What do all mood disorders have in common?

Conclusion

Mood disorders are frequent psychiatric complications of TBI that take place along with prominent anxiety, substance misuse, impulsivity, and aggression. Furthermore, in a significant number of cases, they become chronic and resistant to treatment with the consequent deleterious impact on community reintegration and quality of life.

Mood disorders are associated with structural and functional changes of neural circuits linking brain areas specialized in emotional processing like the prefrontal cortex, basal ganglia and the amygdala. In turn, the onset of mood disorders may contribute to further prefrontal dysfunction among TBI patients. Treatment options are based on logic and current standards of practice rather that empirically based controlled treatment trials. There is a great need for randomized, double blind, placebo controlled trials to establish the most effective treatments for the variety of mood disorders which occur in TBI patients.

In addition, future studies should also examine the effect of therapeutic interventions on the neural systems that are altered in mood disorders. This will ultimately result in optimizing treatment response on an individual basis by selecting the more appropriate intervention for a particular case.

Description

The bipolar and related disorders include bipolar I, bipolar II, cyclothymic, and other specified/unspecified bipolar and related disorders, as well as bipolar and related disorder caused by another medical condition.

Amanic episode is characterized by a distinct period of at least 1 wk in which there is an abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy that is present for most of the day, nearly every day (or any duration if hospitalization is necessary). The episode is associated with characteristic cognitive and behavioral symptoms, including disturbances in self-regard, speech, attention, thought, activity, impulsivity, and sleep (Table 39.5). To diagnosebipolar I disorder, criteria must be met for at least 1 manic episode, and the episode must not be better explained by a psychotic disorder. The manic episode may have been preceded and may be followed by hypomanic or major depressive episodes. Bipolar I disorder is rated as mild, moderate, or severe in the same way as the depressive disorders (seeDescription section ofChapter 39.1).

To diagnosebipolar II disorder, criteria must be met for at least 1 hypomanic episode and at least 1 major depressive episode. Ahypomanic episode is similar to a manic episode but is briefer (at least 4 days) and less severe (causes less impairment in functioning, is not associated with psychosis, and would not require hospitalization) (Table 39.6). In bipolar II disorder, there must never have been a manic disorder, the episodes must not be better explained by a psychotic disorder, and the symptoms of depression or the unpredictability caused by frequent alternation between periods of depression and hypomania must cause clinically significant distress or functional impairment. Bipolar II disorder is also rated as mild, moderate, or severe.

Cyclothymic disorder is characterized by a period of at least 1 yr (in children and adolescents) in which there are numerous periods with hypomanic and depressive symptoms that do not meet criteria for a hypomanic episode or a major depressive episode, respectively.

Other specified/unspecified bipolar and related disorders (subsyndromal bipolar disorder) applies to presentations in which symptoms characteristic of a bipolar and related disorder are present and cause distress or functional impairment, but do not meet the full criteria for any of the disorders in this diagnostic class. Although this diagnosis (formerly known as “bipolar disorder, not otherwise specified”) had frequently been applied to children with severe and chronic mood and behavioral dysregulation who did not precisely fit other diagnostic categories, the empirical support for the validity of this practice has been sparse. Children who formerly received this diagnosis may meet criteria for DMDD (seeChapter 39.1).

VII. Summary

The relationship between brain and mood disorders has been investigated based on numerous brain-related functions, including genetics, neurotransmitters, hormonal activity, anatomical structure, physiological functions, psychosocial aspects, and treatment response. Integrating these diverse areas of investigation into a coherent mechanism of mood disorders has not been accomplished, but significant progress is being made in all these areas of study. Since mood disorders are based on clinical and not laboratory criteria, the definition and classification of mood disorders play a central role in determining which brain changes are associated with mood disorder, and classification of mood disorders, continues to be an evolving area. The study of secondary depression, in which there is a well-defined neuropathology, has also contributed to our understanding of the brain-related mechanism of mood disorders. The exponential growth of genetic research has generated numerous investigations searching for the fundamental abnormality that leads to mood disorders. These studies continue to search for multigenic explanations for these disorders. Similarly, the development and growth of both structural and functional brain imaging techniques have led to a general consensus that the anatomical substrate of mood disorders involves dysfunction of the frontal cortical and basal ganglia–thalamic neuronal loops. In addition, neurotransmitter and neuroendocrine studies have established that changes in brain biochemistry are important elements that must be incorporated into any comprehensive explanation of the brain-related mechanism of mood disorders. Finally, one of the most successful areas of research in mood disorders is empirically based treatment. Although effective treatment suggests neurochemical mechanisms of mood disorder, the fact that controlled treatment trials have established a firm scientific basis for treatment selection has allowed clinicians to effectively manage these disorders while we await a fundamental understanding of the brain mechanisms involved.

Mood and Affective Disorders

Cross-sectional studies have shown some degree of affective disturbance in a significant number of patients with MS (Goldman Consensus Group, 2005). The AAN quality measure set recommends screening for depression and assessing depression as two separate components of comprehensive MS care. Depression is the most common manifestation and may in part be due to the burden of having to cope with an unpredictable and chronic disease. However, it is more prevalent in MS than in other chronic diseases, suggesting a disease-related component as well. The lifetime risk of major depression in patients with MS is up to 50% (Sadovnick et al., 1996). Patients taking multiple medications are prone to depression, and the side-effect profile of the IFN-β medications includes depression. Some data indicate a comorbid association between bipolar illness and MS. Suicide rates are higher in patients with MS than in the general population or when compared to patients with other chronic illnesses (Bronnum-Hansen et al., 2005). Frontal or subcortical white-matter disease may also be a contributory causative factor.

