Comments on Prison Health Care Standards

Health Care Standards in Prisions

August 29, 2001

To: National Commission on Correctional Health Care ncchc@ncchc.org

From: David Oaks - Support Coalition International dendron@efn.org

Subject: Comments about NCCHC HEALTH CARE STANDARDS

Comments about NCCHC HEALTH CARE STANDARDS

As you know, the U.S.A. National Commission on Correctional Health Care (NCCHC) has issued a rough draft of its new "HEALTH CARE STANDARDS," and has requested public comment. We understand the last day for this public comment on your rough draft is on September 15, 2001.

As requested by NCCHC, below are comments from Support Coalition International regarding the rough draft of the NCCHC HEALTH CARE STANDARDS, as posted on the web at the URL: http://208.209.200.23/new/jails.html.

Support Coalition International is a non-profit alliance of 100 grassroots groups working for human rights of people labeled with mental disabilities. Support Coalition International is registered with the United Nations as a Non-Governmental Organization with Consultative Roster Status. Our office is in Eugene, Oregon.

While open to all, the vast majority of leadership and members of Support Coalition International are individuals who have personally experienced human rights violations in the mental health system. For more than a decade we have worked for human rights of people diagnosed with psychiatric disabilities.

We have five main areas requesting changes and additions to NCCHC HEALTH CARE STANDARDS. Our comments are specifically about sections: P52, P69, J51, AND J68.

THE ROUGH DRAFT OF THE NCCHC HEALTH CARE STANDARDS HAS INADEQUATE INFORMATION ABOUT FULL INFORMED CONSENT AND HAZARDS OF PSYCHIATRIC PHARMACEUTICALS.

These cited sections do not adequately require prisons staff to understand the importance of full informed consent about the hazards of prescribed psychiatric pharmaceuticals. We note that in the physical restraint section the problem of "blood clotting" is brought up. However, administration of psychiatric drugs in a prison setting frequently amounts to voluntary or coercive "chemical restraint."

The Physicians Desk Reference lists a wide variety of serious hazards from psychiatric drugs. Among the strongest family of psychiatric drugs is the "neuroleptics," and this category requires special attention. At the bottom of these comments are a few of the many medical citations available in scientific literature regarding neuroleptic-induced changes to the brain, including the structure of the brain.

A related phenomenon is "discontinuation syndrome" after taking neuroleptics for a significant period of time. In other words, this is a form of addiction, dependency and withdrawal. The brain adjusts to the powerful neuroleptics; when the neuroleptics are then removed -- even gradually -- the individual can experience even worse mental and emotional problems than they originally had before the prescription began.

Prison officials have a justifiable need to know about the discontinuation syndrome for neuroleptics for prison security reasons. Similarly, prison officials have a justifiable need to know that stimulants such as Prozac (SSRI's) and Ritalin can help promote mental and emotional problems, including aggressiveness.

It is a compelling statement today in the advocacy field today that "our jails and prisons have become the largest psychiatric wards and these people need care, not just incarceration." However, we note that a number of these advocacy organizations have received a large amount of funding from the pharmaceutical industry; too often, what they mean by "care" is simply the increased use of prescribed psychiatric drugs.

Support Coalition International supports the choice of individuals about prescribed pharmaceuticals; many of our members choose to take prescribed psychiatric drugs. But we do believe the imposition of "chemical prisons" just makes the problems of brick & mortar prisons worse.
INADEQUATE EMPHASIS ON ALTERNATIVES TO PSYCHIATRIC DRUGS.

Individuals in a prison or jail setting should be offered a wide range of voluntary alternatives.

We do note that the draft goes out of its way to say that help should include "more than psychotropics." The implication from this and another reference is that the bedrock of "mental health care" is psychiatric drugs; and *additional* help should be available on top of that. However, we feel that there should be an emphasis that "alternatives to psychotropics" should be included, "instead of" psychiatric drugs, for those who wish it.

The scope of our comments here does not allow an in-depth discussion of the power of the pharmaceutical industry today.

We can only note the irony that many individuals now incarcerated in the prison system are there because of substance abuse problems; yet in prisons and jails many are then prescribed similar neurotransmitter stimulants such as Ritalin, Prozac, etc. You will find a ready acceptance for these drugs among those with dependency problems; but does anyone see the irony? And another irony we can only note: Some incarcerated are even forced to take neurotransmitter suppressors such as neuroleptics; so they are locked up for taking a drug, but then forced to take another drug.

