A It’s All About the Narrative

Patient histories are, fundamentally, stories. As such, their details either hang together in a logical and cohesive fashion or they appear fragmented and mystifying. The challenge for clinicians is to frame the story in a coherent narrative. Purposeful data-gathering allows one to triage information and discern the relevant from the nonrelevant, follow threads that point to a unified phenomenon, formulate testable hypotheses about likely psychopathological processes, and match appropriate treatments to a coherent symptom picture for a given patient. Appropriate treatment options can enter into the picture only after enough pertinent information has been distilled and organized into a cogent summary of symptoms and clinical problems that might otherwise seem disparate and arbitrarily strung together. Clinical reasoning and decision-making hinge on obtaining high-quality data. A cogent summary includes elements such as:

• Affirming that symptom presentations fit within known epidemiological parameters; for instance, it is awfully rare to see new-onset psychosis or mania arise de novo in older adults (suggesting that either an earlier history was concealed, denied, or missed; or that truly new psychiatric symptoms are high-probability secondary manifestations of an underlying medical or toxic-metabolic condition)

• Appreciating the match between symptoms and functioning (e.g., complaints of “anxiety” or “depressed mood” alone may not sufficiently account for pervasively impaired functioning, such as chronic unemployment or a persistent inability to live independently in the community)

• Appreciating behavioral, cognitive, or emotional departures from a baseline versus the static persistence of problems that show little deviation over time (i.e., distinguishing states versus traits)

• Recognizing symptoms that belong together within a known pattern or constellation (for example, complaints of “inattention” that also involve a formal thought disorder may point more to schizophrenia, while those involving vegetative signs may reflect depression, and those involving behavioral apraxias may suggest dementia; or strange ideas that are fixed and resistant to challenge or scrutiny point more toward psychosis, while those that seem odd to the patient himself may more likely reflect obsessional thoughts)

• Formulating a hierarchical explanation about how symptoms are best accounted for under an overarching conceptualization. Occam’s razor favors the simplest and most parsimonious explanation for a phenomenon, as when a single syndrome or cause accounts for multiple signs and symptoms. Parsimony also aligns with the modern nosological principle that symptoms potentially associated with one disorder are not better accounted for by another (e.g., impulsive aggression that results more proximally from alcohol intoxication than “underlying” bipolar disorder)

B Organizing a Coherent History: Start from the Beginning

The core foundation of excellent psychiatric treatment starts with obtaining a coherent history, preferably as a longitudinal narrative that follows a chronological timeline, with an emphasis on parsing relevant pertinent “positives” and “negatives” from that narrative. A simple organizing principle is to have patients present their concerns from a chronological perspective, in order for the clinician to develop a clear narrative. “When was the very first time you recall having any problems involving your mental health?” provides a good starting point, followed by “When was the first time you sought any kind of treatment for those problems?” A chronologically organized narrative gives some sense not only about the backdrop and longevity of a psychiatric disorder but, moreover, clues about the degree of distress and disruption caused by symptoms, the potential duration of untreated illness, and symptom severity as reflected by the kinds of interventions that previously occurred. A clinical timeline that starts with years of psychotherapy differs from one that begins with an involuntary psychiatric hospitalization or a suicide attempt; low-grade symptoms that persist for extended periods unnoticed by others, or cause no outward functional impairment, imply a different level of severity and debilitation, and possible prognosis, from those linked with more obvious outward signs of disability. For persistent problems, one always wonders why the patient is seeking help now and not a week or month or two ago.

Careful clinical assessments are not a race to formulate a diagnostic impression as fast as possible; quite the contrary, when facing symptoms that might overlap across two or more constellations (such as anxiety, psychosis, or inattention), the time spent reasoning through a thoughtful differential diagnosis often pays its eventual dividends in perpetuity. Box 1.1 summarizes a number of basic principles for framing a patient’s history within a meaningful clinical context.

Subjective symptoms should correspond to outward signs that together reflect a distinct core underlying problem. Wise clinicians can anticipate problems almost intuitively when they truly recognize the signature pattern of a particular ailment – such as the anosognostic detachment from reality in psychosis, or the flat vacancy and absence of emotion in negative symptoms versus the presence of sadness and “feelingful” despair in depression, coupled with a sheer absence of hedonic capacity. The art of psychiatric evaluation means more than applying DSM-5 (the fifth edition of Diagnostic and Statistical Manual of Mental Disorders; American Psychiatric Association, 2013) criteria to arrive at a most likely diagnosis – or, for that matter, simply making “just” a diagnosis from checklist criteria. It involves sifting relevant from extraneous information in order to render plausible explanations for symptoms, drug effects, or the environmental contexts in which symptom profiles arise. It is more the clinician’s than the patient’s job to order their narrative, and to understand the context in which symptoms arise.