Depression in MS is a treatable condition, irrespective of whether it is considered a symptom or a comorbidity. SSRIs are the medications of choice for depressive symptoms in patients with MS, and any of the other medications in this class may be used. More stimulating SSRIs may help to address concurrent fatigue; Serotonin and norepinephrine reuptake inhibitors (SNRIs) such as duloxetine are also potentially effective for depression in MS, and may have benefit for MS-related pain in patients with both symptoms. Amitriptyline is a second-line choice because of its anticholinergic side effects. However, anticholinergic properties may also be helpful to patients with symptoms of bladder spasticity or chronic pain.

Euphoria, formerly considered to be common in MS, is actually infrequent and is usually associated with moderate or severe cognitive impairment and greater disease burden on MRI. However, emotional “dyscontrol,” also known aspseudobulbar affect, is quite common, and patients with this condition may oscillate frequently between expressing sad and happy states, at times without clear precipitants and in situations not congruent with the emotional expression. Dextromethorphan with quinidine has been shown to be effective for MS patients with pseudobulbar affect (PBA) (Pioro et al., 2010).

II.C. Epidemiology of Depression

Estimates of the prevalence of major depressive disorder by age and gender have been derived from the The Epidemiological Catchment Area (ECA) study of 18,000 community and institutionalized subjects over 18 years of age at five sites throughout the United States, according to Weissman and colleagues in 1991. The ECA found that the overall lifetime prevalence of mood disorders is 6%. This differs slightly from the 1994 DSM-IV data that suggest a lifetime prevalence of 10 to 25% risk of depression in women as opposed to a 5 to 12% lifetime risk for men. The ECA data indicate a much higher prevalence of all the mood disorders among persons under the age of 45. The ECA also reported a relatively higher prevalence of major depressive disorder in women than in men, which, although consistent across the ages, was more evident among the younger adult group than in the elderly or in childhood. The study also found alcohol abuse and dependence was more prevalent in men than in women, leading some to argue that depressive disorders and alcohol abuse and dependence may be different manifestations of the same biopsychosocial vulnerability.

Sex differences in depression begin in early adolescence and persist at least until midlife. However, women with a previous history of a depressive episode are no more likely to experience a new episode than men with a previous history of a depressive episode. This suggests that the higher risk in women results from women having a higher risk of experiencing major depressive disorder for the first time.

A number of studies performed prior to the ECA study suggested that the prevalence rates of depressive disorders may be changing. The findings seemed to indicate a progressively lowering of the age of onset of depressive disorders and a possible increase in childhood mood disorders as well as an observed reduction in suicide in the elderly.

Mood and Anxiety Disorders

Mood disorders, such as major depression or bipolar disorder, are characterized by dysregulated mood. Anxiety disorders comprise symptoms of anxiety or fear that impair functioning. Both mood and anxiety disorders present additional risk for substance use disorders. Approximately one in three adolescents with SUD also suffer from mood disorders, and one in five with SUD meet criteria from anxiety disorders. Both major depression and bipolar disorder have been associated with structural and functional differences in prefrontal, cingulate, and subcortical regions among adolescents. Adolescent anxiety disorders were associated with frontal and amygdala abnormalities. Thus, comorbid mood disorders or mood symptoms may influence the relationship between substance use and brain structure or functioning. For example, among adolescent marijuana users, those with greater depressive symptoms showed smaller white matter volumes than those who did not show depressive symptoms.

Definition, Prevalence and Course

Mood disorders at times present with psychotic features, and include bipolar disorder and depression with psychotic features. There has been a long held dichotomy between schizophrenia and mood disorders, with Emil Kraeplin differentiating “dementia praecox” from “manic depression” by the presence of psychosis in the former and mood symptoms in the latter. However, more recent conceptualizations, stemming from the evidence of shared genetic vulnerabilities between mood and psychotic disorders, challenge the validity of the dichotomy between mood and psychotic disorders. Psychotic disorders including schizophrenia may thus be best viewed as part of a continuum that includes bipolar disorder and other mood disorders (Craddock & Owen, 2005).

The classification of psychotic disorders is evolving. The current approach, based on DSM-IV, differentiates between diagnoses of schizophrenia, schizoaffective disorder, and mood disorder based on the chronological sequence and duration of symptoms, and overlap of psychosis and mood symptoms. To meet criteria for a mood disorder with psychotic features, the DSM-IV specifies that psychotic symptoms must occur in the presence of a mood disorder—if the patient has delusions or hallucinations for two weeks in the absence of a mood disorder then the diagnosis would be schizoaffective disorder or schizophrenia. Most commonly, psychotic mood disorders include psychotic symptoms that are mood congruent. Depressive delusions include themes of guilt, hypochondriasis, nihilism, persecution, or jealousy. In manic episodes, the content may be grandiose. However, psychotic symptoms do not need to be mood congruent for a person to meet criteria for a mood disorder with psychotic features, so long as the symptoms occur in the context of a mood episode.

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