IN MEMORIUM
ROBERT A. WOODRUFF, JR.
The inspiration for—and co-author of— the first edition of this book
ELI ROBINS
Who, as much as any one person, launched a new era in American psychiatry
SAMUEL B. GUZE
The tough-minded individual who believed that there was only one model of psychiatry: the medical model— which must be part of the mainstream of modern medicine
DON GOODWIN
Gifted writer and co-author of editions two through five
CONTENTS
Preface to the Seventh Edition xi
Preface to the First Edition xvii Looking Forward xxi
1. Evolution of Psychiatric Diagnosis 1
2. Mood (Affective) Disorders 15
3. Schizophrenic Disorders 61
4. Panic and Phobic Disorders 97
5. Posttraumatic Stress Disorder 125
6. Obsessive- Compulsive Disorder 167
7. Eating Disorders 193
8. Somatization Disorder 207
9. Antisocial Personality Disorder 227
10. Borderline Personality Disorder 245
11. Alcohol Use Disorder 271
12. Drug Use Disorder 305
13. Delirium and Dementia (Neurocognitive Disorders) 339
14. The Psychiatric Evaluation 359
Index 377
PREFACE TO THE SEVENTH EDITION
Forty- four years have elapsed since this text was first published. Over this time period, psychiatry has clearly evolved along three noteworthy lines.
First, most psychiatrists have become diagnosticians. The groundwork was set for this in no small part by the authors and collaborators of the early versions of this text, including Eli Robins, Robert A. Woodruff, Donald W. Goodwin, and Samuel B. Guze at Washington University in St. Louis. In particular, their two-pronged philosophical approach to psychiatric illness/diagnosis was to be “agnostic” about the origin of a mental illness and to draw psychiatric conclusions (including diagnostic criteria) based on reliable, reproducible data. The early studies of this group of psychiatric researchers from the 1960s and 1970s eventually produced formal operational criteria sets for the 12 major mental illnesses (adapted from “the Feighner criteria”) (11). While this overall approach to psychiatric illness was described as “narrow” by some (and less charitably by others) in mainstream psychiatry at the time, the criteria sets formed the early basis for a common language among psychiatrists. The diagnostic approach used an “atheoretical” basis for the origin of psychiatric illness, drawing conclusions and developing criteria based on scientific evidence. This approach gained much wider acceptance (and general acceptance by the field) after publication of the best- selling DSM-III (Diagnostic and Statistical Manual of Mental Disorders, 3rd edition, of the American Psychiatric Association) (2) in 1980. The “similarities” between the DSM-III and Washington University approaches were not surprising, as the authors noted earlier were among the DSM-III taskforce contributors, and one- third of the overall taskforce members had trained at Washington University.
Ultimately, the DSM-III solidified a widely acceptable common language and explicit criteria for the major mental illnesses as had long been used in most other areas of medicine. Frustrated by the unknown etiology of most major psychiatric illnesses, young scientifically trained physicians could rely on a published framework as a foundation for communication, research,
( xii ) Preface to the Seventh Edition
diagnosis, and treatment. Many well-respected individuals both inside and outside the specialty would attack the approach over the next two decades, but its utility in almost all psychiatric venues remained undeniable.
Of particular interest was that external forces over the ensuing two decades (1980–2000) further solidified psychiatry’s use of the diagnostic model. Among other developments, diagnosis became a required practice for reimbursement of services (e.g., diagnostic-related groups, or DRGs), with only specific diagnoses (and not others, especially not Axis II disorders) generating payment; accreditation requirements compelled diagnostic uniformity in general medicine; and communication among treating professionals increased, particularly across medical specialties.
In sum, both internal and external forces have driven psychiatry to accept the diagnostic or medical model as THE approach to major mental illness.
The second noteworthy line of evolution is that continuing critical review over time has clarified this empirically based “approach” to the major psychiatric diagnoses is sustainable and has prevailed. The DSM-III has had several subsequent minor revisions (including the DSM-III, revised [DSMIII-R] in 1987 (3), DSM-IV in 1994 (4), and the DSM-IV, text revision [DSMIV-TR] (5) in 2000), but most would argue that the process and the findings withstood the test of time to make DSM-IV/DSM-IV-TR the most widely accepted psychiatric diagnostic criteria in the world. The stability of this empirical approach first espoused by the original authors of the Psychiatric Diagnosis text are a testament to its fundamental inherent strength.
