You do not currently have permission to view the full text for this document. Please sign in to an account with an active subscription or contact support.
It is quite rare to come across cases of infantile autism in which cerebellar abnormalities are discovered and are treated by analytical psychotherapy from very early on in life for a sufficient length of time for considerable improvements to be achieved. Such cases pose the question of etiology. A multi-factorial approach seems to be required in these cases, putting aside any polemic concerning psychogenic as opposed to organogenic etiology. In this chapter, I do not pretend to enter into an exhaustive scientific study. In the aftermath of Martine's treatment, a whole new working-through of hypotheses concerning the interplay of dynamics in this mother-daughter psychotherapy had to be made, taking into account both the neuro-developmental organic anomalies and the problem situation involving mourning that presided over this girl's birth. In my view, the question is still open as regards the impact of congenital lesions per se and the functional aspects of development that may subsequently have modified the brain tissue.
According to Squire and Kandel , all experiences (and all traces of these) physically shape the brain before it reaches full maturity, and perhaps even afterwards too. They argue that long-term memory requires the synthesis of new proteins that stimulate the neuronal growth factors, which play a role in forming new targeted networks.
The cerebellum has long been thought to have a direct impact on the genesis of infantile autism. For the past ten years or so, researchers have used brain imagery to highlight brain and cerebellar anomalies in children with autism. Some investigations were comparative studies that included a sample of non-autistic children. Courchesne et al. showed that the surface of lobules VI and VII of the vermis cerebelli was significantly smaller in a group of 18 autistic persons who did not present any associated neurological syndrome. In 1994, the same research team showed that vermis hypoplasia is associated with a reduction in