PSYCHIATRIC DRUGS THAT WOULD BE USED, MAY LEAD TO CHANGES IN SIZE
AND SHAPE OF BRAIN!
Nearly 40 states in the USA now have laws allowing courts to
order people to take powerful psychiatric drugs against their
will, even while living out in the community in the sanctity of
their own homes. These "involuntary outpatient
commitment" laws are quietly spreading internationally.
NOW is the time to fax/phone/write to the New York State
Commissioner of Mental Health to STOP a bill promoting this
forced outpatient psychiatric drugging. Such a bill can impact
everyone by establishing a precedent.
And this is the same government that says it has a "war
against drugs"?
Whether you live in -- or out -- of New York State, show that the
whole world is watching! Don't let any more homes be made into
wards!
RECENT BRAIN SCAN STUDIES SHOW THESE PSYCHIATRIC DRUGS CAN ALTER
BRAIN
Recent medical studies using CT and MRI scans show that the
chemicals used in these forced druggings -- the
"neuroleptics" such as Haldol, Prolixin, Thorazine,
Mellaril, Stelazine, Navane, etc. -- may in the long run alter
the actual size and shape of the brain. [Citations for these two
important brain scan studies are at THE VERY BOTTOM of this
alert: scroll down.]
These neuroleptic-induced brain changes may explain why quitting
neuroleptics can cause such a hellish "rebound" effect
for months, in which the subject may experience worse emotional
and mental problems than before they even started taking the
neuroleptics. Neuroleptic "discontinuation syndrome" is
often seen in the medical literature. [Citation example: J Clin
Psychiatry 1997 Jun; 58(6):252-5; "Clozapine withdrawal
resulting in delirium with psychosis: a report of three
cases."]
Many people willingly choose to take neuroleptics. But forcing
these drugs into the community is far more insidious than the
cigarettes once pushed by "Joe Camel." Two studies show
African Americans are far more likely to get long-acting depot
neuroleptics, and at higher doses. [Citations: See American
Psychiatric Association's _Psychiatric Services_ 3/96 and 1/94.]
Neuroleptic manfuacturers themselves warn their products are
associated with the ultimate side effect -- death, such as by
neuroleptic malignant syndrome, choking, over-heating,
"sudden unexplained death," etc.
The main pusher of the forced drug bill is the extremist
Treatment Advocacy Center, which is funded by the millionaire
Stanley family, and headed by psychiatrist E. Fuller Torrey. TAC
is misleading the public by calling their forced drug proposal
"assisted treatment."
TAC is now lobbying Commissioner Jim Stone. Let him hear from you
instead! If Commissioner Jim Stone can be convinced not to push
this legislation, your action may help kill the forced outpatient
drugging bill. ACT NOW!
A sample comment you can send to the Commissioner: "If you
endorse 'customer empowerment,' then are you listening to the
thousands of New York State psychiatric survivors and allies who
are united in opposition to this dangerous proposal? Human rights
violations don't help anyone!"
* * * * * A C T I O N * * * * *
WRITE NOW:
Jim Stone, Commissioner
New York State Office of Mental Health
44 Holland Ave
Albany NY 12229 USA
FAX NOW: 518-474-2149
PHONE NOW: 518-474-4403
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ CITATIONS ABOUT
TWO STUDIES LINKING NEUROLEPTIC DRUGS TO CHANGES OF BRAIN SIZE
AND SHAPE: ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
These two brain scan studies link neuroleptics to changes in the
shape of the brain: subcortial brain swelling, and frontal brain
shrinkage.
1. MRI BRAIN SCAN STUDY LINKS NEUROLEPTICS TO BRAIN SIZE/SHAPE
CHANGE
This MRI scan study concludes that neuroleptics seem to be
responsible for subcortical brain swelling.
To read full article and see MRI scan photos go to:
http://ajp.psychiatryonline.org/cgi/content/full/155/12/1711
Citation: American Journal of Psychiatry, December 1998,
"Subcortical MRI Volumes in Neuroleptic-Naive and Treated
Patients with Schizophrenia."
For a copy of article write to: Dr. Raquel E. Gur;
Neuropsychiatry Section; University of Pennsylvania Medical
Center, 10th Floor; Gates Bldg.; Philadelphia, PA 19104 USA.
2. CT BRAIN SCAN STUDY LINKS NEUROLEPTICS TO BRAIN SIZE/SHAPE
CHANGE
Researchers use longitudinal CT scans to reveal frontal brain
shrinkage associated with neuroleptic use. Conclusion: "The
estimated risk of atrophy increases by 6.5% for every additional
10 g neuroleptic drug."
Below is full text. Address to ask researchers in Denmark for a
copy of study is at bottom.
