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There was combat in Nam and I let my hair grow long, went to college, studied orgo until I became draft exempt...

The Pledge

Mr. B is an 85-year-old widower and retired carpenter.

 He is admitted to a psychiatric ward from the dementia care facility where he resides after becoming agitated and striking a caregiver who was trying to bathe him. He has also become increasingly aggressive during any group activities, sometimes pushing other residents.

Mr. B had a small stroke 5 years earlier. Although he was left without any major physical sequelae, he received a diagnosis of vascular dementia that year, and his neurologist prescribed 5 mg of donepezil. A year later he received a diagnosis of depression, and the psychiatrist began treatment with escitalopram at a dose of 10 mg. There was notable improvement with the antidepressant, and Mr. B became more sociable and interested in the various activities at his adult day care.

Six months ago, the dementia progressed and he began to wander. His daughter, who had become his primary caregiver when his wife died 2 years earlier, could no longer safely care for him in her home. A neuropsychologist at the university evaluated the patient and found him to lack capacity for medical, financial, and disposition decisions. Before losing capacity, he had appointed his daughter as his medical power of attorney and his son as his financial power of attorney.

While Mr. B is on the psychiatric ward, escitalopram and donepezil are continued. Medical records from the dementia care facility indicate that several atypical antipsychotics were tried but had little effect on the behavioral disturbances of dementia. They were discontinued after the patient’s daughter raised concern about the black box warning of this class of drugs when used in patients with dementia. The attending psychiatrist prescribes immediate-release valproic acid at 250 mg every 8 hours. Within a few days, Mr. B is calmer and seems less irritable. By the end of the week, Mr. B’s mood and behavior are so much better that at rounds the plan is made to discharge the patient back to his care facility on Monday.

Over the weekend, Mr. B begins to refuse the valproic acid. He tells the staff that “it tastes bad” and then at other times, “You are trying to control me with it.” He is erratic in taking his other medications but closes his mouth and crosses his arms when the nurses try to give him the mood stabilizer. By Sunday night, Mr. B is so aggressive and angry that he requires a crisis team to administer 2.5 mg of olanzapine intramuscularly to keep him from harming himself and the staff. The incident is distressing for Mr. B, for the other patients, and for the staff.

The unit psychologist and occupational therapist try different behavioral techniques and environmental adjustments to form an alliance with Mr. B, but they are unable to persuade him to take the valproic acid willingly. Mr. B’s behavior steadily deteriorates and requires several more episodes of forced medication. The attending geriatric psychiatrist calls the staff together for a case conference with a psychiatric pharmacy consultant to discuss the situation. The pharmacist suggests a trial of divalproex sprinkles that could be put in applesauce or ice cream.

The treatment team is sharply divided over whether it is ethical to administer a medication to a patient -even an incapacitated patient -without his knowledge. The psychologist especially feels that this would be tantamount to deceiving the patient and that it is categorically always wrong to lie to patients. Some of the nursing staff believe that putting the medication in Mr. B’s food is far kinder than the repeated takedowns. The team cannot reach agreement except on the need to request an ethics consultation.

 -and post your comments. I’ll offer a discussion of your comments and commentary about the ethical concerns and questions this case raises in a coming issue of Psychiatric Times.

You are the leader of the 3-person team assigned to perform the ethics consultation. The medical director of the geriatric psychiatry unit has prepared the case summary for you to review before you meet with the team. After you review it, you sketch the following questions as food for thought.

1 When you review the case summary, the opinion of the psychologist is clearly most consistent with which major ethical theory or model?

A. Consequentialist theory that the end justifies the means and if deception will prevent harm to patient and staff in this case, it is ethical.

B. Deontological theory that there are certain near absolutes, one of which is that lying for any reason violates the respect all human beings deserve.

C. Virtue theory that a good clinician puts the patient first and remains faithful to the patient’s well-being.

D. Principlist theory that beneficence may outweigh autonomy when all circumstances are specified and analyzed.

2 Glaringly absent from the summary is any discussion with the daughter, the son, or any other family member. Which of the following is the most accurate statement about the daughter’s ability to consent to concealed medication?

A. As the health care agent, the daughter can legally and ethically provide informed consent for the surreptitious use of the medication.

B. Even as the health care agent, the daughter cannot provide consent for another human being to be deceived with concealed medication.

C. The daughter cannot provide consent for the surreptitious use of the medication because the patient is in a psychiatric hospital; only a court can order it.

D. The daughter would need to be the patient’s guardian to provide consent for a concealed medication.

3 An essential aspect of an ethics consultant’s job is to help the group formulate all of the ethically justifiable conditions under which a particular decision may be made. Assume the daughter consents to the covert administration of medication because she wants the patient to be able to return to his dementia care home. Which of the following conditions would you NOT recommend be included in the treatment plan to enhance the ethical quality of the surreptitious use of medication?

A. The covert administration of the medication should be time-limited and monitored to assess its efficacy and any adverse effects.

B. The treatment plan should not be formally written out but verbally agreed to by all staff.

C. The staff should no longer attempt to persuade the patient to take the medication voluntarily because it endangers the staff and other patients.

D. Staff who object to the use of concealed medication should not be permitted to request recusal from the care of the patient because this places an unfair burden on the rest of the team.

4 One of the primary tasks of the ethics consultant is to help the daughter and treatment team to identify the values conflicts involved in the decision. Which of the following values most strongly argues against the use of covert medication for Mr. B?

A. It is more ethical to use prn medications when all other nonpharmacological means fail to control behavior that can endanger the patient and the staff than to schedule concealed medications.

B. The daughter seems to be consenting only because she wants the patient to go back to his nursing home and so does not appear to be acting in the patient’s best interests.

C. So long as the patient is combative and agitated he cannot be discharged back to his assisted care facility, where he would likely have a better quality of life.

D. Deceiving the patient risks having him discover the covert medication, lose trust in the team, and become even more paranoid and challenging to manage.

MORE ABOUT Cynthia Geppert, MD, MA, MSBE, DPS

I come from a family of musicians and physicians.

