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Results for “Neurodevelopmental Disorders”

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PubMed1986

Pediatric management of nonpervasively "hyperactive" children.

Sixty-five children viewed by their teachers as hyperactive were evaluated as to whether they would benefit from stimulant medication. All underwent extensive neurodevelopmental and educational testing. Additional information was obtained from school and parent questionnaires and interviews. Children were not placed on medication unless they demonstrated characteristic impulsive, inattentive, and/or overactive behavior in two of three environments (home, school, clinic). Fifty-two children (80%) were not placed on medication. Follow-up was completed in 80 percent, and 93 percent of these children were doing well with nonpharmacologic interventions. Initial comparison of children not placed and placed on medication revealed that age, race, SES, amount of resource help and retention could not distinguish groups. Children placed on medication had difficulties earlier in school (chi 2 = 4.88, p less than 0.05), weren't as delayed academically (chi 2 = 6.30, p less than 0.05) and had less neurodevelopmental disorders (chi 2 = 9.01, p less than 0.01). If a careful psychosocial history does not reveal impulsive, inattentive, and/or hyperactive behavior outside of school, a child should be evaluated to rule out neurodevelopmental and educational problems.

Attention↗

PubMed2005

Historical neurotoxins: what we have learned from toxins of the past about diseases of the present.

Throughout history, humans have fallen victim to a variety of neurotoxins, with exposures coming in the form of tainted products, industrial pollution, drugs of abuse, and even the bread and water that sustain them. Despite this long and tumultuous history, neurotoxic outbreaks still occur with regular frequency. Although many difficulties currently exist in linking many of today's unexplained neurologic disorders to toxins, the past suggests a prominent role for neurotoxins in diseases (such as amyotrophic lateral sclerosis and PD), unexplained peripheral neuropathies, neurodevelopmental disorders, and many psychiatric disturbances.

Animals↗

PubMed2002

MMR vaccination and autism: is there a link?

In 1998, a report was published describing 12 patients with inflammatory bowel conditions and regressive developmental disorders consisting primarily of autism. The authors hypothesised that MMR vaccine may have been responsible for the bowel dysfunction which subsequently resulted in the neurodevelopmental disorders. The suggestion that measles vaccine may cause autism through a persistent bowel infection generated much interest since it provided a possible biological mechanism for a causal association. Epidemiological studies, however, have not found an association between MMR vaccination and autism. Autism has a strong genetic component and its associated neurological defects probably occur during embryonic development. It seems unlikely that a vaccination that is given after birth could cause autism. In a minority of cases, autism may have onset after 1 year of age (regressive autism) but the one epidemiological study that included such cases did not find an association with MMR vaccination. Currently, the weight of the available epidemiological and related evidence does not support a causal link between MMR vaccine and autism.

Autistic Disorder↗

PubMed2005

Disruption of the paternal necdin gene diminishes TrkA signaling for sensory neuron survival.

Necdin is a multifunctional signaling protein that stabilizes terminal differentiation of postmitotic neurons. The human necdin gene in chromosome 15q11-q12 is maternally imprinted, paternally transcribed, and not expressed in Prader-Willi syndrome, a human genomic imprinting-associated neurodevelopmental disorder. Although necdin-deficient mice display several abnormal phenotypes reminiscent of this syndrome, little is known about molecular mechanisms that lead to the neurodevelopmental defects. Here, we demonstrate that paternally expressed necdin is required for physiological development of nerve growth factor (NGF)-dependent sensory neurons. Mouse embryos defective in the paternal necdin allele displayed absent necdin expression in the dorsal root ganglia, in which the tropomyosin-related kinase A (TrkA) receptor tyrosine kinase and the p75 neurotrophin receptor were expressed in a normal manner. Necdin interacted with both TrkA and p75 to facilitate the association between these receptors. NGF-induced phosphorylation of TrkA and mitogen-activated protein kinase was significantly diminished in the necdin-null sensory ganglia. Furthermore, the mice lacking the paternal necdin allele displayed augmented apoptosis in the sensory ganglia in vivo and had a reduced population of substance P-containing neurons. These mutant mice showed significantly high tolerance to thermal pain, which is often seen in individuals with Prader-Willi syndrome. These results suggest that paternally expressed necdin facilitates TrkA signaling to promote the survival of NGF-dependent nociceptive neurons.

Animals↗

PubMed2005

Developmental neurobiology and clinical disorders: lost in translation?