In fact, when we elicit a chief complaint by asking the proverbial open-ended question, “Tell me what brings you here,” an enormous amount of data comes forth in the moments that follow. The “sifting” clinician learns the following by not (yet) interrupting the patient’s verbiage:

• Can the patient tell a coherent narrative? Do they present logical threads that can be followed without the need to interrupt for clarification?

• Does the patient lose their train of thought? If flow of thinking is not linear and coherent, what are the possible explanations? Is a formal thought disorder present? Is the patient intoxicated? Is a delirium, dementia, or other major cognitive disorder present? Could they be malingering?

• Does the patient display intact social cognition? That is, do they check in with the clinician to see if they are being understood? Or are they oblivious to their effect on the listener?

• Is the patient reasonable? Entitled? Demanding? Aggressive or threatening? Cognizant of the impact of their words and actions on other people?

• Do they display insight into the nature of their condition and an appreciation for the risks, benefits, alternatives, and consequences of proposed treatment options?

• Do “pertinent positives” occur contemporaneously in ways that point to a cohesive clinical entity? Or are symptoms disjointed and fail to add up to a recognizable syndrome?

C Are Diagnostic Criteria Met?

Meeting the operational definition of a syndrome is often a bugaboo for both clinicians and researchers. The crux of such approaches to diagnosis involves the concept that diagnoses equate to the number, severity, and persistence of signs and symptoms that comprise the criteria for recognizing a clinical entity as unique. Does fleeting psychosis fall under the heading of trauma-related phenomena or micropsychosis during times of stress in someone with borderline personality disorder, rather than a more full-fledged psychotic disorder? Could a thyroid-stimulating hormone level of 5.1 mU/L really be enough to account for current mood symptoms? Clinical investigators can agonize at length over a given patient’s history in order to determine whether or not formal diagnostic criteria for a particular clinical entity are or are not met, in a rigid and binary fashion.

Clinical investigators undergo formal training in how to administer semi-structured clinical interviews, which they then rely on to form operational definitions of a suspected diagnosis. In clinical trials, diagnosticians must gain inter-rater reliability (meaning, they must demonstrate a minimally acceptable level of consensus agreement on the presence of a particular diagnosis based on interviews that elicit concrete information about symptoms and their duration). There is no reason clinicians working “in the trenches” cannot adopt as rigorous an approach to diagnostic assessment, regardless of the use of formal semi-structured clinical interviews.

Diagnostic interviews are keyed to the concept of reviewing specific symptom criteria and durations, as well as ruling out other causes that might better account for a clinical presentation. Though detailed and time-consuming, clinical interviewers who undergo formal training to conduct such diagnostic interviews markedly increase the reliability with which they can identify specific psychiatric disorders and differentiate them from look-alike mimics. An end result is the determination that a patient either does or does not fulfill the operationally defined criteria for a particular diagnosis. Critics of this approach argue that diagnostic “criteria” are established by committee consensus rather than the laws of nature, and often involve arbitrariness (e.g., defining hypomania by syndromal persistence for at least 4 days, or major depression by at least 2 weeks).

Diagnostic categorization also can change over time in ways that may reflect less science and more the sentiments and vagaries of prevailing opinion (e.g., the construct of somatic symptom disorder replaces the concept of “imagined” or inaccurately perceived health problems in hypochondriasis with the concept of “distress” about health problems, regardless of their objective reality; the emphasis has shifted from misperception or impaired reality testing to a focus mainly on how patients react to or feel about their symptoms).

Nosological systems such as the DSM-5 tend not to be particularly lavish in how they account for the context in which symptoms may arise. Frantic psychomotor agitation could superficially look the same in a patient with psychotic mania as someone trapped in an elevator in a burning building. Attributing an adolescent’s poor school efforts “just” to depression may sacrifice a lot of information if one ignores the context of, say, Julie’s parents’ acrimonious divorce process, Isabel’s sexual abuse by a boyfriend, or David’s experience of bullying for identifying as LGBTQ+. Contexts influence treatment decisions, both pharmacologically and psychosocially, as elaborated further in Box 1.2.