The third line of evolution has been the frank failure of psychiatry to discover the neurobiological underpinnings of the major mental illnesses included in this textbook. New students to psychiatry cannot avoid being confronted with animosity from all quarters toward the latest American diagnostic manual, the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th edition) (6). The history of what happened is nearly impossible to locate without extensive literature search; thus we briefly review it for instructional purposes.
Following from the successes just noted, psychiatry embarked upon study of the brain as the major imperative for the 1990s. President Bush declared (Proclamation 6158) 1990–2000 to be the “Decade of the Brain,” and the search was on for the underlying neurobiology. Tremendous resources were expended. Later, some critics jested that one of the main findings of this initiative was that the brain was much more complicated than imagined. Cellular-level analysis was dealing remotely (extracranially) with 100 billion cells with multitudinous overlapping known and unknown tracks, circuits, and functions as opposed to organs devoted to several
metabolic functions. Arising from this early excitement and frank hubris was the notion that neuroscience, imaging, and genetics would yield answers, presumably in short order. The architects of DSM-5 promised inclusion of these “findings” to support the outstanding questions of validity of the major mental disorders. (Also promised by the Task Force for DSM-5 was a dimensional approach to psychiatric diagnosis.)
As the scientific findings failed to materialize and complexities of the tasks expanded beyond current capabilities (dimensionalism without reconciling increasing comorbidity risks), various stakeholders began raising questions. Perhaps the most damning criticism—immediately prior to the 2013 introduction of DSM-5 was a direct rebuke by the National Institute of Mental Health (NIMH) that not only constituted a major funding source for the DSM series but also provided indirect support by requiring DSM language in formal NIMH grant applications.
The failure to identify a single basis for any major (or minor) mental illness accompanied DSM-5’s departure from the careful iterative style of the DSM series (DSM-III-R to DSM-IV-TR) that introduced abrupt major structural changes, acceptance of poor agreement within criteria, ill- conceived theoretical changes, and overly broadening criteria. These missteps and errors have come to light over the ensuing years with the application of DSM-5 criteria particularly to issues within government, insurance, clinical practice, research, and society.
Space does not permit comprehensive review of all of the major changes to the criteria in DSM-5, but some high points may assist the reader. Perhaps most problematic for the acceptance (and credibility) of DSM-5 (and, by direct extension, psychiatry) were major structural changes in the approach to diagnoses, particularly removal of the multi-axial system without much empirical basis or guidance. Over the last 33 years, probably 90% of practicing psychiatrists, as well as many more allied health professionals, were educated under the DSM system of psychiatric diagnosis. Users of the DSM-5 were told that the manual had moved to non-axial documentation of diagnosis, by removing Axes I–III, which were “combined,” and that impinging social and situational factors and functional impairments should be notated. No elaboration was provided on newly created issues for addressing diagnostic primacy, including definition of primary versus secondary disorders (i.e., first onset versus focus of treatment), formal consideration of how the diagnoses integrate in the DSM-5 list format, and determination of amount of overall functional impact on the individual— complexities which had been addressed in previous editions of the criteria.
Problematic for research was the poor interrater reliability (whether two examiners of the same case agree or disagree on the diagnosis) of many
of the diagnostic criteria in the DSM-5 field trials. Particularly concerning was the finding that one of the lowest agreements was for one of the most common psychiatric disorders, major depressive disorder.
Somatization disorder (a historically agreed-upon valid and reliable major diagnosis) was “downlisted” and replaced in DSM-5 with a new major category, somatic symptom disorder. Focusing more on excessive thoughts and feelings related to somatic symptoms, it was opined that the label should also capture most cases of somatization disorder as well as related syndromes. Unfortunately, this new label also captures a large percentage of cancer patients who are “worried” about their disease (and possible death), adding a psychiatric diagnosis to their file.
Concerns for (and by) society centered on the “medicalization” of what some consider normal states and on overdiagnosis. In earlier iterations of the criteria, an exclusion had been included that allowed sadness and grief flowing from the loss of a loved one to be considered within normal for up to two months. This exclusion was removed in DSM-5 (allowing for a diagnosis of major depression earlier in consideration of pharmacological intervention), causing ongoing rancor within psychiatry even 5 years later. Concerns about the overdiagnosis of attention-deficit/hyperactive disorder (ADHD) creating an unreal “epidemic” of this disorder have been voiced for years by both clinicians and researchers. In 2014, Visser et al. (21) reported that nearly one in five high school boys had been diagnosed with ADHD. Irrespective of this well-known ongoing problem with ADHD diagnosis and the resulting untenable rates, the authors of DSM-5 sought to broaden the criteria, which would cause the prevalence rates to climb even higher.