Advances in defining mechanisms of cortical development have been paralleled in recent years by an intense interest in translating these findings into greater insight of both childhood- and adult-onset cognitive and mental health disorders of developmental etiology. Successful integration of basic and clinical findings have been applied to monogenic disorders. The greater challenge lies in studying cortical development in the context of gene x environment interactions, which underlie the pathogenesis of the most common neurodevelopmental disorders. This can occur through an improved delineation of pathophysiological characteristics unique to specific complex disorders and the application of this information to the refinement of the most relevant model systems.

Animals↗

PubMed2000

Regulation of sensorimotor gating of the startle reflex by serotonin 2A receptors. Ontogeny and strain differences.

Sensorimotor gating of the startle reflex can be assessed via measures of prepulse inhibition (PPI), which is the reduction in startle magnitude when the startling stimulus is preceded immediately by a weak prepulse. PPI is reduced in humans with specific neuropsychiatric disorders and in rats after treatment with certain classes of drugs, including serotonin (5-HT) agonists. Because of the relative loss of PPI in inherited, neurodevelopmental disorders such as schizophrenia, there is great interest in understanding the inherited and developmental features of the neurochemical regulation of PPI in animals. In the present study, PPI was disrupted significantly by the 5-HT2A agonist 2, 5-dimethoxy-4 iodopheny-lisopropylamine (DOI) in Sprague Dawley (SDH) and Wistar rat strains (WH). While it was demonstrated that the DOI effects in SDH rats reflected an unequivocal disruption of sensorimotor gating, in WH rats, reduced PPI was observed in the context of a trend for a DOI-induced reduction in startle magnitude. This effect of DOI in SDH rats was evident at the earliest date tested (17 days of age) in male pups, but was not statistically significant in female pups. Thus, the regulation of sensorimotor gating by 5-HT2A receptor stimulation in rats may exhibit subtle differences across strains, and within SDH rats, between sexes. Most importantly, the 5-HT2A regulation of sensorimotor gating in male SDH rats is a "phenotype" that is expressed very early in life, and is sustained through adulthood.

Age Factors↗

PubMed1997

Developmental trajectory and disease progression in schizophrenia: the conundrum, and insights from a 12-year prospective study in the Monaghan 101.

Though conceptualised originally as a deteriorating disorder, some contemporary studies have been interpreted as challenging these foundations; more radically, it has been proposed that schizophrenia may be a 'static encephalopathy' of neurodevelopmental origin. The argument offered here is that schizophrenia is indeed a neurodevelopmental disorder, but that this is not in itself antithetical to later disease progression. Rather, the onset of psychosis may reflect the maturationally-mediated triggering of an active disease process that is associated with progressive deterioration unless attenuated by antipsychotic drugs. A developmental trajectory is proposed to link first or early second trimester dysplasia to the chronic course of the illness; from this, it is argued that schizophrenia is inherently a progressive disorder but that antipsychotic drugs may act to ameliorate this progressive component and thus confer on the disease course some of the characteristics of a 'static encephalopathy'. The 'true' natural history of an illness cannot be determined from studies in treated populations.

Antipsychotic Agents↗

PubMed2005

Prevention of schizophrenia: can it be achieved?

Schizophrenia is a serious mental disorder with a profound impact on patients, their caregivers and society. It is also an expensive disorder to treat, despite being relatively rare. In this paper, prevention of schizophrenia is described in terms of primary, secondary and tertiary prevention. Schizophrenia is regarded as a neurodevelopmental disorder with different phases. Primary prevention essentially involves education programmes about the association of obstetric complications and the increased risk of schizophrenia. Secondary prevention involves intervention at the prodromal phase. We review the literature and discuss the evidence relating to intervention in this phase of the illness. Early intervention could result in reduction in morbidity and better quality of life for the patients and their families. The prodromal phase can now be identified, based on current symptoms, with reliability and predictive validity for the risk of development of schizophrenia in the following year. We also discuss possible risks faced by prodromal patients, such as unnecessary stigmatisation, and the role of drug treatment during intervention at this stage. Any recommendation that anti-psychotic medications be routinely prescribed in this phase should be supported by more research work. Drug and psychosocial intervention is indicated as part of tertiary prevention to prevent further disability in the illness.

Disease Progression↗

PubMed2003

Neuropathology of schizophrenia--a review.

Despite clinical evidence of brain dysfunction in schizophrenia, little progress was made for most of the last century in determining its organic parameters. Neuropathology, over the past few decades, has made a substantial contribution to the understanding of cellular and molecular mechanisms of schizophrenia. During the last 10-15 years the concept of schizophrenia as a 'functional' psychosis has changed to the current paradigm of schizophrenia as a neurodevelopmental disorder. Much still has to be unravelled and learnt. This review gives a brief account of the relevant neuroanatomy, viral hypotheses of schizophrenia etiology, pathologic findings reported, concept of neurodevelopmental model and avenues for the future.

