with cerebral palsy to optimize his or her function in society.

Cerebral Palsy↗

PubMed1997

Schizophrenia: a disorder of neurodevelopment?

For the first time, there is a pathogenic hypothesis of schizophrenia based upon reasonable empirical data. The hypothesis is that schizophrenia is a disorder arising from aberrant brain development. The neurodevelopmental view of schizophrenia is supported by neuropathological, epidemiological and clinical findings. Here, the evidence in favour of the model is summarized, together with a consideration of its weaknesses.

Brain↗