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PubMed2001

Why and how to assess the aetiological diagnosis of children with intellectual disability/mental retardation and other neurodevelopmental disorders: description of the Finnish approach.

One of the most important tasks of a physician who has patients with delayed development is to assess the cause of the problem. To help with this work, an aetiological classification based on timing and type of the injury to the central nervous system (CNS), has been created. The main divisions are: genetic causes; CNS malformations and multiple malformation syndromes of unknown origin; external prenatal factors; paranatally acquired disorders (-1 to +4 weeks from delivery); postnatally acquired disorders; and untraceable or unclassified causes. In the classification, the earliest factor injuring the CNS is the primary diagnosis. The first stage, which consists of a quite simple workup, reveals the timing of the injury and allows the possibility for family counselling. The overview of the second stage assessment is also given. The 'aetiological tree' illustrates the classification method and serves as a reference and teaching aid. It can also be used for genetic counselling to demonstrate the situation. This method has been used for almost 20 years and has been proven to enhance diagnostic activity and family counselling.

Brain Damage, Chronic↗
PubMedDate not supplied

Autism as a neurodevelopmental disorder affecting communication and learning in early childhood: prenatal origins, post-natal course and effective educational support.

Colwyn Trevarthen, working on autism, discussed the importance of time, rhythm and temporal processing in brain function. The brains of new born infants show highly coherent and coordinated patterns of activity over time, and their rhythms are remarkably similar to those of adults. Since the cortex has not yet developed, this coordination must be subcortical in origin. The likely source is the emotional motor system. He noted that the cerebellum might regulate the intricate timing of the development and expression of emotional communication. He also pointed out that emotional and motivational factors have often been seriously neglected in psychology (largely owing to a misplaced focus on 'cognition' as some isolated entity) and emphasized the potential importance of empathetic support and music therapy in helping autistic children.

Adult↗
PubMed1993

Season of birth and neurodevelopmental disorders: summer birth is associated with dyslexia.

OBJECTIVE: Increased risk for certain psychiatric disorders has been associated with season of birth. This study was undertaken to look for hypothesized season-of-birth effects for dyslexia, schizophrenia spectrum disorders, and neurological soft signs in children and adolescents. METHOD: Month of birth and the diagnostic findings in question were examined based on charts from a clinic population of 585 boys. Odds ratios and etiological fractions were calculated. RESULTS: Neurological soft signs showed a sporadic peak for June births and schizophrenia spectrum showed a peak for August and November. A smooth curve suggesting true seasonality was evident in dyslexia for births in May, June, and July. For different 5-year birth cohorts, early summer birth accounts for 24 to 71% of cases of dyslexia. CONCLUSIONS: The authors suggest that viral infection, especially influenza, during the second trimester of pregnancy is the most attractive hypothesis to explain these findings. If this hypothesis is supported, immunization in women of child-bearing age could reduce the incidence of dyslexia. Secondary prevention could also be enhanced by early identification and treatment of children who were exposed in utero.

Adolescent↗
PubMed1982

Minor neurodevelopmental disorders in children born to older mothers.

In order to test the hypothesis that rates of motor and perceptual deficits in children tend to increase with maternal age, 65 children aged five and six years born to mothers with a mean age of 39.4 years were compared with 55 age-matched children born to mothers with a mean age of 27.9 years. The hypothesis was supported in that fine-motor problems were five times more common among the children born to older mothers than among those born to younger mothers. Visuo-perceptual dysfunction and attentional deficit signs also were much more common among the children of older mothers. The contribution of various associated factors to these results is discussed.

Adult↗
PubMed1983

Three-year follow-up at age 10 of children with minor neurodevelopmental disorders. II: School achievement problems.

Part I of this paper considered the behavioural problems at age 10 of groups of children from a total population study of six-year-old children in Gothenburg and diagnosed according to strict criteria as suffering from minimal brain dysfunction (MBD), motor perception dysfunction (MPD) or attention deficit disorder (ADD), and a comparison group of normal children. Part II considers school achievement problems at age 10 among the same groups of children. 80 per cent of MBD children had obvious problems in school achievement, compared with 16 per cent in the comparison group. The MPD and ADD groups did not differ significantly from the comparison group in this respect. There was a considerable overlap between behaviour problems and school achievement problems, and the results indicate a gloomy prognosis for both types of problem among children with MBD.

Achievement↗
PubMed2002

Neurodevelopmental disorders as a cause of seizures: neuropathologic, genetic, and mechanistic considerations.

This review will consider patterns of developmental neuropathologic abnormalities-malformations of cortical development (MCD)--encountered in infants (often with infantile spasms), children, and adults with intractable epilepsy. Treatment of epilepsy associated with some MCD, such as focal cortical dysplasia and tubers of tuberous sclerosis, may include cortical resection performed to remove the "dysplastic" region of cortex. In extreme situations (eg, hemimegalencephaly), hemispherectomy may be carried out on selected patients. Neuropathologic (including immunohistochemical) findings within these lesions will be considered. Other conditions that cause intractable epilepsy and often mental retardation, yet are not necessarily amenable to surgical treatment (eg, lissencephaly, periventricular nodular heterotopia, double cortex syndrome) will be discussed. Over the past 10 years there has been an explosion of information on the genetics of MCD. The genes responsible for many MCD (eg, TSC1, TSC2, LIS-1, DCX, FLN1) have been cloned and permit important mechanistic studies to be carried out with the purpose of understanding how mutations within these genes result in abnormal cortical cytoarchitecture and anomalous neuroglial differentiation. Finally, novel techniques allowing for analysis of patterns of gene expression within single cells, including neurons, is likely to provide answers to the most vexing and important question about these lesions: Why are they epileptogenic?

Brain↗
PubMed1998

Is schizophrenia a progressive neurodevelopmental disorder? Toward a unitary pathogenetic mechanism.

OBJECTIVE: The author 1) reassesses the case against a neuronal degeneration hypothesis for schizophrenia; 2) demonstrates that the hypothesis that schizophrenia is a disorder caused by early (i.e., pre- or perinatal) and static (i.e., fixed, nonprogressive) damage to the brain is unsatisfactory because it cannot readily account for brain imaging results from schizophrenic patients and lacks both satisfactory clinical examples and experimental models of early, static developmental disorders resulting in the late spontaneous functional deterioration that characterizes schizophrenia; and 3) offers an alternative pathogenetic hypothesis for schizophrenia that is consistent with the available imaging and neuropathological data. METHOD: Published data on schizophrenia and relevant clinical and experimental studies of neurodevelopment and its disorders are reviewed. RESULTS: The neuropathological studies provide strong evidence against a classic neurodegenerative pathogenesis of schizophrenia and moderate support for prenatal developmental abnormalities. The imaging data provide strong evidence that excessive brain volume loss occurs after maximum brain volume expansion and equivocal evidence that it continues after onset of overt illness. The available clinical and experimental models of late deterioration after static, early brain lesions are unconvincing. A progressive developmental mechanism can reconcile the neuropathological and imaging data, while being compatible with both early onset and late deterioration. CONCLUSIONS: It matters whether the pathogenetic agent in schizophrenia is static or progressive, since if it is the latter it is worthwhile to search not only for means of prevention but also for interventions that will arrest progression as early as possible.

Apoptosis↗