 My father was an Army doctor during WWII and was one of the founders of military pediatrics. My brother is the award-winning artist Christopher Cross. I spent my youth as a rock and roll drummer and always thought I would end up being a teacher or writer but never a doctor because I was a failure as a student. My teachers thought I had learning disabilities, and I dropped out of high school when I turned 16. Somehow, I managed to graduate from college and spent most of my early career studying and teaching religion and working in various aspects of ministry.

While visiting a sick parishioner, I had a spiritual experience that I needed to try to do more to relieve not just the spiritual but also the physical and mental suffering of human beings. So, in my thirties I decided to go to medical school despite having a third-grade math level and never having taken a chemistry course. It was a very long and difficult journey.

In medical school, I finally found a way to integrate the humanities and medicine in the field of bioethics. I never intended to do a residency, but my philosophy professor in graduate school told me that to be relevant as an ethicist you must take care of patients, and he was right. I was drawn to internal medicine but had some serious health problems that made that impossible and ended up where I should have been all along -in consultation psychiatry.

 that was accepted and am grateful to be involved with the publication ever since. Ron Pies, MD, has been my mentor on this path and though I will never equal his brilliance, my aspiration is to be the same breed of renaissance thinker.

Caring for patients, teaching, and writing are such a privilege and pleasure for me that I cannot really call them work. I guess if I had to name a hobby, it would probably be collecting board certifications and advanced degrees because I love learning. But I also enjoy riding trikes with my wife and hiking with my beloved dogs in the beautiful New Mexico mountains where we live.

When, if ever, is it ethical to administer a medication to a patient-even an incapacitated one-without his knowledge? Read the case, and weigh in.

Ethics case quiz | Food for Thought

I’ve written before about the importance of self-reflection in our clinical practices and in teaching our residents and students to enhance their own skill and to help foster it in their patients. As hectic as the world is today, and with our increasingly busy schedules (as if they weren’t already), we often have little opportunity to consider the future of our profession. So, I’m pleased to suggest you spend a bit of time reading 

The Lancet Psychiatry Commission on the Future of Psychiatry

. The target future selected was a decade from now -far enough that changes would likely be apparent, but not so far into the future that the conclusions would be almost completely speculative.

 has been since the early 1800s one of the most prestigious medical journals in the world. But some may not be as aware that several years ago 

 established a number of specialty journals including 

. I was honored to be asked to serve as a member of the Lancet Psychiatry Commission. (This was a volunteer academic effort, a collaboration of 

 and the World Psychiatric Association, so I receive no benefit from suggesting you read the report.) After a year of work, the final report will have been released by the time you are reading this in early October, timed to coincide with World Mental Health Day.

The report has 6 sections: (1) The Patient and Treatment, (2) Psychiatry and the Health Care System, (3) Psychiatry and Society, (4) The Future of Mental Health Law, (5) Digital Psychiatry Enhancing the Future of Mental Health, and (6) Training the Psychiatrist of the Future. Let me briefly highlight some of the critical issues highlighted in the report. Since most of our readers live in the US, many of the issues of concern will be well known though unsolved.

In the The Patient and Treatment section, one of the key issues addresses the tremendous global disparities in treatment resources, including psychiatrists, other clinical personnel, and treatment facilities. We are aware in the US that although we have among the most extensive treatment availability of any country, substantial segments of our population have limited access to quality care. These groups include those living in urban cores and rural areas; members of many minority groups, including recent immigrants; the elderly; children; and those with significant medical comorbidity.

While recent decades have seen little change in our treatment armamentarium, the development of biomarkers, etiologically based diagnostic classification, and pharmacogenetics hold out promise of dramatic breakthroughs which nonetheless are difficult to predict. How we can maintain the centrality of the therapeutic relationship is an issue we will need to address in the face of increased demand, the rise of telepsychiatry, and the increasingly culturally diverse population.

The Health Care Systems section addresses several important areas familiar to all of us. Given the geographic maldistribution of clinical personnel and resources, how can we engineer a new system that will substantially increase access? The integration of physical and mental care must counter centuries of separation in essentially every country including our own. While collaborative care was a keystone principle when the Affordable Care Act was passed, implementation has been lacking. And who knows how the coming year in Congress will affect our efforts toward integration?

The sections on psychiatry and society and the future of mental health law address thorny issues related to the intersection of individual rights versus societal concerns about safety of individuals with mental illness and those close to them. The United Nations Convention on the rights of persons with disabilities addresses mental health issues and concludes that any compulsory treatment is inherently discriminatory. Since for decades courts in the US have trended toward ruling in this direction -and because we are very aware of how involuntary psychiatric treatment has been used in some countries to suppress political dissent -these matters are very familiar. Another important area involves the social determinants of illness and the amelioration of those types of risks -an issue we have discussed in the US, but for which we have so far found few, if any solutions.

The pace of change in digital communication and the use of digital technology in research and clinical care are highlighted in the section on digital technology. (See the 

 article from September 10, 2017, that discusses the currently publicized IBM Watson project on cancer treatment for a cautionary view.) We already know that widespread use of electronic medical records storage has fostered great risks of identity theft and revelation of personal health information. Figuring out how to maximize the benefits and minimize the risks will take a great deal of work.

Finally, in light of the issues raised by all of the above, the report discusses how we will train the psychiatrist of the future. Certainly we know that in a country like Tanzania, with its 12 million people and fewer than 10 psychiatrists, the role of the psychiatrist is vastly different than one working in London or New York. Thus, training needs to consider both the need to adapt to an increasingly complex body of knowledge and skills, but also to the roles of psychiatrists in very diverse settings in the face of ongoing health care systems changes.

I haven’t tried to address the details of any of these issues in this column as my aim has been to highlight some of the key matters addressed in 

 Commission report and, I hope, to pique your interest in reading all 40 pages. I hope, too, that you will take a little time to read it for yourself, and more important, to reflect on how we’ll address these critically important issues for the future of our profession in the US.

I hope you'll take a little time to read The Lancet Psychiatry Commission on the Future of Psychiatry, and to reflect on how we’ll address a number of issues critically important to the future of our profession. 

