Global Perspectives

Major depression is a chronic and recurrent disorder for many people. It is conceived as an episodic disorder. About 85% of patients who recover from first major depressive episode can experience a recurrence and 58% of these who remained well for at least five years1. Although the afflictions may be long-term and the consequences far reaching, on the whole it is characterized by periods of quiescence and periods of activity. The episodic view of major depression often overshadows the chronic nature of the disorder. The most severe form occurs in people who never achieve remission.

Psychopathology is the most common measure of the outcome of depression. Suicide, psychosocial functioning and general life functioning are important measures of the course of major depression. The level of depressive symptoms serves as a standard measure of long-term outcomes of major depression. Women predominate in prevalence studies of major depression. Female subjects exhibit a higher prevalence of somatic depression than male subjects. It is associated with body aches and onset of depression during early adolescence2. The evidence of age as a predictor of relapse is mixed with some studies showing that younger age is associated with increased rate of recurrence and others demonstrating that age more than 40 years is associated with increased rate of recurrence. Clinical variables that consistently predict increased rates of relapse are an increased number of prior episodes of major depression and secondary depression1,3.

Inspite of the significant levels of depressive symptoms and consequences of these symptoms, there are startling low levels of pharmacologic or psychosocial treatment for major depression3.

Dysthymic disorder is a condition characterized by mild , chronic depressive symptoms. The diagnostic category of dysthymic disorder was introduced in 1980 as DSM-III. It was revised in 1987 with DSM-III R. Clinical studies have proven that major depressive patients have similar or higher rates of more specific symptoms than do dysthymic patients, but there is little evidence of qualitative distinctions in symptomatology between these conditions4.

The phenomenology of major depression is complex involving abnormalities in several areas such as mood, cognition, motor activity and neurovegetative functions. Clinical symptoms may be produced by a neurologic illness, induced by medical illness or drugs (secondary depression) or be idiopathic in etiology (primary depression). Depression may also occur in a single episode or be a recurrent illness. Therefore, major depression is a heterogenous disorder with various subtypes and it is unlikely that all symptonms are mediated by single brain area4.

Basal ganglia and its association with major depression5

Studies have demonstrated that depressive disorders may be related to abnormalities in specific brain systems and networks. Data have pointed to decreased volume, hypometabolism and reduced blood flow in frontal lobes, basal ganglia and temporal structures in patients with mood disorder. Extensive functional and neuroanatomic connections exist between the basal ganglia, the frontal lobe and the limbic system via fronto-subcortical network and studies support the hypothesis pointing to abnormalities in basal ganglia-thalamocortical circuits in major depressive disorder. Ross and Rush were among the first to suggest that the emergence of depression in patients with neurologic lesions. They noticed that focal brain lesions were more likely to produce depressions than lesions in other brain areas. Therefore depression is highly prevalent in basal ganglia disorders. Accumulating evidence implicates the neurotransmitters norepinephrine (NE), serotonin (5HT) and dopamine (DA) in the pathophysiology of depression. There are extensive dopaminergic , noradrenergic, serotonergic and cholinergic projections into the basal ganglia thalamocortical circuits. Although somatic antidepressant therapies influence each of these systems, their therapeutic mechanisms may be associated with enhancing dopaminergic and serotonergic activity. A functional or anatomic disruption at different sites of the basal ganglia thalamocortical circuits may be associated with different forms of depression5.

Headache and depression6

Epidemiologic studies report an association between migraine headache and major depression. In patients with severe headache, prevalence of major depression was higher in patients with migranous disorders. Than in patients with tension headache. In these cases, the onset of headache preceded the onset of major depression. The life time prevalence of major depression was higher in patients with aura than in persons with migraine without aura6.

Major depression and coronary heart disease7

Depressive symptoms are highly prevalent in patients with coronary heart disease (CAD). Depression, particularly geriatric depression, is itself associated with impairment of activities of daily living (ADLs). CAD patients with major depression report significantly greater disability than CAD patients without depression. Microcirculatory cerebral perfusion has been found to be lower in the depressed cardiac patients than in the non depressed patients8. Depression was associated with impairment in both self maintenance and instrumental ADLs. The association between major depression and disability may have important clinical implications. It is found that the functional impairment precedes development of major depression, then efforts to improve functional status and to monitor depressive symptoms closely may prevent development of major depression and ameliorate depressive symptoms7.

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