Atypical Cognitive Deficits in Developmental Disorders: Implications for Brain Function

By Sarah H. Broman; Jordan Grafman | Go to book overview
FIG.6.10. Orienting deficits are seen in autistic and cerebellar patients."% RT Deficit" is the percent increase in reaction time seen at short cue-to-target intervals (100-150 ms) relative to that seen at long intervals (800-900 ms). Adult data are from autistic patients with and without parietal abnormalities, and their normal controls ( Townsend, 1992) and from patients with either parietal or frontal lesions (age 16-54 years) and their controls (age 29-42 years Posner et al., 1984 Petersen, Robinson & Currie 1989;). Child data are from two children with cerebellar lesions in posterior hemispheres ( Townsend, 1992) responding to targets presented contralateral and ipsilateral to lesion sites, and comparison data from similar peripheral cueing tasks for 33 control children, mean age 9 years ( Swanson et al., 1991), and 12 control children age 7-12 years (from the Language Research Center, San Diego). Greater negativity indicates greater slowness in response to target at cued location when there is little time (100-150 ms) between cue and target onset (cb = cerebellar patients). From Townsend ( 1992). Reprinted by permission.

CONCLUSIONS

Autism and Neocerebellar Pathology

Anatomic evidence strongly supports the first central component of the theory linking autism to the neocerebellum: The great majority of autistic patients have specific neural abnormalities of the neocerebellum: (See Table 6.1; Figs. 6.4 and 6.5); the flocculonodular lobe and nonneocerebellar regions of the posterior lobe are also affected, but the anterior lobe appears to be much less affected. In the majority of cases, the key loss is the Purkinje neuron without which the neocerebellar cortex cannot control deep cerebellar nuclei and influence distant brain activity (Fig. 6.1). This reduction in Purkinje neurons may begin as early as the second trimester but not later than the first few months of postnatal life. The anatomic evidence also shows that this reduction seen in the majority of cases and the hyperplasia seen in the minority of cases, is in the portion of the cerebellum that has connections with

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