RE: Kids w/ Classic Autism, PDD-NOS & Speech Delays

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However in psychology any early intervention involving infants/children uses behavioural techniques to promote good behaviours (positive reinforcement) or remove undesirable behaviours (negative reinforcement). Secondly (and this is the tricky part) it also requires consistent and involved parenting

Not really. Most early intervention is child-led, which is different from a behaviourist approach. For example, a speech therapist might play whatever the child wants to play while using that activity to provide language modeling by commenting on the child's actions. It's much less directive. Even if the therapist does suggest an activity, the child is free to refuse it.

I don't really get why there is so much talk about aba distinguishing ASD traits. You teach skills just like you teach any other kid, apart from the focus and how you break it down to smaller chunks. There is no part in our program that includes stopping autistic behaviour. It's not even aimed at behaviour, it's just matching, creating patterns, drawing, brush teeth etc. They get to stim as much as they like and they definitely don't need to stare at me (they will normally look me more in the eyes than I find comfortable).

Hint: For individuals with speech delays, I suggest providing your ASD /PDD-NOS / etc. child a drink he/she likes and keep repeating the word so that sparks interest (e.g. say 'coke' repeatedly while giving him coke) etc.

Not a cure but the kids improve dramatically. Our son all of a sudden speeded up his learning and also improved his comprehensive language. We also met other parents there who were in for a second round. All very pleased with the outcome.

I think Mona Pereth (on a another thread) made the point that developmental delay does not mean intellectual disability. It might be the treatment helped but your son's spontaneous brain maturation might also have contributed.

For us as parents its very hard to work out what worked? but if its showing results and it not harmful then keep going.

I wanted to add a bit more info on his progress. We had a meeting pretty soon after the treatment with our special ed. We were looking at a couple of ABA exercises for our son. A follow up meeting took place about a month after and one of them commented that they couldn't believe the rapid change. At 2 months after the treatment I've got a short film clip of our special ed talking about the incredible improvement and how things that were more or less impossible to do a couple of weeks ago now seemed simple.

My son is still far from being able to attend main stream school. We will have difficulties that are hugely challenging.

Keep us posted about the stem cell treatment. Sweden may be more advanced with this type of treatment.

Acknowledgments

We gratefully acknowledge the participation of the parents and for allowing us to learn from their stories. We would like to thank the anesthetist for his outstanding performance in pediatric anesthesia leading to minimize any postoperative side effects.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Conclusions

Our and previous results by other authors are promising, but mandate further investigations in a larger controlled cohort of patients including objective methods such as biomarkers to possibly better understand the underlying individual dysfunction and potentially allow a stratification of those patients who may benefit most from this treatment strategy.

An important detail reported while interviewing the parents was that children started to respond much better and quicker to their speech and behavior therapy 3–6 months following SCT. Published data suggest that SCT reduces the immunological inflammatory disease of the brain associated with ASD and thus, opens the door for effectiveness of ABA and speech therapy. Indeed, a recent proteomic analysis study discovered nine serum proteins to be significantly different in ASD compared to typically developing boys and a significant correlation with ASD severity according to ADOS (24). Possible mechanisms for the way stem cells improve autism have been discussed more extensively by Liu et al. (25). In summary, two mechanisms seem to prevail: (a) reset of the immunological system and (b) improved vascular perfusion of the brain, two mechanisms that are addressed both by the stem cells but also by the bone marrow plasma, rich in growth hormones.

There is a large body of data pointing at immune-related genetically coupled risk factors and events associated with ASD. A cascade of events, leading disruption of neuronal maturation and dysfunctional networking through dysfunctional astrocytic neuronal support. A comprehensive review on this topic was recently published by Liu et al. (25). More interestingly, neuropathological investigations have recently provided evidence in support of the inflammatory theory, describing perivascular lymphocytic infiltration in the cerebral white, gray matter, and neuronal leptomeninges, this infiltrates were quantitatively accompanied by a corresponding magnitude of astrocytic activation in the affected regions of the brain. In Addition they reported significant loss on neurons and glial cells of the cerebral gray matter immediately adjacent to the leptomeningeal space. Brain micropathology also involved periventricular and other cerebral spinal fluid brain interfaces and vascular ependymal structures, all contributing to a functional disruption of the blood brain barrier (26, 27).

However, in ASD it seems that the overexpression of specific histocompatibility (HLA) genes (chromosome 6) and particularly activating KIR genes (chromosome 19) play an important role in promoting the cellular autoimmune cascade in brain tissue (28). The overexpression of the genes as compared to the general population provides a molecular basis for understanding events triggering a pathological immune response to viral or microbial antigens. BM-derived SCT is capable of targeting these pathological processes in the brain without having immediate and mid-term adverse events. The longevity of the effect of BM-derived SCT on suppressing inflammation and derailed autoimmune processes in the central nervous system (29) requires further investigations in larger cohorts. Furthermore, it is speculated if repeated treatment may have a cumulative effect on ASD. In addition, long-term observation are needed in children following autologous BM-derived SCT, though low likelihood, to rule out potential undesirable complications. Addition issues that require further elucidation involve (a) the efficacy and safety of employed cell types i.e., allogenic vs. autologous, umbilical cord-derived vs. autologous BM-derived, (b) the route of administration (intravenous vs. intrathecal), and (c) the added value of injecting BM-derived plasma. Presently, the rather limited available literature indicates more favorable results when employing intrathecal over intravenous route, probably because with the later, most of the cells will be filtered by the lung parenchyma during their first blood passage.

Autologous SCT have a biological advantages over allogenic stem cells and resemble a novel and promising treatment option for autistic children and adolescent not benefiting from conventional symptom-based and behavioral therapy. In ASD affected children providing intrathecal SCT at an earlier age should be associated with a higher benefit, as the brain plasticity and neurogenesis are at their maximum (30, 31), while perivascular damage to the neuronal circuitry is minimal.