Crystal Ball Gazing

In the early silent era, pianists patched together swatches of prefabricated music to accompany the onscreen action -furious chases, passionate smooches, banana-peel pratfalls, and so forth. During the succeeding century, film scoring evolved into a unique, largely unappreciated art. Today’s reader is likely to be educated in musical history, theory, composition, performance conventions, as well as cinema technology. Skill at apt quotation of music from every nation and category, past and present, classic to rap is also a requisite.

 [1995]) scored most of the music for Christopher Nolan’s magisterial 

 (2017). The film’s central theme, however, was originally written by Sir Edward Elgar. It’s from the famous Nimrod movement of Elgar’s 

, repurposed by Zimmer’s lesser-known but no less accomplished collaborator, David Wallfisch.

Wallfisch retained Elgar’s quintessentially British bell-like clarity and stateliness. But befitting the dire, inglorious circumstances of the 300,000 soldiers stranded on the bloody beach, Wallfisch re-orchestrated the theme, endowing it with a somber, attenuated quality. In musical terms, the music has also been augmented, extending throughout the pivotal scene when a fragile flotilla of weekend sailors materializes out of the murky mist to rescue the wildly cheering multitude.

On each of 2 viewings, Wallfisch’s poignant reinvention of the Nimrod motif brought unaccustomed tears to my eyes. And made me realize -not for the first time -how less powerful a scene like this would be without music. Hence the following examples of the devices used by film composers to stir our emotions.

Cinema scholars theorize that audiences are swept up by a movie by paradoxically effacing the very means of its creation. Resulting from cunning manipulation of camera, lighting, etc, the picture seems to be unspooling from somewhere back in one’s head, instead of being projected upon the screen.

The technology and aesthetics involved in this curious erasure were perfected in Hollywood’s golden studio years. Most films still employ them. A familiar example is “shot-reverse shot” lensing: when 2 characters are speaking together, each is alternately perceived from a camera angle over the other’s shoulder. Unobtrusive “background” music likewise facilitates the “suppressed” process that sweeps a viewer out of his comfortable seat and into a movie’s realm, as it were from the wings.

Wittingly or otherwise, I think we bring some sort of ego-ideal to the multiplex, preparing us in advance to identify with positive qualities in a film’s character -notably, a hero -we want to own. Identification, even a temporary dose of introjection may be evoked via a musical “signature,” the equivalent of a Wagnerian leitmotif that encapsulates a hero’s virtuous intentions or virtuoso kung-fu talent.

Many contemporary blockbusters re-invent the heroic musical signatures found in the simplistic Saturday serials of my youth (eg, John Williams’s robust manly theme for the Indiana Jones franchise). The hero’s leitmotif is usually composed in a major key; then modified according to dramatic vicissitudes (eg, converted to a minor key when the going gets rough). Minor key heroic signatures are rare -the twanging James Bond theme is a notable exception.

The Saturday serial villain rode a black horse to a minor-key theme. Darth Vader’s menacing motif in 

 (1977 [John Williams again]) updates that convention. Comic characters usually have pixilated major-key leitmotifs (the ruinous golf-course excavations of the goofy gopher in 

 [1980] are accompanied by Kenny Loggins’s 

Morally equivalent characters often are given more complex musical signatures (eg, the undulating modulations of David Grusin’s haunting theme for 

’s [1944] enigmatic heroine). Even an inanimate object may be provided with a signature that highlights its dramatic relevance -the 

 (1940) statuette would be merely decorative, were it not for the ominous minor-key chords of Adolph Deutsch’s score that announces its presence.

A film’s opening music frequently establishes the picture’s narrative focus and setting; it is then repeated and modified harmonically and rhythmically, according to the plotline. Maurice Jarre’s grandly sweeping orchestral declaration over the opening credits of 

 (1962) intimates the vast desert reaches that will enrapture the hero, and later accompany his fall from grace.

Background music heightens the viewer’s emotional response across a spectrum of genres. The shock of the shower scene in 

 (1960) is escalated by the high-pitched shrieking violins of Bernard Herrman’s exquisite score. (Herrman, Hitchcock’s favorite composer, rejected the percussion and horns of standard horror fare, and used strings alone, a sonic coup de cinema.)

Music escalates the emotional impact of other genres (eg, the wailing theremin, an electronic instrument invented in the last century, frequently eerily pervaded 1950s sci-fi alien-arrival movies). The redoubtable Herrman used it in 

Background music of one film may reappear, repurposed for radically different psychological ends, in a later film. The eponymous Shane (Alan Ladd) revenges an innocent settler’s shooting by donning his gunfighter outfit (probably for the last time) and riding into town to dispatch villainous Jack Wilson (Jack Palance). In Victor Young’s impressive score, Shane’s return is accompanied by relentlessly pounding tympani in a 5/8 time signature, rare in a 1950s film, rarely used hereafter.

 (1953). Reformed gunslinger Will Munny, his malevolence -and competence -restored by whisky, blows away the sadistic sheriff who tortured his best friend to death. The ominous chords that background Munny’s terminal ride into stygian darkness are in Shane’s 5/8 time signature but are menacingly retarded (again, augmentation) in Danny Elfman’s score, with whispery sinister strings replacing the ear-shattering tympany in 

I prize those few instances when a film’s music emerges from the background to become a narrator in its own right. In Martin Scorsese’s 

 (1980), Lauren Hutton’s hapless socialite, Michelle, trapped in a loveless marriage to a corrupt politico, has fallen in love with Richard Gere’s narcissistic male prostitute, Julian. The politician vengefully manipulates Gere’s arrest, and possible life imprisonment.

The last scene is set in the interview cubicle of a police station. The lovers speak to each other through phones across a screen. Gere murmurs, “It took me so long to come to you . . .” The theme from the second movement of Mozart’s Clarinet Quintet suddenly surges forth and nothing in Moroder’s sizzling electronic score prepares you for it. Mozart’s music is gentle, reflective. Moroder makes it an exultant epiphany. These damaged souls may never meet outside Julian’s confinement; but the music states wordlessly that this unlikely love won’t be confined by paltry prison walls.

Beyond the formal devices I’ve described, one’s response to a film score -as with any other aspect of a movie -can be inflected by subjective experience. The impact may be negligible, and unrecognized. However what one brings to the table from one’s own life may figure prominently -and poignantly -in one’s response to a film score.