Three indisputable facts should be recognized at this point. First, psychiatric illness has existed for thousands of years and it has always represented a descriptive (and treatment) challenge for the “modern medicine” of the time. Second, serious mental illness curiously appears neither to be occurring in epidemics nor disappearing. Third, the machinations of various conceptualizations and unsupported labeling have real potential for harming the credibility that psychiatry has so painstakingly developed over the last 60 years and to directly harm society, the main benefactor of these efforts. We strongly urge readers to maintain focus on the established major diagnoses and the supporting scientifically accumulated evidence (from the last 60 years) which comprises the body of this text.
Two years before his untimely death, Sam Guze asked us (C.S.N. and S.H.Y.) to write the sixth edition of Psychiatric Diagnosis. We share his vision of the evolution of the field and agree with his view that although neuroscience has evolved over the decades, the fundamentals of psychiatric
diagnosis have remained constant. What we have tried to achieve in this latest seventh edition is to incorporate the relevant new scientific research that, not surprisingly, continues to support the fundamental premise of the primacy of psychiatric diagnosis.
Although we remain steadfast in our position that only about a dozen diagnostic entities warrant inclusion as the major psychiatric disorders (see Preface to the First Edition for this heretical view), the field has been working intensely toward validation of other diagnoses, in particular posttraumatic stress disorder and borderline personality disorder. We include chapters on these two diagnoses because they are of considerable recent interest, and to illustrate the state of the art of the validity and reliability status of these disorders (although not because we consider them to have achieved the same level of validation as the first 12 diagnoses in earlier editions of this text).
We have updated references extensively, replacing many of the citations from original research articles with recent review articles to direct readers to currently accessible sources of the material for further study. Readers pursuing historical study of the original work may find the citations in the earlier editions of this text. The current criteria for these major mental illnesses can be found in the DSM-5, except for somatization disorder, which can be found in the DSM-IV-TR. The original criteria sets which are the direct forerunners can be found in Feighner J, Robins E, Guze S, Woodruff R, Winokur G, and Munoz R, Diagnostic criteria for use in psychiatric research, Arch. Gen. Psychiatry, 26:57–62, 1972.
The current authors remain staunchly aligned with the original goal of Psychiatric Diagnosis: to provide a concise compendium of current knowledge in psychiatry, with abundant citations, not much theory, and as little personal opinion as possible.
C. S. N. Dallas, Texas
S. H. Y. Tallahassee, Florida
PREFACE TO THE FIRST EDITION
Because it remains a rose.
A rose is a rose is a rose.
GERTRUDE STEIN
Classification has two functions: communication and prediction. A rose can be defined precisely. It has pinnate leaves, belongs to the rose family, and so forth. When you say “rose” to a person who knows something about the definition, communication results.
A rose also has a predictable life history: It stays a rose. If it changes into a chrysanthemum, it may not have been a rose in the first place. If roses routinely change into chrysanthemums, like caterpillars into butterflies, well and good. Natural history may include metamorphoses but they must be routine to be “natural.”
Classification in medicine is called “diagnosis,” and this book is about diagnosis of psychiatric conditions. Diagnostic categories—diseases, illnesses, syndromes—are included if they have been sufficiently studied to be useful. Like roses, they can be defined explicitly and have a more or less predictable course.
In choosing these categories, the guiding rule was: Diagnosis is prognosis. There are many diagnostic categories in psychiatry, but few are based on a clinical literature where the conditions are defined by explicit criteria and follow-up studies provide a guide to prognosis. Lacking these features, such categories resemble what sociologists call “labeling.” Two examples are “passive-aggressive personality” and “emotionally unstable personality,” which, like most personality diagnoses, have been inadequately studied for us to know whether they are useful or not.
Not every patient can be diagnosed by using the categories in this book. For them, “undiagnosed” is, we feel, more appropriate than a label incorrectly implying more knowledge than exists. Terms like “functional” and “psychogenic” and “situational reaction” are sometimes invoked by
physicians to explain the unexplained. They usually mean “I don’t know,” and we try to avoid them.
Because classification in psychiatry is still at a primitive stage, there are reasonable grounds for questioning our choice of categories. It general, we lump rather than split. Hence we have two affective disorders—primary and secondary—rather than the half-dozen affective disorders cited in the official nomenclature. Schizophrenia is divided into “good prognosis” and “bad prognosis” schizophrenia rather than sliced more finely, as some prefer. Our justification for this is “the literature,” meaning primarily follow-up studies.
