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Wednesday, 8 May 2013

Neurogenesis & Neuroplasticity


Today we have two new N- words and we finally get to the bottom of what autism is and what it is not.   There is nothing revolutionary here, it can all be found in the research and indeed most of it can be found in just one book, but then who would read my blog?
We will start with the bad news and finish with the good news.

Neurogenesis
Neurogenesis sounds like a good thing; it is the birth of neurons in the brain.  This is substantially completed in the pre-natal period, but it can continue in certain parts of the brain throughout life.  After a head injury, or trauma, neurogenesis can take place.

In the case of autism the potential benefit exists, but seems likely to be minimal.
Many studies have already established the pattern of deformities in the autistic brain.  One researcher in particular, Eric Courchesne, seems to have chosen to make this his life’s work.  He has carried out repeated studies over many years focused on examination of brain growth, and overgrowth, in autism using post-mortem brains and later MRI (magnetic resonance imaging).
His findings are unequivocal, and in line with those of his peers.  In his autistic subjects, the brain grows much faster in the first couple of years than typical subjects and then the process slows right down and in later life the autistic brain starts to shrink.  His and other studies show that in later life the brain does seem to try to compensate for its defective development; this is seen as ineffective (but how can anyone possibly know?).

He finds a wide pattern of abnormalities, including the expected presence of a reduced number of Purkinje cells.  He goes on to argue that his evidence shows that this damage was done in the pre-natal period, so he will not be popular with the vaccine damage theorists.

“Thus, given the resulting tight bond between the olivary neurons and the Purkinje cells after this time, loss or damage to the cerebellar Purkinje cells results in an obligatory retrograde loss of olivary neurons. Since, in the autistic brain, the number of the olivary neurons is preserved, it is likely that whatever event resulted in the reduction of the Purkinje cells in these cases has to have occurred before this tight bond has been  established, and thus before 28–30 weeks gestation.”
 
“In addition, microscopic observations of enlarged cells in some brain regions in autistic children and small pale cells that are reduced in number in these same areas in adults strongly indicate changes with age. Clinically and pathologically, this process does not appear to a degenerative one and may reflect the brain’s attempt to compensate for its atypical circuitry over time.”

“This early cessation of growth results in a 2–4 year old autistic brain size that is not different from a normal adolescent or adult in the majority of cases. Thus, at the age of typical clinical diagnosis of the disorder (i.e. 3–4 years), the period of pathological growth and arrest has likely already passed, leaving clinicians and researchers with an outcome, rather than process, of pathology for study and treatment intervention.”

Here are three of Eric’s studies, which include graphs showing autistic brain development vs. the control group at various ages throughout life.


Neuroplasticity
If neurogenesis was the bad news then neuroplasticity is certainly the good news. I think that Eric needs to read up on this subject and perk himself up.  It seems even a deformed brain can do some pretty clever stuff.

Neuroplasticity, also known as brain plasticity, refers to changes in neural pathways and synapses which are due to changes in behavior, environment and neural processes, as well as changes resulting from bodily injury.  Neuroplasticity has replaced the formerly-held position that the brain is a physiologically static organ, and explores how - and in which ways - the brain changes throughout life.
In the field of neuroplasticity we have some pioneering work from  Michael Merzenich is a neuroscientist. He has made some of "the most ambitious claims for the field - that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia - that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning - how we learn, think, perceive, and remember are possible even in the elderly."  Merzenich’s work was affected by a crucial discovery made by Hubel and Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was"… as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself.
Merzenich created a plasticity-based computer aided learning programme called FastForWord, which  offers seven brain exercises to help with the language and learning deficits of dyslexia.

ABA and neuroplasticity.  Then of course, I started thinking about Monty’s  6 years of ABA and endless hours on his computer based learning programmes.  This of course is the link between neuroscience and ABA - the fuzzy science of neuroplasticity; otherwise known as making the most of what you’ve got. 
 
Conclusion
We have established that autistic behaviours are likely caused by stress and inflammation in the cerebellum, and in particular in the region of the Purkinje Cell Layer (PCL).

We have seen that in classic autism this stress and inflammation is associated with physical brain growth abnormalities that occurred in the pre-natal and early post natal period.  The oxidative stress and inflammation is ongoing throughout adulthood.
We have seen that stress and inflammation in the cerebellum can be caused by entirely different causes, that take effect later in life, such as Tuberous Sclerosis Complex (TSC).  There is another truly horrible one called Childhood Disintegrative Disorder (CDD).

With the availability of noninvasive MRI scans, it would be interesting and highly possible to ascertain the level of brain deformity in milder cases of autism and Asperger’s syndrome. 
Given that by the time autistic behaviors are exhibited, the damage to the brain  has already run its course, our main ally would seem to be neuroplasticity and of course to halt the ongoing oxidative stress and inflammation.

In addition, we need to consider countering the apparent ion-channel disfunction, and maybe give the damaged hippocampus a lesson or two about hormone production.

 

 

 

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