To sum up, NCCHC HEALTH CARE STANDARDS should include a greater emphasis on a variety of alternatives.

For example, peer support group is not mentioned as a special and important type of group support, which is only mentioned generally.

Also, prison officials should become aware that a great many innovative alternatives are available that do not necessarily add prohibitive expenses for a prison population. These can include educational approaches, art, spirituality, exercise, yoga, accupuncture, massage. Because the dominant paradigm in the prison system excludes these alternatives, it is especially important that the NCCHC HEALTH CARE STANDARDS include an encouragement to have an open door to these approaches when available and appropriate.
INADEQUATE EMPHASIS ON VOLUNTARY APPROACHES

An extensive amount of information is available that voluntary approaches for mental and emotional healing are key to the long-term sustainable recovery of individuals.

Prison officials should be educated to offer voluntary alternatives. However, the length of the prison sentence, parole, release, privileges, etc. should specifically not be tied to whether or not an individual accepts any particular form of therapy. Individuals should not be forced to take psychiatric drugs as a condition of release from incarceration. Deciding to say "no" to a powerful chemical that can change the structure of the brain should not effect the length of one's sentence.

Also, it is not enough to simply refer to Washington v. Harper and other case law when discussing involuntary procedures.

Since Washington v. Harper, there has been more and more evidence, for example, that neuroleptics can alter the structure of the brain (again, see literature citations at bottom). Therefore, long-term neuroleptics are increasingly in the same category as psychosurgery and electroshock.

In other words, forced neuroleptics in a prison or jail setting amounts to cruel and unusual punishment, and a permanent violation of the First Amendment (by permanently impairing the right to free ideation). Forced neuroleptics can and do feel like debilitating torture to many of those who have received these powerful psychotropics.

The pharmaceutical industry has incorrectly reassured the public and prison officials that newer "atypical" neuroleptics no longer have the danger of previous neuroleptics. However, the atypicals apparently cause less permanent physical twitching such as "tardive dyskinesia" (though all atypicals still produce this phenomenon) But the overall impact of atypicals can be worse than the original neuroleptics, especially in terms of the impact on higher level brain function. The atypicals tend to focus on the receptors in the higher level functioning area of the brain; therefore, the permanent impact there may be greater.

AT THE BOTTOM of this comment you will find citations about neuroleptic-induced brain changes. We very much doubt that prison officials are aware of this. In fact, many medical professionals today are not aware of this issue. This is where the issue of tobacco was back in the 1950's.

While NCCHC may or may not include this information in their new standards, at least the record will show that NCCHC was alerted about these problems. We request that this comment be placed in your permanent records.
NCCHC HEALTH CARE STANDARDS SHOULD INCLUDE EXPLICIT PROHIBITION OF ELECTROSHOCK, AND OTHER INTRUSIVE IRREVERSIBLE PROCEDURES

Support Coalition International has a stand against the medical use of electroconvulsive therapy (ECT). As cited above, psychosurgery is outlawed in the USA prison system (though it does still go on in the non-prison population, such as at Massachusetts General Hospital).

Similarly, electroconvulsive therapy should be strictly and explicitly outlawed from use in the prison and jail systems. You can refer to our web site for more information about that, along with web sites for sponsor groups: http://www.MindFreedom.org, http://www.ect.org, http://breggin.com. You will also find on some of these web sites more information about the hazards of psychiatric drugs, and the funding of some advocacy groups by the psychiatric drug industry. The same applies to other especially intrusive and controversial psychiatric procedures.

This should include explicit prohibition of any "aversive therapy" procedures involving pain.
NCCHC HEALTH CARE STANDARDS SHOULD INCLUDE INPUT FROM THE PSYCHIATRIC AND EX-PRISONER POPULATION

For too many years, our prison and jail systems -- intentionally or not -- have been crushed the spirits of individuals, and actually increased recidivism.

It is important to hear from individuals who have personally experienced human rights violations through the "mental health system," and the jail/prison systems. These individuals often have insight into what can actually decreased recidivism.

The psychiatric survivor and prisoner and ex-prisoner populations are part of the poorest groups in the USA; their input should be sought about designing programs which will actually lead to long-term recovery and rehabilitation.