Citation: The Lancet, Sept 5, 1998 v352 n9130 p784(1).
Title: "Neuroleptics in progressive structural brain
abnormalities in psychiatric illness."
Authors: Al Madsen, N Keiding, A Karle, S Esbjerg, R Hemmingsen
Progressive abnormalities have been reported in schizophrenic
patients.1 We did a prospective, longitudinal study of brain
structure. 31 drug-naive psychotic patients underwent computed
tomography (CT) at first admission to hospital and after 5 years
of illness. We obtained written informed consent from all
patients. A radiologist masked to the patients' identities and
diagnoses, date of scans, and the nature of the study compared
the first and second CT scans. Brain atrophy was assessed on a
visual scale, on which 0-1 meant no changes or dubious atrophy
and 2-3 meant moderate or severe atrophic changes. After 5 years
of illness, we found significant progression of frontal atrophy
in 21 schizophrenic patients, compared with nine consecutively
included healthy volunteers. We saw progressive frontal atrophy
in ten non-schizophrenic patients, but to a lesser degree.
During follow-up, schizophrenic patients received a median of
172040 mg (range 19 540-928450) neuroleptic medication
(chlorpromazine equivalents). Seven non-schizophrenic patients
received a median of 20780 mg (range 678-141596). The only
atypical neuroleptic used was clozapine, administered to three
patients, always in high doses and in combination with
traditional neuroleptics.
Patients were thought to have a chronic, non-remittent course of
illness if all psychiatric records described a state of permanent
psychosis, and if they were psychotic at the time of the
reinvestigation. Some patients were described as remitted, but if
in long interviews they showed firm delusive systems that seemed
to be integrated but not necessarily overt parts of their lives,
and if they were judged to be permanently deluded, despite their
records, they were classified as non-remittent. This
classification was made without knowledge of the results of the
CT scans. Nine schizophrenic patients (eight men and one woman)
had been continuously psychotic during follow-up. At
reinvestigation, non-remittent patients had significantly higher
ratings for psychopathology (SANS and SAPS2) than remittent
patients.
Because of the small sample, we did exact tests in a logistic
regression analysis with LogXact, adjusted for sex, course of
illness, (remission/non-remission), diagnosis, and neuroleptic
load. Course of illness and diagnosis had no significant impact
on the development of frontal atrophy. Sex was significant
(p=0.035) if course of illness was not included into the model,
but sex became non-significant (p=0.138) if course of illness was
included. Neuroleptic load was significant whether sex was
included or not (p=0.013 and 0.0003, respectively). The estimated
risk of atrophy increases by 6.4% for each additional 10 g
neuroleptic drug. Non-remittent patients received a higher
neuroleptic dose than remittent patients, but the model was
corrected for this interaction.
Association has been shown between frontal atrophy or aplasia and
non-respondence to antipsychotic drugs,3 and neuroleptic
side-effects as tardive dyskinesia and akathisia have been
associated with wider sulci.4 These studies do not include
neuroleptic load as a possible explanatory factor for the
anormalities found. Traditional neuroleptics have been shown to
affect brain structure because they enhance the volume of basal
ganglia,5 but the potential impact of neuroleptics, on frontal
cortex, for example, is not known.
Factors causing progression of brain atrophy have not yet been
identified. Our study showed an unexpected effect of neuroleptic
medication on cerebral cortex, but our analysis suggests that the
results cannot be taken as accidental. Future longitudinal
studies of brain structure in schizophrenia are needed to show
whether atypical antipsychotic drugs may be more beneficial.
1. DeLisi LE, Sakuma M, Tew W, Kushner M, Hoff AL, Grimson R.
Schizophrenia as a chronic active brain process: a study of
progressive brain structural change subsequent to the onset of
schizophrenia. Psychiatr Res 1997; 7: 129-40.
2. Andreasen NC, Black DW, Introductory textbook of psychiatry.
Washington DC: American Psychiatric Press, 1991.
3. Friedman L, Knutson L, Shurell M, et al, Prefrontal sulcal
prominence is inversely related to response to clozapine in
schizophrenia. Biol Psychiatry 1991; 29: 865-77.
4. Sandyk R, Kay SR, Sulcal size and
neuroleptic-induced akathisia. Biol
Psychiatry 1990: 27: 466-67.
5. Frazier JA, Giedd JN, Kaysen D, et al. Childhood-onset
schizophrenia: brain MRI rescan after 2 years of clozapine
maintenance treatment. Am J Psychiatry 1996; 153: 4.
For copy of study write:
A. Madsen; Department of Psychiatry E
Bispebjerh Hospital
DK 2400 Copenhagen NV Denmark