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PubMed2002

A selective reduction in the relative density of parvalbumin-immunoreactive neurons in the hippocampus in schizophrenia patients.

OBJECTIVES: To determine the relative densities of the GABAergic subpopulation defined by calcium-binding proteins and to further study the importance of changes in GABAergic interneurons on neuropathology in the hippocampus in schizophrenia cases. METHODS: The relative densities and neuronal body size of cells immunoreactive for the calcium-binding proteins parvalbumin and calretinin as well as the area size of the hippocampal sub-fields were determined from the hippocampal tissue sections taken from schizophrenic patients and well-matched control subjects (15 per group). RESULTS: No significant difference in the density of calretinin-immunoreactive neurons and the neuronal body size of calretinin-positive neurons was found between subject groups. Relative to normal controls, schizophrenic patients showed a significant and profound deficit in the relative densities of parvalbumin-immunoreactive neurons in all hippocampal sub-fields. These reductions were more apparent in male schizophrenic patients and were unrelated to antipsychotic drug treatment, age or duration of illness. CONCLUSION: The findings provide further evidence to support a profound and selective abnormality of a sub- population of GABAergic neurons in the hippocampus in schizophrenia cases, and are consistent with the etiological hypothesis of the neurodevelopment of schizophrenia.

Adult↗
PubMed2002

[Genetic hypothesis of schizophrenia].

It is now well demonstrated from family, adoption or twin studies, that genetic factors are involved in schizophrenia. Yet, the nature of these factors remains unknown. The disappointing results of the classical linkage studies are explained by the complex non mendelian inheritance, involving several genes interacting with environmental and/or maturation processes, and the heterogeneity of the clinical expression. The identification of genes having an influence on schizophrenia requires thus new strategies including statistical analysis with no assumption on the inheritance mode (non parametric methods) and the dissection of the heterogeneous syndrome using endophenotypes and/or relevant clinical features. Beside the hypothesis of a dysfunctional neurotransmission in schizophrenia (i.e. dopaminergic), evidence suggests that genes involved in neurodevelopment could also be candidate. The observation of caryotypic anomalies could also lead to new candidate regions or genes.

Brain↗
PubMedDate not supplied

[Long-term psychiatric and behavioural consequences of prenatal exposure to psychoactive drugs].

A growing body of evidence supports the hypothesis that exposure to prenatal environmental risk factors increases the vulnerability for a broad range of psychiatric disorders. Although the association between exposure to obstetric complications and increased vulnerability for psychiatric disorders is well documented, few studies have explored the putative deleterious impact of psychoactive substances and xenoestrogens on subsequent liability for psychological disturbances. Cohort studies suggest that prenatal exposure to nicotine is a risk factor for conduct disorders, and some case-control studies have reported an association between prenatal nicotine exposure and attention deficit hyperactivity disorder. Studies on the long-term behavioural consequences of prenatal exposure to other licit and illicit psychoactive substances are hampered by methodological flaws limiting the interpretation of the findings. Regarding prenatal exposure to hormones, sparse findings suggest that exposure to xenoestrogens such as diethylstilbestrol may be a risk factor for psychiatric disorders, mediated by a deleterious impact of these substances on the foetal neurodevelopment. However, this hypothesis is largely speculative due to the low number of studies and their methodological limitations. Further studies are required to explore the long-term cognitive and behavioural consequences of prenatal exposure to psychoactive drugs and xenoestrogens.

Alcohol Drinking↗
PubMed2002

Neurodevelopmental issues in the assessment and treatment of deficits in attention, cognition, and learning during adolescence.

Adolescent growth and development occur over multiple domains of function and represent the neurodevelopment process of maturation. Adolescents who have experienced normal development will transition through this complex process and will achieve mastery and integration of those domains by late adolescence (ages 17-21 years). Those youth who do not experience normal development can experience deficits in one or all of the domains of function. These deficits are better understood by examining the neurodevelopmental aspects of maturation. Identifying the interactive effects of strengths and weaknesses in each domain of function will give the clinician access to methods of refining and individualizing treatment.

Adolescent↗
PubMed2001

Neurodevelopmental models of schizophrenia: pathophysiologic synthesis and directions for intervention research.

