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Psychiatric Neuroethics Studies in Research and Practice
Walter Glannon
1
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For Yee-Wah
Advance praise
‘This book is extraordinary as it addresses central and sometimes controversial issues in psychiatry, including its model of the mind–brain relation and ethical issues such as euthanasia. Walter Glannon, one of the leading experts in the philosophy of psychiatry, delivers an outstanding book which will, I am sure, become standard reading in the field and beyond.’
Georg Northoff
Mind, Brain Imaging and Neuroethics Research Unit
University of Ottawa Institute of Mental Health Research, Canada
‘As the big pharma have withdrawn from investing in the development of psychopharmaceuticals, the therapeutic void needs to be filled, and one of the ways to do so is by noninvasive and invasive neuromodulation. Walter Glannon bravely takes the lead in addressing and providing ethical guidance in how to embrace the new technology in real-world settings. A must-read and highly needed work for everybody who is interested or involved in the treatment of psychiatric brain disorders.’
Dirk De Ridder
Neurological Foundation Professor of Neurosurgery
University of Otago, New Zealand
‘In Psychiatric Neuroethics: Studies in Research and Practice, Walter Glannon combines a philosophical sensibility with an appreciation of psychiatry as a psycho-biological science of the brain as well as the mind. With precision, Glannon adroitly teases out ethical conflicts, treating a range of psychiatric interventions such as psychosurgery, neuromodulation, control of psychopathic behavior, and rationales for assisted suicide for psychiatric and neurodegenerative conditions. His critical analysis is an original contribution to psychiatry and neuroethics.’
Laurence R. Tancredi Clinical Professor of Psychiatry
New York University School of Medicine, USA
‘Walter Glannon’s Psychiatric Neuroethics provides keen insights into the intersecting domains of brain science, mental health practice, philosophy, ethics, and law. In addressing longstanding philosophical questions about the nature of the mind, self, and psychiatry as a discipline, Glannon presents a detailed examination of the ways in which ongoing neuroscientific research has been used, or in some cases misused, in the understanding, classification, diagnosis, and care of mental illness. This book affords a prudent perspective on neuroethical issues, questions, and possible solutions that are important in guiding applications of brain science in the clinical practices of the field-inevolution that is psychiatry.’
James Giordano Professor, Departments of Neurology and Biochemistry Chief, Neuroethics Studies Program Pellegrino Center for Clinical Bioethics Georgetown University Medical Center, USA
Acknowledgments
I thank my editors at Oxford University Press, Martin Baum, Charlotte Holloway, and Janine Fisher, for supporting and guiding this project. Three anonymous reviewers and the editors of the International Perspectives in Philosophy and Psychiatry (IPPP) series gave me helpful comments on the book proposal. For their comments on earlier versions of Chapter 5, I thank Nicole Vincent, Allan MacCay, Karen Rommelfanger, and Syd Johnson. Special thanks go to John Sadler for extensive and very helpful comments on earlier versions of Chapters 3 and 4 and to Dirk De Ridder for equally extensive and helpful comments on earlier versions of Chapters 4 and 5. Some sections of the book have appeared previously in journal articles and book chapters. I have benefited from the thoughtful and constructive reviews of the referees.
I presented some of the ideas in the book to audiences at the Neuroethics Unit of the Institut de recherches cliniques de Montreal, a conference on neuromodulation at the Brocher Foundation in Hermance, Switzerland, the Department of Neurosurgery of the University of Zurich Hospital, a philosophy colloquium at the University of Turku, and a conference on Neurointerventions and the Law at Georgia State University.
For discussion and correspondence, I am grateful to Jean-Pierre Changeux, Dirk De Ridder, Thomas Fuchs, Christian Ineichen, Nir Lipsman, Georg Northoff, Roger Pitman, Ulrike Rimmele, John Sadler, Daniel Schacter, Sigrid Sterckx, Teresa Yu, and Adam Zeman. I am especially grateful to John Sadler for encouraging me to submit my project proposal for consideration in the IPPP series and his continued support.
