This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Investigators have attempted to define the neural pathophysiology of autism ever since the hypothesis of “refrigerator parents” as its cause was replaced by the view that it is a developmental disorder of the immature brain. As the article by Minshew et al.1 and the Views & Reviews by DeLong2 in this issue of Neurology show, consensus has yet to be reached. Minshew et al. examine whether abnormal control of eye movements is best explained by impaired vermal or frontal lobe dysfunction; DeLong’s focus is on the temporal lobes and on abnormal maturation of serotonergic pathways. These are by no means the only brain regions implicated; earlier studies have invoked maldevelopment or, rarely, damage of the cerebellum and some brainstem and diencephalic nuclei, involvement of the basal ganglia and thalamus, frontal neuronal migration deficits, thinness of parietal gyri and posterior corpus callosum, and dysfunction of dopamine and opiate neurotransmitter pathways.
Similar to dementia in the elderly, autism (pervasive developmental disorder [PDD] in Diagnostic and Statistical Manual of Mental Disorders, 4th ed. [DSM-IV] and International Classification of Diseases [ICD]-10 parlance) is not a medical diagnosis but a behaviorally defined syndrome of early childhood with a variety of biologic causes. Its severity varies so widely that DSM-IV divides it into five behavioral subtypes. All have in common impaired sociability, language, nonverbal communicative skills, and imagination, together with stereotypic behaviors and preoccupations. Other features are lack of cognitive flexibility, poor organizational skills and insight into what others may be thinking, rigidity, perseveration, and often heightened anxiety. Intelligence is affected in many but not all individuals, although intelligence quotient (IQ) is not a defining feature of autism. DSM-IV specifies that the behavioral deficits must be out of proportion to the individual’s cognitive level, without defining this discrepancy in quantitative terms.
The five DSM-IV …
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