This paper examines contemporary models of the pathophysiology of schizophrenia from a neurodevelopmental perspective. Specifically, this article reviews recent research in the neuropathology, neuroimaging, and developmental psychopathology of schizophrenia, with an aim to critically evaluate several recent proposals concerning the nature and timing of both the neuroanatomic abnormalities underlying the disorder and their behavioral manifestations. Findings from the empirical literature are synthesized from the perspective of dual cytoarchitectonic trends theory of neurodevelopment, as well as in relation to current conceptions of the schizophrenia prodrome. The evidence shows that sufficient groundwork has been laid to begin longitudinal neuroimaging studies of adolescents at clinical risk for schizophrenia, to determine more definitively the pathophysiology of the disorder. Such information could have significant implications in terms of understanding the prediction, treatment, and, ultimately, prevention of schizophrenia.

Adolescent↗
PubMed2002

[Neurotrophic factors and neural stem cells].

Neurotrophic factors includes nerve growth factors (NGF) family, glial cell line-derived neurotrophic factors (GDNF) family and other neurotrophic factors. NGF, BDNF, NT-3, NT-4/5 and NT-6 constitute NGF family (the neurotrophins), which may enhance both survival and differentiation of neurons from the EGF-responsive hippocampal and the subventricular zone neural stem cells. GDNF family includes GDNF, NTN, PSP and ART, whose major role is in peripheral neurodevelopment. This family enhance proliferation and survival of enteric neural crest precursor cells and is critical for the development of peripheral sensory nerve. Other growth factors such as bFGF and EGF can enhance proliferation and survival of neural stem cell. CNTF and LIF are critical for differentiation of neural stem cells.

Animals↗
PubMedDate not supplied

[Pascual graphomotor test in children with attention deficit hyperactivity disorder, combined type].

INTRODUCTION: Different neuropsychological batteries are used in order to define the neurocognitive profile of the patient with attention deficit hyperactivity disorder (ADHD). Pascual graphomotor test has recently been presented; it is useful to study the neurodevelopment in drawing and the non verbal cognitive level in normal children and others with neuropsychiatric disabilities. METHOD: We have studied 45 patient with ADHD, combined type. Pascual and Wechsler tests were performed in all cases before any kind of therapies. No relation was observed between the scores obtained in both tests. A linear correlation was demonstrated between age and graphomotor score with statistical significance. Pascual graphomotor test showed a good sensibility in the screening of mental retardation although a low specificity. CONCLUSIONS: We propose that Pascual graphomotor test should be included in neuropsychological batteries which will be applied in patients with ADHD.

Adolescent↗
PubMed1998

Progressive changes in schizophrenia: do they exist and what do they mean?

Schizophrenia is a disorder characterized by multiple symptoms, with a varied course and outcome. The etiology is yet unknown, but multiple pathological processes or, equally likely, a unique pathophysiological process, may be involved. Here, we review evidence for progressive changes in schizophrenia in order to understand further the pathophysiology of this disorder. We first present evidence for clinical and psycho-social changes over time, followed by evidence from structural brain studies that suggests that schizophrenia is a brain disorder. We then review findings from the small number of longitudinal studies that have evaluated structural brain changes in schizophrenia, followed by a review of the evidence for neurophysiological changes, both cross-sectional and longitudinal. This is followed by a discussion of possible cellular mechanisms, including NMDA receptor abnormalities, that might account for structural and functional brain changes (temporal and frontal), and we discuss how these abnormalities might be related to not only the specific signs and symptoms of schizophrenia but also to the onset and course of the illness. Finally, we discuss neurodevelopment (static and perhaps non-static alterations) and neurodegenerative theories of schizophrenia. We propose that the two are not mutually exclusive, but instead likely reflect a "two-hit" model for some subtypes of schizophrenia.

Journal Article↗
PubMed2003

Detrimental effects of hypoxia-reoxygenation injury on development of rat embryos during organogenesis in vitro.

AIM: To analyse the effects of hypoxia-reoxygenation on the development of rat embryos during early stages of gestation in vitro. METHODS: Whole embryo culture techniques were used to culture Wistar rat embryos under a range of gassing regimes, some of which included periods of mild hypoxia. After the termination of cultures, embryos were morphologically examined and assessed, and their protein content was determined. RESULTS: Cultured embryos exposed to 4 h of mild hypoxia did not show any significant growth or differentiation, as expected during this developmental stage. The ensuing 20 h reoxygenation period appeared to exacerbate the effects of the hypoxia. CONCLUSION: The effects of hypoxia during the perinatal or late fetal stages are well documented, but less is known of the effects at earlier stages of gestation. Our results indicate that during organogenesis, even short-term exposure to hypoxia may impose detrimental effects on growth and neurodevelopment of embryos.

