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Abstract

For any diagnostic system to be clinically useful, and go beyond description, it must provide an understanding that informs about aetiology and/or outcome. DSM-III and DSM-IV have provided reliability; the challenge for DSM-V and DSM-VI will be to provide validity. For DSM-V this will not be achieved. Believers in DSM-III and DSM-IV have impeded progress towards a valid classification system, so DSM-V needs to retain continuity with its predecessors to retain reliability and enhance research, but position itself to inform a valid diagnostic system by DSM-VI. This review examines the features of a diagnostic system and summarizes what is really known about mood disorders. The review also questions whether what are called mood disorders are primarily disorders of mood. Finally, it provides suggestions for DSM-VI.

Keywords

bipolar disorder depression diagnostic systems mood disorders

The classic book by Robert Kendell (1975), The role of diagnosis in psychiatry, remains a timeless contribution to discussions on the purpose and features of any diagnostic system [1]. In that book Kendell outlined that in all settings, including health services; people have three sets of features: those that are unique to the individual; those that are shared with some people but not others; and those features common to all people. These three sets of features are all of importance, but to varying degrees in different circumstances. In mental health unique features include an individual's life story; shared features include diagnosis, while common features include beliefs that all people should be treated with respect.

An individual's unique features include their life story, and has four domains: the story of their genes; the story of life experiences; the story of the life lived; and the story of lives created. We can start with the story of our genes, which includes our immediate family history and ancestors, but also our further distant human ancestors [2] and our more distant human and non-human ancestors [3]. Evolutionary psychology and psychiatry are critical components for any comprehensive understanding of mood and other mental disorders [4–6]. Contrary to earlier sociological myths, human biological evolution is ongoing [7]; it has not been replaced by social evolution. Indeed, the rate of genetic change in humans may be increasing rather than decreasing.

Of the four domains in an individual's life story, psychiatry has most concentrated on life experiences, particularly adverse life experiences. There is a large amount of research on the consequences of adverse early life experiences, particularly abnormalities of mother–child bonding, of physical and sexual abuse, of neglect and of parental overprotectiveness. At times psychiatry has viewed the family environment as being of particular importance, but the evidence is now clear that outside of eating disorders, shared family environment makes a minimal contribution to the aetiology of most mental disorders [8]. There is also a large amount of research on recent adverse life events, especially in relationship to the onset of mental disorders such as depression. Psychiatry, perhaps because the information is difficult to obtain within the context of usual practice, has tended to ignore life experiences during the first 9 months of life despite growing data that in utero drug [9], [10], alcohol and nicotine exposure [11], and that maternal mental state and nutritional status during pregnancy are of considerable importance to an individual's later mental and physical health.

Psychiatry has also tended to neglect the story of the life lived and the story of lives created. This may be because these are more relevant to psychological health rather than to psychopathology. Psychiatry has tended to be more focused on the consequences of the ending of relationships, rather than the making of relationships. One of the most protective factors for young women from abusive and disrupted family backgrounds, however, is to ‘marry well’ [12]. Adolescent offending is associated with deviant peer association [13], which is no surprise to the many parents who work hard to get their children to mix with the right group. Similarly we do not focus on success in the face of adversity, despite George Vaillant highlighting how one positive relationship with an adult can compensate for considerable childhood adversity [14]. There is a similar lack of clinical and research focus on lives created, despite evidence that the number of young children is a major protective risk against suicide in young women, and despite suggestions that happiness is better correlated with what you give than with what you have. Finally, understanding development and life stories is not nature versus nurture, but nature via nurture [15].

The features that an individual shares with some but not with others includes, in a mental health setting, diagnosis. Diagnosis is the primary focus of this review and will be discussed in further detail. Other shared features, of varying importance to health, include ethnic identification, community and sport group identification, height and weight. There is considerable evidence that ethnic identification impacts on health inequalities, as is only too apparent when the data on the health of indigenous people are considered [16].

