Book contents
- Frontmatter
- Contents
- Preface
- Foreword
- List of Contributors
- Introduction
- Part I Classification and Diagnosis
- Part II Genetics, Neurology and Biochemistry
- 2 Unravelling the genetics of autism spectrum disorders
- 3 Brain imaging and the neuroanatomical correlates of autism
- 4 Magnetoencephalography (MEG) as a tool to investigate the neurophysiology of autism
- 5 Autism and epilepsy
- 6 Biochemistry of autism: changes in serotonin, reelin and oxytocin
- Part III Cognition, Development and Education
- Index
- Plate section
- References
5 - Autism and epilepsy
Published online by Cambridge University Press: 04 February 2011
- Frontmatter
- Contents
- Preface
- Foreword
- List of Contributors
- Introduction
- Part I Classification and Diagnosis
- Part II Genetics, Neurology and Biochemistry
- 2 Unravelling the genetics of autism spectrum disorders
- 3 Brain imaging and the neuroanatomical correlates of autism
- 4 Magnetoencephalography (MEG) as a tool to investigate the neurophysiology of autism
- 5 Autism and epilepsy
- 6 Biochemistry of autism: changes in serotonin, reelin and oxytocin
- Part III Cognition, Development and Education
- Index
- Plate section
- References
Summary
Epilepsy, autism and cognitive impairment are over-represented in all studies that take one of these major categories as the starting point. The rates of epilepsy and autism are related to the severity of cognitive impairment. Those with primary or early regressive autism show a steadily rising rate of epilepsy with age reaching 30–50% in some adult studies but without evidence of causative relationship. Seizures of all types occur with complex partial attacks being prominent but we have no convincing explanation for this relationship. However, in several particularly early onset epilepsies, autism and cognitive impairment develop with the epilepsy suggesting causation (i.e. an epileptic encephalopathy). This process seems to preferentially involve the temporal neocortex and medical or surgical treatment of the epilepsy may cause remission of autistic symptoms in these cases.
Introduction
In 1943, Kanner described 11 children with his then new ‘autistic disturbances of affective contact’ (Kanner, 1943). One of these 11 suffered from epilepsy. In 1971, Kanner reported on a follow-up of the 11 patients; by now, two patients – 18% of his original series – were suffering from epilepsy (Kanner, 1971). Thus, in this seminal report, which defined autism, the patients already formed a clinically heterogeneous group – those with and those without seizures.
What has become clear over the years since Kanner's writings is that patients with autism are, in fact, at greater risk of seizures than are children with other types of developmental problems, such as developmental dysphasia or Down syndrome (Wong, 1993).
- Type
- Chapter
- Information
- Researching the Autism SpectrumContemporary Perspectives, pp. 176 - 189Publisher: Cambridge University PressPrint publication year: 2011