Today, the new US Secretary of HHS, Robert F. Kennedy Jr., announced a new initiative to uncover the cause(s) of autism. Click HERE to read today’s news about this announcement. He hopes to make major progress by this coming September. I wish him luck!
Last week, on Autism Awareness Day, I posted my experience treating a child who had autistic regression with intravenous immunoglobulin (IVIG). Over the course of treatment, this five-year-old’s communicative and social skills fully normalized. He was dismissed from his autism school program because he had become normal. Due to the tragic death of his father, this treatment program could not be continued and over three months he gradually regressed into severe autism with no communicative abilities.
My own explanation for autistic regression, which usually occurs around 18 months of age, is that it is an autoimmune disease which attacks the central nervous system. This child’s response to IVIG strongly supports my hypothesis. This line of clinical research should be continued.
Autistic regression does not match any of the well-recognized childhood autoimmune brain disorders. Therefore, autistic regression is a form of atypical neuroinflammation.
In the May 13, 2025 issue of Neurology, there is a review article about this topic: “Diagnosis and Management of Children With Atypical Neuroinflammation”. It appeared online a few days ago. Neurology is the most widely read neurology publication in the world. Even I have published several of my research reports in this journal.
There are several notable statements in this article. In the section entitled Seronegative AE (autoimmune encephalitis), the authors wrote: “…subacute polysymptomatic encephalopathy with neuropsychiatric symptoms…. is highly suggestive of immune-mediated encephalitis.” This is a precise description of autistic regression.
Concerning treatment, their recommendation appears in the abstract. In the text itself they wrote: “Acute first-line immunotherapy for most neuroimmune disorders consists of steroids, IVIGs, and plasma exchange, alone or in combination.”
Thus, their treatment recommendation strongly supports what I did. When I organized my study, not knowing the length of treatment that may be required, I avoided the use of steroids because of their side effects. Plasma exchange would have required hospitalization—the arrangements and costs would have been prohibitive. IVIG could and was easily administered in my outpatient clinic.
In addition, the authors recommend another medicine as a second-line treatment, and in some cases as the first-line treatment: rituximab. This is an intravenous immunoglobulin used to treat several cancers and autoimmune disorders. It has been FDA approved for the treatment of rheumatoid arthritis, an autoimmune disorder.
They suggested several other second-line medicines: tocilizumab (intravenous medicine, FDA approved for the treatment of juvenile idiopathic arthritis); anakinra (administered subcutaneously and FDA approved to treat DIRA, a rare autoinflammatory disease of infancy); mycophenolate mofetil (oral pills, used to prevent organ transplant rejection and treat many autoimmune diseases).
Thus, there are many new possibilities in treating the atypical neuroinflammation of autistic regression.
I published my results in the Journal of Child Neurology in 1998. This article, and all of my autism-related research results can be accessed HERE. I also gave a one-hour interview about this topic on Komentaras TV which can be accessed HERE (in Lithuanian). I am gratified that aspects of this work is continuing in the clinical and research activities of Lithuania based LukoLab.
The incidence of autism is increasing dramatically. The most likely explanation is that environmental factors are triggering more anti-central nervous system immunologic attacks.
I did my share of the work 27 years ago—it is due time for other clinical researchers to continue. Hopefully Secretary Kennedy will make this happen.