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PubMed1999

Correlation between lead-induced changes in cerebral ornithine decarboxylase and protein kinase C activities during development and in cultured PC 12 cells.

Exposure to lead (Pb) interferes with neurodevelopment and disturbs ornithine decarboxylase (ODC) activity. ODC the key regulatory enzyme of the polyamine pathway, is a potential substrate for protein kinase C (PKC). Therefore, we examined developmental changes in PKC activity and its relationship to ODC activity. Male rats were lactationally exposed to 0.2% Pb-acetate from birth to weaning. PKC and ODC activity were measured on postnatal days (PND) 3, 5, 10, 20 and 30. We found that the basal patterns of ODC and PKC activities resembled each other in both the neocortex and cerebellum and Pb-exposure attenuated both enzymes in a similar manner. To determine whether any link existed between these enzymes, ODC and PKC activities were induced to increase using nerve growth factor (NGF) in the presence and/or absence of ODC (difluoromethylornithine, DFMO) and PKC (staurosporine) inhibitors, in control and Pb-exposed Pheochromocytoma (PC-12) cells. Staurosporine decreased both ODC activity and PKC activity, while DFMO had no effect on PKC activity. These data suggest that ODC may be regulated by PKC and that Pb-induced developmental alterations in ODC activity may be secondary to changes in the integrity of PKC.

Animals↗

PubMed2002

Melatonin production in infants.

This study investigated the relationships of the excretion of the melatonin metabolite, 6-sulfatoxymelatonin, to prenatal, natal, and postnatal variables and its possible relation to psychomotor development. nocturnal urinary excretion of 6-sulfatoxymelatonin was studied over a 13-hour period in 355 term infants at 8 weeks of age (n = 320) and 16 weeks of age (n = 96). data on a variety of perinatal factors including pregnancy course, delivery, early postnatal course, birth weight, medical problems, growth (length, weight, and head circumference), and psychomotor development were collected at 1, 3, 6, 9, 12, and 18 months. the relationship between nocturnal 6-sulfatoxymelatonin excretion at 8 and 16 weeks of age and these factors was investigated and analyzed. 6-sulfatoxymelatonin levels at 16 weeks of age were significantly lower in infants with abnormal vs normal development at 3 months of age (7.27 + 1.44 vs 7.97 + 1.06, p = 0.05) as well as at 6 months of age (7.15 + 1.29 vs 7.95 + 1.10, p = 0.04). no other significant relation was evident among growth, perinatal complications, medical problems, and 6-sulfatoxymelatonin excretion at 8 weeks of age and at 16 weeks of age. low melatonin excretion in the first weeks of life correlates with delayed psychomotor achievements at 3 and 6 months of age. this association suggests a causal or predictive link between melatonin and neurodevelopment in infants.

Analysis of Variance↗

PubMed1998

Epilepsy in children with cerebral palsy.

Epilepsy occurs in 15-60% of children with cerebral palsy; however, its clinical course is not well defined. This retrospective study reviewed the prevalence, nature, and prognosis of epilepsy in cerebral palsy. Thirty-two of 85 children with cerebral palsy seen in the Neurodevelopmental Clinic in Tuen Mun Hospital between 1990 and 1995 had epilepsy. A control group of 59 epileptic children with normal neurodevelopment status was seen during the same period. Epilepsy most commonly affected patients with spastic tetraplegia and those with mental subnormality. When compared with controls, children with cerebral palsy had a higher incidence of epilepsy with onset within the first year of age (47% vs 10%), history of neonatal seizures (19% vs 3%), status epilepticus (16% vs 1.7%), polytherapy (25% vs 3%), and treatment with second-line antiepileptic drugs (31% vs 6.7%). They had a lower incidence of generalized seizures (28% vs 59%) and remaining seizure free (37% vs 90%). Factors associated with a seizure-free period of 1 year or more in epileptic children with cerebral palsy were normal intelligence, single seizure type, monotherapy, and spastic diplegia. Epilepsy was common in children with cerebral palsy. Further larger studies are required to delineate other prognostic factors.

Anticonvulsants↗

PubMed1998

The impact of prenatal drug exposure on the neonate.