Introduction 1
1 A paradigm for psychiatry 15
2 Disorders of consciousness, memory, and will 51
3 Treating psychiatric disorders: Less invasive and noninvasive interventions 87
4 Psychiatric neurosurgery 135
5 Neuromodulation: Control, identity, and justice 185
6 Intervening in the psychopath’s brain 219
7 Euthanasia and assisted suicide for psychiatric disorders 251
8 Prediction and prevention 291 Epilogue: Psychiatry, neuroscience, philosophy 327
References 333 Index 369
Introduction
In 2013, data from the World Health Organization (WHO) World Mental Health Surveys indicated that mental illness constituted 7.4% of the global burden of disease and that its incidence and burden would increase exponentially in the future (Alonso, Chatterji, and He, 2013; Becker and Kleinman, 2013). This followed a 2012 estimate by the WHO that depression would be the leading cause of the global burden of all diseases by 2030 (World Health Organization, 2012). Schizophrenia, which is the most functionally disabling psychiatric disorder, affects approximately 24 million people worldwide. Mental illness is untreated or undertreated in many countries. These facts and estimates underscore the need for continued research that will lead to a better understanding of psychiatric disorders. This research may in turn lead to the development of safer and more effective therapies that will relieve or prevent the burden of disease experienced by millions of people.
Psychiatric Neuroethics is an analysis and discussion of questions at the intersection of psychiatry, neuroscience, philosophy, and law that have arisen from advances in psychiatric research and clinical psychiatric practice in the last 30 years. Are psychiatric disorders diseases of the brain, caused by dysfunctional neural circuits and neurotransmitters? What role do genes, neuroendocrine and neuroimmune interactions, and a person’s response to the environment play in the development of these disorders? How do different explanations of the etiology and pathophysiology of mental illness influence diagnosis, prognosis, and decisions about treatment? How do psychiatric disorders affect consciousness and agency? Could the presumed salutary effects of neural interventions for pathological thought and behavior change one’s mental states in undesirable ways? What are the ethical and social justice issues regarding access to treatment and experimental and innovative interventions for treatment-refractory conditions? What are the obligations of clinicians and researchers to patients and research subjects in psychiatry? Could the interests of society in preventing public harm override the cognitive liberty of criminal offenders with a psychiatric disorder to refuse an intervention in the brain? Would it be rational for a person with a chronic treatment-resistant disorder to request euthanasia or assisted suicide (EAS) as
the only way to end his suffering? Could psychiatric disorders be prevented? If so, then how could they be prevented? I raise and discuss these questions in a comprehensive, systematic, and thematically integrated way. The book is written for a multidisciplinary audience, including psychiatrists, neurologists, neurosurgeons, philosophers, psychologists, legal theorists, and informed lay readers.
These questions fall within the domain of neuroethics. This is an interdisciplinary field at the intersection of the brain sciences, radiology, cognitive psychology, philosophy, and law. In a seminal paper, Adina Roskies distinguished between two branches of neuroethics: the ethics of neuroscience and the neuroscience of ethics (2002, pp. 21–22). The first branch generally considers the risks and potential benefits to patients and research participants whose brains are mapped or monitored by structural and functional imaging, as well as when they are altered by drugs, surgery, and electrical or magnetic stimulation. The ethics of neuroscience also considers the decisions that patients and research subjects make in receiving treatments and participating in research in light of the potential benefits and risks. In addition, this branch of neuroethics pertains to the obligations of clinicians and investigators to benefit patients and protect them and research subjects from harm. The neuroscience of ethics generally pertains to the neurobiological basis of the mental capacity for rational and moral decision-making. In particular, this branch pertains to the capacity to understand the nature of one’s medical condition and make informed decisions to consent to treatment or participate in research. At a deeper level, Roskies asked whether future developments in neuroscience might cause us to revise our definition of “normal” behavior (2002, p. 22). She concluded by arguing that neuroethics should not be confined to specialists in neuroscience, philosophy, and law. It should also include public debate and broad social participation from all members of society in considering the implications of reading and changing people’s brains (2002, p. 23).
