On 27 May 1996 lpacker at nyc.pipeline.com wrote:
> "Fact?" Keep in mind that many unmedicated patients develop dyskinesias,
> too, and a lot of what was originally attributed to neuroleptics may have
> _not_ been iatrogenic but related to the disease process itself. The only
> subpopulation where the relationship to increased risk really seems to hold
> up is in elderly schizophrenic patients on neuroleptics.
This is a view which is not even accepted by the very pro-drug
American Psychiatric Association. Tardive dyskinesia as a side effect
of neuroleptic drugs is very well-established and extensively
studied. See http://www.ihr.com/apa/meds.htm for a discussion of
tardive dyskinesia _by the APA_. These are the people who try to
_minimize_ brain-damage effects of psychiatric 'treatments'. There
is also a paper on tardive dyskinesia at
http://vh.radiology.uiowa.edu/Providers/Lectures/Conferences/CPS/
08TardiveDyskinesia.html.
> >Is it your view that David Oaks is wrong to publish her number?
> >If you feel that it is somehow wrong, please explain why you think its
> wrong.
>> There is a difference between education and harassment. What Mr. Oaks is
> doing by suggesting everyone call her is harassment, in my book. Why pick
> out just one person or name?
David Oaks posted the 800 number of the Brain Bank, not someone's office
or lab number. There is no harassment involved there. The 800
number is intended to be called. If she got more calls than she
wanted to deal with through the 800 number it would be very easy to tell
the people who answer the 800 number to not transfer calls to her.
While you are trying to make something out of David Oaks posting an 800
number, NAMI is pushing forced outpatient drugging of about
a million people in the U.S., there is in general *forcible* use of
psychiatric treatments, and neuroleptic-induced and
electroshock-induced brain damage are often minimized in "informed
consent" even when psychiatric treatments are voluntary. These are
major threats to civil liberties and to the psychological and
physical health of millions of people.
> Deal with the issues and let's get away from the individual attacks.
> If you or others feel that what one practitioner is doing is unethical or
> problematic, there are remedies that can be pursued.
No, it's not a matter of individual practitioners. It's a problem with
a corrupt system where psychiatry is intertwined with legal force,
unlike other areas of medicine. I wonder when the massive tardive
dyskinesia class-action lawsuit is going to happen.
Mental patients are sometimes not in a good state to watch out for
themselves and have lost rights and a voice in what happens to their
own minds and brains as a result. The result of their disempowerment
has been a bunch of treatments which often look more like an attack
on the person than any help -- stupefying drugs, turning people into
zombies, zapping brains with electroshock and destroying people's
memories, sometimes seriously disorienting them.
Also, the allegation is that psychiatry and psychiatric research is
corrupted by funding from
drug companies, research on electroshock is done by shock doctors
who make a large part of their income from electroshock -- or, like
Abrams, own part of a shock-machine company -- and so it's often
skewed, invested in minimizing side effects of neuroleptic drugs or
electroshock. Also that research on brain damage from various
psychiatric treatment is inadequate. It's as if tobacco companies
were the major researchers into the cause of lung cancer. I looked
at a book on electroshock written by Abrams -- one of the big pro-shock
doctors -- and it mentioned that there was basically no research on memory
loss from electroshock between 1950 and 1968! Research after that
time substantiated memory loss.
Studies of brain damage from neuroleptic drugs are confused by the
fact that it's hard to locate 'schizophrenic' people who aren't
medicated. So studies of 'schizophrenic' brain changes may actually
be studies of the effects of neuroleptic drugs, although they are
not presented this way. I looked at a paper at
http://splweb.bwh.harvard.edu:8000/pages/papers/bg_hokama_95/bg.html
< CAUDATE, PUTAMEN, AND GLOBUS PALLIDUS VOLUME IN SCHIZOPHRENIA:
< A QUANTITATIVE MRI STUDY
<
<Hiroto Hokama, M.D., Martha E. Shenton, Ph.D., Paul G. Nestor,
<Ph.D., Ron
<Kikinis, M.D.*, James J. Levitt, M.D., David Metcalf, M.A.*, Cynthia G.
<Wible,
<Ph.D., Brian F. O'Donnell, Ph.D., Ferenc A. Jolesz, M.D.* and Robert W.
<McCarley, M.D.+
<
< Key Words: Schizophrenia, Basal Ganglia, Magnetic Resonance Imaging,
< Caudate, Putamen, Globus Pallidus
Note "neuroleptic" is not included as a keyword or in the title of the
study: the assumption is
that one is studying 'schizophrenia' rather than the effects of
neuroleptic drugs, even though all the people in the study were on
neuroleptics. It is a preconceived assumption.
There are a couple of sentences indicating that enlargements in
basal ganglia regions found in 'schizophrenics' could have been
due to neuroleptic drugging:
> With respect to the onset time and cause of increased volumes, Chakos
> et al. (1994) have noted, compared with normal controls, caudate
> enlargement in first episode schizophrenic patients and a further
> increase in caudate volume at 18 month follow-up scans. The degree of
> schizophrenic volume increase was correlated with a longer time to
> remission and a larger cumulative neuroleptic dosage, raising the
> possibility of a neuroleptic-induced effect.
> Since results from a first episode study (Chakos et al., 1994) have
> suggested that the volume increases in schizophrenics might be
> secondary to neuroleptic medication, we examined the correlation
> between relative ROI volumes and several measures relevant to this
> variable, although the absence of detailed medication history
> precluded our using actual dosage, which would have been a more direct
> and desirable variable. There were no large magnitude correlations
> with either current chlorpromazine equivalent neuroleptic dosage level
> or several measures of disease duration and severity: duration of
> illness, age of onset, or percentage and absolute time hospitalized
> since onset. The maximum r value was only -0.279 (with the set of r
> values having p's > 0.2).
In other words, they measured here a rough indication of how long the
people had been 'diseased'; again no separation of neuroleptic effects
vs. 'schizophrenia'.
> Neuroleptic dosage studies in animals
> show that neuroleptics induce plastic changes, including enlargement
> of neural elements, that may be reversible at the ultrastructural
> level, but thus far have not examined whole structure volumetric
> changes (Benes et al., 1983; 1985; Klintzova et al., 1989; Meshul et
> al., 1989). Such animal studies, as well as follow-up studies of first
> episode patients (e.g., Chakos et al., 1994), may help answer the
> question of whether the enlargement is neuroleptic-related, partly or
> completely.
Studies of brain changes in 'schizophrenia' vs from neuroleptics seem
difficult to obtain, since the 'schizophrenics' who aren't medicated
are generally refugees from psychiatry and not likely to come in to be
studied. But, it seems there is a large body of evidence about
brain changes that could be from neuroleptics, only the convention is
that one is studying 'schizophrenia', not major tranquilizers. So
animal studies would seem to be very relevant here: what happens to,
say, a chimpanzee if it's drugged with a neuroleptic for 10 years,
if it hasn't been abducted by an animal-rights activist first?
I don't know of any long-term studies on chimps, but shorter-term
animal studies show brain damage.
Peter Breggin's review article in the Journal of Mind and Behavior,
Autumn 1990, lists a number of animal studies which show cell degeneration
and death in the basal ganglia in rats from neuroleptic drugs. Also
a study about inducing tardive dyskinesia in rats, I guess with
neuroleptic drugs.
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