The term “mood disorder” is a misnomer because it suggests a temporary state of mind or feeling, as in “being in a bad mood.” Another common meaning defines mood as an artifact or precipitate of a socio-psychological situation, as in “the mood of the room.” The DSM however uses the term “mood” in a different, technical way to refer to serious depressive disorders (unipolar depression), bipolar disorders and two disorders based on etiology (mood disorder due to a general medical condition and substance-induced mood disorder). Mood disorders are among the more serious of Axis I DSM diagnoses. As expressed by the neuropsychiatrist Peter Whybrow in his book A Mood Apart (1997), “they actually involve mental processes that extend well beyond mood and also beyond the emotional awareness that sustains social communication. … There is an impairment of the core experience of being – the familiar pattern of thinking, feeling, and behavior that we loosely identify as the ‘self.’ In mood disorders, life’s usual balance is lost.” One of the main reasons why they are serious is because the diagnosis of a mood disorder is permanent. Unlike other psychopathologies it does not resolve and disappear. The best one can hope for is that it goes into permanent remission.
General Medical Conditions, Substance Abuse, NOS
Etiological Considerations. First I would like to uncouple the last general category of mood disorders comprising mood disorders due to a general medical condition, mood disorders to due substance abuse and mood disorders NOS. Their etiology is uncomplicated: a general medical condition (293.83), substance-abuse (29x.xx, where x.xx identifies the substance) or NOS (296.90). They also must meet the other diagnostic criteria set forth in their respective DSM sections.
Symptom/Behavioral Presentations. Their symptom/behavioral presentations are straight-forward: from the standpoint of a differential diagnosis the patient first must present with the underlying pathology as a condition precedent to considering any other diagnostic criteria. While there is a sense in which they are comorbid it would be more accurate to characterize the relationship as one of cause and effect. The underlying pathology is the cause and the mood disorder is the effect. Only after establishing the premise does it make sense to consider whether the mood disturbance is etiologically related. Clinically, evidence of a medical condition or substance abuse is more likely to be apparent (or previously diagnosed) than the subtle nuances of mood disorder. In evaluating patients for mood disorder these conditions are more likely to be markers or pointers in that they can be ruled out quickly, or judged to be decisive in arriving at a diagnosis.
Relevant Treatments. Treatment considerations also are simplified. The first step is resolution (or taking steps to resolve) the underlying general medical condition or physiological effects of a substance (such as commencement of withdrawal). Treatment of the mood disorder goes hand-in-hand with (and will not be effective without) taking this step. Treatment otherwise follows that of the other depressive or bipolar disorders, depending on the diagnosis.
The depressive disorders include: major depressive disorder (296.xx); dysthymic disorder (300.4); and depressive disorder NOS (311). The DSM sets forth several subdivisions and subcategories. For example major depressions can have either a single episode (296.2) or recurrent episodes (296.3). The fifth digit then rates them on a scale of severity from 1 to 4 (thus e.g. recurrent episodes of major depression with psychotic features is 296.34); if full criteria are not currently met the fifth digit indicates their current clinical state. Depressive disorders need to be distinguished from normal depressive mood states such as bereavement or postpartum depression.
Etiological Considerations. The etiology of depressive disorders implicates biological, psychosocial and sociocultural factors. It is highly heritable (2x – 3x higher than the population at large; monozygotic co-twins 2x more likely to develop than dizygotic co-twins). It most likely is caused by neurochemical imbalance, in particular, depletion of neurotransmitters on reuptake by downstream dendrite receptors at the synaptic cleft. Another hypothesis is dopamine dysfunction or abnormal HPA/HPT axis regulation. Neuroanatomically there is a correlation with lower brain activity (measured by EEG or shown by PET neuroimaging) in the left PFC, the orbital PFC or the hippocampus.
From a psychological standpoint depression may be caused by stressful life events such as relationship discord, economic loss or health problems. There also are a variety of at-risk personality traits such as negative affect and early childhood adversity (parental loss, abuse).
Socioculturally depression highly correlates with impaired personal infrastructure. People who lack social support relationships or who are unemployed for example are more likely to be depressed. Their depression develops into a negative feedback loop exacerbating its intensity, further weakening or damaging their future prospects. With plenty of time on their hands to ruminate they descend to a state of hopelessness and helplessness. There is considerable controversy as to whether depression is a disease of Western culture as opposed to Asian or African. Although they may identify it differently it seems likely that people in these cultures can get depressed for the same neurochemical reasons that people in Western cultures do.
Symptom/Behavioral Presentations. For major depressive disorder the DSM requires a major depressive episode, defined as at least two weeks of depressed mood followed by at least four out of nine additional specified symptoms of depression. In summary these are melancholia, anhedonia, weight loss, insomnia, psychomotor agitation, fatigue, feelings of worthlessness or guilt, diminished ability to concentrate and suicidal ideations. They must result in significant distress or social impairment. Dysthymia requires a depressed mood for at least two years with other specified depressive symptoms.