While acknowledging that the ethics of neuroscience and the neuroscience of ethics “can be pursued independently to a large extent,” Roskies noted that “perhaps most intriguing is to contemplate how progress in each will affect the other” (2002, p. 21). One example of overlap between the two branches of neuroethics is when a patient with a psychiatric disorder, such as schizophrenia or major depression, decides to accept or refuse an intervention in the brain or participate in research. This requires informed consent from the competent patient as an expression of his autonomy and ability to act in his own best interests. Respect for patient autonomy obligates the clinician or researcher to respect the patient’s decision regarding the intervention (ethics of neuroscience). Competence and consent presuppose the cognitive and emotional
capacity to weigh the potential benefits and risks of an approved or experimental intervention, the reasons for or against it, and to make an informed decision on this basis (neuroscience of ethics). This can be problematic if the disorder is moderately severe or severe and involves significant impairment in the relevant mental capacities. It may raise questions about whether the patient can meet the criteria of consent to receive therapy or participate in research.
I construe “neuroethics” broadly to include more than questions about the patient’s capacity to weigh the benefits against the risks of different interventions in the brain and the obligations of clinicians and researchers to protect patients and research subjects. In addition, neuroethics pertains to how psychiatric disorders can harm people by distorting the content of their mental states, impairing their will, and altering their identities. It also pertains to how certain therapies can benefit people by restoring mental content, the will, and the self to normal functional levels. In these respects, issues in the philosophy of mind as well as normative ethical theory can influence how we assess ethical issues in psychiatry. At the same time, psychiatry can influence how we assess questions in the philosophy of mind and normative ethics. Some philosophers may question the extent to which neuroscience and psychiatry can elucidate philosophical questions and provide guidance on how to address them. They may hold that psychological explanations are sufficient and that appeals to the brain add nothing to them. Yet the use of brain imaging in psychiatric research provides evidence that neural circuits and networks mediate psychomotor, cognitive, emotional, and volitional capacities associated with the mind, the will, and identity. Although imaging has its limitations, techniques such as computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), and functional magnetic resonance imaging (fMRI) showing structural and functional abnormalities in these circuits and pathways can help to explain why these capacities become impaired in major psychiatric disorders.
One of the best examples of how impaired reasoning and decision-making is traceable to brain damage and dysfunction is the case of Phineas Gage. This man lost many of his rational and moral capacities due to damage to his ventromedial prefrontal cortex from a metal projectile that penetrated this region of his brain while he was working on the Burlington and Northern Railroad in Vermont in 1848. The changes in Gage’s personality and behavior were so significant that “in the words of his friends and acquaintances, ‘Gage was no longer Gage’ ” (Damasio, Grabowski, Frank et al., 1994, p. 1102). In addition, functional neurosurgery on awake patients with neurological and psychiatric disorders can confirm that cognitive and emotional processing is mediated by different regions in the brain. Patients’ reports of their experiences from techniques that probe and modulate neural circuits validate the neurobiological basis of
their mental states. They can also confirm when dysfunction at the neural level manifests in dysfunction at the mental level.
Some cognitive psychologists and neuroscientists have claimed, or suggested, that knowledge of brain structure and function and its effects on the mind can completely explain, or explain away, the psychological aspects of concepts such as free will and personal identity (Wegner, 2002; Seung, 2013). They ignore the many ways in which the mind, body, and environment influence the brain, which rejects the neuroreductionism behind these claims. Although neuroscience in general and psychiatry in particular cannot provide a complete account of the mind, they can yield a better understanding of ordered and disordered mental states. As Georg Northoff points out, neuroscience enables us to “study the unwell brain for clues about the healthy mind” (2016, p. ix). Because the brain–mind relation underlies thought, identity, and agency, the implications of psychiatry for these philosophical questions are significant (Kendler and Parnas, 2012, 2014, 2017).