I have always loved the Nimrod theme; had played a piano rendition not long ago. The night after hearing it in 

 and weeping a second time, I dreamed about my Uncle Bernie. He enlisted in the Army Air Corps, illegally, at 17; survived 25 bombing missions over Germany; and died with all his comrades when his Flying Fortress blew up during a routine training flight back in England.

I hadn’t thought of Bernie for years -yet here he was in my dream -just as the last time I saw him: on leave, in a crisp uniform filled with stripes and medals, with his typical goofy smile, holding out a huge bunch of bananas boosted from his unit’s kitchen. The poignant evocation of Elgar’s lustrous harmonies had resurrected him from the sepulcher of memory.

What one brings to the table from one’s own life may figure prominently -and poignantly -in one’s response to a film score. 

Multiplex Melodies

The potential for therapeutic applications of electromagnetic energy to the brain has long been recognized. The earliest recorded report of neurostimulation was that of Mesopotamian physician Scribonius Largus who applied a live torpedo fish on the scalp to treat headache. The modern era has seen an exciting emergence of research and clinical applications in neurostimulation-based therapeutics for psychiatric disorders. Such therapeutics offer a set of alternatives that are mechanistically distinct from and fundamentally different in mode of delivery and adverse-effect profile from pharmacologic interventions.

Neurostimulation is often referred to as “neuromodulation,” which the International Neuromodulation Society more broadly defines as “the alteration of nerve activity through targeted delivery of a stimulus, such as electrical stimulation or chemical agents, to specific neurological sites in the body.” Thus, electrical or magnetic neurostimulation is one method of altering nerve activity in a targeted fashion and represents a paradigm shift in the conceptualization and development of therapeutics for brain disorders. Accordingly, it confers some unique therapeutic advantages over medications but may also elicit different kinds of potential adverse effects that need to be thoughtfully studied and mitigated.

“Targeted fashion” is perhaps the most critical aspect of neurostimulation that distinguishes it from medications, which generally have no substantive neuroanatomic specificity in their application. In contrast, neurostimulation approaches have much better spatial resolution. At a minimum, all brain stimulation methods have limited or no effects “below the neck.”

Some approaches such as standard applications of transcranial direct current stimulation (tDCS) have poor spatial selectivity (centimeters), but the most selective approach in the form of deep brain stimulation (DBS) can have a spatial resolution of approximately 1 mm. Most other neurostimulation approaches have spatial resolutions intermediate to these 2 extremes, with the exception of convulsive approaches (ECT and magnetic seizure therapy).

One of the great advantages of neurostimulation as a therapeutic is the focality of application, which spares other brain regions as well as other organ systems of the body from exposure to the treatment. In addition to differences in spatial resolution, neurostimulation approaches vary in other aspects including their depth of penetration, whether they are invasive or non-invasive, convulsive or non-convulsive, and whether energy is delivered in electric or magnetic form (

While this mechanistically novel and spatially selective array of therapeutics offers a beacon of hope against a backdrop of a relatively poor track record in the development of novel pharmacologic interventions, we should be clear about the underlying assumptions regarding the mode of action. Such clarity will help us in demarcating the potential theoretical limits of therapeutic efficacy, in pointing to potential adverse effects, and in refining treatment parameters as advances in basic and clinical science prompt updating of these assumptions.

The advantage of a spatially selective therapeutic rests on the assumption that there is a well-defined brain region or structure that if stimulated could directly (through involvement in the pathophysiology) or indirectly (by ameliorating a pathophysiologic process even if the region is not itself involved) derive a therapeutic benefit. Limiting stimulation to the targeted brain region would then ideally elicit the desired effect while sparing stimulation of adjacent regions, thereby avoiding any undesirable effects. Such reasoning assumes a certain model of brain function and by extension pathophysiology of the illness being treated. Specifically, the brain is assumed to have a modular organization where the brain is divided into functional anatomically distinct regions and that through over- or under-activation can serve as the pathophysiologic basis for disease states. Accordingly, correcting such altered activations could ameliorate the disease state.

This framework for understanding brain functional organization and pathophysiology has proved useful in the development and application of successful neurostimulation-based therapies for a number of psychiatric disorders. That this simple framework could serve at least as a useful heuristic is remarkable given all of the brain’s known intricacies involving neurochemistry, molecular mechanisms, cellular subtypes, cytoarchitectural organization, connectivity to other regions, etc.

This surprising outcome can be poignantly illustrated by repetitive transcranial magnetic stimulation (rTMS) treatment for refractory depression. This well-established therapy targets the left dorsolateral prefrontal cortex (DLPFC) and is the only FDA-approved noninvasive neurostimulation treatment for refractory depression. That delivery of electromagnetic energy to this critical brain structure might lead to therapeutic effects needs to be appreciated in the context of its connectivity to other brain regions as well as its functional role. It is interesting to note that the effects of rTMS of the DLPFC may be mediated by engagement of the subgenual cingulate cortex, a region that is consistently identified as an important node in the distributed network affected by depression.

 In this study Fox and colleagues found that the strength of functional connectivity between the specific stimulation site in the DLPFC and the subgenual cingulate was correlated with treatment response. Thus, the local stimulation of DLPFC by rTMS appeared to be effective only inasmuch as it was engaging other structures in a broader network implicated in the pathophysiology of depression.

The finding that neurostimulation’s therapeutic effects could be mediated by distal effects downstream to the site of stimulation or perhaps modulating the connectivity with those regions offers an important insight regarding treatment mechanisms. That stimulation of the DLPFC might lead to such therapeutic benefits may be surprising given the important cognitive functions that it supports such as working memory and cognitive control. Discussions of rTMS therapeutic mechanisms in depression at such gross neuroanatomic levels of analysis typically sidestep how such stimulation may affect cognitive functions and the underlying local circuitry. Indeed, rTMS of the DLPFC may be considered to be relatively nonselective given how highly specialized and refined the local circuitry connectivity must be to support such cognitive processes. It may also be surprising that the stimulation of this structure does not obviously disrupt its function but rather can actually enhance its functioning with high-frequency stimulation.