Several social or recreational drugs singly or together have demonstrated effects on the fetus and neonate, with those effects extending into adulthood. The use of recreational drugs during pregnancy remains a major health problem, with adverse effects including higher rates of fetal distress and demise, lower Apgar scores, growth retardation, and adverse neurodevelopmental outcome. Ethanol has the most profound effects, with physical stigmata of the drug seen in one third of exposed infants. In children without the affected physical appearance, profound neurodevelopmental sequelae have been demonstrated. Other drugs, such as cocaine, heroin, amphetamines, and nicotine, have been associated with impaired fetal growth and acute withdrawal during the neonatal period. Subsequently, these infants and children have an increased risk for altered neurodevelopment and long-term health status. Long-term follow-up and assessment are essential. The risk of neonatal withdrawal or abstinence syndrome is greatest with narcotic drugs but has been found to occur in neonates following exposure to cocaine, nicotine, and amphetamines. Early treatment with tincture of opium, paregoric, or phenobarbital is crucial. Assessment of the overall health status of the infant should include growth parameters, signs and symptoms of infection (especially hepatitis, syphilis, and immunodeficiency viruses), and neurobehavioral function. Such assessments should not be limited to the newborn period, as neurodevelopmental sequelae may not be manifest until later in infancy and childhood. In addition, evaluation of the social milieu is warranted because of the increased risk for neglect and abuse of drug-exposed infants and children. Early intervention, maternal drug rehabilitation treatment, and parenting classes are frequently prescribed, but their efficacy is variable. Further investigations should study the potential benefits of these recommendations.

Developmental Disabilities↗

PubMedDate not supplied

Chlorpyrifos exposure of developing zebrafish: effects on survival and long-term effects on response latency and spatial discrimination.

Chlorpyrifos (CPF) is a widely used insecticide, which has been shown to interfere with neurobehavioral development. Rat models have been key in demonstrating that prenatal CPF exposure causes choice accuracy deficits and motor alterations, which persist into adulthood. Complementary nonmammalian models can be useful in determining the molecular mechanisms underlying the persisting behavioral effects of developmental CPF exposure. Zebrafish with their clear chorion and extensive developmental information base provide an excellent model for assessment of molecular processes of toxicant impacted neurodevelopment. To facilitate the use of the zebrafish model and to compare it to the more typical rodent models, the behavioral phenotype of CPF toxicity in zebrafish must be well characterized. Our laboratory has developed methods for assessing spatial discrimination learning in zebrafish, which can differentiate response latency from choice accuracy in a three chambered fish tank. Low and high doses of CPF (10 and 100 ng/ml on days 1-5 postfertilization) both had significant persisting effects on both spatial discrimination and response latency over 18 weeks of testing. The high, but not the low dose, significantly accelerated mortality rates of the fish during the study from 20-38 weeks of age. Developmental exposure to either 10 or 100 ng/ml of CPF caused significant spatial discrimination impairments in zebrafish when they were adults. The impairment caused by 10 ng/ml was seen during early but not later testing, while the impairment caused by 100 ng/ml became more pronounced with continued testing. The higher dose caused a more pervasive impairment. The 10 and 100 ng/ml doses had opposite effects on response latency. The low 10 ng/ml dose significantly slowed response latency, while the high 100 ng/ml dose significant increased response latency. Both of these effects diminished with continued testing. CPF exposure during early development caused clear behavioral impairments, which lasted throughout adulthood in zebrafish. The molecular mechanisms by which early developmental CPF exposure produces these behavioral impairments expressed in adulthood can now be studied in the zebrafish model.

Animals↗

PubMed1998

The transmembrane Semaphorin Sema I is required in Drosophila for embryonic motor and CNS axon guidance.

The semaphorins comprise a large family of conserved glycoproteins, several members of which have been shown to function in repulsive neuronal growth cone guidance. We show here that Drosophila Semaphorin I (Sema I), a transmembrane semaphorin expressed on embryonic motor and CNS axons, is required for correct guidance of motor axons and for the formation of CNS pathways. In mutant embryos lacking Sema I, motor axons stall and fail to defasciculate at specific choice points where normally they would project to their muscle targets. In addition, a specific CNS fascicle fails to form correctly in these embryos. Rescue and ectopic expression experiments show that Sema I is required in neurons to mediate axon guidance decisions. These studies further suggest that like secreted semaphorins, transmembrane semaphorins can function as repulsive guidance cues for specific axon guidance events during neurodevelopment.

Animals↗

PubMed1998

Feeding the disabled child.