Since the declaration of the 1990s as the “Decade of the Brain,” much of the research in psychiatry has endeavored to explain psychiatric disorders in terms of dysfunctional neural circuits and neurotransmitters mediating motor and mental functions (Insel, 2010, p. 188). The gradual shift in focus from observed and reported symptoms in patients to the underlying neurobiology of mental illness has driven the field of biological psychiatry (Walter, 2013). In particular, this shift motivated the 2009 National Institute of Mental Health (NIMH) strategic plan that included the Research Domain Criteria (RDoC) as a research classification system for mental disorders (Insel, Cuthbert, Garvey et al., 2010; National Institute of Mental Health, 2011; Casey, Craddock, Cuthbert et al., 2013). While the RDoC focuses mainly on neural circuits, it also examines how genetics, the environment, and other processes influence brain structure and function, and how a synthesis, or “matrix,” of all of these factors can result in a better understanding of how psychiatric disorders develop and persist in people. The neural circuit-based criteria of the RDoC provide a necessary framework to complement the symptom-based criteria of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American Psychiatric Association, 2013) which until recently was the dominant paradigm for conceptualizing and classifying mental illness (Kendler and Parnas, 2017).
I avoid discussing mental disorders whose nosological status is ambiguous. Instead, I focus on what have been classified unambiguously as major psychiatric disorders. These include schizophrenia, major depressive disorder (MDD), bipolar disorder I and II (BD I and BD II), obsessive–compulsive disorder (OCD), generalized anxiety disorder (GAD), post-traumatic stress
disorder (PTSD), and anorexia nervosa (AN). I mention other disorders as well, though I consider them to be variants of the major disorders. I focus mainly on moderately severe to severe psychiatric disorders because most of the contentious ethical questions in psychiatry arise from predicting, diagnosing, and intervening in the brains of people who are affected by them. One possible exception to this categorization is psychopathy, which I discuss in Chapter 6. Although it should not be included in the same category as other disorders I have listed in terms of symptom severity and burden of disease, psychopathy is included in the DSM-5 as a specifier for antisocial personality disorder (p. 765). More importantly, this disorder has significant implications for the field of forensic psychiatry, particularly regarding the justification of interventions in the brains of criminal psychopaths to alter their behavior.
I do not take “mental disorder” to be a natural kind. A natural kind is defined in terms of how its properties combine in the natural world. It has an objective ontological status and is not the product of concepts we apply to the world. The criteria psychiatrists use to classify psychiatric disorders are the product of these concepts. Psychiatric nosology is not a naturalistic but an interpretive enterprise. It is objective in the sense that classification of major psychiatric disorders results from agreement among a community of researchers and clinicians in psychiatry. This is not just an empirical process but also a normative one. Psychiatrists interpret and agree, or disagree, on what data from brain imaging, overt symptoms, and other measures reveal about thought and behavior in diagnosing and treating psychiatric disorders. John Sadler points out that there are nonmoral and moral senses of normativity in psychiatry. He raises the question of whether psychiatric disorders should be considered “moral bads” warranting some form of moral judgment, or “nonmoral bads” like “medical diseases or surgical injuries” (2004, p. 221). Sadler writes, “I would like to make the, perhaps controversial, argument that mental disorders . . . should involve, substantively, non-moral evaluations in the core concepts, and such normative evaluations ‘filter up’ to define and constrain diagnostic criteria as well” (2004, p. 221).
The “moral bad” attribution to major psychiatric disorders has diminished over the last 50 years, thanks largely to research elucidating the processes underlying their etiology and pathophysiology. This research has helped to reduce some of the stigma attached to them (Sadler, 2009). Mental illness continues to be stigmatized to an unacceptable degree. Different interpretations of some of the causal factors of psychiatric disorders have impeded rather than promoted the elimination of stigma. Psychiatric genetics is one example. Raising ethical concerns about translating psychiatric genomics
research into mental healthcare, Camilla Kong, Michael Dunn, and Michael Parker state that “the genetic essentialism that is commonly associated with the genomics revolution in health care might inadvertently exacerbate stigma toward people with mental disorders” (2017, p. 1). In contrast, in their analysis and discussion of schizophrenia, Michael Owen, Akira Sawa, and Preben Mortensen state that “a genetic diagnosis might . . . have psychological benefits for patients and their families by reducing internalized stigma and self-blame” (2016, p. 88). Each of these comments attributes too much of a causal role to genetics in psychiatric disorders. How genes express themselves in the brain and influence brain function depends on epigenetic and environmental factors. This refutes any hint of genetic essentialism in psychiatry.
