Boundary With Normality

"In DSM-IV, each of the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning) or with a significantly increased risk of suffering death, pain, disability, or an important loss of freedom" (APA, 2000, p. xxxi). If one considers the fundamental, defining features of a mental disorder, it is perhaps apparent that it would not be realistic for a qualitative distinction between normal and abnormal functioning to exist. This will be illustrated with respect to dyscontrol, impairment, and pathology— fundamental components of most concepts of mental disorder (Bergner, 1997; Klein, 1978, 1999; Spitzer & Williams, 1982; Wakefield, 1992; Widiger & Sankis, 2000; Widiger & Trull, 1991).

Dyscontrol

Central to the concept of a mental disorder is dyscontrol (Bergner, 1997; Klein, 1999; Widiger & Trull, 1991). A mental disorder as an "involuntary organismic impairment in psychological functioning" (Widiger & Trull, 1991, p. 112; our emphasis). "Involuntary impairment remains the key inference" (Klein, 1999, p. 424). Dyscontrol is not within the concept of a physical disorder, but it is fundamental to a mental disorder, as the latter concerns impairments to feelings, thoughts, and behaviors over which normal, healthy persons attempt to exert volitional or regulatory control.

Persons who freely choose to engage in harmful or impairing behaviors would not be said to have a mental disorder. Presumably, persons can choose to consume alcohol, take anabolic steroids, shoot heroin, gamble, steal, assault, or engage in deviant sexual acts without being compelled to do so by the presence of a mental disorder. Gambling, drug usage, theft, assaults, and deviant sexual acts can be harmful and maladaptive, but the occurrence of a harmful (or deviant) act would not itself constitute a mental disorder (Gorenstein, 1984; Wakefield, 1992; Widiger & Trull, 1991). Similarly, to the extent that a person can control, modulate, manage, or regulate painful or harmful feelings of sadness, anxiety, or anger, the person would not be considered to have a mood or anxiety disorder (Widiger & Sankis, 2000). "It is the ability to flexibly adjust the way one regulates one's emotions to environmental exigencies that is related to mental health" (Gross & Munoz, 1995, p. 151). It is when a person lacks sufficient control of mood, anxiety, or a harmful behavior pattern that a person might be diagnosed with a mental disorder (Frances, Widiger, & Sabshin, 1991).

There is, however, no qualitative distinction between the presence and absence of self-control. It is not even clear how much volitional or regulatory control a normal, healthy person has over adaptive, healthy behaviors (Bargh & Ferguson, 2000; Howard & Conway, 1986; Kirsch & Lynn, 2000; Wegner & Wheatley, 2000). Both normal and abnormal human functioning is, at best, the result of a complex interaction of apparent volitional choice with an array of biogenetic and environmental determinants.

A continuum (or ambiguity) of self-control is particularly evident in those disorders that involve behaviors that provide immediate benefits or pleasures to the person, such as pedophilia, intermittent explosive disorder, transvestic fetishism, kleptomania, antisocial personality, bulimia nervosa, anorexia nervosa, pathological gambling, and substance-related disorders such as alcohol abuse, cocaine abuse, anabolic steroid abuse, and nicotine dependence. These disorders are difficult to diagnose and are often controversial precisely because there is no distinct point at which dyscontrol occurs (Widiger & Smith, 1994). At one time, persons with alcohol dependence were thought to have a discrete pathology that rendered them entirely incapable of any control of their drinking. However, there is now sufficient research to indicate that persons vary in the extent to which they have inadequate control (Hyman, 2005; Kalivas & Volkow, 2005; Peele, 1984). Treatment for the purpose of controlled drinking is controversial because there is no absolute point of demarcation and persons who lack sufficient control will also lack an adequate awareness of their dyscontrol (Vaillant, 1995). In sum, determination of adequate versus inadequate self-control is fundamental to many social and clinical decisions, but the boundary is at best grossly ill-defined and poorly understood (Alper, 1998; Hyman, 2005; Kalivas & Volkow, 2005).

Impairment

An additional fundamental feature of mental disorders is impairment (APA, 1994, 2000; Wakefield, 1992; Widiger & Trull, 1991). "The definition of mental disorder in the introduction to DSM-IV requires that there be clinically significant impairment" (APA, 2000, p. 8). The purpose of this requirement is to distinguish between a mental disorder and simply a problem in living. "The ever-increasing number of new categories meant to describe the less impaired outpatient population raises the question of where psychopathology ends and the wear and tear of everyday life begins" (Frances, First, & Pincus, 1995, p. 15).