We feel there has been inadequate outreach to this population, and inadequate opportunity to comment by this population, regarding the NCCHC HEALTH CARE STANDARDS. Therefore, we request an extension of time for this population to provide input. Further, we request that some NCCHC resources be specifically devoted to the difficult and challenging work of reaching out, locating and obtaining comments from these marginalized, disenfranchized, poor, powerless, and silenced populations.

Sincerely,
David Oaks,
Director Support Coalition International
454 Willamette, Suite 216
PO Box 11284
Eugene, OR 97440-3484
USA e-mail: oaks@mindfreedom.org
general info: office@MindFreedom.org
web: http://www.MindFreedom.org
phone: (541) 345-9106
toll free in USA: 1-877-MAD-PRIDE
fax: (541) 345-3737

Support Coalition International is a non-profit federation of 100 grassroots groups united to win human rights and humane alternatives for people labeled with mental disabilities.

Recent evidence of brain changes in humans associated with neuroleptic drugs:

Gur, R.E., Maany, V., Mozley, P.D., Swanson, C., Bilker, W., & Gur, R.C. (1998). Subcortical MRI volumes in neuroleptic-naive and treated patients with schizophrenia. American Journal of Psychiatry, 155 (12), 1711-1717. Using MRI imaging, this study monitored changes in the size of the basal ganglia and thalamic regions of the brain as patients were treated with neuroleptic drugs. Treatment by neuroleptics increased the area of both regions. For typical neuroleptics, a higher dose was associated with a size increase in multiple areas, while atypcal neuroleptics increased the volume only of the thalamic portion. Furthermore, these researchers reported that increased size of these portions of the brain is associated with greater severity of symptoms. In other words, the patient's brains were being changed in ways that would likely make it more difficult for them to ever withdraw from neuroleptic

Chakos, M.H., Lieberman, J.A., Bilder, R.M., Borenstein, M., Lerner, G., Bogerts, B., Wu, H., Kinon, B., & Ashtari, M. (1994). Increase in caudate nuclei volumes of first-episode schizophrenic patients taking antipsychotic drugs. American Journal of Psychiatry 151 (10) 1430- 1436. Based on MRI measurements of patients who initially had under 12 weeks of lifetime exposure to neuroleptics, and comparison with data after 18 months of treatment, the authors concluded that "caudate enlargement occurs early in the course of treatment in young first-episode schizophrenic patients. This may be a result of an interaction between neuroleptic treatment and the plasticity of dopaminergic neuronal systems in young patients." It was known prior to this study that chronically treated patients had increased volumes in this portion of their brains, but it had been thought this was due to the disease and not the treatment...drugs.

1998. Neuroleptics in progressive structural brain abnormalities in psychiatric illness.(Research Letters). The Lancet, 352 (9130) 784. This was a longitudinal study of patients, some schizophrenic, some not, from the beginning of their treatment with neuroleptics until 5 years later. Before and after scans of the brain were done using computed tomography (CT). The finding was that diagnosis had no significant impact on the development of frontal atrophy, but that "the estimated risk of atrophy increases by 6.4% for each additional 10 g neuroleptic drug."

Gur, R.E, Cowell, P., Turetsky, B.I., Gallacher, F., Cannon, ?, Bilker, W., & Gur, R.C. (1998) A follow-up magnetic resonance imaging study of schizophrenia. Archives of General Psychiatry, 55 145-152. This study looked at changes in the frontal and temporal lobes of the brains of schizophrenics over a period of about 31 months. They found that for first episode patients, "higher medication dose was associated with greater reduction in frontal and temporal volume r = -0.75 and -0.66 respectively; P<.001)." Volume reduction was associated with decline in some neurobehavioral functions.

Evidence that Tardive Dyskinesia [TD - a well-established form of neuroleptic-induced brain damage that can result in permanent twitching of face and limbs] involves brain changes that impact cognitive functioning:

Paulsen, J. S., Heaton, R.K., & Jeste, D.V. (1994). Neuropsychological impairment in tardive dyskinesia. Neuropsychology,8 (2), 227-241. The authors reviewed 31 published studies of neuropsychological testing comparing schizophrenics with and without TD. 24 of these studies, or 77%, found TD patients did worse on such tests. In an attempt to improve on past studies, the authors did their own study which matched patients with and without TD on a variety of measures, including duration and severity of illness. Those with TD demonstrated greater neuropsychological impairment, and those with more severe TD manifested greater neuropsychological impairment. The authors go on to discuss brain changes which may be associated with both TD and neuropsychological impairment, and concludes that "it is likely that TD involves an alteration of brain function that affects both motor and cognitive control."