The idea of a genetic diagnosis based on identifiable mutations is equally problematic. Thomas Insel points out that “the diversity and private nature of these mutations preclude a simple genetic explanation for schizophrenia,” even though “these findings may yield important clues to pathophysiology” (2010, p. 188). Insel acknowledges that genetics is an important causal factor, but it is not the only causal factor in this disorder. While the genetic component is more significant in schizophrenia than in other psychiatric disorders, it is also a factor in bipolar disorder and depression. Yet the same qualifications about the causal import of psychiatric genomics in schizophrenia apply to these disorders as well. What contributes to the persistence of stigma is a primary or exclusive focus on one dimension of mental illness. Focusing solely or mainly on the psychological dimension may facilitate the dismissive comment that psychiatric disorders are “all in the mind.” The most effective way to reduce the stigma is for researchers and clinicians to educate the public that psychiatric disorders develop and persist not because of biological, psychological, or social processes operating independently of each other, but because of the interactions between all of them. This education should emphasize that therapies can take weeks, months, or even years to be effective. It should also point out that some disorders are treatment-resistant. For example, as many as 20% of depressed patients fail to respond to multiple treatments over many years (Holtzheimer and Mayberg, 2010, p. 1437, 2011, p. 2). The rate of treatment-resistance is even higher in other disorders. Knowledge of these facts could help to dispel the view that controlling symptoms and “curing” mental illness is simply a matter of taking the “right” pill. It could help to disabuse people of the attitude that, if symptoms persist, then the patient must be taking the “wrong” pill or otherwise doing something wrong. It may also help to emphasize that no two people’s brains are alike. How genes and other biological factors shape brain structure and function, how the brain responds to stress, and how it responds to drugs or techniques can vary considerably from one person to the
next. Ultimately, reducing stigma depends on families and colleagues of affected individuals making the necessary effort to inform themselves of the many causes and dimensions of mental illness (Thornicroft, Mehta, Clement et al., 2016).
Methodologically and structurally, Psychiatric Neuroethics is divided roughly into two parts. In Chapters 1 and 2, I examine and discuss different conceptions of psychiatric disorders in terms of their etiology, pathophysiology, and symptomatology and the ways in which they impair thought and behavior. In Chapters 3 through 8, I describe different interventions in the brains of people who have psychiatric disorders, as well as interventions in processes that occur before they exist, and discuss the ethical and broader philosophical questions these interventions raise. I interweave the science of psychiatry with the philosophy of psychiatry. Philosophical questions can be appropriately addressed only when they are appropriately framed by the science of the brain and mind. These questions arise from less and more invasive interventions to control and ameliorate symptoms. They become more pressing and controversial the more resistant the disorder is to treatment and the more invasive the treatments are. Most controversial is EAS for patients with treatment-resistant depression (TRD) and other disorders, where the intervention does not control but eliminates symptoms by ending the life of the person who experiences them. This underscores the need to prevent the onset of psychiatric disorders, or to slow or stop their progression at an early stage.
My discussion of the normative dimensions of psychiatry is not driven by a single ethical theory. Instead of selecting a theory and then discussing particular issues around it, I first raise the issues and then explicitly or implicitly appeal to a theory to explain why a particular course of action or policy is justifiable or unjustifiable. Questions about what to do in a particular case, or which policy to adopt, drive the application of the theory, rather than the other way around. A competent patient’s right to receive or refuse treatment or participate in research is based on deontology, as is the duty of clinicians and investigators to respect competent patients’ decisions and protect patients and research subjects. Concern about treatment outcomes in ameliorating symptoms and reducing side effects rests on consequentialism. Yet insofar as these outcomes are in the best interests of consenting patients, nonconsequentialism may guide ethical assessment of the key issues. Outcomes matter, but they are not the only factor that matters in evaluating an action or policy. Indeed, deontological, consequentialist, and nonconsequentialist considerations may all be relevant to a single issue.