There are both advantages and disadvantages in adopting a “criteria-based approach” to diagnosis. The most obvious disadvantage involves the notion that operational criteria may be reliable (and even then, not always) but not valid. This latter point makes it rather disingenuous to speak of diagnostic “accuracy,” if in fact diagnoses by operational criteria are mainly heuristic constructs that provide a way of organizing narrative information but involve elements of arbitrariness that undermine accuracy. A compelling example might be the categorization of excessive worry as a diagnostic entity. Known as “overanxious disorder” in DSM-III-R (American Psychiatric Association, 1987), the construct was revised in DSM-IV (American Psychiatric Association, 1994) to generalized anxiety disorder (GAD) but criticisms have surrounded both its reliability and validity based on several of its operational criteria. Some authors suggest that determining “excessiveness” of anxiety and worry (an “A” criterion) is subjective and may vary depending on the evaluator; the imposed duration criteria of at least 6 months also has been associated with poorer inter-rater reliability than if a shorter duration (such as 1 month) were acknowledged; and that many of the associated symptoms listed as “C” criteria for GAD are highly nonspecific (e.g., fatigue, poor concentration, insomnia) and unduly overlap with other disorders (such as major depression) (Reference Andrews, Hobbs and BorkovecAndrews et al., 2010).

An obvious advantage of using operationally based diagnostic criteria for clinical decision-making is that doing so minimizes subjectivity or ambiguity about how to characterize the phenomenon being treated; the definition is agreed upon, regardless of whether it is accurate. However, without an appreciation for context, this approach could lend itself to overly concrete thinking among practitioners. Imagine if one concluded that because stimulants treat inattention in attention deficit–hyperactivity disorder (ADHD), they might equally improve attention in people with delirium or dementia; or, if tryptans improve migraine headaches, they should expectably improve all other forms of headache; or, if nitrates help chest pain from angina, why not assume they should also alleviate chest pain from a peptic ulcer or rib fracture? Diagnosticians cannot undertake clinical reasoning without ruling out look-alike conditions that might superficially imitate other clinical entities (phenocopies; see Box 1.3) lest we resign ourselves to clinical decision-making as being no more than a wild-West lawless enterprise.

The nature of enrolling patients in a clinical trial hinges on affirming the specificity of diagnosis – for example:

• A patient with suspected major depressive disorder must manifest at least five of nine symptoms for at least 2 weeks, uncontaminated by other factors that might better account for the presenting features (such as, active substance use or clinically meaningful hypothyroidism); or

• A patient whose “mood swings” are called “cyclothymia” has never been fully manic, nor had a sufficient number or duration of hypomanic or depressive symptoms to constitute a full syndrome of either polarity; or

• “Panic disorder” connotes the occurrence of specific autonomically driven events with physical (not just psychic) manifestations; or

• PTSD is not a catch-all phenomenon that encapsulates any and all forms of highly stressful events – such as difficult relationship break-ups, job losses, or reversals of financial fortune; in fact, the treatments geared to PTSD focus on its recognized clusters, such as avoidance, autonomic hyperarousal (e.g., exaggerated startle response) or involuntary intrusive thoughts and memories causing physiological distress in response to associated cues; or

• A patient who periodically smokes cannabis would not formally be identified as having cannabis use disorder unless they use for increasingly longer periods in larger amounts, their use adversely affects their work and social functioning, physical or psychological problems ensue from use, and other formal diagnostic criteria are met that differentiate “use” from a “use disorder”

Real-world patients do not always fully meet formal diagnostic definitions of a categorical disorder, and real-world clinicians often do not painstakingly appraise every item within a diagnostic checklist. Nevertheless, for better or worse, there is objective merit behind the phrase “the diagnostic criteria are (or are not) met.” Why? In large part, it allows apples-to-apples comparisons between a real-world patient’s presentation relative to the patient descriptions found in clinical trials or textbooks. Disparities mean extrapolation, which in turn means that “real-world” outcomes may differ substantially from “prototypical” patients who embody the characteristics of a textbook presentation.

D Are DSM Criteria Written Mainly for Clinicians or Researchers?