To further complicate the story, working memory ability involves the ability both to maintain stable representations and to flexibly update them when necessary. It is well recognized that there is a tradeoff between stability and flexibility, with much interest in the neural mechanisms that map to these opposing requirements.

 However, since these mechanisms largely operate at the level of local neural circuitry within the DLPFC, any benefits that may accrue from neurostimulation for stability requirements may come at the expense of flexibility and vice versa. In other words, since this tradeoff may be inherently “built-in,” the spatial selectivity of neurostimulation does not confer the ability to avoid this tradeoff, since it is part and parcel of the functioning of the DLPFC.

The example spelled out here highlights 2 important considerations in the realm of neurostimulation therapeutics. First, the therapeutic effects of stimulation may not be caused solely by local circuit modulation but may be mediated by effects on distal sites and/or modulation of the connectivity of distributed networks. Second, stimulation of a brain region can lead to pleiotropic effects; ie, multiple clinical and cognitive effects -desirable and undesirable -may result.

Neurostimulation approaches offer an exciting set of therapeutic alternatives to traditional pharmacologic treatments for psychiatric disorders. One of the greatest advantages most of the approaches confer is their spatial selectivity that minimizes or avoids effects on non-targeted brain tissue or other organ systems. Given that the modes of delivery and mechanisms of action are so different from pharmacologic approaches, we must utilize a framework that is specifically informed by our understanding of electromagnetic energy and its effects on neural systems. This will help us develop and refine the optimal treatment protocols for enhancing clinical effects as well as properly evaluating and mitigating any potential adverse effects.

Dr. Cho is Associate Professor, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center, McGovern Medical School, Houston, TX.

 Fox MD, Buckner RL, White MP, et al. Efficacy of transcranial magnetic stimulation targets for depression is related to intrinsic functional connectivity with the subgenual cingulate. 

 Bagherzadeh Y, Khorrami A, Zarrindast MR, et al. Repetitive transcranial magnetic stimulation of the dorsolateral prefrontal cortex enhances working memory. 

 D’Esposito M, Postle BR. The cognitive neuroscience of working memory. 

Neurostimulation approaches offer an exciting set of therapeutic alternatives to traditional pharmacotherapy for psychiatric disorders. 

Neurostimulation Therapeutics in Psychiatry -The Promise and Potential Pitfalls

Many psychiatric disorders are more prevalent in women during their reproductive years and at stages of life associated with changes in the hormonal milieu. The neuroendocrine system, including central brain circuits, gonadal functions, and other target organs, has been implicated in the development of psychiatric conditions, such as mood, anxiety, and cognitive disorders. The hypothalamic-pituitary-gonadal (HPG) axis coordinates a tightly regulated feedback loop that consists of gonadotropin-releasing hormone (GnRH) produced by the hypothalamus; follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary; and the sex steroids estrogen, progesterone, and androgens, produced primarily by the ovary, corpus luteum, and adrenals (

). Cyclic and episodic alterations in the HPG axis across the menstrual cycle and during important reproductive health events, such as pregnancy and menopause, are hypothesized to alter the sensitivity of neurotransmitter systems and the function of neural circuits in ways that increase vulnerability to psychiatric symptoms for some women.

This article reviews basic neuroendocrine function and discusses the evidence base of hormonal contribution to psychiatric symptoms in polycystic ovary syndrome (PCOS), premenstrual dysphoric disorder (PMDD), and perimenopause. Strategies for psychiatrists for both clinical assessment and management of female patients with neuroendocrine dysfunction are provided, and the role of hormonal therapies in exacerbating or alleviating neuropsychiatric symptoms in these conditions is explored (

PCOS is one of the most common endocrine disorders in women of childbearing age and is a leading cause of menstrual irregularity and anovulatory infertility. In the US prevalence is 6% to 15%, depending on the criteria used for diagnosis.

 The core features of PCOS include hyperandrogenemia, menstrual irregularities/oligovulation or anovulation, and polycystic ovaries. Women with PCOS also commonly have metabolic disturbances such as reduced insulin sensitivity and obesity.

The characteristic problems of PCOS can be separated into reproductive/menstrual abnormalities, hyperandrogenemia, and metabolic dysfunction. Hyperandrogenemia is identified clinically by hirsutism, acne, and male-pattern alopecia; or biochemically, with elevated levels of testosterone, dehydroepiandrosterone sulfate, or androstenedione. Irregular or absent ovulation leads to the menstrual abnormalities typical of PCOS, including oligomenorrhea/amenorrhea and dysfunctional uterine bleeding (breakthrough bleeding and menorrhagia).

Infertility is common, and ovulation induction is often necessary for conception. There are increased rates of spontaneous abortion, premature delivery, pregnancy-induced hypertension, and gestational diabetes -independent of weight. Women with PCOS have an elevated risk of endometrial cancer because of less frequent exposure to ovulatory surges of progesterone and menstrual bleeding. They are also more likely to be obese, with rates varying according to environmental and cultural factors.

Insulin resistance affects more than three-quarters of women with PCOS, even those who are lean. Rates of type 2 diabetes and gestational diabetes are higher in those with PCOS, as is metabolic syndrome.

 The menstrual irregularities of PCOS may improve as women age and androgen levels decrease. Women with a history of PCOS may have persistent hyperandrogenemia and metabolic disturbances after menopause, and they may experience less severe vasomotor symptoms during the menopausal transition.

PCOS appears to be a multifactorial disorder, with genetic and environmental contributions.

 Excessive androgen production in the ovary leads to hyperandrogenemia, as well as the maturation and premature arrest of maturing follicles, which creates the characteristic polycystic ovary morphology. Insulin resistance and hyperinsulinemia further aggravate ovarian androgen production by stimulating the ovarian theca cells to produce androgens in response to LH and disrupting central control of gonadotropins. Circulating androgens may negatively and positively modulate the gamma-aminobutyric acid (GABA) and 

-methyl d-aspartate (NMDA) systems, respectively.

Disturbances of mental health are prevalent in PCOS.