Waddington, J.L., & Youssef, H.A. (1996). Cognitive dysfunction in chronic schizophrenia followed prospectively over 10 years and its longitudinal relationship to the emergence of tardive dyskinesia. Psychological Medicine, 26 681-688. Often the relationship between cognitive dysfunction and TD has been explained by suggesting that those with underlying cognitive dysfunctions are more prone to TD. This study sharply contradicts that explanation. The authors followed the cognitive functioning of a group of chronic schizophrenic patients over 10 years. Most were stable in regards to cognitive functioning: the exceptions were the individuals who developed TD during the course of the study. The authors write that "Those patients demonstrating prospectively the emergence of orofacial dyskinesia showed a marked deterioration in their cognitive function over the same time-frame withing which their movement disorder emerged, but this decline did not progress thereafter." The authors conclude that the cognitive changes are related to the patho-physiological process which also results in TD.

Sachdev, P., Hume, F., Toohey, P., & Doutney, C. (1996). Negative symptoms, cognitive dysfunction, tardive akathisia and tardive dyskinesia. Acta Psychiatrica Scandinavica, 93 (6), 451-459. The authors, in their literature review, point out that while there are some studies that do not find a relationship between TD and cognitive deficits, there are many that do show a positive relationship between TD and cognitive deficits and none that show the opposite relationship. In the current study, TD was shown to be related to cognitive deficits, while tardive akathisia was shown to be even more strongly related to cognitive deficits. While the authors do not see this as proving that neuroleptics cause cognitive deficits, they recommend considering the possibility, and they compare TD and TA with other movement disorders such as Parkinson's disease and Huntington's disease, in which neuropsychological deficits and even subcortical dementia are known to occur.

Wade, J.B., Lehmann, L., Hart, R., Linden, D., Novak, T., & Hamer, R. (1989). Cognitive changes associated with tardive dyskinesia. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 1 (3), 217-227. "The results of multip regression analysis revealed a modest linear relationship between TD and cognition (p<.04) after controlling for the effects of years of illness, duration of hospitalization, motor speed, severity of illness, and medication." The authors conclude that "our findings suggest that TD may represent both a motor and dementing disorder regardless of major psychiatric diagnosis."

Famuyiwa, O.O., Eccleston, D., Donaldson, A.A., & Garside, R.F. (1979). Tardive dyskinesia and dementia. British Journal of Psychiatriy, 135 500-504. Schizophrenics both with and without tardive dyskinesia were compared with both EMI scans and psychological tests of intellectual function. Those with TD did worse on the tests, and it was suggested that the higher incidence of pathology in that group might be related to chronic neuroleptic toxicity.

Edwards, H. (1970). The significance of brain damage in persistant oral dyskinesia. British Journal of Psychiatry, 116, 271-275. The author sought to discover whether brain damage could be an important contributory cause of TD. To examine that possibility, he compared two samples matched for phenothiazine intake and age, one sample with TD, the other without. Both groups were checked for brain damage and dementia. 28 out of 34 in the group with TD, versus 14 out of 34 controls, showed at least some brain damage. Edwards mostly focused on brain damage putting patients at risk for TD, but he also raised the possibility that the drugs themselves cause permanent neurological damage.

Wade, J.B., Taylor, M.A., Kasprisin, A., Rosenberg, S., & Fiducia, D. (1987). Tardive dyskinesia and cognitive imparment. Biological Psychiatry, 22 393-395. Because not all studies have found a relationship between tardive dyskinesia and cognitive functioning, the authors conducted a study using tasks known to find cognitive impairment in Parkinson's and Huntington's diseases. These tasks were chosen because the authors believed these diseases might provide a neuropsychological, as well as a biochemical, model for TD. The authors found a modest but significant linear relationship between TD and reduced cognitive functioning, where those with the most severe forms of the disorder were most impaired cognitively.