Relevant Treatments. Freud thought he could treat depression using psychoanalytic methods such as dream analysis, transference and interpretation. This belief continued through the object relations school. Klein and Bowlby for example believed depression arose from deficiencies in early attachment relationships. Psychoanalysis was replaced by CBT in the 1960s. Beck for example believed that depression was the result of dysfunctional “core beliefs” or “schema” that develop early in life from personal experiences and identification with significant others. They are cognitive structures comprising an individual’s fundamental beliefs and assumptions about self, others and the nature of reality. They are latent during non-stressful periods but activate when triggered by specific stressors or circumstances.
These theories now by and large have been replaced with psychotropic medications, primarily SSRIs. Serotonin is a neurochemical diffused by axon terminals into the synaptic cleft during the neurochemical transfer of information. It is however subject to reabsorption by the presynaptic cell limiting the amount available to bind to the postsynaptic receptor. SSRIs inhibit this reuptake thereby increasing the extracellular level available to transmit neural impulses. Psychodynamic approaches still may be slightly efficacious in connection with a psychopharmacological treatment regimen.
The major criterion for bipolar disorders is a manic episode. In many respects mania is the counterpart to depression – a distinct period of abnormally and persistently elevated or expansive (or irritable) mood, lasting at least one week. Mania also requires three or more of seven additional specified symptoms. (1) In summary these are inflated self-esteem, hypersomnia, logorrhea, idea fugue, distractibility, hyperteleological activity or hyperhedonia-like activity. Bipolar disorders in turn are divided into Bipolar I (296.xx), Bipolar II (296.89), cyclothymic disorder (301.13) and bipolar disorder NOS (296.80). As with depression each bipolar disorder is divided into various sub-categories depending on frequency and features of episodes.
From a differential diagnosis standpoint the most important criterion distinguishing Bipolar I from Bipolar II is the presence or absence of both mania and depression. Bipolar I, single manic episode (296.0) specifically excludes a major depressive episode; Bipolar I, most recent episode hypomanic (296.40) or most recent episode unspecified (296.7) do not necessarily exclude it; and Bipolar I, most recent episode manic (296.4x), most recent episode mixed (296.6x) or most recent episode depressed (296.5x) require it. Bipolar II (296.89), Cyclothymia (301.13) or NOS (296.80) require a combination of both.
Etiological Considerations. As with depression BPD is highly heritable. Approximately 8 – 9% of BPD patients have first-degree relatives who also have it. Approximately 67% of monozygotic twins who have it also have a co-twin who has it (versus 12% for dizygotic twins). Neurochemically BPD is associated with increased norepinephrine activity during manic episodes. Given the role of dopamine in activating the brain’s pleasure system it is not surprising that BPD correlates with increased dopaminergic activities. Abnormalities of the HPT axis frequently accompany changes in mood. PET studies show that increased blood flow to the left PFC also is associated with BPD.
From a psychological standpoint there is some evidence that stressful life events precipitate BPD however this relationship is not as well developed as it is with depression. This makes sense because stress seems more likely to provoke anxiety and rumination (both characteristic features of depression) rather than hyperactivity. It is not surprising that BPD patients have a high level of cognitive functioning and during manic episodes have expansive, outgoing personalities (contra of course when cycling through a depressive state).
There also is some evidence that poor social infrastructure contributes to BPD however this is not as persuasive as it is with depression. As with depression some social psychologists suggest BPD predominantly is a phenomenon resulting from the stressful dynamics of Western culture. It may even differ within different SES strata in the United States and Europe. These studies are not persuasive given the precipitating ontogenic neurochemical factors.
Symptom/Behavioral Presentations. Although it shares many symptoms with depression (and can be misdiagnosed as such) the primary feature of BPD is emotional lability possibly accompanied by psychotic features such as delusional thinking, magical ideations and feelings of grandiosity or invulnerability. BPD patients most likely will be insomniac. They tend to experience more episodes of it than do patients with depression and can rapidly cycle from states of depression to mania. Interestingly many artists and creative people show BPD-like symptoms though exactly how this works isn’t known.
Relevant Treatments. Psychopharmacologically the preferred treatment is lithium, which stabilizes mood. A regimen of purely antidepressant medication is contra-indicated because it actually has the possibility of exacerbating manic episodes. There is some evidence that ECT and TMS are effective but these are second-order treatments that should be pursued only in refractory cases. As with depression patients should consider psychodynamic or CBT therapy however it is unlikely this standing alone will be efficacious.
Mixed Disorders, Hypomania
Finally (in the interest of completeness) mood episodes may be mixed, characterized by a period of at least a week during which the criteria are met for both a major depressive episode and a manic episode nearly every day. The DSM also describes hypomania as a separate mood episode lasting at least four days with at least three manic symptoms of lesser severity. Etiological considerations, symptom/behavioral presentations and relevant treatments are a combination of those for their component elements.
It is interesting that depression requires two weeks of symptoms whereas mania requires only one; and depression requires four out of nine symptoms whereas mania requires only three out of seven. This suggests that mania should be more readily diagnosable than depression.
Whybrow, P. (1997). A Mood Apart. New York, NY: HarperCollins.