Within a mental health setting, features that should be common to all who use mental health services will include service philosophies, standards and practices. In reality unfortunately, some patients within services are treated better than others, with the most common blatant injustice being the maltreatment of those labelled as only having a personality disorder. Against current diagnostic criteria, personality disorders are markedly under-diagnosed in usual clinical practice [17], because clinicians do not enquire about the diagnostic features that currently constitute the criteria for making such a diagnosis. Conversely, audit of clinical notes suggests that they seldom contain the information to justify any personality disorder diagnosis that is made, again because clinicians do not enquire about the features that justify making such a diagnosis. Therefore, false positive and false negative personality disorder diagnoses are the norm in most mental health services, and this has considerable impact on what should be universal standards of non-stigmatizing acceptable practice [18].

Reliability and validity of diagnostic systems

As highlighted by Kendell two key features for any diagnostic system are reliability and validity [1]. Reliability is easier to define, measure and achieve with diagnostic systems, but without reliability we cannot achieve the more elusive goal of validity. Research leading up to DSM-III during the 1970s highlighted the low reliability of psychiatric diagnoses across countries. In principle the introduction of diagnostic criteria should enhance reliability, although it is surprising the number of clinicians who, despite saying that they are using DSM-IV criteria, cannot actually recall what the diagnostic criteria are. Or even if the criteria are known they are not used; for instance, how often is a patient with mania described as having hypomania, despite them having impairment or hospitalization as a consequence of their manic symptomatology. Or how often is the diagnosis of adjustment disorder with depressed mood made, even though the individual has had five depressive diagnostic criteria for at least 2 weeks?

Validity has a variety of definitions, but in relationship to diagnostic systems we are mainly interested in predictive validity. In brief, a valid diagnosis will provide us with additional information about the aetiology and/or prognosis about an individual's clinical state (beyond description). When an individual presents to health services they often have three key questions to which they are seeking answers. These questions are: what is wrong, why has this happened, and what will happen. Our answers, in medical jargon, are in terms of diagnosis, aetiology and prognosis.

For mood disorders a valid diagnostic system will provide additional information relevant to understanding the aetiology of both the current mood episode, as well as the longitudinal pattern of mood episodes. For mood disorders, thinking separately about episode and diagnosis is vital for clarity. In the case of bipolar disorder, the single largest risk factor relevant to understanding a lifetime diagnosis is knowledge about genetics and family history. The major exception is with late-onset bipolar disorder, when a key risk factor may be structural brain changes. To understand the aetiology of a manic episode in someone with bipolar disorder, it is most relevant to know about compliance with prescribed medications such as lithium, use of antidepressants, use of non-prescribed medications including alcohol, seasonality, and disruptions to circadian rhythms and sleep. Underlying some of these risk factors, a clinician will need to understand the patient's views about their bipolar disorder, their attitudes to medications, their ability to recognize and act on early signs of a manic relapse and recent life events that may have contributed to sleep disruption [19–21].

In relationship to prognosis, a valid diagnostic system should provide additional information about the natural history of the current episode, including the likelihood of both remission and recovery from the current episode and the likelihood of future recurrence. In the case of a depressive episode we also wish to know the likelihood of a future manic episode. For instance we now know that young people who present in a depressive episode with some or all of the following features have a high probability of developing bipolar disorder when followed over time: psychotic symptoms, loaded family history of bipolar disorder, hypersomnia, and retardation [22], [23]. Beyond natural history, patients want to know whether there are any effective treatments for the condition they have, whether those treatments may work for them, and whether the treatment options may have potential adverse effects.

What have DSM-III and DSM-IV achieved?

DSM-III and its successor DSM-IV have potentially achieved a reliable diagnostic system, which should be the first step towards a valid diagnostic system. The ‘followers of Spitzer’, however, believed that DSM-III provided a valid diagnostic system, and in so doing fostered research that has enshrined current non-valid diagnostic entities (e.g. major depression) and have stifled research that may have led to a valid diagnostic system. In addition the tick-box mentality promoted by the checking off of diagnostic criteria has meant that clinicians have failed to understand and grasp the full phenomenology associated with depressive and manic states. Of the potential criteria for making a diagnosis of depression, nine symptoms were chosen by a committee and enshrined. Some key symptoms, such as anger, irritability and social withdrawal in depression have been ignored, while of the existing nine criteria some are almost certainly redundant for the purposes of making a diagnosis [24].

