Schizophrenia on Death Row: How Neuropsychiatry Could Help Protect Civil Rights

Introduction:

I write this piece today because, as a nurse, I feel it’s my professional obligation to educate and advocate. I only learned about the Scott Panetti case last weekend and was thoroughly disturbed, like many others, upon hearing media reports of the impending ethical disaster scheduled for this Wednesday, December 3rd. To understand my heavy-hearted and conflicted feelings, I read as many articles, research studies, and legal documents as I could up until writing this. I am a nursing student and am by no means a neurolaw or neuropsychiatric expert. Mental health professionals have indeed weighed in on the hearings, confirming symptoms and presence of disability; however, I did notice what seemed to be a lack of discussion revolving around the bias of stigma and societal misrepresentation of mental illness that undoubtedly influenced to the Court’s decision. To negate bias and bolster the past psychiatric testimonies confirming mental incompetence, the basic pathophysiology of the disease must be presented to the Court and should be supported by neuropsychiatric evidence to emphasize the true, organic, and degenerative nature of schizophrenia. I have presented my thoughts below in two related sections: The Ethical Dilemma and Much Needed Neuroscience and Education for Justice.

The Ethical Dilemma:

In less than two days, Texas will execute Scott Panetti, a severely mentally ill man who was convicted of murder in 1995 after representing himself in court dressed in a purple cowboy costume. Panetti, who had been hospitalized for acute exacerbations of schizophrenia several times throughout his life, was not taking his medications and was floridly psychotic, yet the court somehow deemed him competent enough to insist on representing himself. During the trial, he presented his medical records, which were covered in drawings and scripture, and he called upon over 200 witnesses including Jesus, Pope John Paul II, and John F. Kennedy. When he testified in court he appeared agitated and spoke of delusions in disorganized, tangential phrases. At some point, he spoke to the jury as his alter-ego “Sarge” whom he says committed the murders of his mother-in-law and father-in-law in 1992. Panetti has been on Death Row ever since.

Scott Panetti’s handwritten list of witnesses to be subpoenaed.

 Over the past several years, Panetti’s execution has been stayed many times, largely on the grounds of the 8th Amendment, which bans states from “inflicting the death penalty upon a prisoner who is insane”. Texas continued to battle with attorneys, essentially saying Panetti is sane enough to be executed. This prompted the US Supreme Court decision in 2007’s Panetti v. Quarterman, 551 U.S. 930 stating “A prisoner’s awareness of the State’s rationale for an execution is not the same as a rational understanding of it.”

Scott Panetti may be aware of his impending execution, however he clearly cannot rationally comprehend the reason: Panetti currently believes Satan, working through the State of Texas, wants to kill him this week to prevent him from preaching scripture to fellow inmates. Despite the above stated legislature designed to protect the mentally ill; despite extensive evidence of mental disability; and despite numerous international petitions for clemency, the Texas Court of Criminal Appeals continues to uphold its decision to execute Scott Panetti on December 3, 2014. As Ron S. Honberg, J.D., National Director of Policy and Legal Affairs at NAMI, the National Alliance on Mental Illness, writes in his recent Los Angeles Times Op-Ed piece, if the State of Texas carries out Panetti’s death sentence, it will be one of the “most outrageous executions of our time” demonstrating the United States’ failure “to protect the inherent dignity and civil rights of Americans with mental illness when they come into the criminal justice system.”

Much Needed Neuroscience and Education for Justice:

The media too often represents sufferers of schizophrenia as scary, erratic, crazy people who hear voices and see things that don’t exist. It’s important to correct this inaccurate portrayal and educate the public about the lesser-appreciated trademarks of the disease, such as progressive cognitive deterioration and delusions.

Perhaps the most striking and telling form of evidence that could be easily appreciated by the untrained layperson is a set of MRIs, or magnetic resonance images, comparing a healthy brain image with a schizophrenic brain. With a bit of basic background information about the pathophysiological process, the layperson could be guided in analyzing the basic differences between the images.

fMRI Comparison of a normal brain (L) and a brain with chronic schizophrenia (R); exhibits decreased total volume, decreased gray matter and white matter, and enlarged ventricles commonly seen in patients with schizophrenia.

Challenging jurors to learn and to replace stigma with unbiased pathophysiology could possibly lead to better-informed decisions and a more just justice system.

We as mental health professionals can and should cite every bit of current research that could allow us to correct media misrepresentations and stress the true gravity of a schizophrenia diagnosis. In this case, neuroscientific evidence could have helped influenced a life or death decision and thwarted a civil rights disaster.

References

Ahmed, A., Buckley, P., Hanna, M. (2013). Neuroimaging Schizophrenia: A Picture Is Worth a Thousand Words, but Is It Saying Anything Important? Current Psychiatry Reports, 15.345. doi: 10.1007/s11920-012-0345-0.

Appelbaum, P. S. (2006). Insanity, guilty minds, and psychiatric testimony. Psychiatric Services, 57, 1370-1372. http://ps.psychiatryonline.org/doi/pdf/10.1176/ps.2006.57.10.1370.