Animals↗
PubMed2003

Effect of prenatal PAH exposure on birth outcomes and neurocognitive development in a cohort of newborns in Poland. Study design and preliminary ambient data.

Preliminary data suggest an association between infant mortality rates and several measures of ambient air pollution, including dustfall and polycyclic aromatic hydrocarbons (PAH). The effects of airborne PAH components on fetal growth and early childhood development are of primary interest since we have previously demonstrated that these pollutants were associated with significant decrements in birthweight, length and head circumference in Polish newborn babies. The undertaken research combines a state-of-the-art environmental monitoring and molecular approaches with comprehensive neurodevelopment assessments. A further innovation is the incorporation of biomarkers (lead and antioxidants in cord blood) to control for potential confounding of exposure-effect. The mean overall concentrations of specific PAH compounds in Kraków were highest for benzo(b)fluoranthene (23 ng/m3), benzo(a)anthracene (16 ng/m3), indeno(l,2,3-cd)pyrene (14 ng/m3), chyresene (13 ng/m3) and benzo(a)pyrene (12 ng/m3). In general, concentrations of the PAH compounds measured by personal monitoring were considerably higher among the residents of the higher polluted area of the city. The comparison between the Kraków and New York City monitoring ambient data demonstrates that the concentrations and proportions of specific compounds in the total PAH mixture differ widely across these cities. Thus, one may expect that the PAH-related health risks would differ between the two areas not only because exposures are different, but also because the PAH profile differs. Presumably, this different profile is a consequence, at least in part, of variations in the sources of fossil and solid fuels used in production of energy. In Poland, solid fuels such as coal is used to a much greater extent than in New York City, where fossil fuels are the universal source of energy production. Auto emissions for example, are low in benzo(a)pyrene, whereas such emissions from refuse burning are high.

Air Pollutants↗
PubMed2003

Synapse number and synaptic efficacy are regulated by presynaptic cAMP and protein kinase A.

The mechanisms by which neurons regulate the number and strength of synapses during development and synaptic plasticity have not yet been defined fully. This lack of fundamental knowledge in the fields of neurodevelopment and synaptic plasticity can be attributed, in part, to compensatory mechanisms by which neurons accommodate for the loss of function in their synaptic partners. This is generally achieved either by scaling up neuronal transmitter release capabilities or by enhancing the postsynaptic responsiveness. Here, we demonstrate that regulation of synaptic strength and number between identified Lymnaea neurons visceral dorsal 4 (VD4, the presynaptic cell) and left pedal dorsal 1 (LPeD1, the postsynaptic cell) requires presynaptic activation of a cAMP-PKA-dependent signal. Experimental activation of the cAMP-PKA pathway resulted in reduced synaptic efficacy, whereas inhibition of the cAMP-PKA cascade permitted hyperinnervation and an overall enhancement of synaptic strength. Because synaptic transmission between VD4 and LPeD1 does not require a cAMP-PKA pathway, our data show that these messengers may play a novel role in regulating the synaptic efficacy during early synaptogenesis and plasticity.

Animals↗
PubMed2003

The phenotype of patients with 4q-syndrome.

The 4q-syndrome comprises all microscopically visible deletions of the long arm of chromosome 4. Here we review the phenotypical characteristics of 101 literature cases and delineate this evolving deletion syndrome further. The most common anomalies observed in these patients were craniofacial (99%), digital (88%), skeletal (54%) and cardiac (50%). Nearly all of the surviving probands were delayed in their neurodevelopment and approximately two third of the study group showed ante- or postnatal growth deficiency. The overall mortality was twenty eight percent.

Chromosomes, Human, Pair 4↗
PubMed2003

Infant formulas. Recent developments and new issues.

Infant formulas on the market today should be aimed at providing the best alternative to breast milk for infants of those women who are unable to continue breastfeeding until 6 months of age and substituting ideally for human milk after 6 months of age approaching the structural and functional effects observed in breastfed infants. The aim is to mimic the functional outcome of the breastfed infant (e.g. growth and development), and not to copy the composition of human milk. For this purpose, the following compounds have been added to formulas and are reviewed: long-chain polyunsaturated fatty acids (LCPUFA) for brain composition and neurodevelopment, probiotics and prebiotics for the fecal flora and the local intestinal defense, and nucleotides for promoting the immune response. Changes in protein quantity and quality allow to balance the blood amino acid pattern (possibly relevant to the early stages of brain development for the neurotransmitter function) and reducing the protein intake could be important for the prevention of later overweight. Hydrolysed proteins are important in the prevention of atopic disorders. Many trials have been published so far with short-term assessments, most of them with positive findings. However, we need more data on the long-term follow-up of infants who were fed the new formulas. Such data will allow to look at neural performance, prevention of overweight and obesity, and effects on the immune-allergic pattern.