To highlight the importance of considering this issue, the criteria sets for most disorders include a clinical significance criterion (usually worded ". . . causes clinically significant . . . impairment in social, occupational, or other important areas of functioning"). This criterion helps establish the threshold for the diagnosis of a disorder in those situations in which the symptomatic presentation by itself (particularly in its milder forms) is not inherently pathological and may be encountered in individuals for whom a diagnosis of "mental disorder" would be inappropriate. (APA, 2000, p. 8)

DSM-III-R (APA, 1987) failed to include this requirement within the criterion sets for many of the disorders, contributing to a confusion of apparently harmless deviances, eccentricities, peculiarities, or annoyances with the presence of a mental disorder (Frances et al., 1991). For example, in DSM-III-R the attention-deficit hyperactivity and oppositional defiant disorders were diagnosed even if the behaviors resulted in "only minimal or no impairment in school and social functioning" (APA, 1987, pp. 53, 58). Similarly, transvestic fetishism could be diagnosed with DSM-III-R simply on the basis of intense sexual urges, fantasies, and behaviors involving cross-dressing that continued for more than six months (APA, 1987). A man who engaged in this behavior for longer than six months but experienced no impairment in functioning would still have been considered in DSM-III-R to have been mentally ill solely because he engaged in deviant sexual acts for longer than six months. It is possible that a six-month duration is a valid indicator for impairment (as well as dyscontrol) but (assuming that volitional behavior does exist) deviant sexual preferences could also be largely harmless. Therefore, DSM-IV required that "the fantasies, sexual urges, or behaviors cause clinically significant distress or impairment in social, occupational, or other important areas of functioning" (APA, 1994, p. 531).

However, nowhere in DSM-IV is a "clinically significant" impairment defined, not even within the section of the manual identified by the heading "Criteria for Clinical Significance" (APA, 2000, p. 8). It is only stated that this "is an inherently difficult clinical judgment" (APA, 2000, p. 8), and it is advised that the clinician consider information obtained from family members and other third parties. Frances et al. (1995) in fact stated that "the evaluation of clinical significance is likely to vary in different cultures and to depend on the availability and interests of clinicians" (p. 15). Absence of a clear basis for the judgment has also helped fuel the considerable controversy of premenstrual dysphoric disorder, a mental disorder that is diagnosed when normal premenstrual experiences (that occur in a substantial proportion of normal adult women) reach an ill-defined level of clinically significant impairment (Winstead & Sanchez, 2005).

Spitzer and Williams (1982), the original authors of the DSM-IV definition of mental disorder, defined a clinically significant impairment as that point at which the attention of a clinician is indicated. "There are many behavioral or psychological conditions that can be considered 'pathological' but the clinical manifestations of which are so mild that clinical attention is not indicated" (p. 166). They provided three examples: caffeine withdrawal, jet lag syndrome, and insomnia because of environmental noise. Impairments in each case were considered by Spitzer and Williams to be too small to be "justified as syndromes that were clinically significant to mental health professionals" (p. 166). These three examples, however, proved to be ironic, as jet lag syndrome was actually included within DSM-III-R as a variant of sleep-wake schedule disorder (APA, 1987, p. 306); caffeine withdrawal was subsequently included in the appendix to DSM-IV (APA, 1994); and a strong case has been made for the inclusion of caffeine dependence (Hughes, Oliveto, Helzer, Higgins, & Bickel, 1992).

What is considered to be a sufficient level of impairment to warrant treatment probably varies substantially across patients and across clinicians (Samuel & Widiger, in press) as well as often being below the threshold for many of the existing DSM-IV criterion sets. Clark, Watson, and Reynolds (1995) documented well the reliance of clinicians on the category of "not otherwise specified" (NOS) to diagnose subthreshold cases. Whenever this catchall diagnosis is included within a study, it is often the most frequent diagnosis, as in the case of mood disorders (Angst, 1992), dissociative disorders (Spiegel & Cardena, 1991), and personality disorders (Verheul & Widiger, 2004).

New additions to the diagnostic manual rarely concern newly discovered forms of psychopathology; instead, they are typically efforts to plug holes in between existing diagnosis and normal functioning (as well as filling gaps among the existing diagnoses). For example, acute stress disorder is essentially posttraumatic stress disorder with a shorter duration; recurrent brief depressive disorder is major depression with shorter episodes; mixed anxiety-depressive disorder concerns sub-threshold cases of mood and anxiety disorders; binge eating disorder concerns subthreshold cases of bulimia nervosa; and mild neurocognitive disorder concerns subthreshold cases of dementia, delirium, or amnestic disorder (Frances et al., 1995). A fundamental difficulty shared by all of these diagnoses is the lack of a clear distinction with normal functioning. Two cases that illustrate well the absence of a clear boundary between normal and abnormal functioning are minor depressive disorder (which is considered to be a mental disorder, although not yet officially recognized) and age-related cognitive decline (which is not considered to be a mental disorder).

