The name is absent

Autism prodrome 30 of 89

circumference might contribute to clinical surveillance needs to be interpreted with
caution.

However, this finding has attracted enormous interest in the idea that a
trajectory of abnormal brain growth that occurs pre-symptomatically might be a
marker of underlying neurodevelopmental disturbances that contribute (or at least
‘signpost’) the later emergence of the autism phenotype. The window of this
abnormal brain growth coincides with the period of Synaptogenesis and subsequent
pruning when cortical connections are developed, refined and stabilized. This process
is interactive with the infant’s experience of the environment, a process that
Greenough et al. (1987) termed ‘experience expectant development’, and the
consequences of a developing brain whose connections are not undergoing the usual
refinement on information processing may result in a secondary pathogenic process
that impacts on future development in the process of the emergence of the ASD
phenotype.

A recent study identified an intriguing finding that might be related to this
overall pattern of abnormal brain growth. Mosconi et al. (2009) found that by the age
of 2 years children with autism had enlarged amygdalae, particularly in the right
hemisphere over and above an increase in total brain volume and that this increase
maintained (but did not increase further) up until the age of 4 years. This indicates
that prior to this age brain growth in this particular structure is likely to have been
abnormal. Furthermore, amygdale volume at age 4 was positively associated with
joint attention skills at the same age. Joint attention behaviors involve co-ordination
(initiating, response) between objects and caregivers or other adults; often involving
the shifting of gaze to and from the gaze of the adult. It is well-established that the
amygdala is recruited in facial emotional recognition tasks and in particular in

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