Typing and Correction
Toxicity, infection, and inflammation converge on the limbic brain. This, it has been argued, is responsible for the behavioral features of ASD. The question then arises of whether such damage can be reversed. Unlike most brain regions, the limbic brain has some capacity for repair. In most of the brain, neurons once formed lose the capacity to divide and, following damage, are unable to regenerate new neurons. In contrast, dividing neuronal cells are seen in the limbic brain until adulthood.1,2 In monkey brains, neuronal division in the hippocampus was seen at the grand age of 23 years.3 Even so, the rate of division was much lower than in the youngest animals examined, suggesting that repair capacity declines with age.
There are therefore prospects of some degree of recovery if the specific problem can be identified and treated. Whereas in high-functioning ASD it is questionable whether any therapy is at all advisable, in low-functioning individuals restorative treatment is clearly justified. There are many examples where remedial therapy can ameliorate the behavioral deficits. In one child with a urea cycle metabolic disorder, the autistic symptoms and hyperactivity disappeared on appropriate therapy.4 Because neuronal proliferation in the limbic brain declines with age, therapeutic intervention should be put in place as early as possible.
There is an urgent need to match therapy to the specific deficits, and guidelines for good clinical practice, for instance as set out authoritatively by Filipek and co-workers,5 recommend genetic testing and selective metabolic analysis. Clearly, each individual with autism is distinct, and underlying biochemical,