hippocampal 'atrophy'

Kenneth Collins k.p.collins at worldnet.att.net
Thu Aug 22 03:25:23 EST 2002


Ian Goddard wrote in message <3d62f359.92179446 at news.erols.com>...
>
> The following reviews a new book by Douglas Bremner, an Emory
> University psychiatrist who argues that many major psychiatric
> conditions are the result of environmental stressors.
>[...]

>"When patients are having flashbacks, as my veteran was, they are
>unaware of what is going on in the present," said Dr. Bremner.
>"Patients often describe flashbacks as if a movie were playing in
>front of their eyes, complete with visual images, sounds and
>smells." Dr. Bremner theorized that the flashbacks could involve the
>same brain areas that are affected by seizures, most importantly the
>hippocampus, which is affected in 80% of epilepsy cases. Subsequent
>PET (positron emission tomography) studies with trauma victims
>showed a significant and direct link between a reduction in the
>volume of the hippocampus and PTSD.

The relatively-recent [~3 years ago] findings with respect to
hippocampal stem-cell proliferation probably indicate that such
hippocampal 'atrophy' is, at least to a degree, 'reversible'.

The 'atrophy' correlates strongly with the survival-necessity
inherent in prolonged 'stressful' environmental circumstances, and
is, itself, commensurate with TD E/I-minimization in that it would
reduce information-processing options to a relatively-small subset
that's dictated by the environmental stressors, thereby, augmenting
the information-processing 'power' that can be 'poured-into' a
relatively-narrow range of survival-pertinent behavioral
manifestations.

'Reversibility' of stress-induced hippocampal 'atrophy' would enable
post-stress-reaction return to 'normal' information-processing.

The 'catch' is that, if 'modern' psychiatric practice 'intervenes'
inappropriately, such might, itself, interfere with post-stress
hippocampal stem-cell proliferation. The 'treatment', itself,
interferes with, and 'blocks' return to 'normal'
information-processing because the 'treatment' is, itself, a
stressor - so the 'treatment' does just the opposite of it's intended
purpose.

This's all testable.

I'm not familiar with the state of the art in animal-stress
experiments, but a swim-tank design should work.

Use no blood relative subjects. All subjects same-sex.

Populate an enriched environment with 3-times the subjects that will
be subjected to the stressor [1/3 will just remain in it]

Populate an impoverished environment with the same number of
subjects.

Pre-stress, have subjects gain relatively-long-enduring familiarity
within a generously-rich experiential environment. Minimal handling,
plenty of food, lots of 'toys', exploration opportunities, exercise
equipment, etc. 'Shoot the moon' on enriching their environment.
Allow them relatively-long opportunity to become familiar with the
environment. Do not introduce new subjects after a set of subjects is
inserted into the environment [mid-test unfamiliar stuff confounds
results].

Do the stressor. 2/3 of subjects from the enriched environment

Post-stress, allow half the subjects to return to the enriched
environment with which they're familiar. [Since there're no blood
relatives, the absent 1/3 enriches the environment further.]

Remove 1/3 of the animals in the impoverished environment, and place
the other half of the stressed animals into it.

Get it? The pre- and post-experiment impoverished population has the
same number of animals, but some were replaced by stressed animals.

Allow an aclimation period of the same length as the pre-experiment
acclimation period.

Get-it? The impoverished environment is, itself, a stressor because
1. it's unfamiliar, and a large change from the familiar
pre-experiment enriched environment, and 2. because there'll be
'conflict' between the animals long-familiar with the impoverished
environment and the post-stress animals unfamiliar with the
impoverished environment.

Prediction: there'll be an observable hippocampal-rebound
differential between the subjects that're returned to the enriched
environment with which they're familiar, and the subjects that're
placed into the impoverished environment with which they're
unfamiliar. Latter-group, less-rebound.

The experimental design needs to be precise in all it's facets.
Freedom in the enriched environment. Limited opportunity, and
'obnoxious' strangers in the impoverished environment.

Tweak-it to enhance it from this "top-of-the-noggin'" description to
conform with best-practice with respect to the experimental designs
that demonstrate the hippocampal atrophy in animals.

What you've got here is an analogue for what a stressed-out human
encounters when he's virtually incarcerated in a
psychiatric-'helping' place.

Other trials might replace the impoverished environment with
excessive handling, chemical intervention, etc.

The hippocampal-rebound differential will disclose the impact of not
just enabling folks to be Free to find themselves, post-stress.

If you do this experiment, since I proposed it, you are
Ethically-bound to allow me to review your experimental design and
results [no self-fulfilling-prophecy-via-sloppy-design allowed :-]

Get in the spirit of it. Work to develop as close an analogue of a
post-stress 'hospitalization' experience as is possible.

What I'm getting at is that what has become 'deemed to be helpful'
with respect to recovery from 'stress', is actually deleterious with
respect to such recovery.

There're =many= variations of this general experimental design, all
of which will yield significant results with respect to 'helping'
environments.

The thing that makes this possible is that, animal or Human, it's all
'just' TD E/I :-]

k. p. collins

>[...]





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