Animals↗

PubMed2003

Antibodies to neuronal targets in neurological and psychiatric diseases.

The role of antibodies to specific neuronal and muscle ion channels in the etiology of neuromuscular transmission disorders is now well accepted. In addition, maternal antibodies can cross the placenta and cause neonatal disease or even alter the development of the infant, raising the possibility that some neurodevelopmental conditions could be caused by maternal antibodies. Voltage-gated ion channels are expressed in the brain as well as at the neuromuscular junction, and in recent years it has become clear that antibodies to some central nervous system (CNS) channels can be associated with CNS disease. This review highlights features of these conditions, preliminary investigations into neurodevelopmental disorders, and areas for further study.

Antibodies↗

PubMed1987

CSF monoamines in autistic syndromes and other pervasive developmental disorders of early childhood.

Spinal fluid concentrations of the three major monoamine metabolites were examined in 25 infantile autistic children and 12 children with other childhood psychoses, and were contrasted with results obtained in normal children and in groups of children with neurological and neurodevelopmental disorders. Autistic children showed absolute and relative increases of the dopamine metabolite homovanillic acid. The group with other childhood psychoses also showed an increase in HVA level; in this group there were also indications of high levels of serotonin and norepinephrine metabolites. The results are discussed in the context of a pathogenetic model for autism involving hyperfunction of dopaminergic nerve fibres in the brain stem-mesolimbic system.

Adolescent↗

PubMed2005

Ataxia, autism, and the cerebellum: a clinical study of 32 individuals with congenital ataxia.

The suggested link between autism and cerebellar dysfunction formed the background for a Swedish clinical study in 2001. Thirty-two children (17 females, 15 males; mean age 12y, SD 3y 10mo; range 6 to 21y) with a clinical suspicion of non-progressive congenital ataxia were examined, and parents were interviewed about the presence of neuropsychiatric problems in the child. Twelve children had simple ataxia, eight had ataxic diplegia, and 12 had 'borderline' ataxia. All but one of the 32 children had a mild to moderate gross motor disability according to Gross Motor Function Classification System (15 were categorized as level I, 16 as level II, and one child as level IV). Neuroimaging and neuropsychological testing were achieved in most cases. There was a strong association between learning disability* and autism spectrum disorder (often combined with hyperactivity disorder) on the one hand, and both simple and borderline 'ataxia' on the other, but a weaker link between ataxic diplegia and neuropsychiatric disorders. A correlation between cerebellar macropathology on neuroimaging and neuropsychiatric disorders was not supported. Congenital ataxia might not be a clear-cut syndrome of cerebellar disease, but one of many signs of prenatal events or syndromes, leading to a complex neurodevelopmental disorder including autism and learning disability.

Adolescent↗

PubMed2000

Neuroimaging in child and adolescent psychiatric disorders.

Neuroimaging in child psychiatry is a rapidly developing field and the number of different techniques being used is increasing rapidly. This review describes the current status of neuroimaging in childhood psychopathology and discusses limitations of the various studies. As yet, no specific and consistent abnormality has been detected in childhood psychiatric disorders. Obsessive compulsive disorder has shown the most consistent findings so far, with orbitofrontal cortex and the caudate nucleus being implicated. Better understanding of the corticostriatal neural networks will shed more light on the neurodevelopmental disorders of childhood.

Adolescent↗

PubMedDate not supplied

[Management of children with autism spectrum disorders].

INTRODUCTION: Autistic spectrum disorders (ASD) are characterized by qualitative deficits in communication, social skills and a restrictive repertoire of interests and behaviors. Recent studies suggest that they may represent one of the most prevalent neurodevelopmental disorders. METHOD: Treatment of core deficits of ASD are primarily speech and language, behavioral and educational interventions. Clinical management of ASD requires a multidisciplinary approach to identify behaviors that could interfere with the individual s ability to benefit from those interventions. Medications, such as neuroleptics, antiepileptic drugs, SSRI s, neurostimulants and others have been used to target specific behaviors. CONCLUSIONS: Further research is much needed if medications are eventually to have a greater role in the treatment of core ASD symptoms. Recent attempts at neurosurgical interventions cannot be justified by our present level of knowledge

Anticonvulsants↗

PubMed2006

[Attention deficit hyperactivity disorder and mental retardation].

