Serotonin in autism and pediatric epilepsies

Chugani, Diane C.

doi:10.1002/mrdd.20021

Cited by 83 publications

(51 citation statements)

References 72 publications

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“…The high incidence of hyperactivity in the autistic children of our study can be explained by, parents sought medical advice because of hyperactivity was a distressing problem in their families and causing scholastic inachievement.In the present study, the blood serotonin level was higher in autistic than control group, the plasma serotonin level was elevated in (31.8%) of autistic children, and this is in agreement of the previous studies of (Anderson G. et In the present study, the blood serotonin level was higher in the low functioning group (2.6±0.531) than high functioning group (2.5±0.8), and there might be a relation between high plasma serotonin levels and lower verbal ability scores (Chugani D., 2004). Form the previous result, there is a possibility of correlation between high plasma serotonin level and severity of the disorder.…”

Section: Discussionsupporting

confidence: 93%

Clinical Manifestations, Blood Serotonin Level, Electroencephalography and Brain Magnetic Resonance Imaging in Autistic Children

hadi¹

2017

IOSR JDMS

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Section: Discussionsupporting

confidence: 93%

Clinical Manifestations, Blood Serotonin Level, Electroencephalography and Brain Magnetic Resonance Imaging in Autistic Children

hadi¹

2017

IOSR JDMS

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“…Others have posited that the defect lies at the inhibitory synapse 31 ; this model could also account for the seizures that are observed in a subset of patients with ASDs. At the same time, strong arguments exist for the involvement of serotonin 91 , potentially accounting for abnormalities both in the brain and outside the central nervous system. Abnormal calcium signalling has likewise been suggested as a possible mechanism 92 .…”

Section: Box 3 Neurobiological Hypotheses In the Asdsmentioning

confidence: 99%

Advances in autism genetics: on the threshold of a new neurobiology

2008

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Autism is a heterogeneous syndrome defined by impairments in three core domains: social interaction, language and range of interests. Recent work has led to the identification of several autism susceptibility genes and an increased appreciation of the contribution of de novo and inherited copy number variation. Promising strategies are also being applied to identify common genetic risk variants. Systems biology approaches, including array-based expression profiling, are poised to provide additional insights into this group of disorders, in which heterogeneity, both genetic and phenotypic, is emerging as a dominant theme.Autistic disorder is the most severe end of a group of neurodevelopmental disorders referred to as autism spectrum disorders (ASDs), which share the common feature of dysfunctional reciprocal social interaction. A meta-analysis of ASD prevalence rates suggests that approximately 37 in 10,000 individuals are affected 1 . ASDs encompass several clinically defined conditions (see BOX 1 and the Diagnostic and Statistical Manual of Mental Disorders), pervasive developmental disorder -not otherwise specified and autistic disorder are the most common, whereas Asperger syndrome appears less frequently. Boys are at increased risk for the ASDs, an effect that becomes even more pronounced in so-called high-functioning cases.A chronological overview of research in the ASDs underscores the short history of genetic work in this area as well as the diversity of the methods used. Before the 1970s, autism was not widely appreciated to have a strong biological basis. Instead, various psychodynamic interpretations, including the role of a cold or aloof style of mothering, were invoked as potential causes. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript co-occurrence of chromosomal disorders and rare syndromes with the ASDs were noted 2 . Subsequent twin and family studies provided additional support for a complex genetic aetiology, but these were limited by the lack of uniform diagnostic criteria. The development of validated diagnostic and assessment tools in the early 1990s, most notably the Autism Diagnostic Interview -Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS), addressed these concerns and these tools have proven crucial to the advancement of international research into the ASDs. This work, in concert with important technical advances, made it possible to carry out the first candidate gene association studies and resequencing efforts in the late 1990s. Whole-genome linkage studies followed, and were used to identify additional loci of potential interest. Although the application of genome-wide techniques to assess copy number variation (CNV) has only just begun 3-5 , these studies have already identified a large number of potentially important novel candidate loci.Thus, in contrast to the complete absence of any biological understanding of the ASDs as recently as 30 years ago, we now know that defined mutations, genetic syndromes and de novo CNV acco...

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“…Another possibility for future treatment is that critical periods may be extended, or even reopened, via pharmacological intervention to treat children with autism. For example, autistic children do not experience the period of high serotonin synthesis during childhood that typically developing children do (Chugani 2004). Serotonin is critical to postnatal synaptogenesis, and so one possibility would be to treat very young children with serotonin agonists in an attempt to replicate for autistic children a more typical period of early brain plasticity (Chugani 2004).…”

Section: Boosting Recovery Via Biomedical Treatmentmentioning

confidence: 99%

Can Children with Autism Recover? If So, How?

et al. 2008

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Although Autism Spectrum Disorders (ASD) are generally assumed to be lifelong, we review evidence that between 3% and 25% of children reportedly lose their ASD diagnosis and enter the normal range of cognitive, adaptive and social skills. Predictors of recovery include relatively high intelligence, receptive language, verbal and motor imitation, and motor development, but not overall symptom severity. Earlier age of diagnosis and treatment, and a diagnosis of Pervasive Developmental Disorder-Not Otherwise Specified are also favorable signs. The presence of seizures, mental retardation and genetic syndromes are unfavorable signs, whereas head growth does not predict outcome. Controlled studies that report the most recovery came about after the use of behavioral techniques. Residual vulnerabilities affect higher-order communication and attention. Tics, depression and phobias are frequent residual co-morbidities after recovery. Possible mechanisms of recovery include: normalizing input by forcing attention outward or enriching the environment; promoting the reinforcement value of social stimuli; preventing interfering behaviors; mass practice of weak skills; reducing stress and stabilizing arousal. Improving nutrition and sleep quality is non-specifically beneficial.

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Serotonin in autism and pediatric epilepsies

Cited by 83 publications

References 72 publications

Clinical Manifestations, Blood Serotonin Level, Electroencephalography and Brain Magnetic Resonance Imaging in Autistic Children

Clinical Manifestations, Blood Serotonin Level, Electroencephalography and Brain Magnetic Resonance Imaging in Autistic Children

Advances in autism genetics: on the threshold of a new neurobiology

Can Children with Autism Recover? If So, How?

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