Autism: Neurodevelopmental disorder
 OTSOPOULOS S.

Evidence from imaging and anatomical studies has started to shed light on the developmental deviation that occurs in the brain of autistic individuals. The aetiology however and the pathological mechanisms that underlie the deviation of the autistic brain development remain unknown. Clinical observations at first and systematic measurements of the head circumference on follow up studies have shown an unusual growth of the brain of the autistic child. A study showed that the head circumference, which at birth was smaller (25th percentile) than normally expected, increased fast to reach the 84th percentile by the middle of the second year. Further increase ceased and by the 4rth year no difference was observed with normally developing children. Imaging studies of young children have shown that the growth of the brain volume is primarily due to increase in white matter in the hemispheres and the cerebellum and mediocre increase of grey matter. Reduced volume of grey matter and increase of cerebrospinal fluid (CSF) have been reported among older autistic children. The same imaging studies have shown specific structural abnormalities in the anatomy and connectivity between cortical of areas, parts of the limpic system and amygdala. In addition, abnormalities have been observed in the configuration of the minicolumns of the neurons in layer III in Brodmann aresa 9 (prefrontal cortex) and areas 21 and 22 (temporal lobe). The miniculomns were more numerous, smaller in size, less compact and more dispersed. The alterations in the neural structure of the brain reduce intracortical connectivity which results in deficits in integration of information at the neural and cognitive levels. Study that has examined brains post-mortem of autistic individuals has shown evidence of an active neuroinflammatory process in the white matter and notably in the cerebellum in the cerebral cortex. Increase was observed in microglia, astroglia and cytokines. Presence of cytokines has also been found in the CSF of young children with autism. It has been hypothesized the neuroinflammatory process may be triggered off by toxic or viral insults on the CNS in early stages of in utero development. Studies of high functioning autistic individuals with fMRI have shown lower levels of activation at resting state and disruption under testing on executive functions tasks in areas that underlie social cognitive functions of the brain. It is hypothesized that neurotrophic and autoimmune factors are possibly involved in the pathogenesis of autism. These are currently intensively studied.

Key words: Autism, neurodevelopmental disorders.