Baskak, B., Baran, Z., Ozguven, H. D., Karaboga, I., Oner, O., Ozel Kizil, E. T., & Hosgoren, Y. (2014). Prefrontal activity measured by functional near infrared spectroscopy during probabilistic inference in subjects with persecutory delusions. Schizophrenia Research, doi:http://dx.doi.org/10.1016/j.schres.2014.11.011

Bo, S., Abu-Akel, A., & Kongerslev, M. (2014). Chapter 8 – metacognition as a framework to understanding the occurrence of aggression and violence in patients with schizophrenia. In P. H. L. D. Brüne (Ed.), Social cognition and metacognition in schizophrenia (pp. 137-149). San Diego: Academic Press. doi:http://dx.doi.org/10.1016/B978-0-12-405172-0.00008-9

Bo, S., Abu-Akel, A., Kongerslev, M., Haahr, U. H., & Simonsen, E. (2011). Risk factors for violence among patients with schizophrenia. Clinical Psychology Review, 31, 711-726. doi:http://dx.doi.org/10.1016/j.cpr.2011.03.002

Butters, M., Davies, S.J.C., Kalache, S.M., Kern, R.S., Liu, A.Y., Menon, M., Miranda, D., Mulsant, B.H., Voineskos, A.N., Rajji, T.K. (2014). The Impact of Aging, Cognition, and Symptoms on Functional Competence in Individuals With Schizophrenia Across the Lifespan. Schizophrenia Bulletin. doi: 10.1093/schbul/sbu114.

 

Kahn, R.S., Sommer, I.E. (2014). The Contribution of Neuroimaging to Understanding Schizophrenia; Past, Present, and Future. Schizophrenia Bulletin. doi:10.1093/schbul/sbu141

Bristow, E., Tabraham, P., Smedley, N., Ward, T., & Peters, E. (2014). Jumping to perceptions and to conclusions: Specificity to hallucinations and delusions. Schizophrenia Research, 154, 68-72. doi:http://dx.doi.org/10.1016/j.schres.2014.02.004

Corlett, P. R., Taylor, J. R., Wang, X. -., Fletcher, P. C., & Krystal, J. H. (2010). Toward a neurobiology of delusions. Progress in Neurobiology, 92, 345-369. doi:http://dx.doi.org/10.1016/j.pneurobio.2010.06.007

Hodgins, S. (2014). Among untreated violent offenders with schizophrenia, persecutory delusions are associated with violent recidivism. Evidence Based Mental Health, 17, 75-75. doi:10.1136/eb-2014-101859

Menon, M., Addington, J., & Remington, G. (2013). Examining cognitive biases in patients with delusions of reference. European Psychiatry, 28, 71-73. doi:http://dx.doi.org/10.1016/j.eurpsy.2011.03.005

Perlin, M. L. (2010). Good and bad, I defined these terms, quite clear no doubt somehow?: Neuroimaging and competency to be executed after panetti. Behavioral Sciences & the Law, 28, 671-689. doi:10.1002/bsl.955

Poletti, M., & Sambataro, F. (2013). The development of delusion revisited: A transdiagnostic framework. Psychiatry Research, 210, 1245-1259. doi:http://dx.doi.org/10.1016/j.psychres.2013.07.032

Stilwell, E. N., Yates, S. E., & Brahm, N. C. (2011). Violence among persons diagnosed with schizophrenia: How pharmacists can help. Research in Social and Administrative Pharmacy, 7, 421-429. doi:http://dx.doi.org/10.1016/j.sapharm.2010.11.002

Walsh, A., & Yun, I. (2013). Schizophrenia: Causes, crime, and implications for criminology and criminal justice. International Journal of Law, Crime and Justice, 41, 188-202. doi:http://dx.doi.org/10.1016/j.ijlcj.2013.04.003

 

Nicotine and Schizophrenia

Smoking rates are extremely high in schizophrenic patients. Currently, in the United States 25-30% of the general population smokes: However, nearly 90% of schizophrenics are smokers (Schizophrenia and Smoking, 2006).

Many theories have been investigated as to why the prevalence of smoking is nearly three times higher in schizophrenics. There has been evidence indicating that nicotine might be therapeutic towards the negative symptoms of schizophrenia. Negative symptoms of schizophrenia can be a lack of interest in or inability to complete activities, a lack of emotion, a lack of motivation, social withdrawal and/or lack of personal hygiene. A large study in China found smokers (regardless of pharmacologic intervention) had significantly fewer negative symptoms according to the Positive and Negative Syndrome scale than non-smoking schizophrenics. However, smoking had no effect on positive, cognitive, or depressive symptoms (Pederson, 2013).  Also, two independent studies by Yale in 2005 and Columbia in 2004 found that nicotine was associated with better concentration and short term memory in schizophrenic patients (Schizophrenia and Smoking, 2006). Additionally, a study at the University of Colorado found that schizophrenics were less likely to be ‘startled’ by external stimuli if they had nicotine in their system (Schizophrenia and Smoking, 2006).