Dietary Proteins↗
PubMed2003

Incipient neurovulnerability and neuroprotection in early psychosis.

The objective of this study was to review the implications of altered regulatory mechanisms of progenitor cell generation and death for neurodevelopment and adult brain functioning in early intervention in schizophrenia and related disorders. MEDLINE databases were searched from 1966 to 2002 using the following key words: stem cells, progenitor cells, glia, neurogenesis, apoptosis, and combined with brain and schizophrenia. Necropsy evidence suggests alterations in synaptic connectivity and a reduction in glial cell numbers with no substantial signs of neuronal cell loss or necrotic neurodegeneration (gliosis). Neuroimaging data propose dynamic structural changes with some evidence of volume loss of the hippocampus during the transition to psychosis. Central and peripheral tissues of patients with schizophrenia give indirect evidence of reduced neurotrophic and anti-apoptotic factors relevant for generation, and atrophic degeneration of cells of glial and, in some brain areas, even neuronal origin. In vivo brain magnetic resonance spectroscopy data in schizophrenia support the loss of neuropil (reduction in n-acetylaspartate) and increased membrane turnover (decrease in phosphomonoesters [PMEs], increase in phosphodiesterases [PDEs]) at the onset of illness, which potentially corresponds with increased apoptotic activity of progenitor cells. In conclusion, dysfunctional regulation of generation and degeneration of progenitor cells of glial and, in some brain areas, neuronal origin may potentially explain early and late neurodevelopmental abnormalities in early psychosis. A reduced genesis or an increased death of glial cells in the grey matter may provide the cellular substrate for synaptic and dendritic changes resulting in local atrophy and disconnectivity. Neuroprotective strategies counteracting the loss or supporting the generation of progenitor cells may therefore be a potent therapeutic avenue to explore.

Animals↗
PubMedDate not supplied

[Phenotypic variability of deletion 22q11.2. An analysis of 16 observations with special emphasis on the neurological manifestations].

INTRODUCTION: The microdeletion 22q11.2 affects 1/4000 live births and constitutes the most frequent interstitial chromosomal alteration in humans. It is involved in a heterogeneous series of phenotypic expressions. AIMS: To determine the most important clinical characteristics in a series of patients with this genetic molecular disorder. PATIENTS AND METHODS: We conducted a retrospective study of 16 patients who had been diagnosed, by means of FISH or PCR, as having microdeletion 22q11.2, and the following data were evaluated in a protocolised manner: sex, age, family background, characteristics of the pregnancy, birth, neonatal and post-neonatal periods, clinical and semiological data, as well as the results from the complementary explorations carried out according to the predominant pathology. RESULTS: The age at which the diagnosis was made oscillated between newly born and 8 years, with a predominance of males over females in a ratio of 3.2/1. In all, 81% of patients presented neurological disorders. Brain malformations were seen in six, hypoplasia of the anguli oris muscle in five, congenital facial palsy in three which was associated with brain malformations in one patient, retarded neurodevelopment in six cases and neurogenic arthrogryposis in one. Other findings such as congenital heart disease (75%), skeletal disorders (37%), peculiar phenotypes (31%), nephrourological disorders (19%) and hypoacusis (19%) constitute significant manifestations of the process. Some of the most noteworthy occasional events include retarded height and weight development, hypocalcemia and cleft palate. In one case involving a child whose mother suffered from chronic alcoholism, there were both phenotypic traits of this entity and of foetal alcohol syndrome at the same time. In four of the patients the FISH technique did not detect the deletion, which was confirmed by a technique involving DNA amplification with PCR. CONCLUSIONS: The presence of central and peripheral neurological alterations, together with cardiac, skeletal, renal and auditory disorders was confirmed, as was the existence of neurodevelopmental retardation and a peculiar phenotype. Both the frequency and the kind of disorder coincided with what has been described earlier. A number of facts stand out owing to their novelty. These include the high incidence of asymmetric crying facies, the existence of data compatible with foetal alcohol syndrome in one of the patients with this clinical entity, and the association with neurogenic arthrogryposis in another, which are circumstances that suggest the possibility of a causal relation with the deletion 22q11.2. Using DNA amplification with PCR is seen to be of greater diagnostic efficacy than the FISH technique.