Dilemmas for DSM-V and DSM-VI

If DSM-III and DSM-IV have increased research and provided reliability, how should we proceed with the classification of mood disorders in DSM-V and DSM-VI? The time to DSM-V is too short to allow the development of a research agenda that will provide a valid diagnostic system. Funding bodies should, however, be actively encouraging research projects to ask questions about the validity of existing diagnostic criteria, while asking other research questions. For instance, in a recent psychotherapy clinical trial in anorexia nervosa we knowingly changed the DSM-IV criteria by dropping the requirement for amenorrhoea and changing the weight loss requirement [25]. There were no notable differences between those subjects who did or did not meet the weight loss criteria currently specified by DSM-IV, while anorexic women with and without amenorrhoea differed with regard to cigarette smoking and personality traits, but not on core features of anorexia nervosa [26].

It is therefore strongly recommended that DSM-V does not make many changes from DSM-IV, and when it does then it should be for very clear reasons that are based on research rather than politics. This will help maintain a continuity of knowledge and practice. DSM-V, however, should be structured to promote, rather than stifle, the search for validity, and could add additional domains that may be relevant to the search for validity-driven changes in DSM-VI.

What do we know about the aetiology of mood disorders?

In contemplating how diagnostic systems for mood disorders should change it is relevant to review what we know about the aetiology of these disorders. We also need to keep in mind that depressive states are common; manic states are less common than depressive states [27–30]; depressive states often coexist with anxious or agitated states; and depressive and manic states may coexist (mixed mood states). Psychotic symptoms may occur in both depressive and manic episodes, and are especially common in mixed states. What we know includes the following: (i) depressive states are familial and genetic, but the genes for depression are likely the same genes for generalized anxiety and for negative affect personality traits, often called neuroticism or harm avoidance [8]; (ii) adverse childhood experiences, including abuse and neglect, increase the risk for depression [31–33]; (iii) past experiences of depression increase the risk for future episodes of depression; (iv) anxious personality traits definitely increase the risk of depression, while perfectionistic and impulsive traits may increase the risk of future depression [8]; (v) certain drugs and alcohol may induce depressive episodes; (vi) recent adverse life events and ongoing life adversity increase risk for the onset of depressive episodes avoidance [8]; (vii) a personal or family history of mania increases the risk of depression; (viii) manic states are familial and genetic, but the genes for mania and depression may only partially overlap [34]; and (ix) depressive states become more common during the adolescent years, and are highly likely influenced by sex hormones [35], [36].

What do we know about the outcome of mood disorders?

In considering what we know about the outcome of mood disorders it is relevant to think about both the outcomes and consequences of them. What we know includes the following: (i) even without any specific treatment people may recover from both depressive and manic episodes; (ii) depressive episodes are usually recurrent and/or chronic [37], [38]; (iii) manic episodes are usually recurrent, and only occasionally chronic; (iv) incomplete recovery (residual symptoms) from a depressive episode predicts future depressive episodes [39–41]; (v) depressive episodes are associated with a markedly increased rate of suicide attempts and of suicide [42], [43]; (vi) depressive episodes may markedly interfere with usual functioning and life satisfaction; (vii) manic episodes may markedly impact upon usual judgement, and disrupt usual social and occupational functioning; (viii) depressive episodes respond to a variety of treatments, including psychotherapies (e.g. cognitive therapy, interpersonal psychotherapy), pharmacological treatments (e.g. selective serotonin re-uptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs)) and electroconvulsive therapy; (ix) manic episodes respond to a variety of treatments including antipsychotic drugs and mood stabilizers; and (x) future mood episodes can be prevented by ongoing treatment [44–47].

Boundaries of mood disorders

We often like to think that disorders should have clear boundaries, but why would nature be designed to have such clear boundaries? If there is an abnormality in one aspect of human functioning why should that be independent of abnormalities in other domains of functioning? If the prefrontal cortex is critical to the integration of emotions, thoughts and behaviours, why should disorders of emotion be distinct to disorders of thinking or disorders of behaviour? But please do not think that this represents a call for the misguided notion of a unitary psychosis or a single dimensional view of mental disorder. Instead, it is more appropriate to think about disorders as groups of overlapping ‘fuzzy sets’. Furthermore, there is and will continue to be debate about whether our disorders are best conceptualized as categories or dimensions. While modern statistical approaches can provide answers to such questions, the answer as to whether clusters of symptoms are best seen as categories or dimensions can depend upon which symptoms are included. Even to date, however, some of the results of such modelling may not have produced the results expected by some; for instance anxiety may be categorical but depression dimensional, and some personality disorders may well be categorical and not dimensional [48–52].