Feeding difficulty and malnutrition are common in disabled children. Intake may be reduced because of anorexia, chewing and swallowing difficulties, or vomiting. Feeding is often time consuming, unpleasant, and may result in aspiration. Malnutrition may result in impaired growth and neurodevelopment, and impaired cardiorespiratory, gastrointestinal, and immune functions. Multidisciplinary assessment is recommended and should include a feeding history, oral-motor examination, and nutritional assessment. The energy requirements of most disabled children are less than those for a normal child of the same age but may be increased by spasticity, athetosis, convulsions, and recurrent infections. Micronutrient deficiencies may occur even in children receiving nutritionally complete feeds if the volume is reduced because of low energy requirements. Oral intake may be improved by a change of posture, special seating, feeding equipment, oral desensitization, mashing or pureeing of lumpy food, thickening of liquids, use of calorie supplements, and treatment of reflux/esophagitis. Non-oral feeding should be considered when oral feeding is unsafe, not enjoyable, inadequate, or very time consuming. Long-term support requires a gastrostomy. This is less obtrusive than a nasogastric tube, less likely to become displaced, less traumatic, and is associated with improved quality of life, but is also associated with significant morbidity. If there is symptomatic reflux a fundoplication may be required, but this is associated with significant mortality and substantial morbidity.

Child↗

PubMed2002

Characteristics of epilepsy in focal cortical dysplasia in infancy.

To describe the poorly known characteristics of epilepsy during infancy in focal cortical dysplasia (FCD), one of the most frequent cause of infantile epilepsy. All 28 patients with FCD referred to two specialized centres were retrospectively studied regarding seizure characteristics, psychomotor evaluation, and response to medical and surgical treatment. All patients presented with early partial seizures. Semiology, but not the age of onset, depended on the topography of the dysplasia, with abnormal eye movements in all cases of posterior FCD. Eleven patients also developed infantile spasms (IS), mainly asymmetrical. IS were easily controlled with Vigabatrin or ACTH, but no partial seizures could be medically controlled except in one patient. All patients except one had abnormal neuropsychological findings. Fifteen patients had surgery, eight became seizure free, and seven were significantly improved regarding psychomotor development. Very early and refractory partial seizures, but easily controlled IS are the main characteristics of FCD in infancy. Only the focal ictal semiology may help differentiate the localization of FCD. Its intrinsic epileptogenicity could sustain this clinical pattern. Since the chances for medical control and normal neurodevelopment are poor, surgical treatment should be considered early in infants with FCD.

Age Factors↗

PubMed2001

Low GSK-3 activity in frontal cortex of schizophrenic patients.

Glycogen synthase kinase-3 (GSK-3) (EC 2.7.1.37) is a protein kinase highly abundant in brain and involved in signal transduction cascades of multiple cellular processes, particularly neurodevelopment. Two forms of the enzyme, GSK-3alpha and -3beta have been previously identified. We have previously reported reduced GSK-3beta protein levels in postmortem frontal cortex of schizophrenic patients. In an attempt to explore whether reduction of GSK-3beta levels is brain region specific we examined it in occipital cortex. In order to find out if the reduction in frontal cortex is reflected in altered activity we measured GSK-3 enzymatic activity in this brain region. Western-blot analysis of GSK-3beta was carried out in postmortem occipital cortex of 15 schizophrenic, 15 bipolar, and 15 unipolar patients, and 15 normal controls. GSK-3 activity was measured by quantitating the phosphorylation of the specific substrate phospho-CREB in the frontal cortex specimens. GSK-3beta levels in occipital cortex did not differ between the four diagnostic groups. GSK-3 activity in the frontal cortex of schizophrenic patients was 45% lower than that of normal controls (0.196+/-0.082 and 0.357+/-0.084 pmol/mg proteinxmin, respectively; Kruskal-Wallis analysis: chi-square=8.27, df=3, p=0.04). The other two diagnostic groups showed no difference from the control group. Our results are consistent with the notion that schizophrenia involves neurodevelopmental pathology.

Bipolar Disorder↗

PubMed2002

Season of birth in Japanese patients with schizophrenia.

A number of North American and European studies have observed a higher proportion of winter births in schizophrenia patients. Fewer studies have investigated this issue in Asian populations, and the findings are not as consistent as in the studies of Western populations. A statistically significant excess of winter births has not been observed in Japanese or Korean studies, while some of the studies found a decreased number of summer births among their patients. We further investigated the issue in Japanese patients with schizophrenia (n=2985). No significant excess of winter births was observed. Spearman correlation between schizophrenia births and ambient temperature was not significant. However, a decrease in the summer births was found, consistent with most of the previous Japanese studies. When analyzed by gender, a decrease in summer births was found in males, but not in females. In addition, a trend towards an increase in winter births was observed and Spearman correlation between low ambient temperature and schizophrenia births was significant in male subjects. More significant seasonality of birth in male patients than in female patients might be related to more susceptibility to pre- or perinatal disturbances in neurodevelopment in males than in females.

