These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Autism, epilepsy and temporal lobe pathology].
    Author: García-Peñas JJ.
    Journal: Rev Neurol; 2009 Feb 27; 48 Suppl 2():S35-45. PubMed ID: 19280573.
    Abstract:
    INTRODUCTION: The social, language, and behavioral problems that occur with autism suggest that the syndrome affects a functionally diverse and widely distributed set of neural systems. The temporal lobe is an important part of the social brain, and manifests morphological and functional alterations in autism spectrum disorders (ASD). AIM. To describe the relationship between autism, epilepsy and temporal lobe dysfunction. DEVELOPMENT: Psychopathology is common in children with temporal lobe epilepsy, with over-representation of ASD and unusual disruptive behaviour disorders. Behaviors associated with damage to the amygdala and related temporal lobe structures in humans and nonhuman primates are strikingly similar to those seen in autism. The anatomic alterations observed in patients with temporal lobe epilepsy involve those structures responsible for social brain functioning, mainly amygdala, hippocampus and superior temporal sulcus. This is supported by studies demonstrating associations among temporal lobe epilepsy, ASD, and neuroimaging alterations in the hippocampus and amygdala. CONCLUSIONS: The complex relationship between autism and epilepsy, as reflected in the autism-temporal lobe epilepsy phenotype, provides a bridge to further knowledge of shared neuronal networks that can account for both the autisms and the epilepsies. There is a critical early stage of brain maturation during which temporal lobe epilepsy perturbs the development of brain systems that underpin social intelligence and possibly other cognitive skills, disrupting normal cortical organization and circuitry, thereby inducing an ASD. It's difficult to know if these patients became autistic because of repetitive epileptic seizures and/or persistent epileptiform activity on the EEG or because of the epileptogenic and psychopathological effects of temporal lobe lesions during early development (infancy and early childhood).
    [Abstract] [Full Text] [Related] [New Search]