We have to assess which theory has more weight in adjudicating competing moral claims about a course of action. In terms of the bioethical principles
corresponding to the ethical theories, I frame the ethical discussion by appealing to the standard principles of autonomy, nonmaleficence, beneficence, and justice (Beauchamp and Childress, 2012, Chapters 4–7). While these principles are limited in their scope of application to ethical debates in medicine, they serve my framing purpose for psychiatric neuroethics as well as any alternatives. Much of the discussion in this book addresses how psychiatric disorders impair control of thought and behavior, and how interventions in the brain can restore it. Control is a measure of autonomy in the sense that one’s motivational states and actions are one’s own. Autonomy is also germane to informed consent to participate in psychiatric research. This is significant given that many interventions for psychiatric disorders are still experimental. Nonmaleficence grounds researchers’ obligation to protect subjects enrolled in clinical trials from harm. Beneficence grounds clinicians’ obligations to provide patients with proven therapies consistent with best practices. Justice is germane to the question of whether patients with treatment-resistant psychiatric disorders have a right to participate in clinical trials testing experimental drugs and neuromodulation techniques. It is also germane to the question of whether subjects in clinical trials testing deep brain stimulation are entitled to retain a brain implant after the conclusion of these trials. I base most of my examples on actual cases, or hypothetical variants of them. This gives substance to the principles and the ethical and broader philosophical issues better than the fanciful thought experiments that are so common in armchair philosophy.
In addition to ethical questions surrounding standard forms of psychopharmacology, I examine some questions emerging from experimental use of the psychotropic drugs ketamine, psilocybin, and 3,4-methylenedioxymethamphetamine (MDMA) for depression and PTSD. I discuss newer closed-loop forms of deep brain stimulation (DBS) as a potentially safer and more effective form of neuromodulation than open-loop DBS. I also discuss optogenetics, focused ultrasound, and temporal interference as novel neuromodulating techniques for a range of psychiatric disorders. My discussion of ethical issues arising from historical, current and emerging interventions in the brain and mind shows the evolution of psychiatric neuroethics.
In Chapter 1, I define psychiatric disorders as disorders of the brain, mind, and the person’s relation to the world. The etiology, pathophysiology, and symptomatology of these disorders is influenced by interactions between the brain, mind, immune and endocrine systems, the subject’s perception of the body, and how the person responds to the environment. A biopsychosocial model provides the best account of the development of these disorders and a guide
for research and treatment. I discuss some of the merits and limitations of the symptom-based DSM-5 and the more recent circuit-based RDoC and claim that they can be complementary models in a paradigm for psychiatry research and clinical practice. Noting the considerable overlap in pathophysiology between neurological and psychiatric disorders, I argue that there are sound reasons for relaxing the strict distinction between the two disciplines. However, there are distinctive features of psychiatric disorders that warrant treating them separately in some respects. I defend nonreductive materialism as the theory best able to account for the different dimensions of the brain–mind relation in psychiatry. In addition, I propose that the self in psychiatry should not be defined solely in terms of conscious mental processes but as a complex set of conscious and nonconscious processes that emerge from and are shaped by many factors inside and outside of the brain.
I discuss major psychiatric disorders as disorders of consciousness, memory, and will in Chapter 2. Schizophrenia, major depression, and OCD are disorders of consciousness in the sense that they involve disturbances in how the brain processes and integrates information about the body and external world. Anxiety, panic, some forms of depression, and PTSD are disorders of memory content. The emotionally charged representation of a memory of a traumatic or disturbing experience can cause hyperactivation in the brain’s fear memory system and result in maladaptive responses to environmental stimuli. The distorted mental content in these psychopathologies impairs the capacity to consider different action plans, and to form and execute particular plans in particular actions. Dysfunctional mental states correlating with dysfunctional neural states impair the capacity for flexible behavior and adaptability to the environment. This dysfunction also impairs the capacity for insight into a psychiatric disorder and understanding the need for and motivation to seek treatment. In these respects, neural and mental dysfunction impairs free will. As disorders of consciousness, memory, and will, psychiatric disorders disable the capacity for autonomous agency.
