Cerebellar and cortical systems in 26 high-functioning adolescents and young adults with autism were examined and compared to 26 healthy controls at the University of Pittsburgh School of Medicine. Reflexive, visually guided (cerebellar modulated) saccadic eye movements were normal whereas volitional (neocortical) saccade tasks (oculomotor delayed-response and antisaccade) were abnormal. The results demonstrate neocortical, not cerebellar, dysfunction in autism, suggesting deficits in higher cognitive mechanisms and impairments in spatial working memory and executive control over reflexive behavior. [1]

COMMENT. Both cerebellar and neocortical dysfunctions have been proposed as a neurologic basis for autism. Dysfunction of cerebellar vermal lobules VI and VII should be associated with dysmetric saccadic eye movements. In the present study, cerebellar-mediated saccades were normal but neocortical control of oculomotor eye movements was impaired. The findings support neuropsychological evidence of deficits in cortical, voluntary regulation of attentional focus in autism.

A new hypothesis for autism is proposed by DeLong GR, Duke University Medical Center [2]. Autism occurs in two forms: 1) Secondary to early infantile, bilateral brain damage (eg. epileptic medial temporal sclerosis, herpes simplex encephalitis, infantile spasms, tuberous sclerosis, congenital rubella); 2) idiopathic autism, with regression in the second year, prominent affective symptoms, and a more favorable prognosis. Idiopathic autism is characterized by a left-hemisphere serotonin deficiency, and is benefited by selective serotonin reuptake inhibitors (eg fluoxetine). Secondary autism caused by bilateral hemisphere damage has a poor prognosis, whereas idiopathic autism with a learning and memory deficit due to single hemisphere damage is compatible with higher functioning levels.

Brain weight in autism. The serotonin deficiency in autism, by permitting excessive branching of thalamocortical axons, may result in postnatal brain enlargement. Megalencephaly has been reported in some autopsied cases of autism, but a brief report of brain weights of 21 postmortem cases found the majority were normal, one micrencephalic, and only 3(15%) were megalencephalic. [3]

Polydipsia in autism. The incidence of polydipsia in 49 autistic children was higher than in retarded children studied at the Noto Second Hospital, Ishikawa, Japan [4]. This finding suggests a hypothalamic-pituitary dysfunction in autism.

Placental insufficiency as a risk factor for early onset schizophrenia. Hultman CM et al, University of Uppsala, Sweden, report the association of small size for gestational age and bleeding during pregnancy as risk factors for early onset schizophrenia and affective psychosis in males [5]. This was a large population based, case-control study, including 167 patients with schizophrenia. The findings support the concept of environmental risk factors and prenatal or natal brain damage in some cases of early onset schizophrenia.

These articles and others in the adult literature, concerning the recent evidence for a neurological basis for autism and schizophrenia, are important to pediatric neurologists who will be consulted by child psychiatrists regarding the diagnosis and treatment of underlying neuropathology.