Boundaries of major depression

DSM-IV defines a major depressive episode as at least five symptoms for a period of at least 2 weeks; but neither five criteria nor a duration of 2 weeks is a valid cut-off. Some of the most interesting data on this issue come from an examination of subthreshold depression. In the Christchurch Health and Development Study, Fergusson et al. showed that at age 18: 18% had met criteria for major depressive disorder (MDD) during the preceding year, 7% had subthreshold depressive symptoms (STDS) and 75% reported no depressive symptoms (NoDS) [53]. Seven years later, at age 25: 39% of those with MDD at 18, 33% of those with STDS at 18, and 16% of those with NoDS at 18 experienced depression. At 25 years: 9% of those with MDD, 7% of those with STDS and 2% of those with NoDS made a suicide attempt. At age 25: 27% of those with MDD, 26% of those with STDS and 11% of those with NoDS sought treatment for depression. Therefore, the most relevant cut-off for predicting future depression and suicide attempts from information at age 18, is not the boundary between major depression and subthreshold depression, but the boundary between the 75% with no depressive symptoms and the 25% with any depressive symptoms.

Currently a DSM-IV major depressive episode is not diagnosed if the symptoms are due to uncomplicated grief. Recent research has challenged whether a wider range of loss experiences should not also be included as exclusion criteria [54]. This issue would then be related to the criteria for an adjustment disorder with depressed mood, or indeed should any diagnosis be made. In other words, under what circumstances would the presence of depressive symptoms be deemed normal and not justify any diagnosis?

Boundaries of mania

DSM-IV arbitrarily defines mania as being of at least 1 week's duration and association with impairment, psychosis or hospitalization. Hypomania is defined as being of at least 4 days duration and the absence of impairment, psychosis or the need for hospitalization. It is difficult to find any data that support either the duration or the impairment requirements specified in DSM-IV; perhaps they were first approximation reasonable guesses by a committee in the absence of data. DSM-IV has no criteria for episodes of mania/hypomania <4 days duration, although it is possible to make a diagnosis of bipolar disorder not otherwise specified in some such situations. Hypomanic episodes of <4 days are relatively common (approx. as common as hypomanic episodes of ≥4 days), and the presence of hypomanic episodes of <4 days appears to have comparable relevance to a bipolar family history and to personality traits as ≥4 day hypomanias. The impairment criteria, especially hospitalization, are extremely arbitrary, and the impairment criteria in clinical practice are applied with little consistency [55–60].

Boundaries with anxiety disorders

Genetic studies across the range of depressive and anxiety disorders suggest that there is an overlap of genes between major depression and generalized anxiety disorders, while the genes for phobic disorders (and probably obsessive–compulsive disorder) may be distinct [8]. At minimum, this suggests that what is currently called generalized anxiety should be combined with major depression under one diagnostic category. It has been suggested that depression and generalized anxiety should be combined under a broader grouping of the distress disorders, while the phobias and obsessive–compulsive disorder would be lumped as the fear disorders [61]. Indeed, it is difficult to find any aetiological, treatment or outcome data that really differentiate major depression from generalized anxiety disorder, except perhaps that loss events trigger depressive symptomatology, while fear and uncertainty trigger anxiety symptomatology? Both major depression and generalized anxiety disorder share genes, early life and recent life events as aetiological factors; they both respond to a variety of antidepressant drugs and psychotherapies, and they are both prone to be chronic and/or recurrent.

While less relevant to classification, the patterns of comorbidity between mood disorders and anxiety disorders are worthy of more attention. Phobic, panic and obsessive–compulsive disorders are frequently comorbid with depression. What is less well recognized, however, is that the comorbidity of these disorders with bipolar disorder are even greater, yet clinicians seeing patients with panic and obsessive symptoms seldom enquire about bipolarity [62], [63].

Boundaries of mood disorders with personality

DSM-III separated axis I disorders such as mood, anxiety and psychotic disorders from the axis II personality disorders. This separation contributed to research into personality disorders, including the reliability of the personality disorder diagnoses, but was this separation valid? This review has already highlighted that the genes for axis I depressive and anxiety disorders are shared with the genes for negative affect/anxious personality traits. It is also likely that some of the early adverse life experiences that are risk factors for depression are also risk factors for increasing negative affect personality traits. For instance childhood abuse and neglect may make individuals more anxious.