In Chapter 3, I analyze and discuss different types of psychopharmacology. I cite the view held by some psychiatrists that drugs targeting monoamines to treat psychiatric disorders may be based on a mistaken hypothesis about the pathophysiology of these disorders. I mention recent research on the role of dysfunctional glutaminergic signaling and how novel pharmacological treatments such as ketamine and psilocybin for depression, and MDMA for PTSD, have considerable therapeutic potential. Questioning the distinction between noninvasive and invasive treatments in psychiatry, I point out that some presumably noninvasive treatments could be described as invasive because they can cause changes in the brain. This can occur in the absence of intracranial
surgery. I propose that the invasive–noninvasive distinction be replaced by a distinction between less and more invasive interventions, where the degree of invasiveness corresponds to the extent of changes the intervention induces in the brain. I discuss the potential benefits and risks, as well as the limitations of electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), and transcranial current stimulation (tCS). The indications for using TMS, tCS, and psychotropic drugs to treat psychiatric disorders support reasons for maintaining the distinction between therapy and enhancement. Placebos and neurofeedback (NFB) are distinct from the other interventions I consider because the cognitive and emotional responses of the patient to the physician or images of the patient’s brain can ameliorate symptoms without psychotropic drugs or neurostimulation. While deception and potential erosion of trust are the main ethical issues in using placebos, in some cases even deceptive use of placebos can be justified in psychiatric treatment. I raise some social justice issues regarding access to and affordability of NFB. Yet this and other techniques that induce psychological responses from patients may not be effective in treating moderately severe and severe forms of psychiatric disorders. With a view to potential future therapies, I consider how the neurostimulating technique of temporal interference could potentially result in higher response rates and better control of disease progression and symptoms.
I discuss a range of ethical issues in psychiatric neurosurgery in Chapter 4. This is functional neurosurgery designed to modulate dysfunctional neural circuits mediating sensorimotor, cognitive, emotional, and volitional capacities. Because it is largely still experimental and investigative, functional psychiatric neurosurgery falls within the domain of psychiatric research. It is used for psychiatric disorders that have not responded to other interventions. After surveying the history of this practice, I assess the comparative benefits and risks of neural ablation and DBS as the two most invasive forms of neuromodulation. This includes neural ablative techniques of radiofrequency neurosurgery, Gamma Knife® radiosurgery, and high-intensity focused ultrasound. It also includes open-loop and closed-loop versions of DBS. I discuss the question of whether individuals with a severe or moderately severe psychiatric disorder have enough cognitive and emotional capacity to weigh the reasons for and against DBS and give informed consent to undergo it. This question includes consideration of whether some patients might be motivated by a therapeutic misconception to participate in a functional neurosurgery clinical trial. It also considers whether the idea of DBS as a treatment of “last resort” unduly influences their perception of risk. In addition, I discuss the obligation of investigators conducting these trials to research subjects and the medical and ethical justification for a sham control arm in psychiatric neurosurgery trials.
Social justice issues are relevant here as well. I examine the issue of fairness in patients having or lacking access to neurostimulation when it is the only intervention that can control and relieve symptoms of a psychiatric disorder. In the last section of the chapter, I describe the mechanisms of optogenetics and discuss the therapeutic potential of this novel form of neuromodulation. The ability of this technique to control gene expression in the brain and a broad range of neural activity could make it a superior form of neuromodulation to DBS. Yet the fact that optogenetics manipulates both genetic material and neural circuits and has been tested only in animal models makes it unclear what its benefit-to-risk ratio would be.
In Chapter 5, I address concerns that people with devices in their brains regulating neural and mental functions are not in control of their thoughts and actions. I argue that DBS or any other neuromodulating system that operates safely and effectively does not undermine control or agency. Rather, by restoring motor and mental capacities, DBS enables autonomous agency that has been impaired or undermined by a psychiatric disorder. There is shared control between the person and the device, and this allows enough control for autonomy and free will. Nor does neuromodulation necessarily cause substantial changes in a person’s mental states and alter her identity. When it functions properly, neuromodulation does not alter but restores the mental capacities impaired by the disorder. Rather than disrupting psychological connectedness and continuity, DBS and other techniques can re-establish these relations and return the patient to her premorbid self. Nevertheless, the control a patient has with a device may entail certain expectations about operating it to maintain normal neural and mental functions. I discuss whether these expectations impose an unfair burden of control on these patients compared with people who do not need a device to maintain these functions
Extending the discussion of interventions aimed at restoring control of mental capacities in psychiatric disorders, I explore some of the implications of this desired outcome for forensic psychiatry in Chapter 6. I discuss whether pharmacological intervention in the brains of criminal psychopaths to modify and enable them to control their behavior could be justified as an alternative to continued incarceration. I consider the question of whether treatment designed to rehabilitate the offender could be forced on him against his wishes and whether it would violate his cognitive liberty. One of the key issues is weighing the interests and rights of the offender against the interests of society in preventing recidivism and protecting the public from harm.