Minor depressive disorder was a new addition to DSM-IV that attempted to plug the gap between DSM-III-R mood disorder and normal sadness. There is considerable reluctance to add a new diagnosis for subthreshold depression (Pincus, McQueen, & Elinson, 2003), but it has been estimated that up to 50% of depressive symptomatology is currently being treated by primary care physicians without any consultation or involvement of a mental health clinician in part because the depression is below the threshold of a mood disorder diagnosis (Munoz, Hollon, McGrath, Rehm, & VandenBos, 1994). Many of these persons would meet the DSM-IV criteria for minor depressive disorder. However, it is acknowledged in DSM-IV that "symptoms meeting . . . criteria for minor depressive disorder can be difficult to distinguish from periods of sadness that are an inherent part of everyday life" (APA, 2000, p. 776). Only two distinctions are provided, one of which is a two-week duration. If a person is sad for less than two weeks, it is normal sadness. If it lasts longer than two weeks, it is a mental disorder. This is comparable to diagnosing cross-dressing as a transvestic fetishism if it is done longer than six months (APA, 1987). The second distinction is that "the depressive symptoms must cause clinically significant distress or impairment" (APA, 2000, p. 776) but, again, clinical significance is left undefined.

Age-related cognitive decline was a new addition to the section of the manual for conditions that are not mental disorders but might be the focus of clinical attention. "Cognitive decline in the elderly can be considered dimensionally . . . , involving aging-associated cognitive decline, mild cognitive impairment, and dementia" (Caine, 1994, p. 335). "It may be very difficult to establish an arbitrary or numerical level where a disease state should be proclaimed" (Caine, 1994, p. 334). Age-related cognitive decline concerns "problems remembering names or appointments or . . . difficulty in solving complex problems" (APA, 2000, p. 740). Persons with this condition are often troubled by their cognitive deterioration and they seek the help of clinicians who specialize in the treatment of dementia, thereby meeting the threshold for a clinically significant level of impairment proposed by Spitzer and Williams (1982). However, the DSM-IV Task Force decided that age-related cognitive decline should not be classified as a mental disorder because the decline in cognitive functioning is the result of "the aging process that is within normal limits given the person's age" (APA, 2000, p. 740). The level of impairment is sufficient to warrant professional intervention but it is not considered to be a mental disorder because the level of impairment is normative for that time in life. One might question, however, whether being close to the norm is any more relevant for a diagnosis than being deviant from the norm (Frances et al., 1991; Gorenstein, 1984). The fact that age-related cognitive decline is the result of the normal (i.e., common) process of aging does not indicate that it is adaptive, healthy, or without an underlying neuropathology. The aging process is part of the explanation for the development of neuropathology. Fortunately, physicians do not apply the same reasoning by judging that deteriorations in the functioning of one's vision, liver, or bladder are not disorders because they are simply the result of aging and are common to persons within one's age group.

PAtHoLogy

Fundamental to many definitions of mental disorder is the presence of some form of pathology (Klein, 1978; Wakefield, 1992, 1997). "The necessary crucial inference is that something has gone wrong, not simply that something is undesirable or rare" (Klein, 1999, p. 421). Clinicians do not treat normal, healthy functioning; clinicians treat pathologies in cognitive, interpersonal, neurochemical, or psychodynamic functioning. Textbooks of psychopathology, such as this one, are largely efforts to identify and characterize pathologies that are the bases for each respective mental disorder. Presumably, there are persons who lack these pathologies. Such persons could be described as having normal, healthy psychological functioning. The boundary between normal and abnormal psychological functioning might then be identified by the presence versus absence of a respective pathology (Klein, 1978).

Missing from the diagnostic criterion sets in DSM-IV, however, are references to underlying pathologies (Wakefield, 1997). Explicit within the DSM-IV definition of mental disorder is that the condition "must currently be considered a manifestation of a behavioral, psychological, or biological dysfunction in the individual" (APA, 2000, p. xxxi) but few, if any, of the criterion sets refer explicitly to a behavioral, psychological, or biological dysfunction or abnormality. The diagnostic criterion sets emphasize instead the distress or impairment that is presumably the manifestations of an underlying pathology. Perhaps inclusion of the underlying pathology within a diagnostic criterion set would provide a scientifically and clinically meaningful distinction between a respective mental disorder and normal (nonpathological) functioning (Spitzer & Wakefield, 1999; Wakefield, 1997; Wakefield & Spitzer, 2002).