The operational criteria captured in nosologies such as the DSM or the International Classification of Diseases (ICD) are collections of symptoms and duration criteria arrived at by consensus agreement among experts, rather than “absolute truths” found in nature. They are subject to change and can sometime even become eliminated altogether (as in the case of Asperger syndrome) or “voted” into existence by committee opinion (as in the case of disruptive mood dysregulation disorder or major depressive disorder with mixed features). “Cardinal” symptoms are also subject to greater or lesser importance as consensus opinions about psychiatric diagnoses change over time. For example, neologisms, bizarre delusions, and so-called first-rank symptoms of psychosis (e.g., believing one’s thoughts or actions are controlled by outside forces) were once strongly associated with schizophrenia, but eventually were felt to lack diagnostic specificity and consequently “demoted” to the status of holding less pathognomonic importance based on clinical consensus of opinion.

As noted in Section C above, investigators think about psychiatric diagnoses differently than practitioners; like bookkeepers, they focus on whether or not the requisite number and duration of symptoms have been met, and the phrase “the criteria are not met” becomes a ubiquitous refrain when deciding that a patient is ineligible to qualify as a research subject in a clinical trial. Twists occur along the way with regard to problems like “double counting” symptoms that could be attributed to more than one condition. A well-known example is the DSM-5 “mixed features” course specifier, which was conceptually meant to embrace the notion that mania and depressive symptoms could occur on a continuum across all mood disorders. Four particular symptoms – distractibility, irritability, insomnia, and psychomotor agitation (“DIIP”) could occur in the context of either a mania or depression and, consequently, crafters of the DSM-5 suggested that none of these symptoms could be used to constitute a “tie-breaker” when deciding on the presence of an opposite affective pole. Critics of this stipulation have argued that DIIP symptoms can be integral to the construct of mixed states, and to exclude them (as polarity-deciding factors) would be akin to excluding fever as a criterion when differentiating an infection from an autoimmune process. Both perspectives are correct in their own way, and underscore the dilemma for the practitioner (who may be altogether less fastidious in even registering DIIP symptoms as casting a decisive diagnostic vote).

E Hierarchical Diagnostic Treatment Approaches: How to Triage

It should come as no surprise to in-the-trenches practitioners that most patients with significant psychiatric symptoms often have more than one diagnosable psychiatric condition. Part of the assessment challenge is parsing symptoms that could overlap between two or more disorders in trying to understand “overarching” diagnostic constructs from the collision of multiple separate ailments. When is inattention or distractibility an indication of comorbid ADHD rather than an intrinsic component of depression, anxiety, or psychosis? When are problems with impulse control or emotional self-regulation artifacts of a broader condition such as bipolar disorder rather than manifestations of a comorbidity such as PTSD or a significant personality disorder? And perhaps most important of all, when and how does one determine which is the “core” or predominant psychiatric condition and which are – for want of a better term – subsidiary coexisting conditions?

There is often an implicit assumption that if a predominant or overarching condition is recognized, perhaps its successful treatment will lead to some attenuation of the comorbid or subsidiary conditions. This is an interesting but largely empirically untested hypothesis. Some comorbid conditions may spring from a common underlying process but, once initiated, follow their own trajectories and require their own independent treatment. Outside of psychiatry, diabetes may be the most illustrative example. Diabetic patients who develop neuropathy, retinopathy, nephropathy, poor wound healing, and worsening of cardiovascular disease can ultimately attribute blame to how their body manages glucose – and yet, once the wheels have been set in motion for these end-organ consequences of impaired glucose metabolism, fixing the initial source of the problem will not necessarily repair the collateral downstream damage.

In psychiatry, perhaps substance use disorders represent a comparable dilemma when they are viewed as incidental to some larger, overarching clinical problem. When substance use disorders involve problems with mood or anxiety, patients or their families (and sometimes also their clinicians) sometimes may hypothesize that comorbid substance use might evaporate if only a more effective therapy were in place for the more fundamental problem being “self-medicated.” There may very well be instances in which optimal control of mood or anxiety (or other) disorders can help make inroads in active substance use disorders, but a reductive approach such as this discounts the notion that addictions often constitute ailments that exist unto themselves (i.e., disorders of the reward pathway), which typically require their own treatment. Moreover, unmanaged substance use disorders may in turn aggravate and perpetuate a comorbid psychiatric condition such as depression or anxiety. Which condition is subsidiary to which? Or should the preferred rule of thumb be to assume that multidiagnostic clinical presentations are just that, and require separate but coordinated treatments?

Examples of common comorbidities associated with major psychiatric disorders are summarized in Table 1.1. As alluded to above, it is sometimes difficult (and subjective) to classify the “primary” from the “comorbid” condition for many of the scenarios listed below, and it never hurts at least to consider the possibility that many complex/multidiagnostic presentations are two-way streets with traffic that interacts bidirectionally.