Abnormalities, Multiple↗
PubMed2003

[Prenatal and postnatal cardiologic evaluation of normal twin from acardiac twin pregnancy--case report].

The aim of the paper was to describe dynamic changes in 'pump twin's' circulatory system within clinical observation, indication analysis for premature delivery due to cardiovascular findings and long-term postnatal follow up. In echocardiographic examination of 'pump twin' no structural heart defects but functional changes in cardiovascular system have been detected (cardiomegaly, right heart disproportion, tricuspid valve regurgitation). Within 10-week observation polyhydramnios did not increased significantly, no amnioreduction procedures had been performed. Due to single umbilical artery in 'pump twin' a cytogenetic examination had been performed revealing a normal karyotype. When the first signs of abnormal Doppler flows appeared such as increased PI of umbilical artery and DV and cardiomegaly with TR--caesarean section was performed at 33 weeks of gestation. Echocardiography performed in the first day of life findings: right atrium and ventricle enlargement, significant tricuspid valve regurgitation (V max 3 m/s), a prenatally undetected, small perimembrane-part ventricular septal defect. At the age of 6-months a non-significant VSD with tricuspid valve septal leaflet closure and ASD II has been confirmed. The infant is systematically followed-up by paediatricians, cardiologists and neurologists and her further neurodevelopment appears to be slightly retarded.

Adult↗
PubMed2004

Developmental function of very-low-birth-weight infants and full-term infants in early childhood.

BACKGROUND AND PURPOSE: Despite general recognition that surviving very-low-birth-weight (VLBW) infants are at risk for neurodevelopmental impairments and educational achievement difficulties, there has been relatively little study on their functional status in areas such as locomotion, communication, cognition, self-care, and interpersonal relationships. This study assessed the functional status of VLBW infants and full-term infants in early childhood, and sought to identify risk factors for functional morbidity. METHODS: A total of 238 VLBW infants and 91 full-term infants were included in this prospective follow-up study. The functional status of the infants was assessed using the Chinese Child Development Inventory (CCDI) and neurodevelopment was evaluated using the Bayley Scales of Infant Development, second version (BSID-II) at 3 years of corrected age. Perinatal and sociodemographic data were collected through review of medical records. RESULTS: The VLBW infants had lower scores on all the CCDI measures compared with the full-term infants. Functional limitation (defined as more than 2 standard deviations below the means of the full-term infants) occurred more frequently in the VLBW infants than in the full-term infants: gross motor, 23% vs 3%; fine motor, 12% vs 1%; expressive language, 21% vs 2%; comprehension-conceptual, 23% vs 4%; situation comprehension, 17% vs 4%; self-help, 17% vs 1%; and personal-social, 19% vs 3% (all p < 0.01). Significant risk factors associated with functional morbidity included gestational age < 30 weeks, grade III-IV intraventricular hemorrhage, chronic lung disease, stage III-IV retinopathy of prematurity, male gender, and maternal education below high school. CONCLUSION: VLBW infants have a higher risk of functional morbidity than their full-term counterparts in early childhood. Infants with functional limitations on CCDI screening might require comprehensive developmental assessment and continued follow-up.

Developmental Disabilities↗
PubMed2004

Mercury exposure and child development outcomes.

Mercury is ubiquitous in the global environment, ensuring universal exposure. Some forms of mercury are especially neurotoxic, including clinical signs at high doses. However, typical human exposures occur at low to moderate doses. Only limited data about neurotoxicity at low doses are available, and scientists differ in their interpretation. Dose-response data on neurodevelopment are particularly limited. Despite or perhaps because of the lack of sufficient or consistent scientific data, public concern about a link between mercury exposure and developmental disabilities has been rising. After reviewing the data, the US Environmental Protection Agency proposed a reference dose (an estimate of a daily dose that is likely to be without a risk of adverse effects over a lifetime) for methyl mercury that is substantially lower than previous guidelines from the World Health Organization, the US Agency for Toxic Substances and Disease Registry, and the US Food and Drug Administration. Some questions have been raised about the Environmental Protection Agency's guidelines, but the issue remains unresolved. Meanwhile, consumer groups have raised questions about the potential link between mercury exposure and autism spectrum disorders as well as other adverse neurodevelopmental outcomes. This hypothesis has prompted some parents to seek regulatory, legal, or medical remedies in the absence of firm evidence. This article reviews what is known about mercury neurotoxicity and neurodevelopmental risk. Our intent is to focus the debate about mercury on 1) additional research that should be sought and 2) defining the principal issues that public policy makers face.

Child↗