Age of Onset↗

PubMed2002

Schizophrenia and schizotypal personality: a tribute to Peter H. Venables.

Peter Venables made multiple contributions to the field of schizophrenia and schizotypy, most notably in the areas of psychophysiology, neurocognition, and assessment. On the 50th anniversary of the start of his research career in 1951, a conference on schizophrenia and schizotypy was held in his honor in Tuscany, Italy. This special edition encapsulates many of the presentations given at that meeting, covering the areas of neurodevelopment, assessment, genetics, psychophysiology, neurocognition, brain imaging, psychopharmacology, intervention, and prevention. A key theme of this special edition concerns the integration of schizophrenia and schizotypy research in a manner that will allow for a more comprehensive understanding of both of these disorders.

History, 20th Century↗

PubMed2003

Increased developmental deviance and premorbid dysfunction in early onset schizophrenia.

Abnormal neurodevelopment and poor premorbid function have been described in schizophrenia. It is unclear whether abnormalities in these domains are increased in patients with early onset schizophrenia (EOS; onset before the 18th birthday) and whether they act to precipitate the earlier onset of the disorder. To address these questions, we collected information based on maternal interviews about the premorbid function of 40 adolescents with recent onset schizophrenia and an equal number of healthy controls using the Developmental Scale Score, the Premorbid Schizoid and Schizotypal Trait Scale (PSST) and Premorbid Adjustment Scale (PAS). Data on the PSST and PAS were also available in 54 patients with adult onset schizophrenia (AOS; onset after the 20th birthday). Compared to healthy controls, EOS patients had (a). delayed speech milestones, difficulties in reading and spelling and greater overall developmental deviance; (b). poor premorbid adjustment in childhood, which became even more deviant in adolescence particularly in boys and (c). more schizophrenia spectrum traits. Both premorbid adjustment and personality traits were more abnormal in patients with increased developmental deviance suggesting the possibility that they represent different manifestations of ongoing abnormalities in developmental processes. EOS patients had more impaired premorbid adjustment in adolescence and schizophrenia spectrum traits compared to AOS cases. Age of onset was related to developmental deviance, premorbid schizophrenia spectrum traits and childhood adjustment in EOS patients only.

Adolescent↗

PubMed1997

Glutamate in schizophrenia: clinical and research implications.

The excitatory amino acids, glutamate and aspartate, are of interest to schizophrenia research because of their roles in neurodevelopment, neurotoxicity and neurotransmission. Recent evidence suggests that densities of glutamatergic receptors and the ratios of subunits composing these receptors may be altered in schizophrenia, although it is unclear whether these changes are primary or compensatory. Agents acting at the phencyclidine binding site of the NMDA receptor produce symptoms of schizophrenia in normal subjects, and precipitate relapse in patients with schizophrenia. The improvement of negative symptoms with agents acting at the glycine modulatory site of the NMDA receptor, as well as preliminary evidence that clozapine may differ from conventional neuroleptic agents in its effects on glutamatergic systems, suggest that clinical implications may follow from this model. While geriatric patients may be at increased risk for glutamate-mediated neurotoxicity, very little is known about the specific relevance of this model to geriatric patients with schizophrenia.

Aging↗

PubMed1999

A hyperglycinergic rat model for the pathogenesis of schizophrenia: preliminary findings.

There is evidence of high glycine concentrations in the brains and periphery of schizophrenics. In the forebrain, glycine plays a major role as a co-agonist with glutamate at the excitatory N-methyl-D-aspartate (NMDA) receptors. This activity of glycine is involved in the normal functioning of the brain in adulthood and during neurodevelopment, and it may also cause neurotoxicity and brain abnormalities when its concentrations are high. To test the hypothesis that the high glycine concentrations observed in schizophrenics play an etiologic role in schizophrenia, an animal model was tested where rats were made hyperglycinic from life in utero to adulthood. The hyperglycinic rats showed abnormalities in sensory gating mechanisms, enlarged cerebral ventricles and diminished hippocampal dimensions. All of these abnormalities closely parallel observations reported in patients with schizophrenic psychoses. These results from a rat model suggest an etiologic role for high glycine concentration in the behavior and brain abnormalities of schizophrenic patients.

Animals↗

PubMed2000

Type of feeding during infancy and later development of schizophrenia.