In Chapter 7, I discuss reasons for and against euthanasia and physician-assisted suicide for patients with TRD or other psychiatric disorders. Although these actions may seem anathema to the goal of treating psychiatric patients in
order to prevent suicide, there may be cases in which it would be permissible to bring about or assist in the death of a person with one of these disorders. The permissibility of these actions depends on four conditions. First, the patient must be competent enough to weigh the reasons for and against EAS. Second, the patient must make an informed and persistent request for it. Third, the suffering the patient experiences from the disorder must be unbearable and interminable. Fourth, the disorder must be resistant to all indicated treatments given to the patient over many years. A corollary to the fourth condition is that there must be a reasonable limit to the time a patient could be expected to wait for a possible treatment to relieve symptoms. When these conditions obtain, continued life may not be in the patient’s best interests. He could make a rational request for a psychiatrist or other physician to end his life or assist him in ending it.
Shifting the focus from events occurring in early adulthood and adolescence to events occurring perinatally and prenatally, I discuss different ways of predicting and preventing psychiatric disorders in Chapter 8. After considering reasons for and against intervening with psychotropic drugs during the prodromal phase of disease, I discuss how the identification of biomarkers for psychiatric disorders in childhood or adolescence might predict who would be at risk of developing them. Biomarkers could indicate which interventions could reduce this risk or eliminate it altogether. I raise questions about the predictive value of biomarkers in psychiatry and discuss some of the ethical and social issues arising from how different parties might interpret them. In some cases, the identification and interpretation of biomarkers may be more harmful than beneficial to those who have them. Abnormal neuroimmune and neuroendocrine interactions may disrupt normal rates of synaptic pruning and myelination in childhood and adolescence and increase the risk of schizophrenia and other disorders. I discuss how immune-modulating drugs could reverse this process and how to balance the potential benefits against the risks of intervening in the brain in this way. I speculate on the possibility of using focused ultrasound to open the blood–brain barrier (BBB) to allow the infusion of growth factors at an early stage of pathogenesis when neurodevelopmental abnormalities may signal early neurodegeneration. This might reverse the disease process in severe disorders such as schizophrenia and change what would have been a life of mental illness into a life of mental health. I also consider noninvasive interventions such as altering the environment to prevent epigenetic factors from influencing gene expression in the brain and making a person susceptible to mental illness. This could obviate the need for psychotropic drugs or neurotrophic factors that could have permanent adverse effects in the brain. In the last section of the chapter, I explain how prenatal and perinatal events
can increase the risk of developing a psychiatric disorder in the second or third decade of life. I consider different interventions before birth that might prevent people from having a disorder after birth. These interventions include not conceiving, terminating a pregnancy, or having and carrying a pregnancy to term at one time rather than another. If potential parents knew that a child they had would be at risk of developing a psychiatric disorder, then they could control to a certain extent whether they brought into existence a person who would have a disorder or a different person who would not have it.
After briefly summarizing the main points from the preceding chapters, in the Epilogue I consider whether an artificial or purely mechanistic model of the brain could lead to a better understanding of mental health and mental illness. It is doubtful that such a model could simulate the processes of a natural brain. It is also doubtful that it could simulate the complex interactions between biological, psychological, and social factors necessary to explain how psychiatric disorders develop and how they might be treated or prevented. In addition, I point out that mental illness can be as disabling and impose more of a burden on more people than physical illness. On grounds of fairness, diseases of the brain and mind should have priority over diseases of the body in the allocation of funding for research into treatment and prevention. This is necessary to relieve the burden of disease, enable functional independence for people with major psychiatric disorders and ideally eliminate this burden altogether.