Autism: A Disorder of Conflicting Causes and Treatments
Despite its 50 year-old diagnosis, autism is still one of the mostly commonly contracted and rarely treated childhood diseases. Studies suggest that as many as 1 in 500 children may display autistic symptoms. Manifestations of this disability include the stereotypical physical contortions and hand-flapping motions commonly associated with autism, as well as inability to relate to the outside world, limited social skills, lack of concentration, and hypersensitivity to certain stimuli-particularly noise (1). Perceived causes include poor fetal development, genetics, allergies, and a lack of crucial enzymes. Because for many years the disorder was thought to be a result of poor parenting, only recent studies have begun any attempts to identify the causes of childhood autism. Many diagnosis and potential treatments have been tried only by the parents of autistics; undergoing research is still slow and often under-funded.
Eric Courchesne (2), a leading scientist whose studies of the cerebellum have opened a new field of belief for the region's potential functions, suggested that autistics have a marked propensity for cerebellar lesions and Purkinje neuron loss, leading to an inability to "rapidly and accurately" change attention from one focus to another, particularly in the areas of visual and auditory stimuli.
Dr. Margaret Bauman, (Dept. of Neurology, Harvard Medical School and a child neurologist at Massachusetts General Hospital in Boston), and Dr. Thomas Kemper (Depts. of Neurology, Anatomy, and Pathology, Boston University School of Medicine) have a different hypothesis (3) which nonetheless correlates with Courchesne's theory. They believe that a dysfunctional neural structure may result in autistic behavior. Bauman and Kemper have discovered that the amygdala and hippocampus (parts of the limbic system which regulate memory and emotional reactions) are packed densely with neurons in the dissected brains of autistics. This complements Courchesne's idea that there are fewer Purkinje neurons in the cerebral regions of autistic children. Because Purkinje neurons are responsible for programmed cell death, a lack of them could result in an overabundance of neurons in the brains of autistic infants. If it is to be believed that humans develop many more neurological connections than are needed (the unnecessary neurons undergoing cell suicide in early development), then it stands to reason that a high neural density will result if there is an insufficient number of Purkinje cells. Likewise, the overabundance of neurons in the amygdala and hippocampus can potentially explain why autistics have difficulty responding to too much stimulus at a given moment: their systems overreact to the given input, and they respond by simply not reacting at all. These theories imply that autism has a genetic origin.
Studies of a Massachusetts town have attributed autism to congenital environmental...