DSM-III and DSM-IV assume that mood disorders are episodic and that personality disorders have an early onset, are persistent and stable. There is now considerable evidence, however, that this differentiation is not tenable. Early onset depressive disorders are frequently chronic, and the stability of many personality disorders, especially cluster B disorders such as borderline personality disorder, frequently remit with time and treatment of associated axis I disorders, or treatment of the personality disorder itself [64–66]. The differentiation between rapid cycling bipolar disorder (especially ultra-rapid) and affective instability in borderline personality disorder is not as clear as some believe; and both may sometimes respond to treatment with antipsychotic drugs and/or mood stabilizers [67], [68].

Cloninger, in his evolving psychobiological model of personality, was one of the first to explicitly state that risk for axis I disorders is due to the inheritance of genes for personality traits [69–71]. Therefore, if we inherit the genes for high harm avoidance we are at increased risk, not only of being anxious, but of having axis I depressive and anxiety disorders, and of having axis II avoidant and other cluster C personality disorders. If we have the genes for high novelty seeking, we are likely to be impulsive, at risk for early onset alcohol dependence, and for borderline and antisocial and other cluster B personality disorders. Novelty seeking decreases with age, so people may become less impulsive, recover from early onset alcohol dependence and grow out of their cluster B personality disorders.

If the same genes influence anxious personality traits, cluster C personality disorders and axis I depressive and anxiety disorders, does it make sense in a diagnostic system to make them into three distinct groups of disorders? Older psychiatry textbooks sometimes had one chapter on personality and neurotic disorders; perhaps that was more valid than having three distinct chapters on depressive, anxiety and cluster C personality disorders?

Researchers such as Akiskal et al. have also highlighted affective temperaments, especially hyperthymia, cyclothymia and dysthymia [72], [73]. These temperaments may either be forme fruste of full blown disorders or may represent the personality substrate from which mood disorders develop. But although clinicians may frequently use such terms, they are not currently captured in any classification system. These affective temperaments have considerable face validity and require more research so that they may be included in future classification systems.

Boundaries with psychotic disorders

Psychotic-like symptoms appear to be relatively common in the population at large and likely occur in many people when suffering from a moderate or severe depressive or manic episode. Full blown delusions, and sometimes hallucinations, may occur during depressive or manic episodes. The boundaries of inflated self-esteem, grandiosity and grandiose delusions, however, are not well demarcated, and there is no real evidence that the demarcation has any prognostic or treatment relevance. Similarly, the boundaries of low self-esteem, self-blame, and ideas of guilt and delusions of guilt are difficult to clearly define.

At another boundary, there can be considerable uncertainty about the differential diagnosis of psychotic mania and schizophrenia. With schizophrenia and bipolar disorder there may be some shared genes, but there are also genes that are not shared. Current approaches to the classification of psychotic disorders will likely evolve as our understanding of the genetics and neurocircuitry of these disorders advances [74]. The childhood precursors of bipolar disorder and schizophrenia are, however, quite distinct [75]. Therefore, despite some diagnostic uncertainty and some shared genes, there remain very good reasons for not lumping bipolar disorder with schizophrenic disorders in any future diagnostic systems. Schizoaffective disorder, bipolar type, however, should almost certainly be moved from the schizophrenic disorders and into the mood disorders [76], [77]. This author believes that the most common presentation of schizoaffective disorder, bipolar type arises from partial treatment of bipolar disorder with psychotic features, which results in the affective syndrome being less prominent than the persisting psychotic symptoms; it is speculated that withdrawal of medications in most people with schizoaffective disorder, bipolar type would lead to the clear re-emergence of the full affective syndrome.

Interfaces of mood disorders with organic and drug-induced states

This is a substantial topic and beyond the scope of this review, but there are some limited issues relevant to mood disorder diagnosis, which require a brief comment. When mania or hypomania is induced by antidepressant or related drugs, it is recommended that the diagnosis should not be that of an organic or drug-induced disorder, but should be classified primarily as a mood disorder, with the rider or specifier that the episode was substance induced. Perhaps the same should apply to drug- or alcohol-induced depressive states as well?