 Hirsutism and obesity may have a negative impact on body image and feelings of attractiveness; menstrual dysfunction and anovulation may raise concerns about female identity; and challenges with fertility may cause emotional suffering and relationship disruption. Higher rates of depression and anxiety appear to be associated with features of PCOS, including obesity and signs of hyperandrogenemia. PCOS has also been associated with lower quality of life and higher distress scores. Disordered eating, particularly binge eating, appears to be more common in women with PCOS than in controls.

Associations have been found between bipolar disorder and PCOS, and this appears to be most closely linked to the use of valproate. There is limited convincing evidence that women with bipolar disorder are more likely to have PCOS than women without bipolar disorder, when they are not treated with valproate.

 A study that evaluated menstrual abnormalities and hyperandrogenemia in women with bipolar disorder did not find either measure to be significantly higher in patients with bipolar disorder than in a control group.

 On the other hand, bipolar disorder may be more common among women with PCOS than in the general population. A screening study of women with PCOS found higher rates of bipolar disorder than in women without PCOS, independent of valproate treatment, although the findings are limited by sample size, lack of a control group, and non-standardized diagnostic criteria for PCOS.

The moderating effect of valproate on the risk of PCOS is clearer, although the same limitations of inconsistent PCOS diagnostic criteria and methodological differences among studies exist. Valproate appears to increase the risk of PCOS in women with epilepsy, a population with high baseline rates of PCOS and reproductive abnormalities, thought to be related to the effect of epileptic activity on hypothalamic function.

The association between valproate on the incidence and prevalence of PCOS in women with bipolar disorder has been studied. Rates of PCOS are higher in women who take valproate than in those who take other antimanic agents.

 Valproate may contribute to PCOS via the alteration of androgen production and insulin metabolism and functioning, and is less likely to be a direct effect of weight gain.

While there remains uncertainty about the specific relationship between valproate and PCOS, and its clinical significance, prescribers should be mindful of this potential risk when making treatment decisions. In the context of other negative or undesirable effects such as weight gain, hair loss, and teratogenicity in the case of pregnancy, alternate treatments should be strongly considered before recommending valproate in women of reproductive age.

Treatment must address the common features of PCOS: menstrual dysfunction, infertility, acne and hirsutism, metabolic disorder, and mental health disturbances. The reproductive, dermatologic, and metabolic aspects of the syndrome should be managed by a primary care provider or relevant specialist. Weight loss is recommended for overweight or obese women with PCOS; it may be associated with direct improvement of reproductive functioning, metabolic health, and cosmetic appearance. For women who are not actively pursuing pregnancy, hormonal contraception is a first-line treatment. Estrogen in oral contraceptive pills suppresses hyperandrogenemia, and cyclic progestin exposure prevents endometrial hyperproliferation.

Metformin has demonstrated benefit on menstrual functioning as well as weight and insulin sensitivity. Antiandrogens, such as spironolactone and flutamide, may improve cutaneous features of hyperandrogenemia as well as menstrual function.

 Cosmetic treatments can be used to ameliorate acne and hirsutism. In refractory cases, pituitary suppression of gonadal hormones, or surgery, may be recommended by the medical provider. Ovulation induction and other fertility treatments are commonly needed for those who seek pregnancy. Psychiatric disorders, including anxiety, depression and eating disorders, should be actively screened for and addressed.

The psychiatrist plays a pivotal role in the management of patients with PCOS and should be knowledgeable about the condition, because of its prevalence in women of reproductive age. In addition to identification and management of the co-occurring mental health conditions in women with established PCOS, the mental health provider should assess for the features of PCOS such as menstrual abnormalities and dermatologic features in women who present with depression, anxiety, bipolar disorder, and eating disorders. Facilitating appropriate referral to a primary care provider for further evaluation, treatment, and specialist involvement allows for more women with PCOS to receive a diagnosis as well as needed attention -with significant implications for reproductive, metabolic, and mental health.

Psychological and physical symptoms that present in the second half of the menstrual cycle comprise premenstrual syndrome (PMS) and the more severe PMDD. Common symptoms include bloating, mood swings, lethargy, irritability, breast tenderness, anxiety or tension, and rejection sensitivity.

The American College of Obstetricians and Gynecologists defines PMS as the presence in the 5 days prior to menses of at least one physical or emotional symptom causing impairment in social or occupational functioning that must recur for a minimum of 3 consecutive cycles.

 A diagnosis of PMDD, as described in DSM-5, requires at least 5 symptoms from a list of psychological, physical, and behavioral symptoms, confirmed by the use of prospective daily ratings (eg, The Daily Record of Severity of Problems) over a minimum of 2 cycles. The symptoms, which should occur in the week leading up to menses and be largely absent following menses, must be present in the majority of cycles, cause impairment, and be distinct from an exacerbation of another mental disorder or a medical condition. Women who do not menstruate because of hysterectomy or an intrauterine device may still be ovulating, and they can have PMDD if their symptoms follow a pattern consistent with a menstrual cycle.

Although up to 85% of menstruating women may experience at least one menstrual-related symptom, conservative estimates indicate a prevalence of 5% for clinically significant premenstrual disorders.

 PMDD affects women across different cultures and ethnicities. Factors associated with a diagnosis of PMS and PMDD include increased weight, a history of sexual abuse or trauma, and additional psychiatric disorders including other depressive disorders, anxiety disorders, and substance use disorders. Women with a history of PMS/PMDD may be at elevated risk for postpartum depression and for depression during perimenopause. Moreover, there appears to be a genetic contribution to susceptibility to PMDD.

PMDD occurs exclusively in ovulating women and is thought to require fluctuating gonadal hormones. No studies have demonstrated significant differences in any specific hormone in women with PMDD; therefore, leading theories posit that the clinical expression of PMDD is related to increased sensitivity to changes in gonadal hormones, and their modulation of neurotransmitter systems, predominantly serotonin and GABA.

Differences in serotonin activity, improvement of symptoms in response to serotonin agonists and serotonin-reuptake inhibitors (SRIs), and worsening of symptoms in response to serotonin antagonists and depletion of the serotonin precursor tryptophan have been seen in women with premenstrual mood changes.