In addition to the cognitive effects nicotine has on the schizophrenic mind, nicotine also affects the metabolism of many anti-psychotic drugs. Nicotine activates the P-450 1A2 (CYP1A2) hepatic enzyme so anti-psychotic drugs (particularly the atypicals such as clozapine and olanzapine) are metabolized more quickly (Eden Evins, 2008). Interestingly, nicotine helped prevent some of the adverse effects of the drugs such as weight gain and extrapyramidal symptoms, even with the higher doses given to smokers to counteract increased enzymatic activity (Levin, 1996). Also, in animal studies nicotine had been shown to improve the inattention brought on by haloperidol, risperidone and clozapine (Eden Evins, 2008). If the drug is not titered in smokers to compensate for its rapid metabolism, symptoms may return at varying levels: Some patients find might find this to be a positive or negative effect and might subconsciously alter their smoking habits accordingly.

While there is evidence explaining why schizophrenics might ‘self-medicate’ by smoking, either to improve everyday functioning by limiting their negative symptoms of schizophrenia and/or to counter the effects of the often unpleasant drugs practitioners prescribe to patients, we must consider the negative effects of nicotine products on our patient’s physical and mental health. According to the Center for Disease Control and Prevention smoking puts one at risk for cancer, heart disease, diabetes and stroke (2014). Patients on atypical anti-psychotics are already at risk for developing metabolic side effects from the drugs, putting these patients at high risk for heart disease, stroke and diabetes without smoking. So there is a huge concern with allowing smoking from a physical health standpoint in schizophrenic patients who are on the currently recommended drug treatment plan due to increased health risks.

From an addiction standpoint, it had been found in autopsies that schizophrenics have fewer nicotine receptors throughout their brain and in their hippocampus (Eden Evins, 2006). This lack of receptors leads to heavy smoking and a stronger dependence nicotine delivering devices, as schizophrenic patients need more nicotine than a non-schizophrenic person to achieve the desired effects of smoking. As biologically prone schizophrenics are to nicotine dependence, the effects of addiction can be more harmful than in other patient populations and might lead to increased impairment of mental, physical, and social functioning.

The risks of using tobacco products for schizophrenics to get any amount of therapeutic nicotine is dangerous from an addition and physical health standpoint. However, the question then becomes what about using pure nicotine as a pharmaceutical agent? Many of the positive effects schizophrenics have had from smoking have been seen with nicotine patches and gums. However these ‘smoke-less’ nicotine products are still extremely addicting to patients. It can also assumed that most insurance companies with only supply these products for smoking cessation, but not as a long term therapeutic until more research is done on the topic.

Currently there a few cholinergic agonists on the market, but most of these drugs work on muscarinic receptors as opposed to nicotinic receptors. Of the cholinergic agonist drugs on the market none are approved for psychiatric treatment. However, companies such as Targacept, Roche, and Abbott Laboratories have clinical trials focusing on treating major depressive disorder, Alzheimer’s disease and attention deficit hyperactivity disorder respectively by focusing on nicotinic receptors (Wikipedia, 2014). While it is still early in the process in a few years hopefully there will be a new range of nicotinic psychiatric drugs for many mental illnesses and another schizophrenia drug on the market.

As it stands today most schizophrenic patients are smokers and with the metabolic risks associated with atypical anti-psychotics, practitioners should not be promoting the use tobacco products to use nicotine as therapy. A discussion between the patient (or caregiver) and the practitioner should promote smoking cessation.  Information on quitting smoking can be found on the Center for Disease Control’s website at http://www.cdc.gov/TOBACCO/quit_smoking/cessation/.

 

 

References

Aden Evins, A. “Nicotine Dependence in Schizophrenia: Prevalence, Mechanisms, and Implications for Treatment.” Psychiatric Times. N.p., 1 Mar. 2008. Web. 30 Nov. 2014. <http://www.psychiatrictimes.com/schizophrenia/nicotine-dependence-schizophrenia-prevalence-mechanisms-and-implications-treatment>.

“Health Effects of Cigarette Smoking.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 06 Feb. 2014. Web. 29 Nov. 2014. <http://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_cig_smoking/>.

Levin ED, Wilson W, Rose JE, McEvoy J. Nicotine-haloperidol interactions and cognitive performance in schizophrenics. Neuropsychopharmacology. 1996; 15:429-436. – See more at: http://www.psychiatrictimes.com/schizophrenia/nicotine-dependence-schizophrenia-prevalence-mechanisms-and-implications-treatment/page/0/2#sthash.dnlx5UNI.dpuf

“Nicotinic Agonist.” Wikipedia. Wikimedia Foundation, 29 Nov. 2014. Web. 01 Dec. 2014. <http://en.wikipedia.org/wiki/Nicotinic_agonist>.

Pederson, Traci. “Nicotine Therapy for Schizophrenia?” Psych Central.com. N.p., 7 Sept. 2013. Web. 30 Nov. 2014. <http://psychcentral.com/news/2013/09/08/nicotine-therapy-for-schizophrenia/59285.html>.

“Schizophrenia and Smoking.” Schizophrenia. N.p., 1 Mar. 2006. Web. 30 Nov. 2014. <http://www.schizophrenia.com/smokereport.htm>.