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From the end of a long medically challenging for me read. My #2 Grandson is currently undergoing treatment at Shands in Florida for "GAD65 Positive Autoimmune Limbic Encephalitis". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3513425/
Post mortum examinations have show a very high incidence of Brain encephalitis in the Autistic.

"Discussion

The dramatic rise in ASD began in the 1990s, and in the past two decades, the rates of ASD have increased by 289% (Boyle et al., 2011). The sudden and dramatic rise in ASD prevalence has, in some ways, caught the medical community “off guard.” In the midst of the meteoric rise in rates of autism and ASD, significant new research into the physical symptoms has been done. The challenge now is to incorporate this new research about the physical symptoms of autism into the practice of medicine that historically has stereotyped autism as a purely psychiatric disorder. For the benefit of patients, the physical symptoms of autism must be recognized and treated. For children with ASD, particularly those who have begun to regress into ASD and show other signs of neurological regression, testing for encephalitis may be warranted. Particularly, given the documented cases of children with regressive ASD and NMDA Encephalitis who tested positive for anti-NMDA receptor antibodies, routine testing for anti-NMDA receptor antibodies in ASD should be seriously considered. The study by Scott et al. (2014), mentioned earlier, of the child who regressed into autism and recovered from treatment for NMDA, indicates that there is benefit to recognizing the possibility of encephalitis in children with ASD. The delay in incorporating new research findings into medical practice standards is unfortunate because if a diagnosis of autism or ASD were recognized in the medical community as having a possible component of encephalitis that could be tested and treated appropriately, such treatment for encephalitis would likely reduce, and possibly eliminate, ASD symptoms in some children. Future studies should include treatments for neuroinflammation in ASD."

I hope your grandson does well.

Best wishes for a full recovery.

RMD

I would expect that, as individuals with autism are extremely affected by a high carb/sugar diet. Any time I learn of a health problem where the symptoms are dramatically reduced with a low carb/low sugar diet, as with autism, I pretty much assume that an infection is the underlying cause. The infection would most likely be bacterial or fungal, but probably not viral.

quote:

Originally posted by c1steve:
I would expect that, as individuals with autism are extremely affected by a high carb/sugar diet. Any time I learn of a health problem where the symptoms are dramatically reduced with a low carb/low sugar diet, as with autism, I pretty much assume that an infection is the underlying cause. The infection would most likely be bacterial or fungal, but probably not viral.

Thanks for your input as the article mentioned it the cause can be many different things including inoculations. If memory and understanding serves,it seems to be a genetic abnormality that's triggered by various means.

quote:

Originally posted by Fla. Jim:

quote:

Originally posted by c1steve:
I would expect that, as individuals with autism are extremely affected by a high carb/sugar diet. Any time I learn of a health problem where the symptoms are dramatically reduced with a low carb/low sugar diet, as with autism, I pretty much assume that an infection is the underlying cause. The infection would most likely be bacterial or fungal, but probably not viral.

Thanks for your input as the article mentioned it the cause can be many different things including inoculations. If memory and understanding serves,it seems to be a genetic abnormality that's triggered by various means.

Found possible causes in the article.
"Thus, it is plausible that systemic inflammation and/or infection could trigger the inflammation or encephalitis seen in the brains of children with an ASD.

In addition, the production of brain autoantibodies, notably found in children with ASD and in specific cases of autistic regression and encephalitis, could also be secondary to various types of external triggers. Researchers have suggested various exposures that can contribute to the production of brain autoantibodies in autism (Mostafa and Refai, 2007; Mostafa and Al-Ayadhi, 2015).

To this point, a study by Vojdani et al. (2003) provides evidence to support the hypothesis that there are external triggers, such as the ones mentioned previously, that can instigate the production of brain autoantibodies in children with autism. Vojdani et al. (2003) measured IgG, IgM, and IgA antibodies against CD26, CD69, streptokinase (SK), gliadin, and casein peptides and against ethyl mercury bound to human serum albumin in patients with autism. From the results, they proposed that bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69 and induce antibodies against these molecules. Their study demonstrated that dietary peptides, bacterial toxins, and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in and autoimmune reaction in children with autism.

It is conceivable that this process could begin with a single exposure or trigger; however, a combination of exposures or factors could also trigger a cascade of events resulting in brain inflammation and production of brain autoantibodies. Numerous studies have shown that toxins and pathogens can work synergistically – where the effect of the combination of their presence is greater than the sum of their individual effects (Kern et al., 2012)."