 Differences in sensitivity to and regulation of the progesterone metabolite allopregnanolone -a stress-responsive GABA receptor agonist -have also been implicated in the symptoms of PMDD.

Despite a lack of strong evidence, first-line management of PMDD is with lifestyle modifications (ie, sleep hygiene, exercise, stress management).

 Psychotherapy such as CBT may help women avoid stressors and better tolerate distress during symptomatic days. For moderate to severe symptoms, SRIs (including SSRIs and SNRIs) are recommended, with a response rate of up to 70%. Doses can be effective at the low end of therapeutic doses for depression, but moderate doses are often required. SRIs can be dosed during the luteal phase or at the start of symptoms, or they can be dosed continually throughout the month. Factors such as cycle and symptom regularity, adverse-effect profile, and personal preference may guide the dosing schedule.

In contrast to depression, the benefits of SRIs for PMDD are observed soon after the first dose, and patients on luteal-phase dosing do not appear to experience withdrawal symptoms when dosing stops each month.

If symptoms persist following an adequate trial of SRIs, hormonal therapy with an oral combination of ethinyl estradiol and the progestin drospirenone is indicated for ovulation suppression. Drospirenone may be particularly effective for PMDD because of its antiandrogenic effects; however, the risk of venous thromboembolism appears to be higher than that of other progestins.

There is evidence that continual dosing of oral contraceptive pills, skipping placebo pill days for several consecutive months, provides symptom relief, likely because of better suppression of ovulation. Antiandrogenic agents, such as spironolactone, finasteride, and flutamide, may be useful for women who cannot take SRIs or hormonal therapies. Brief use of alprazolam during the symptomatic period may also benefit some women. The GnRH antagonist leuprolide, with add-back estrogen and progesterone, or surgical removal of the ovaries may be required for refractory cases.

The menopausal transition occurs in the setting of reduced numbers of ovarian follicles, lower levels of follicle-derived inhibin B, and increased production of FSH from the anterior pituitary gland. Menstrual cycles become longer and more variable in duration, and non-ovulatory cycles are more prevalent. Progesterone levels drop, and levels of physiologic estrogen (estradiol [E2]) become more variable than with premenopausal cycles. Subsequently, menstrual cycles cease, and ovarian E2 and progesterone production fall to minimal levels, characterizing the postmenopausal state. The perimenopausal period can be associated with vasomotor symptoms, alterations in sexual functioning, and mood and cognitive changes.

Depressive disorders are twice as common in women, with rates diverging at puberty and aligning again in the postmenopausal period. Some women appear to be more prone to depressive symptoms and disorders at particular points of the reproductive cycle, such as during the luteal phase of the menstrual cycle, the postpartum period, and the perimenopause. In addition to such epidemiological data, basic and translational studies have elucidated connections between gonadal steroids and neurotransmitters, neurotrophic factors and inflammation, the hypothalamic-pituitary-adrenal (HPA) axis, and systems of the brain related to emotional processing.

 Together, the available research suggests that changes in ovarian hormones play a key role in the development of depressive syndromes in at least a subset of women.

While most women do not experience significant depression during the perimenopause, there may be a 2-fold risk of depression during this period. Women with a history of depression may be at greater risk for recurrence during the menopausal transition. The degree of fluctuations in levels of E2 and FSH and the severity of self-reported vasomotor symptoms have been associated with a higher risk of perimenopausal-onset depression.

 Such findings suggest that mood symptoms may develop in response to highly variable hormone levels, and depend on the ability of the brain to adapt to those fluctuating levels. The finding that perimenopausal women with depression benefit from estrogen therapy, while exogenous estrogen does not appear to improve depression later in the postmenopausal period, further supports the premise that it is the instability of gonadal steroids and trophic factors that drives the depressive symptoms, rather than a primary hormone deficiency.

Ovarian hormones may contribute to perimenopausal-onset depression in several ways. E2 raises levels of available serotonin and norepinephrine through reduced degradation and increased synthesis, modulates the serotonin reuptake transporter and receptors, and may affect levels of neurotrophins, such as brain-derived neurotrophic factor. E2 appears to be implicated in reward circuitry.

 E2 and progesterone are active in areas of the brain associated with mood and emotional processing, such as the prefrontal cortex, hippocampus, and brainstem. Perimenopausal depression may be related to dysfunction of the GABA system and the HPA axis in response to stress in the presence of changing ovarian hormone and neurosteroid levels.

Options for pharmacologic management of perimenopausal depression include antidepressants and hormone therapy. Despite some inconsistencies in the literature, there appears to be a benefit of E2 replacement in women within the perimenopausal period, whereas there was no improvement seen in women who have transitioned into menopause, which suggests a “critical window” for E2 replacement in depressive disorders.

The efficacy of E2 may be related to stabilization of circulating estrogen and FSH levels. Transdermal E2 may be more effective than oral formulations, although the literature is discrepant. Exogenous progestins, indicated if the patient has an intact uterus, may reduce the antidepressant benefit of E2 therapy. Menopausal hormone therapy carries an increased risk of adverse cardiovascular outcomes and cancer -among other risks -although evidence for short-term use (ie, 5 years) during the perimenopausal period and early menopause may be considered after discussion of individual risks and benefits with the patient’s medical provider.

SRIs have demonstrated efficacy in women with perimenopausal depression and may have the added benefit of improving vasomotor symptoms. Head-to-head studies of hormone therapy versus antidepressants for perimenopausal depression are lacking.

Uncertainties exist about the effect of the menopausal transition on neurocognitive functioning, although there is an emerging literature on the effect of ovarian hormones and neurosteroids on the aging brain. While women may report changes such as impaired memory and concentration, there is a dearth of studies that demonstrate specific changes in neurocognitive profiles. Estrogen depletion, either in the natural menopausal period or due to oophorectomy before menopause, appears to be associated with cognitive decline. This finding is supported by compelling human and animal studies and has led to interest in estrogen therapy after menopause to prevent or ameliorate age-related cognitive decline.

Estrogen’s potential benefits on cognition may be mediated through effects on the acetylcholine system, prefrontal cortex functioning, and dendritic spine density. Early studies of postmenopausal exogenous estrogen use suggested reduced risk of cognitive disorders, which was later questioned by results of the Women’s Health Initiative that suggested no cognitive benefit or an increased risk of cognitive impairment in some groups.