Nutrition may be critical for neurodevelopment and can affect the later development of schizophrenia. Recently, a marked reduction in breast-feeding was reported in infants that developed schizophrenia in later life (McCreadie, R.G., 1997. The Nithsdale Schizophrenia Surveys. 16. Breast-feeding and schizophrenia: preliminary results and hypothesis. Br. J. Psychiatr. 170, 334-337). In the present study, we investigated feeding patterns during the infancy of 100 schizophrenia patients, 37 of their siblings and 200 age-matched healthy controls using a structured written questionnaire. Having been breast-fed was not negatively associated with schizophrenia.

Adult↗

PubMed1999

Computed tomography study of pineal calcification in schizophrenia.

Computed tomography studies concerning pineal calcification (PC) in schizophrenia have been conducted mainly by one author who correlated this calcification with several aspects of the illness. On the basis of these findings the aim of the present study was to analyze size and incidence of pineal gland calcification by CT in schizophrenics and healthy controls, and to verify the relationship between pineal calcification and age, and the possible correlation with psychopathologic variables. Pineal calcification was measured on CT scans of 87 schizophrenics and 46 controls divided into seven age subgroups of five years each. No significant differences in PC incidence and mean size between patients and controls were observed as far as the entire group was considered. PC size correlated with age both in schizophrenics and controls. We found a higher incidence of PC in schizophrenics in the age subgroup of 21-25 years, and a negative correlation with positive symptoms of schizophrenia in the overall group. These findings could suggest a premature calcific process in schizophrenics and a probable association with 'non-paranoid' aspects of the illness. Nevertheless the potential role of this process possibly related to some aspects of the altered neurodevelopment in schizophrenia is still unclear.

Adult↗

PubMed2002

GSK-3 and the neurodevelopmental hypothesis of schizophrenia.

The Neurodevelopmental Hypothesis of schizophrenia suggests that interaction between genetic and environmental events occurring during critical early periods in neuronal growth may negatively influence the way by which nerve cells are laid down, differentiated and selectively culled by apoptosis. Recent advances offer insights into the regulation of brain development. The Wnt family of genes plays a central role in normal brain development. Activation of the Wnt cascade leads to inactivation of glycogen synthase kinase-3beta (GSK-3beta), accumulation and activation of beta-catenin and expression of genes involved in neuronal development. Alteration in the Wnt transduction cascade, which may represent an aberrant neurodevelopment in schizophrenia, is discussed. Programmed cell death is also an essential component of normal brain development. Abnormal neuronal distribution found in schizophrenic patients' brains may imply aberrant programmed cell death. GSK-3 participates in the signal transduction cascade of apoptosis. The possible role of aberrant GSK-3 in the etiology of schizophrenia is discussed.

Animals↗

PubMed2002

Amygdala-hippocampal shape differences in schizophrenia: the application of 3D shape models to volumetric MR data.

Evidence suggests that some structural brain abnormalities in schizophrenia are neurodevelopmental in origin. There is also growing evidence to suggest that shape deformations in brain structure may reflect abnormalities in neurodevelopment. While many magnetic resonance (MR) imaging studies have investigated brain area and volume measures in schizophrenia, fewer have focused on shape deformations. In this MR study we used a 3D shape representation technique, based on spherical harmonic functions, to analyze left and right amygdala-hippocampus shapes in each of 15 patients with schizophrenia and 15 healthy controls matched for age, gender, handedness and parental socioeconomic status. Left/right asymmetry was also measured for both shape and volume differences. Additionally, shape and volume measurements were combined in a composite analysis. There were no differences between groups in overall volume or shape. Left/right amygdala-hippocampal asymmetry, however, was significantly larger in patients than controls for both relative volume and shape. The local brain regions responsible for the left/right asymmetry differences in patients with schizophrenia were in the tail of the hippocampus (including both the inferior aspect adjacent to parahippocampal gyrus and the superior aspect adjacent to the lateral geniculate nucleus and more anteriorly to the cerebral peduncles) and in portions of the amygdala body (including the anterior-superior aspect adjacent to the basal nucleus). Also, in patients, increased volumetric asymmetry tended to be correlated with increased left/right shape asymmetry. Furthermore, a combined analysis of volume and shape asymmetry resulted in improved differentiation between groups. Classification function analyses correctly classified 70% of cases using volume, 73.3% using shape, and 87% using combined volume and shape measures. These findings suggest that shape provides important new information toward characterizing the pathophysiology of schizophrenia, and that combining volume and shape measures provides improved group discrimination in studies investigating brain abnormalities in schizophrenia. An evaluation of shape deformations also suggests local abnormalities in the amygdala-hippocampal complex in schizophrenia.

Adult↗