your doctor should be using this to help your recovery in the first week. But I'd be willing to bet a hell of a lot of money that s/he is doing absolutely nothing to stop the neuronal cascade of death.
Ask your doctor how many neurons are dying in the first week. My calculations for me are here:
How many neurons is your doctor responsible for killing/not saving?
http://link.springer.com/referenceworkentry/10.1007/978-1-4614-5836-4_145
Abstract
Excitotoxicity has been
implicated as a key pathogenic pathway in a number of neurodegenerative
diseases and conditions including Alzheimer’s disease, amyotrophic
lateral sclerosis, multiple sclerosis, brain trauma, and stroke. While
acute excitotoxicity can result in the initiation of cell death
pathways, chronic or low levels of excitotoxin exposure may result in a
more slowly progressing pathological cascade. In this respect, there is
emerging evidence that excitotoxicity can result in axonal degeneration
and pathology, a key pathological feature of many of these
neurodegenerative conditions. Recent evidence supports the notion that
axon degeneration can be a separate and independent process from cell
death, and thus mechanisms involved need to be understood in order to
provide axonal protection in neurological disease. While axon
degeneration following transection (Wallerian degeneration) has been
well documented, less is known about axon degeneration following other
insults such as excitotoxicity and the mechanistic relationships they
bear to Wallerian degeneration. In particular, how a primarily
somatodendritic insult, such as excitotoxicity, results in a
pathological cascade within the axon is unclear. This chapter reviews
our current understanding of the pathological changes and mechanisms of
excitotoxin-induced axon degeneration with particular reference to our
understanding of other forms of axonal degeneration and potential
mechanisms involved. An increased understanding of the mechanisms of
axon degeneration in neurological disease is essential to the
development of therapeutic agents targeting axon protection.
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