Oculomotor evidence for neocortical systems but not cerebellar dysfunctionin autism

Citation
Nj. Minshew et al., Oculomotor evidence for neocortical systems but not cerebellar dysfunctionin autism, NEUROLOGY, 52(5), 1999, pp. 917-922
Citations number
34
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
52
Issue
5
Year of publication
1999
Pages
917 - 922
Database
ISI
SICI code
0028-3878(19990323)52:5<917:OEFNSB>2.0.ZU;2-R
Abstract
Objective: To investigate the functional integrity of cerebellar and fronta l systems in autism using oculomotor paradigms. Background: Cerebellar and neocortical systems models of autism have been proposed. Courchesne and col leagues have argued that cognitive deficits such as shifting attention dist urbances result from dysfunction of vermal lobules VI and VII. Such a verma l deficit should be associated with dysmetric saccadic eye movements becaus e of the major role these areas play in guiding the motor precision of sacc ades. In contrast, neocortical models of autism predict intact saccade metr ics, but impairments on tasks requiring the higher cognitive control of sac cades. Methods: A total of 26 rigorously diagnosed nonmentally retarded aut istic subjects and 26 matched healthy control subjects were assessed with a visually guided saccade task and two volitional saccade tasks, the oculomo tor delayed-response task and the antisaccade task. Results: Metrics and dy namics of the visually guided saccades were normal in autistic subjects, do cumenting the absence of disturbances in cerebellar vermal lobules VI and V II and in automatic shifts of visual attention. Deficits were demonstrated on both volitional saccade tasks, indicating dysfunction in the circuitry o f prefrontal cortex and its connections with the parietal cortex, and assoc iated cognitive impairments in spatial working memory and in the ability to voluntarily suppress context-inappropriate responses. Conclusions: These f indings demonstrate intrinsic neocortical, not cerebellar, dysfunction in a utism, and parallel deficits in higher order cognitive mechanisms and not i n elementary attentional and sensorimotor systems in autism.