When depressive and manic symptoms occur simultaneously

Mixed mood states are common in people with bipolar disorders; recognition of them is poor, and understanding of them is necessary to developing any satisfactory classification system for mood disorders [78]. That depression and mania may coexist means that depressive and manic states are not opposites. Perhaps the conceptualizing of mania and depression as being orthogonally related allows that any mixture of depressive and manic states is feasible. It is also likely, however, that in some situations mixed states are transitional states, and reflect that an individual is moving from a more pure manic state when euphoria, activation and thought content are highly linked, into a mixed state with loss of euphoria and the emergence of negative thought content but persistence of activation, into a depressive state with linked dysphoria, anergia and negative thought content.

Mood disorder specifiers

DSM-III and DSM-IV use specifiers, beyond episodes and disorders, as a method of providing additional information to clinicians that may be relevant to aetiology or outcomes. Most specifiers provide further information about current mood episodes, but rapid cycling and seasonal portray information about the pattern of episodes. Rapid cycling suggests a poorer response to lithium treatment [79], while seasonal opens the question of whether lack of light is a risk factor, and suggests light treatment as an option to improve outcomes. The specifier single episode or recurrent is relevant to making estimates about the likelihood of further recurrences and to treatment planning decisions on continuation or maintenance treatment. The mild, moderate or severe specifier assists with treatment planning, because in depression of mild severity most specific treatments may not be better than placebo, while in severe depressions there may be poor responses to both placebo and perhaps to psychotherapies [80–82]. The presence of psychotic features in depression predicts a minimal response to placebo, a poor response to TCAs, and probable benefit from combined antidepressant and antipsychotic drugs or electroconvulsive therapy [83], [84]. The limited studies to date, however, have not shown that psychotic depression has a poor response to SSRIs [85]. In young people with depression the presence of psychotic features predicts a higher likelihood of current or future bipolar disorder [22], [23]. The specifier melancholia is controversial; some believe it is a clear and distinct subtype, but epidemiologically it is not distinct, it may respond to psychotherapies, and it does not breed true across recurrent episodes. DSM-IV did retain the melancholic specifier, to promote further research, because it did not want to see it prematurely discarded from diagnostic consideration [86], [87]. The specifier atypical depression provides recognition that some depressions respond much better to monoamine oxidase inhibitor (MAOI) antidepressant drugs than to TCAs [88]. Before the SSRIs became the usual first-line antidepressants, knowing which depressed patients had a low likelihood of responding to a TCA was very important, but is probably of lesser importance in current clinical practice. The symptoms that comprise atypical depression, however, do not make a coherent syndrome [89], and it may be the personality trait of sensitivity to interpersonal rejection that best differentiates TCA and SSRI or MAOI responders [90].

But are they really mood disorders?

So far in this review I have accepted the prevailing paradigm that episodes of depression and mania are best conceptualized as disorders of mood. But is mood disturbance really the critical and defining feature? By calling them mood disorders we may well be limiting the way in which we are thinking about and researching these disorders.

It can be argued that depressed mood is one of the least relevant criteria for identifying the core features of a depressive episode. Perhaps the more fundamental features are anergia (loss of energy and motivation) and anhedonia (loss of pleasure). Perhaps dysphoria arises from being in an anergic and anhedonic state, rather than being a fundamental feature. Similarly, it can be argued that euphoria is not the defining feature of mania, but that activation and increased drive and energy are more fundamental features. If an individual is activated and energized they are likely to feel great (euphoric), especially when they are getting their own way, but in an activated and energized state euphoria may quickly turn to irritability, anger or dysphoria when an individual is frustrated by other people or by their current circumstances. Mood itself is probably an epiphenomenon, rather than the fundamental abnormality.

Speculative options for DSM-VI

Because there is insufficient time for DSM-V to obtain validity data to justify many changes to current diagnostic systems, it should just be altered with a view to promoting a better and more valid DSM-VI. By DSM-VI it will have become accepted that mood disorders are better called disorders of energy and drive; anxiety disorders, mainly the notably phobias, will be called the fear disorders. Obsessive–compulsive disorder will be distinct from the disorders of energy and drive and may be included within the disorders of fear, or may be distinct again.