INTRODUCTION: Attention deficit hyperactivity disorder (ADHD) is a common condition in children with mental retardation (MR), with a prevalence rate of between 4 and 15%. It is therefore necessary to examine the epidemiological characteristics of neurodevelopmental disorders in patients with MR, evaluate diagnostic protocols and especially update the pharmacological treatment of ADHD in children with MR. DEVELOPMENT: The study of ADHD in patients with mild mental retardation is no different to that carried out in children without MR. No neuropsychological instruments are available to measure the executive functions properly in patients with severe mental retardation. Neuroleptic and psychostimulant agents are the two groups of drugs that are most commonly used to treat behavioural problems in children with MR. Methylphenidate is effective in three quarters of the children with MR at preschool ages. It has proved to be effective in the clinical profiles and in psychometric studies. Other forms of treatment, such as clonidine or fenfluramine, have also proved to be effective to a certain extent in patients with MR, especially in the clinical setting. CONCLUSIONS: ADHD is more frequent in patients with MR than in the general population. The diagnostic methodology is usually the same as that used in patients without MR. Stimulation treatment is the most specifically indicated for the treatment of attentional and behavioural problems in these children.

Attention Deficit Disorder with Hyperactivity↗

PubMed1999

Brain maturational processes and delayed onset in schizophrenia.

The central feature of schizophrenia is its onset in adolescence. Although this clinical observation is consistent with the view that schizophrenia may be a neurodevelopmental disorder, debate has focused on when the proposed brain maturational deviations may begin and what might be the nature of such defective development. Conflicting models of this illness (e.g., the early and late neurodevelopmental models) have been proposed. In this paper, we will first review concepts from basic developmental neurobiology pertinent to these issues; we then summarize aspects of the neurobiology of schizophrenia that have a particular bearing on the adolescent onset of this illness. We propose that the schizophrenic syndrome may result from early brain adversity and late maturational processes of brain development interacting with adverse humoral, biochemical, and psychosocial factors during adolescence and early adulthood. The onset of schizophrenia in adolescence may be related to the "plasticity switch" secondary to the peripubertal brain maturational changes, perhaps involving an alteration in glutamate receptor function. This loss of plasticity could result in social and nonsocial cognitive deficits that are central to the pathophysiology of schizophrenia; the vulnerable person may therefore utilize prepubertal processing styles that are insufficient to the adaptive and "gistful" abstraction requirements of adult cognition. Schizophrenia onset might occur in the context of psychosocial developmental challenges to a delayed social cognitive capacity among neurodevelopmentally compromised individuals. We review therapeutic implications as well as testable predictions generated by this model, and discuss research strategies that might further our understanding of the brain maturational abnormalities in schizophrenia.

Adolescent↗

PubMed2005

Developmental coordination disorder (dyspraxia): an overview of the state of the art.

A large number of school-aged children present with motor-based performance problems that have significant negative effects on their ability to participate fully in the daily activities of home, school, and play. These children have a neurodevelopmental disorder most commonly known as developmental coordination disorder (DCD). These children are frequently brought to the attention of the family doctor and referred to health care professionals in search of answers and services. Therapists treating these children have a large number of intervention approaches at their disposal. This paper presents an overview of these approaches and a review of the available evidence. The evidence for the older, deficit-oriented approaches remains inconclusive, at best; whereas the task-oriented approaches, seem to be better supported. While more work is needed to validate the use of the task-oriented approaches, the results suggest that a shift in perspective from a deficit-oriented to a task-oriented perspective would be appropriate.

Apraxias↗

PubMed2001

Sculpting the developing brain.

The developing brain experiences major construction during fetal life and for at least the first decade of childhood. Many more neurons and synoptic connections are produced than are needed for later function, and the mature brain is what remains after these excess building materials are "sculpted" away. This process is thought to be the basis for the developing brain's plasticity, or the capacity to adapt its behavior and circuitry to stimulation from the external environment. Plastic reorganization of the brain is now being studied in children and adults with new noninvasive tools such as functional brain magnetic resonance imaging. This exploratory tool and other new clinical methods demonstrate how the brain's functional "maps" undergo major reorganization in response to early environmental changes. The neurobiology of brain reorganization during development is also being studied with use of new insights into the molecular mechanisms for activity-dependent neuronal plasticity. Clinical disorders such as lead poisoning, metabolic and epileptic encephalopathies, and psychosocial deprivation may arise from disrupted brain plasticity. Several mental retardation syndromes and cognitive disorders recently recognized as being secondary to genetic disruption of intracellular signaling cascades may also disrupt this process. Understanding how the brain's circuitry is sculpted during development provides an important perspective for thinking about neurodevelopmental disorders.

Brain↗