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.