“The follow-up is the great exposer of truth, the rock on which many fine theories are wrecked and upon which better ones can be built,” wrote P. D. Scott. “It is to the psychiatrist what the postmortem is to the physician.” Not all such studies are perfect, but we feel they are better than no studies. And inevitably there are instances where our “clinical judgment” has prevailed in evaluating the merit of individual studies. No text in psychiatry could be written today without a certain amount of this, but we have tried to limit personal opinion to a minimum. Many if not most assertions have a citation, and the reader can check the references to form his own judgment.
When the term “disease” is used, this is what is meant: A disease is a cluster of symptoms and/or signs with a more or less predictable course. Symptoms are what patients tell you; signs are what you see. The cluster may be associated with physical abnormality or may not. The essential point is that it results in consultation with a physician who specializes in recognizing, preventing, and sometimes, curing diseases.
It is hard for many people to think of psychiatric problems as diseases. For one thing, psychiatric problems usually consist of symptoms— complaints about thoughts and feelings—or behavior disturbing to others. Rarely are there signs—a fever, a rash. Almost never are there laboratory tests to confirm the diagnosis. What people say changes from time to time, as does behavior. It is usually harder to agree about symptoms than about signs. But whatever the psychiatric problems are, they have this in common with “real” diseases— they result in consultation with a physician and are associated with pain, suffering, disability, and death.
Another objection to the disease or medical “model” arises from a misconception about disease. Disease often is equated with physical abnormality. In fact, a disease is a category used by physicians, as “apples” is a category used by grocers. It is a useful category if precise and if the encompassed phenomena are stable over time. Diseases are conventions and may not “fit” anything in nature at all. Through the centuries, diseases
have come and gone, some more useful than others, and there is no guarantee that our present “disease”— medical or psychiatric— will represent the same clusters of symptoms and signs a hundred years from now that they do today. On the contrary, as more is learned, more useful clusters surely will emerge.
There are few explanations in this book. This is because for most psychiatric conditions there are no explanations. “Etiology unknown” is the hallmark of psychiatry as well as its bane. Historically, once etiology is known, a disease stops being “psychiatric.” Vitamins were discovered, whereupon vitamin-deficiency psychiatric disorders no longer were treated by psychiatrists. The spirochete was found, then penicillin, and neurosyphilis, once a major psychiatric disorder, became one more infection treated by nonpsychiatrists.
Little, however, is really known about most medical illnesses. Even infectious diseases remain puzzles in that some infected individuals have symptoms and others do not.
People continue to speculate about etiology, of course, and this is good if it produces testable hypotheses and bad if speculation is mistaken for truth. In this book, speculation largely is avoided, since it is available so plentifully elsewhere.
A final word about this approach to psychiatry. It is sometimes called “organic.” This is misleading. A better term, perhaps, is “agnostic.” Without evidence, we do not believe pills are better than words. Without evidence, we do not believe chemistry is more important than upbringing. Without evidence, we withhold judgment.
Advocacy is not the purpose of this book. Rather, we hope it will be useful in applying current knowledge to those vexatious problems— crudely defined and poorly understood— that come within the jurisdiction of psychiatry.
D. W. G.
Saint Louis December 1973
LOOKING FORWARD
PSYCHIATRIC DIAGNOSIS— AN UPDATE AND CONTINUING LOOK FORWARD
Diagnosis is the cornerstone of medicine. It allows physicians to communicate effectively with their patients and other healthcare professionals and serves as a prediction about the future. It is the means by which physicians make treatment decisions and are able to assess whether an intervention has a beneficial effect. In the absence of accurate, reliable and valid diagnosis, medicine becomes a “Tower of Babel” in which clinical information is very difficult to interpret. This lesson has been learned more slowly in psychiatry than in other fields of medicine, but thanks to psychiatrists at Washington University in St. Louis, the field has moved to a reliable, criteria-based system of classification over the past 50 years. Early pioneers included Eli Robins, Sam Guze, George Winokur, and a host of others at Renard Hospital in the 1960s and ‘70s. Their efforts were highlighted with the publication of a set of criteria for psychiatric diagnoses by John Feighner and colleagues in 1972 (11). Subsequently, Bob Woodruff, Don Goodwin, and Sam Guze published the first edition of this text, Psychiatric Diagnosis, in 1974 (22). The book has subsequently undergone several revisions. In 2010, Carol North and Sean Yutzy, former members of the Department of Psychiatry at Washington University, published the sixth edition of this classic text, providing major updates from prior editions and doing a tremendous service for the field of psychiatry. In the latest edition, they have provided us with an outstanding and thoroughly updated version taking into account recent advances in the field.