F Signs and Symptoms

Signs are objective, outward manifestations of an underlying problem, while symptoms are subjective complaints. In general medicine, a stomach ache is a symptom and abdominal tenderness or grimacing is its corresponding sign. In psychiatry, we expect subjective complaints of sadness or feeling blue to correspond with outward signs of weepiness, a low voice, psychomotor slowing, and exasperation. Patients who identify their mood as depressed would expectably appear unanimated, not so loquacious, and at least somewhat impoverished in their generation of ideas and details, with diminished spontaneity in the course of an interview. In mania, where excess energy and psychomotor activation are fundamental elements, we expect patients to talk fast and be hard to interrupt, use animated gestures, sleep fewer hours, and perhaps make interpersonally provocative or boundary-bending comments to the people with whom they interact; psychomotor retardation with impoverished speech does not reconcile with subjective complaints of euphoria.

Because patients can misidentify their symptoms it is important to clarify the intended meaning of terms they use. Someone who is worried about their cognitive function and reports problems with memory or concentration may be depressed or anxious. Someone who says they feel anxious may mean they have a vague sense of apprehension or anticipation of an imagined catastrophe, or they could mean they are worried their food is being poisoned and someone is following them with malicious intent. Intensity of belief-conviction and the patient’s own willingness to consider more than one explanation for their symptoms provide important context for understanding the nature of an underlying problem.

G Depression as a Disorder of Information Processing

Fundamentally, clinical depression has less to do with life adversities per se than with how the brain processes emotional information. Perhaps nowhere is that more evident than in the case of an impaired hedonic tone. Think of the capacity to detect and experience pleasure as tantamount to the 13th cranial nerve. It can be tested. The diminished ability to perceive pleasure (anhedonia) when an inherently pleasurable sensation or experience occurs reflects a sensory process, on par with intact olfaction or hearing. Significant forms of depression, where medications can be especially useful, tend to involve impaired hedonic capacity. We can assess whether the reward pathway is intact in an analogous way to testing if the olfactory nerve is intact when we ask someone to smell coffee beans or soap. Often this is accomplished more by history-gathering than by performance-based in-office testing. Are inherently pleasurable things still as pleasurable as they have ever been? The distinction between the ability to feel pleasure versus the extent to which life itself is inherently enjoyable is fundamental, inasmuch as clinicians want to differentiate complaints about unfavorable existential circumstances from an impaired capacity to feel positive emotions.

What does this have to do with clinical reasoning and decision-making? In the case of identifying clinical depression, and contemplating the role of pharmacotherapies versus psychotherapies versus, say, prescribing exercise, we are interested in determining if the brain circuits believed relevant to processing pleasurable experiences – the ventral striatum, aka the reward pathway – are intact. This is a critical point when assessing depression as a brain disorder, no different from identifying anosmia or a sinus infection. An impaired capacity to process sensory information lies at the heart of the dysfunctional brain circuitry of depression, and treatment decisions may very much may be targeted to distinct symptom domains such as anhedonia, attentional impairment, or aberrant anxiety processing. Symptom clusters as they may inform differential therapeutics are discussed further in Chapter 9, Section G.

H Interface Symptoms: When Delusions Meet Obsessions

“Overvalued ideas” are isolated, strongly held concepts that take on greater salience for an individual than might seem called for in a given situation. The term may reflect a level of intensity that falls along a continuum influenced by factors such as belief-conviction, awareness of plausibility, insight, idiosyncratic thinking, and cognitive flexibility (where one can consider and vet alternative conclusions behind a given belief). Overvalued ideas move closer to delusions when their content is false, conviction is fixed, and there is generally little to no awareness or recognition about either the falsehood or fixity of thinking. (Contrast this process with either lying (where a false proposition is intentionally brought forth not because it accurately reflects someone’s interpretation of reality but more for the sake of manipulating someone else’s interpretation of reality) or denial (in which someone refuses to acknowledge an objective reality because of its undesirable consequences, rather than an inability to perceive objective reality due to psychosis).) Obsessions are persistent intrusive thoughts, ideas, impulses, or images that cause distress. They differ fundamentally from delusions because they tend to make no sense to the individual who experiences them, and in fact may very well conflict directly with their sense of objective reality (in other words, obsessions involve intact reality testing). Box 1.4 offers further discussion on the concept of schizo-obsessive disorder as a fusion of persistent psychosis with obsessive–compulsive features.