A limitation of this proposal, however, is the absence of consensus as to fundamental pathologies that should be required. Pathologies are not currently included within diagnostic criterion sets in part because there is insufficient empirical support favoring one particular cognitive, interpersonal, neurochemical, or psycho-dynamic model of pathology over another (Widiger, 2004). Wakefield (1997), for example, indicated that in order to provide a meaningful distinction between major depressive disorder and normal bereavement, it is "necessary to formulate some account . . . of the evolutionary programming of the mechanisms with respect to what kinds of triggering circumstances are supposed to cause which kinds of responses (e.g., loss-response mechanisms are designed so that perceptions of major losses trigger roughly proportional sadness responses)" (p. 647). Wakefield's (1992) conceptualization of mental disorder is tied to evolutionary theory. Evolutionary theory has enriched current understanding of the etiology and pathology of many mental disorders but it is unclear whether the normal and pathologic behavioral response mechanisms from the perspective of evolutionary theory can be adequately specified for the purposes of a clinician's diagnosis. In addition, because it is a model of psychopathology that is derived from a particular theoretical perspective, it may not be capable of serving as a general definition of mental disorder that would be compatible with or suitable for alternative theoretical models (Bergner, 1997; Lilienfeld & Marino, 1999; Widiger & Sankis, 2000).

Even if clinicians and researchers agreed on a particular theoretical model of pathology, it is unclear whether qualitative distinctions between normal functioning and abnormal pathologies could be identified. Klein (1999) believes that there are qualitative distinctions between normal and abnormal neurochemical functioning that would provide a compelling basis for classification. As suggested by Klein, "currently, positive experience with psychopharmacological agents, which have little effect on normal people but have marked benefits on patients with chronic disorders, leads to the inference of something chronically but reversibly wrong" (p. 425). However, there has not in fact been much research on the effects of current psychopharmacological agents on normal neurochemical functioning, and what limited research there is contradicts Klein's assertion.

For example, Knutson et al. (1998) administered paroxetine, a selective serotonin reuptake inhibitor (SSRI), for four weeks in a double-blind study to 23 of 48 normal volunteers. None of the participants met currently, or throughout their lifetime, the DSM-IV diagnostic criteria for a mental disorder, as assessed with a semistructured interview. None of them had ever previously received a psychotropic medication, had ever abused drugs, or had ever been in treatment for a mental disorder, nor were any of them currently seeking or desiring treatment for a mental disorder. In sum, they were in many respects above normal in psychological functioning. The parox-etine and placebo treatments continued for four weeks. Knutson et al. reported that SSRI administration (relative to placebo) reduced negative effects and increased social facilitation. The magnitude of changes in functioning even correlated with the plasma levels of SSRI within the treatment group. "This is the first empirical demonstration that chronic administration of a selective serotonin reuptake blockade can have significant personality and behavioral effects in normal humans in the absence of baseline depression or other psychopathology" (p. 378). More generally, effectiveness of anxiolytics and antidepressants for clinical treatment might be their ability to impair, inhibit, or block normal neurochemical mechanisms of sadness and anxiousness rather than reversing or altering pathological neurochemical processes.

Mayberg et al. (1999) investigated with positron emission techniques two complementary alterations in mood: transient sadness provoked in healthy volunteers and treatment-induced resolution of dysphoria in clinically depressed patients. The results indicated "reciprocal changes involving nearly identical limbic-paralimbic and neocortical regions" (pp. 678-679). In other words, the neurophysiology of a mood disorder might be, at best, only quantitatively different from the neuro-physiology of normal sadness. Kendler (2005) goes further to suggest for anxiety disorders that neurophysiologically "a panic attack during a near-fatal climbing accident in a psychiatrically healthy individual or in a crowded shopping mall in a patient with agoraphobia are probably the same" (p. 437).

No neurophysiological laboratory technique is currently able to identify the presence of psychopathology independent of or blind to a clinical diagnosis (Steffens & Krishnan, 2003). Substantial attention is being given to structural and functional brain imaging with the hope that these instruments could be used eventually to diagnose neurophysiological pathology (Drevets, 2002; Epstein, Isenberg, Stern, & Silbersweig, 2002). However, there is a virtual absence of research indicating their ability to provide independent, blind diagnoses. Despite enthusiasm for their potential diagnostic value, there are no studies that have assessed the sensitivity and specificity of neuroimaging techniques for the diagnosis or differential diagnosis of specific mental disorders (Steffens & Krishnan, 2003). The diagnosis of a mental disorder requires instead an assessment of the person's behavior within an environmental context, as "functional impairment or disability, not the presence of a lesion, is the essential element in the medical concept of disease" (Bergner, 1997, p. 245).

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