At the time of the last edition, I wrote a preface discussing a prospective view of psychiatric diagnosis, and described the field as being at an important period in its history. It is now appropriate to take a look at what has happened since that time and how this has influenced psychiatric diagnosis. One of the major developments since the last edition of
this text was the publication of DSM-5 in 2013 (6). DSM-5 was highly anticipated in 2010 and provided some advances in the criteria for psychiatric illnesses, some new illness classifications, and some changes in how illnesses are categorized. As many in the field thought at the time, DSM-5 is a thoughtful, but incremental, extension of work that originated with the publication of the Feighner criteria in 1972 (11), the first edition of Psychiatric Diagnosis in 1974 (22), and DSM-III in 1980 (2). Unfortunately, DSM-5, while useful, has not fundamentally altered conceptualization of psychiatric illnesses and may be viewed as a relatively small step forward for the field, remaining consistent with traditional categorical descriptions of disorders. Categorical approaches remain extremely helpful for clinicians, and psychiatric categorical diagnoses can be applied highly reliably, consistent with other recent editions of the DSM. As noted in all editions of this book, validation of the major psychiatric syndromes remains problematic and is largely based on clinical criteria initially developed in the 1970s (18). The field continues to lack mechanistic explanations and meaningful biomarkers.
In parallel to DSM-5, other attempts have considered psychiatric symptoms from dimensional perspectives, in which specific symptoms and traits are viewed as being continuously distributed in the population with disorders representing far ends of the distribution spectra. The most notable example of this approach is found in the Research Domain Criteria (RDoC) project, launched by the National Institute of Mental Health (NIMH) in 2010 (9). RDoC attempts to relate psychiatric symptoms more closely to advances in brain science and in understanding brain systems that likely underlie these symptoms. This has had a significant impact on research (as would be expected from an NIH-driven initiative), but the impact on psychiatric diagnosis and practice has been much less clear. Nonetheless, a possible marriage of categorical and dimensional approaches remains possible and could have a significant impact going forward, particularly as brain sciences and behavioral genetics continue to evolve.
The past eight years have witnessed major advances in neuroscience and genetics that hold great, but not yet realized potential for psychiatry. In 2009, the first round of the Human Connectome Project (HCP) was launched. This project sought to map functional connectivity neural networks in the normal human adult brain using an array of sophisticated imaging and neuroscience tools, including state-of- the-art functional connectivity magnetic resonance neuroimaging (fcMRI) and sophisticated analytical methods based on graph theory and network analysis (12). HCP provides important information about the brain networks that can be identified in humans, networks that underlie cognition, perception,
emotion and motivation, key components of the human mind, and aspects of information processing that are altered in all major psychiatric illnesses. HCP is being extended across the human lifespan and will continue to produce major new insights into how the brain functions in health and illness.
A major challenge going forward concerns how to relate the understanding that has derived from studies of relatively large groups of individuals to the connectomes of individual humans (13), particularly those with psychiatric illnesses. Again, progress is being made in this arena, but it is still not possible to use fcMRI for diagnostic purposes at the level of individual patients. This latter situation could change dramatically before the next editions of Psychiatric Diagnosis and the DSM are published. Already, significant inroads are being made in using connectivity neuroimaging to subclassify groups of patients with major depression and other illnesses and to make predictions about possible treatments targeted to illness subtypes (10). This work will undoubtedly continue to advance over the next decade and continues to hold great promise for the field.
While advances in human neuroscience have been dramatic over the past eight years, they arguably pale in comparison to the accomplishments in preclinical neuroscience. Neuroscientists now have at their disposal an array of highly sophisticated methodologies to probe the activity of cells and networks of cells in live animals as they perform a variety of behaviors likely related to psychiatric symptoms and syndromes. These techniques include ways to manipulate the expression of specific genes using CRISPRCas9 gene editing technology (Clustered Regularly Interspersed Short Palindromic Repeats) (16), the ability to study the anatomy of circuits in exquisite detail using CLARITY methods (7), and the ability to manipulate the activity of neurons and others cells within neural circuits using optogenetics and visible light pulses to activate ion channels and other proteins expressed in specific brain cells (15). This work has advanced greatly in recent years, and studies using these methods are now routinely conducted in major neuroscience laboratories around the world. Studies using these methods have provided new insights into how the mammalian brain processes information, how emotions are coded in the brain, and how specific neural circuits underlie motivated behavior. Coupled with these methods have been advances in animal behavioral studies, including models of animal behavior that may have relevance for psychiatric disorders. As with human neuroscience, studies using these methods and derivatives of these methods are in their infancy, although progress is being made rapidly. How these studies in animals, particularly in rodent models, translate into insights about human disorders and into new treatments
remains uncertain, but this is an active sphere of investigation and one that warrants cautious optimism.