I The Longitudinal Stability of Psychiatric Diagnoses

Are psychiatric diagnoses fluid? Obviously, as additional information or new symptoms can become apparent over the long-term course of managing a chronic or recurrent condition, clinicians would be remiss not to periodically reassess their diagnostic formulations. It is never a bad idea for practitioners to wear a clinical investigator hat and attach their own confidence rating to the diagnoses they make (say, “low,” “medium,” or “high”). Chances are, diagnoses will be less prone to modification the higher one’s initial confidence rating is. If we look to the empirical literature on diagnostic stability, we find the results shown in Table 1.2.

Let us turn next to the interpersonal context in which psychiatric symptoms can present, and the ways in which levels of emotional security or insecurity around important relationships can color the experience of life adversity as well as the experience of symptoms caused by faulty information processing. Here, the concept of attachment theory becomes relevant for diagnostic assessment and subsequent clinical reasoning.

J Understanding Attachment Styles as a Clue to Diagnostic Formulations

British psychiatrist John Bowlby was perhaps the first innovator in the field to draw attention to the ways in which, during development, people form emotional bonds or attachments to identified caregivers with varying degrees of security or insecurity. In adulthood, attachment styles (summarized in Table 1.3) can influence how people form relationships and interact with others, procure emotional supports, and cope with adversities or negative emotions. Interpersonally, attachment styles can be somewhat like A/B/O blood types – relationship incompatibilities may arise when attachment styles clash. Attachment styles can dramatically influence how individuals present with an interpersonal crisis, or color the presentation of a psychiatric condition such as depression or anxiety as it impacts psychosocial functioning. The attachment style of significant others may also influence collateral information provided when a loved one incurs a psychiatric disorder. For example, avoidant/dismissive family members may minimize the magnitude or significance of emotional distress associated with a loved one’s depression; or anxious/preoccupied significant others may overamplify their own sense of distress in response to a loved one’s psychiatric disorder when the disorder threatens to make the loved one less emotionally available to the significant other.

How exactly does an understanding of attachment styles help us make sense of the ways in which a psychiatric problem presents, in order to both better understand the nature of the problem and devise an appropriate treatment? To the extent that both life adversities and psychiatric disorders in and of themselves can evoke distress, the interpersonal ramifications and mode of presentation provide context and colorization to almost any underlying problem. Let us illustrate this with the case of Carlos in Clinical Vignette 1.1.

Let us hope Carlos follows through with the C–L team’s recommendation; it is not simply a “dispo plan” but more importantly probably the best opportunity for fleshing out missing details. What more lies beneath the surface of Carlos’s narrative than we now know? Probably a lot. He could certainly be clinically depressed and, if that is the case, time will help reveal that. He could have an impulse control disorder, although the lack of known previous events makes it hard to draw a pattern, and we are looking for patterns. Collateral history about Carlos would be nice to have. Is he psychotic, and well-compensated (or guarded) enough not to tip his hand on that for the C–L team to appreciate? His attachment style is far from secure. Is he disorganized or preoccupied? Does loss represent to him an unrecoverable catastrophic event, placing him at risk for more of the same depending on what emotional threats await him tomorrow? And is DBT the right psychotherapy modality just for now, or for the long-term? An important point around clinical decision-making will be the extent to which other clinicians find themselves preoccupied with a desire to see Carlos taking some medication, at the expense of trying to better elucidate his risk for self-harm and the nature of his distress.

K Information Flow

Once we have one or more working diagnostic impressions, we tend to structure the flow of an interview to corroborate (or refute) our developing hypotheses. In suspected depression, we often ask about hopelessness as a precursor to questions about suicide, and we ask about suicidal thoughts before asking about actions because thought precedes action. Questions about a patient’s outlook lead to more direct inquiries about negativism and hopelessness, in turn leading to more questions about magnitude of hopelessness and fixed nihilism. In psychosis, we express neutral curiosity about the basis for someone’s expressed beliefs – what makes someone so sure about an idea or perception, or is their belief-conviction not so fixed?

Some symptoms within a syndromal constellation also carry more weight than others. If one were assessing depression, suicidal features would have more centrality and gravitas than, say, poor concentration or initial insomnia. Anhedonia, as noted above in Section G, is another cardinal symptom that likely reflects diminished functioning of the ventral striatum and reward pathway.