Because neuroscience research will have advanced sufficiently we will know the brain circuitry of energy and drive and the brain circuitry of fear. Although there will be distinct abnormalities of neural circuitries for each group of disorders, they will not be independent of each other.

Given that disorders of energy and drive are so often chronic and/or recurrent there will need to be a method to collect and collate both the current mental state/episode and the longitudinal history. Indeed, often the critical information for making a diagonsis of an energy and drive disorder is obtained from the longitudinal history of both the patient and a relative.

Current episode (most recent episode)

The nature of the current or most recent episode will need to be noted, perhaps as one of the four A syndromes: (i) anergic, anhedonic syndrome (retarded depression); (ii) activated, driven syndrome (mania); (iii) anxious dysphoric syndrome (anxious depression or generalized anxiety); and (iv) agitated syndrome (mixed states).

For any such episode there will need to be additional information about severity, duration, impairment, risk and specifiers or subtypes. Any episode can be coded as severe, moderate, mild (as per current criteria), subthreshold or absent; with subthreshold being the key additional severity rating. There will also be the opportunity to note what phase a current episode is at, with options such as prodrome, evolving, peak, early remission, partial remission or full remission. The duration of the current or most recent episode will be noted in days (including <24 h), weeks, months and years; perhaps on a 1–9 scale such as follows: <24 h, 1; 1–3 days, 2; 4–6 days, 3; 1–2 weeks, 4; 2–4 weeks, 5; 1–6 months, 6; 6–12 months, 7; 1–2 years, 8; or >2 years, 9. Impairment will be coded and current risk to self and others noted. In risk to self, both suicidality and self-harm or self-mutilation will be recorded separately.

Specifiers or subtypes of episodes that may be of relevance to treatment planning will be retained or expanded, and may include: with psychotic features, reactive, or reversed diurnal variation [91]. The coding of psychotic features will be completely separated from the issue of severity; and there will be the opportunity to note delusional-like features, delusions, brief hallucinations and persistent hallucinations. The nature and context (e.g. sleep related, grief related) of hallucinations will also be noted. The reason for dropping atypical and replacing it with reactive (i.e. the presence of mood reactivity) is to re-encourage the exploration of the key features of atypical depression, because the current symptoms do not create a coherent set. The subtype of reversed diurnal variation will have been added because it may represent a subtype with poor response to SSRIs [91]. Of note, the melancholic subtype will have been dropped, due to lack of validation data [86], [87].

Longitudinal history

The longitudinal data coded in DSM-VI will include information about past mood episodes. There will be the opportunity to code mood disorders over three time frames: (i) past 5 years: number and nature of episodes, severity of episodes, notable features (e.g. with psychotic features, with marked impairment, with high suicide risk, difficult to treat), extent and duration of inter-episode recovery; (ii) lifetime worst episode(s), including severity and notable features; and (iii) first symptoms/episode(s), including evolution, prodrome and age of onset(s).

Affective temperament and personality

Given that axis I and axis II disorders are not independent there will need to be the opportunity to code for relevant temperamental, personality styles and personality disorders in conjunction with the mood disorder. Furthermore, there are shared genetic and environmental risk factors between anxious personality traits (neuroticism or harm avoidance) and depression. How personality and its disorders will be classified by DSM-VI is beyond the scope of this paper, but for the classification of mood disorders, personality disorders, dimensional personality models and affective temperaments are all likely to have their places. Perhaps by DSM-VI the personality disorders will have been reduced to the four As [92]: (i) asthenic (cluster C, except obsessive–compulsive personality disorder); (ii) anankastic (obsessive–compulsive personality disorder); (iii) antisocial (cluster B); and (iv) asocial (schizoid and schizotypal).

The personality trait with the greatest relevance to depression is negative affect. In dimensional personality models this will equate to introverted neuroticism or harm avoidance, and when pathological and pervasive it will be avoidant personality disorder. The corresponding affective temperament is dysthymic temperament.

For bipolar disorders it will be relevant to note the presence of hyperthymic or cyclothymic temperaments. Hyperthymia is somewhat related to extraversion or to novelty seeking; and there is no associated personality disorder. Cyclothymia is likely a composite temperament involving a combination of neuroticism with extraversion, or a combination of harm avoidance and novelty seeking. If mood instability is of early onset, pathological and pervasive, then such people will likely meet the criteria for borderline personality disorder. By DSM-VI, however, it is doubtful that borderline personality disorder will retain that name, or have the same diagnostic criteria; and the overlap with bipolar disorder will have been greatly clarified [67], [68].