We have also witnessed an explosion of information in psychiatric (and complex disease) genetics over the past eight years. The field of psychiatric genetics has long been plagued by identification of genes of small effect size that often have not held up to replication, in part because of underpowered samples.
Advances in genetics including the evolution of more sophisticated analytical methods, coupled with the realization that studies must have very large numbers of participants in order to identify replicable changes, have had a major recent impact. Understanding of numerous psychiatric illnesses, such as autism and schizophrenia, has advanced and provided new insights into the complexity of the genetic structure of these sets of disorders. This includes findings that over 100 genes (likely more) contribute to schizophrenia (1), with perhaps an even higher number of genes being associated with autism. These genes involve complex signaling systems within the brain, including genes that contribute to neuroinflammation, neurodevelopment, and synaptic plasticity, among others (1, 19). Again, it is not certain how this new information will translate into better psychiatric diagnoses, but we can expect increasing use of polygenic risk scores in future studies with the hope of translating this information to the diagnosis and care of individual patients (17).
We are also getting a much clearer understanding of the complexity of psychiatric genetics and recognizing that there is genetic overlap among multiple major psychiatric phenotypes. Phenotypic and genetic pleiotropy will likely become even more complex going forward and could have a major impact on how we think about the diagnostic system. The continuing evolution of sophisticated methods for sequencing genes and for understanding the factors that regulate gene expression, including the important area of epigenetics, will be part of the process. In this latter area lies the critical ability to understand the impact of the environment on gene expression and brain function. Importantly, the cost of studying individual genomes continues to plummet and will be aided by rapidly advancing technologies and analytical methods. Advances in cellular science and the conversion of patient-derived inducible pluripotent stem cells (iPSCs) into neurons and other brain cells, including growth of these cells in organoid models, offer the hope of studying how an individual patient’s genetics contribute to changes in brain cell and network function (20).
While advances in neuroscience and genetics have not yet translated into improved diagnosis or validated biomarkers for psychiatric illness, it appears that new treatments are on the horizon, based, at least in part, on
sophisticated neuroscience. Eight years ago there was considerable hope about the development of novel pharmacological treatments, including the possibility that ketamine and other antagonists of N-methyl-D-aspartate (NMDA) glutamate receptors could be brought to clinical practice as rapidly acting but transient antidepressants for patients with treatmentresistant major depression. This work has continued to advance and has gained increasing scientific acceptance. While it is still premature to use ketamine in clinical practice and there are concerns about how to maintain the short- term benefits and the possible consequences of long- term use, it appears likely that drugs of this type will be approved and become available over the next few years (23).
The evolution of ketamine marks a major change in the types of drugs that will be available for treating complex psychiatric illnesses. Similarly, other novel agents are in development, again based on advances in neuroscience, including neurosteroids that target gamma aminobutyric acid (GABA) receptors and are at advanced stages of development for treatment of severe postpartum depression, and possibly other forms of depression (14). Newer developments in structural biology using cryo electron microscopy are providing novel insights into how protein structure affects function and how pharmacological agents interact with proteins (8). This latter work offers the hope of identifying much more specific drugs with high therapeutic efficacy and fewer side effects. Another hope going forward is that the combination of functional neuroimaging with neuromodulation methods such as transcranial magnetic stimulation (TMS) can offer more effective treatment strategies with fewer side effects than with current treatments.
In summary, as we enjoy North and Yutzy’s insights in this latest edition of Psychiatric Diagnosis, psychiatry remains at a critical crossroad. Science will continue to advance and this bodes well for the field and for patients with these devastating and disabling illnesses. North and Yutzy are to be congratulated once again for their efforts in this updated version of Psychiatric Diagnosis. Their clarity of thought and tough-minded approach to psychiatry remain a beacon for our field and will serve us well as science advances. It is now up to science to take advantage of its opportunities to provide the next revolution in understanding and treating psychiatric illnesses. Only when that occurs will we be ready for the next edition of the DSM.
Charles
F. Zorumski, MD Washington University in St. Louis