L Those Who Do Not Learn from the Pharmacological Past Are Doomed to Repeat It

A branch of statistics known as Bayesian analytics teaches that subsequent decisions are influenced by prior experiences. Unlike flipping a coin – where the umpteenth toss has the same 50–50 chance for calling “heads” as does the first or second toss – past therapeutic undertakings convey information about the probability of future treatment outcomes. The nature and results of past treatments can inform present and future refinements of a given clinical impression. Table 1.4 summarizes a number of pertinent historical features related to previous treatments that, more often than not, provide useful information about a current working diagnosis and evolving treatment plan.

M The Art of Interpreting Gathered Clinical Information

What separates a cub reporter from a seasoned investigative journalist? Consider the inferential and at times forensic qualities that a superb information gatherer must call upon in order to recognize the significance of the very findings they unearth. The essence of clinical decision-making rests on a solid foundation of skills in not simply gathering and ordering relevant information but interpreting it and using the conclusions as a kind of launching pad for knowing pertinent next steps. In medical education, the so-called “RIME” framework has been established to describe the phases of professional growth and development for physicians in training. Formulated originally by Reference PangaroPangaro (1999) for evaluating the development of professional expertise among medical student clerks, the core tenets of the RIME mnemonic focus on transitioning a clinician from a data gatherer to a data interpreter to a problem solver capable of devising strategies to remedy clinical problems, as summarized in Table 1.5.

Let us see how these concepts surrounding clinical reasoning play out in the case of Warren (Clinical Vignette 1.2).

What does the RIME manager or educator notice about Warren? His SNRI (serotonin–norepinephrine reuptake inhibitor) dose has been optimized for more than long enough to judge its success, placing him in the categories of both chronic depression and treatment-resistant depression. The RIME reporter or interpreter may fail to recognize Warren’s physical symptoms as probable discontinuation effects from duloxetine, which he likely has either stopped (if his bodily sensations are recent) or taken erratically (if they have been occurring for an extended period of time). They might also innocently wonder about the possibility of serotonin syndrome until the RIME educator advises them to perform a MedLine search linking the terms “buspirone” + “SNRI” + “serotonin syndrome” or “high-dose buspirone” and “serotonin syndrome” and they discover there are no relevant entries. Hierarchical prioritization demands ruling in or out life-threatening conditions. The RIME reporter/interpreter thinks Warren’s tremor cannot reflect alcohol withdrawal given his more-than-respectable blood alcohol level in the emergency department, but the educator wonders if chronic alcohol use places Warren’s usual blood alcohol level at much higher than 50 mg/dL, meaning that a dip downward from a higher norm could certainly equate to acute withdrawal.

The RIME reporter orders a toxicology screen to see what other substances Warren may have ingested, while the interpreter readies a benzodiazepine test dose to see if his tremor and autonomic signs improve (with an eye toward – depending on the results – likely admitting Warren for alcohol detoxification and gearing up fluid hydration, supplemental thiamine and folate, and an aftercare dual-diagnosis intensive outpatient program). Meanwhile, the RIME manager/educator wonders why Warren has remained for so long on a medication regimen that clearly has done nothing to improve his condition. Does that reflect disengagement or nihilism on the part of the prescriber? Or has the prescriber encouraged changes to his regimen that Warren may not have followed through on? The outpatient prescriber was clearly impressed enough with Warren’s alcohol use and/or risk for gobbling up controlled substances to construct an aggressive regimen of lowish-potency anxiolytic medications that steers clear of sedative-hypnotics. Are we sure Warren has not gotten a hold of benzodiazepines elsewhere?

Unless Warren’s prior follow-through has been poor, his prescriber must have been underwhelmed with Warren’s depression to have left his optimally dosed duloxetine unchanged for so long. There have been no past hospitalizations or suicide attempts to up the ante of how impressive his depression symptoms come across as standout features. But the history also does not reflect aggressive attention being paid to comorbid alcohol use disorder. Where are the prior detoxes? Why no trail of failed naltrexone or disulfiram or acamprosate or even topiramate trials? Is this really Warren’s first rodeo when it comes to addressing his alcohol use, and implicating it as a potential exacerbator, if not even a cause, of his persistent depression?

Detoxing Warren from alcohol is probably the easiest part of this case. The remaining threads are left hanging without so clear a narrative, at least as yet, in order to construct a more cogent and comprehensive treatment plan.