The other personality dimensions of note for mood disorders are perfectionism (persistence or obsessiveness) and schizotypy (self-transcendence). Schizotypy is of particular relevance for bipolar disorder, and not just schizophrenia [93].

Risk behaviours

By DSM-VI we should have made important advances on the assessment of risk, within the context of mood disorders. Risk to self will be separated into four components, although these are not independent. These components will be risks for suicide, suicide attempts, self-mutilation, and neglect. There will be debate as to whether financial risk (during mania) should also be included as risk behaviour. It will be better recognized that most of these risks are mood state dependent, and that the optimal approach to minimization of risk is optimal treatment of the individual's mood disorder.

Risks to others include those uncommon situations related to murder–suicide, which are most commonly associated with psychotic depressive states. Mania, or the activated-driven syndrome, poses risks to others through recklessness, especially reckless driving. Neglect of others, especially of children and dependents, will also be noted.

Risk factors

DSM-VI should debate whether established risk factors for mood disorders should be included in emergent diagnostic systems. This will be especially important with the development of neuroimaging and molecular genetics, but because genetic or imaging findings will influence our understanding of aetiology and treatment/prognosis planning, then we will need to consider how these new data will be used in clinical practice.

It may be that there will be the development of risk factor groupings under which relevant risk factors can be coded, such as: (i) familial/genetic/developmental; (ii) childhood; (iii) last 5 years; (iv) last 3 months; (v) physical; and (vi) neuroimaging.

Familial/genetic/developmental risk factors will include not only traditional family history data, but also the results from genotyping (e.g. short-short genotype of serotonin transporter) and data about in utero environmental risk factors. Attachment difficulties, abuse and neglect can be coded under childhood risk factors. Coding of risk factors over the past 5 years will allow for comments on enduring personality traits, enduring burdens (e.g. caring for a parent with Alzheimer's disease) and conflicts at home and at work. The category ‘last 3 months’ allows for the coding of immediate episode precipitants, including recent life events (dependent and independent) and variables such as circadian rhythm disruptions and seasonal risk factors. Physical risk factors should be separated into disorders of the central nervous system, vascular risk factors and systemic disorders. The new neuroimaging risk factor code will allow for the systematic coding of a wide range of emerging imaging data, including variables such as hippocampal and amgydala size (structural imaging) and activation under selected paradigms (functional imaging).

Conclusion

There is too little time for DSM-V to make any meaningful advances in the classification of mood disorders. DSM-V should retain continuity with the past (i.e. make few changes from DSM-IV), but create a framework that will enhance (rather than enshrine) a DSM-VI diagnostic system based upon the concepts of validity. One dilemma will be how to create an international research agenda that will provide the new validity data required. Another dilemma will be how complicated to make the diagnostic system; the proposal given here, with headings such as current episode, specifiers, longitudinal history, personality, risk behaviours and risk factors may be too complex for real-life busy clinical practice. Although I recommend few changes for DSM-V due to lack of real validity data to justify changes, I anticipate that the committees appointed to write DSM-V will not be able to resist making more changes than can be justified, if only to self-justify their time spent on such important committees!

Footnotes

Acknowledgements

Research by the author is primarily funded by a programme and project grants from the Health Research Council of New Zealand.

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Classification of Mood Disorders in DSM-V and DSM-VI

Abstract

Keywords

Reliability and validity of diagnostic systems

What have DSM-III and DSM-IV achieved?

Dilemmas for DSM-V and DSM-VI

What do we know about the aetiology of mood disorders?

What do we know about the outcome of mood disorders?

Boundaries of mood disorders

Boundaries of major depression

Boundaries of mania

Boundaries with anxiety disorders

Boundaries of mood disorders with personality

Boundaries with psychotic disorders

Interfaces of mood disorders with organic and drug-induced states

When depressive and manic symptoms occur simultaneously

Mood disorder specifiers

But are they really mood disorders?

Speculative options for DSM-VI

Current episode (most recent episode)

Longitudinal history

Affective temperament and personality

Risk behaviours

Risk factors

Conclusion

Footnotes

Acknowledgements

References