Neuroleptics increase cognitive decline in elderly people with dementia:

McShane, R., Keene, J., Gedling, K., Fairburn, C., Jacoby, R., & Hope, T. (1997). Do neuroleptic drugs hasten cognitive decline in dementia? Prospective study with necropsy follow up. British Medical Journal, 314 (7076), 266-271. This study looked at the impact of long term use of neuroleptics on the cognitive function of elderly people with dementia. It found that cognitive function declined twice as fast in those taking neuroleptics as in those not on neuroleptics. Brain differences were not found at autopsy, which means either that the cognitive decline was functional only, or that the brain differences escaped detection by the methods these researchers used.

A sampling of some of the animal studies showing brain changes afer neuroleptics:

Benes, F.M., Paskevich, P.A., Davidson, J., & Domesick, V.B. (1985) The effects of haloperidol on synaptic patterns in the rat striatum. Brain Research, 329, 265-274. This study finds changes in cell size and in number of vesicles in rats in a particular part of their brain. The authors cite other studies which have also found changes in rat brains caused by neuroleptics. In their conclusion the authors state that "The results of this study provide further evidence that haloperidol can induce synaptic alterations in the rat central nervous system, an effect which we first noted in the rat substantia nigra."

Muller, P. & Seeman, P. (1977). Brain Neurotransmitter receptors after long-term haloperidol: dopamine, acetylcholine, serotonin, -Noradrenergic and naloxone receptors. Life Sciences 21, 1751-1758. This study looked at the effect of chronic haloperidol on a variety on neurotransmitters in rats. The authors concluded that "these results indicate that long-term haloperidol treatment produces rather selective increases in dopamine/neuroleptic receptors, without much change in 4 other types of receptors." The dopamine receptor changes were very significant though, ranging from 34 to 45%.

Burt, D.R., Creese, I., & Snyder, S.H. (1977). Antischizophrenic drugs: Chronic treatment elevates dopamine receptor binding in brain. Science, 196, 326-328. Another study looking at changes in dopamine receptors. "Chronic treatment of rats with the neuroleptic drugs haloperidol, fluphenazine , and reserpine elicits a 20 to 25 percent increase in striatal dopamine receptor binding assayed with Haloperidol."

Jeste, D.V., Lohr, J.B., & Manley, M. (1992). Study of neuropathologic changes in the striatum following 4, 8 and 12 months of treatment with fluphenazine in rats. Psychopharmacology, 106, 154-160. In the literature review of research over 3 decades, most studies listed found brain changes. The current study also found brain changes: a lower density of large neurons in the striatum of middle aged rats. Older rats did not show significant differences, which the authors felt was because the neuroleptics were accelerating the loss of large neurons which naturally die later as a result of aging.

Nielsen, E.B., & Lyon, M. (1978). Evidence for cell loss in corpus striatum after long-term treatment with a neuroleptic drug (flupenthixol) in rats. Psychopharmacology, 59 85-89. The authors found a 10% cell loss in one region of the rat's brains, which they concluded "further suggest that persistent irreversible anatomical changes can follow long-term neuroleptic treatment."

Pakkenberg, H., Fog, R., & Nilakantan, B. (1973) The long term effect of perphenazine enanthate on the rat brain. Some metabolic and anatomical observations. This study found a significant decrease in the number of nerve cells in the basal ganglia of rats under long-term treatment.

Chakos, M.H., Shirakawa, O., Lieberman, J., Lee, H., Bilder, R., & Tamminga, C.A. (1998). Striatal enlargement in rats chronically treated with neuroleptic. Biological Psychiatry, 44 (8), 675-684. The authors sought to find out whether the striatal enlargement found in humans treated with neuroleptics also occurred in rats. This was seen as important, since there remained the possibility that the changes in striatal volume seen to occur with neuroleptic treatment might be part of some disease process in human subjects with schizophrenia. Also, there had been some speculation that the apparent growth in the striatum of humans seen with MRI scans really were just changes in blood flow or metabolism. This study found, however, that rats experienced a similar growth in their striatum, as measured at autopsy. It also found that rats with movement disorders experienced greater growth in their striatum than did rats without such disorders. The authors, in their conclusion, state that "It is possible that neuroleptic-induced striatal volume changes play a role in the development of subtle cognitive impairment as well as the development of a movement disorder in vulnerable patients. An association between striatal enlargement and cognitive impairment has, in fact, been reported by Hokama et al (1995)."

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