Abstract
Autism is a neurologic disorder with impairments in language, social communication, and behavior, which may improve over time, but which persist throughout the lifetime. The evaluation of autism requires a separation of clinical and research objectives and is done best in close cooperation with professionals in the fields of communication, education, and psychology. There are no biologic markers of autism. Regression in language and social communication is present in approximately 30% of children with autism and is most likely to occur between 18 and 24 months of age. Early deficits in social communication can be identified by the assessment of joint attention, affective reciprocity, and metacognition. Current evidence suggests that deficits in social cognition and communication in autism may be related to dysfunction in the amygdala, hippocampus, and related limbic and cortical structures. Other neuroanatomic structures, such as the cerebellum, also may form part of a distributed neuronal network responsible for social cognition and communication. Genetics play a major role in autism, but what is inherited and how broad the inheritable phenotype is remain unclear. At a neurochemical level, the principal neurotransmitter implicated in autism is serotonin. Seizures and epileptiform discharges are common in autism and are linked to cognitive dysfunction. The role of medication is to target specific symptoms and open windows of opportunity that allow implementation of a multimodal individualized educational plan.
| Original language | English |
|---|---|
| Pages (from-to) | 915-932 |
| Number of pages | 18 |
| Journal | Neurologic Clinics |
| Volume | 21 |
| Issue number | 4 |
| DOIs | |
| State | Published - Nov 1 2003 |
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ASJC Scopus subject areas
- Clinical Neurology
Cite this
Autism. / Tuchman, Roberto.
In: Neurologic Clinics, Vol. 21, No. 4, 01.11.2003, p. 915-932.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Autism
AU - Tuchman, Roberto
PY - 2003/11/1
Y1 - 2003/11/1
N2 - Autism is a neurologic disorder with impairments in language, social communication, and behavior, which may improve over time, but which persist throughout the lifetime. The evaluation of autism requires a separation of clinical and research objectives and is done best in close cooperation with professionals in the fields of communication, education, and psychology. There are no biologic markers of autism. Regression in language and social communication is present in approximately 30% of children with autism and is most likely to occur between 18 and 24 months of age. Early deficits in social communication can be identified by the assessment of joint attention, affective reciprocity, and metacognition. Current evidence suggests that deficits in social cognition and communication in autism may be related to dysfunction in the amygdala, hippocampus, and related limbic and cortical structures. Other neuroanatomic structures, such as the cerebellum, also may form part of a distributed neuronal network responsible for social cognition and communication. Genetics play a major role in autism, but what is inherited and how broad the inheritable phenotype is remain unclear. At a neurochemical level, the principal neurotransmitter implicated in autism is serotonin. Seizures and epileptiform discharges are common in autism and are linked to cognitive dysfunction. The role of medication is to target specific symptoms and open windows of opportunity that allow implementation of a multimodal individualized educational plan.
AB - Autism is a neurologic disorder with impairments in language, social communication, and behavior, which may improve over time, but which persist throughout the lifetime. The evaluation of autism requires a separation of clinical and research objectives and is done best in close cooperation with professionals in the fields of communication, education, and psychology. There are no biologic markers of autism. Regression in language and social communication is present in approximately 30% of children with autism and is most likely to occur between 18 and 24 months of age. Early deficits in social communication can be identified by the assessment of joint attention, affective reciprocity, and metacognition. Current evidence suggests that deficits in social cognition and communication in autism may be related to dysfunction in the amygdala, hippocampus, and related limbic and cortical structures. Other neuroanatomic structures, such as the cerebellum, also may form part of a distributed neuronal network responsible for social cognition and communication. Genetics play a major role in autism, but what is inherited and how broad the inheritable phenotype is remain unclear. At a neurochemical level, the principal neurotransmitter implicated in autism is serotonin. Seizures and epileptiform discharges are common in autism and are linked to cognitive dysfunction. The role of medication is to target specific symptoms and open windows of opportunity that allow implementation of a multimodal individualized educational plan.
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UR - http://www.scopus.com/inward/citedby.url?scp=0142043289&partnerID=8YFLogxK
U2 - 10.1016/S0733-8619(03)00011-2
DO - 10.1016/S0733-8619(03)00011-2
M3 - Article
C2 - 14743656
AN - SCOPUS:0142043289
VL - 21
SP - 915
EP - 932
JO - Neurologic Clinics
JF - Neurologic Clinics
SN - 0733-8619
IS - 4
ER -