DESCRIPTION

Autism is a neurobiological disorder that covers a broad spectrum of syndromes. The main characteristics of autism are problems in social interaction, communication, and restrictive and repetitive interests and activities.

Autism may be initially noted in infancy as impaired attachment, but it is most often first identified in toddlers, mostly boys, from 18 to 30 months of age. Boys are 3 to 4 times more likely to be afflicted with autism than girls. Girls as a group, however, may be more severely affected.

Correct diagnosis of autism depends on an accurate developmental history focused on types of behaviors typical of autism and on evaluation of current functional skills. Approximately 75 percent of persons with autism are mentally retarded. Less than 5 percent of children with autistic traits have fragile X or some other, known chromosomal abnormality.

The stereotype of severe withdrawal in autism is in reality a fairly rare condition. While language skills are affected, when care is taken to carefully invite communication on the child's terms, connections frequently take place. These connections form readily when the child is treated with respect and compassionate insight.

Although there is no cure, autism is treatable. Symptoms associated with autism often improve, as children start to acquire language and learn how to communicate their needs.

CAUSE

The causes of autism are unknown in most cases. In a few cases, biologic causes have been identified, although none are unique to autism. Some prenatal factors include intrauterine rubella; tuberous sclerosis; chromosomal abnormalities, such as Down's syndrome; as well as brain abnormalities, such as hydrocephalus. Frequently cited postnatal conditions associated with autism are untreated phenylketonuria, infantile spasms, and herpes simplex encephalitis. In the majority of cases, however, no underlying cause can be identified.

The current theory favored by many experts is that autism is a genetically-based disorder that occurs before birth (Piven 1997). Studies of persons with autism are finding abnormalities in brain structures that develop in the first few weeks of gestation (that is, while the fetus is in the womb) (Rodier 1998). Evidence that genetics is an important, but not exclusive, cause of autism includes a three to 8 percent risk of recurrence in families with one affected child. A working group convened by the National Institutes of Health in 1995 reached a consensus that autism is a genetic condition. An issue unresolved by the group was the role of immune factors in autism spectrum disorders; it was suggested that studies to clarify the situation are needed.

A new and dramatic treatment protocol for Autism has been developed at The Center For Complex Infectious Disease (CCID)in Rosemead, Californis. According to CCID, "Autism is often mistakenly viewed as a precise clinical entity, rather than as variable sets of symptoms resulting in abnormal social behaviors among young children. Clinical emphasis is given to an early onset (generally before the third year of life); a failure to express empathy for others; poor development, and even regression, of meaningful speech; hypersensitivity to various stimuli; and an apparent need for repetitive self-stimulated sensations.

Discussions concerning a possible infectious cause for autism have met with little interest, especially since the vast majority of those providing medical care for autistic children are not well versed in microbiology. Such discussions also raise disturbing inferences regarding possible sources of infection and modes of disease transmission. This is especially true for any suggestions that live viral vaccines might either cause or exacerbate autistic illnesses.

The Center For Complex Infectious Disease (CCID) has performed viral cultures on blood samples from well over 100 autistic children. In greater than 80% of the samples, a marked cytopathic effect (CPE) has occurred. The strongly positive CPE is similar to that induced by "stealth-adapted" viruses. The term stealth was chosen because certain cytopathic viruses seemingly lacked components targeted by the cellular immune defense mechanisms. This conclusion has been substantiated in detailed DNA sequencing studies conducted on a prototype stealth virus. This particular stealth virus originated from an African green monkey simian cytomegalovirus (SCMV), and presumably was derived from an SCMV-contaminated batch of poliovaccine. While the virus lacks genetic sequences coding for the major target antigens for anti-cytomegalovirus cell mediated immunity, it has acquired many additional genes of both cellular and bacterial origins.

Among the viral sequences, a notable finding is the expansion of a viral gene that provides a receptor for cell migration regulatory molecules termed "chemokines". Rather than a single copy of this gene, the virus has at least five copies in a linear array. There is sufficient indirect evidence for chemokines driving the replication of other stealth-adapted viruses to consider therapeutic trials with chemokine regulatory medicines in stealth virus infected individuals.

In preparation for such trials, CCID has tabulated many of the herbal and proprietary medicines reported to suppress various stages of the complex processes leading to chemokine production. Interestingly, a number of these medications have been used individually, with some apparent success, in patients with stealth virus-associated diseases. Following the lead of rheumatologists, there may be advantages to using lower doses of various combinations of differently acting chemokine regulatory agents, rather than relying upon a single medication. Especially for children, the initial priority should be given to those medications without appreciable risks of significant toxicity.