Current theories suggest that -as with depression -there may be a critical period for estrogen treatment during perimenopause or early postmenopause (ages 50 to 60) that may lead to improved cognition and/or prevention of age-related cognitive decline, perhaps with sustained benefit well beyond the cessation of hormone therapy. By comparison, initiation of estrogen treatment in the late postmenopausal stage (ages 65 to 79) may be associated with an increased risk of neurocognitive disorders.

While there is no approved indication for perimenopausal use of hormone treatment for cognition, women who undergo early surgical menopause or experience premature menopause should be considered for hormonal treatment until the average age of natural menopause. There are insufficient data at this time to make recommendations for hormone therapy in women who experience natural menopause at the expected age. If a woman chooses to begin treatment because of menopausal symptoms such as vasomotor symptoms, vaginal dryness, or mood instability, it is suggested that short-term use may have added benefit for her neuorocognitive health.

Women experience higher rates of several common psychiatric disorders, and they appear to be at elevated risk during their reproductive years and at specific reproductive transitional points. Pituitary and ovarian hormones have been implicated in these sex- and phase-specific differences. The mental health provider should be knowledgeable about prevalent psychiatric presentations related to reproductive functioning, including those reviewed in this article. Gaining appreciation for the effect of the HPG axis on neurobiology and mental health, as well as learning to recognize, assess, and manage or refer to the appropriate specialist, will enhance the mental health clinician’s capacity to serve the needs of women across the reproductive life cycle -as provider, liaison, and advocate.

The authors acknowledge the Academy of Psychosomatic Medicine (APM) for helping to bring this article to fruition. The APM is the professional home for psychiatrists providing collaborative care bridging physical and mental health. Over 1200 members offer psychiatric treatment in general medical hospitals, primary care, and outpatient medical settings for patients with comorbid medical conditions.

Dr. Gordon-Elliott is Assistant Professor of Clinical Psychiatry, New York-Presbyterian/Weill Cornell Medicine; Dr. Ernst is Associate Professor of Psychiatry, Icahn School of Medicine at Mount Sinai Hospital, New York; Dr. Fersh is Assistant Professor of Psychiatry, Long Island Jewish Medical Center/Hofstra Northwell School of Medicine, Hempstead, NY; Dr. Albertini is Assistant Professor of Psychiatry, Icahn School of Medicine at Mount Sinai Hospital; Dr. Lusskin is Clinical Professor of Psychiatry, Obstetrics, Gynecology, and Reproductive Science, Icahn School of Medicine at Mount Sinai Hospital; Dr. Altemus is Associate Professor of Psychiatry, Yale School of Medicine, New Haven, CT.

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The authors review basic neuroendocrine function and the evidence base of hormonal contribution to psychiatric symptoms in PCOS, PMDD, and perimenopause. They also offer strategies for psychiatrists for both clinical assessment and management of women with neuroendocrine dysfunction.

The Hypothalamic-Pituitary-Gonadal Axis and Women’s Mental Health: PCOS, Premenstrual Dysphoric Disorder, and Perimenopause

Once a year, the National Center for Health Statistics (NCHS), the federal agency responsible for the use of the International Classification of Diseases – 10th revision (ICD-10) in the US, releases an updated version of the ICD-10-CM, the HIPAA-adopted code set for medical diagnoses used by medical providers, insurers, and health care administrators. The 2018 update of the ICD-10-CM took effect on October 1, 2017, meaning that users of the ICD-10-CM are required to start using the updated codes as of that date.

Coding updates affect the ICD-10-CM codes across all areas in medicine and typically are made to improve coding specificity. For example, the diagnostic code for Type 2 Diabetes Mellitus with Ketoacidosis (E11.1) has been altered to allow the clinician to indicate whether the ketoacidosis was accompanied by coma. This year, there are several coding updates that affect the diagnostic coding in the Mental, Behavioral, and Neurodevelopmental chapter (F00-F99) and thus affect the diagnostic codes used by mental health practitioners. As is the case with most of the other coding updates, the changes to the mental disorder codes aim to improve the coding specificity of the diagnoses, which in turn can help optimize medical reimbursement.

One important update involves the diagnostic codes for substance use disorders. The ICD-10-CM diagnostic codes recommended by DSM-5 are F1x.10 for the diagnosis of mild substance use disorder, and F1x.20 for both moderate substance use disorder and severe substance use disorder, where x indicates the class of substance: 0 for alcohol use disorder; 1 for opioid use disorder; 2 for cannabis use disorder; 3 for sedative, hypnotic, or anxiolytic use disorder; 4 for cocaine use disorder; 5 for amphetamine or other stimulant use disorder; 6 for phencyclidine or other hallucinogen use disorder; 7 for tobacco use disorder; 8 for inhalant use disorder; and 9 for other or unknown substance use disorder. Currently, the clinician indicates that the substance use disorder is in early or sustained remission either by writing in the applicable specifier on the chart or by selecting it from a drop-down menu on an electronic health record. Either way, the fact that the substance use disorder is in remission is not reflected in the diagnostic code. For example, mild alcohol use disorder and mild alcohol use disorder in sustained remission have the same diagnostic code: F10.10.

The October 1 update remedies this by providing different ICD-10-CM codes for active substance use disorder and substance use disorder in remission. Whereas mild substance use disorder continues to be F1x.10, moderate substance use disorder continues to be F1x.20, and severe substance use disorder continues to be F1x.20, mild substance use disorder in remission is now coded as F1x.11 and moderate and severe substance use disorder in remission is now coded as F1x.21 (

The other coding update effective October 1, 2017, involves the ICD-10-CM code for avoidant/restrictive food intake disorder (ARFID). It is now changed from F50.89 (a diagnostic code which is shared by other specified eating or feeding disorder) to F50.82, which will be unique to ARFID.

Dr. First is Professor of Clinical Psychiatry at Columbia University in New York.

Several updates to ICD-10-CM affect the diagnostic codes used by mental health practitioners. One important update involves the codes for substance use disorders. Details here.