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persons, but this difference may reflect the early onset and the resulting marital
discord characteristic of the disorder.
Socioeconomic and Cultural Factors
No correlation has been found between socioeconomic status and major
depressive disorder. A higher-than-average incidence of bipolar I disorder is found
among the upper socioeconomic groups. Bipolar I disorder is more common in
persons who did not graduate from college than in college graduates, however, which
may also reflect the relatively early age of onset for the disorder. Depression is more
common in rural areas than in urban areas. The prevalence of mood disorder does
not differ among races. A tendency exists, however, for examiners to underdiagnose
mood disorder and overdiagnose schizophrenia in patients whose racial or cultural
background differs from theirs.
COMORBIDITY
Individuals with major mood disorders are at an increased risk of having one or
more additional comorbid Axis I disorders. The most frequent disorders are alcohol
abuse or dependence, panic disorder, obsessive-compulsive disorder (OCD), and
social anxiety disorder. Conversely, individuals with substance use disorders and
anxiety disorders also have an elevated risk of lifetime or current comorbid mood
disorder. In both unipolar and bipolar disorder, men more frequently present with
substance use disorders, whereas women more frequently present with comorbid
anxiety and eating disorders. In general, patients who are bipolar more frequently
show comorbidity of substance use and anxiety disorders than do patients with
unipolar major depression. In the Epidemiological Catchment Area study, the
lifetime history of substance use disorders, panic disorder, and OCD was
approximately twice as high among patients with bipolar I disorder (61 percent, 21
percent, and 21 percent, respectively) than in patients with unipolar major
depression (27 percent, 10 percent, and 12 percent, respectively). Comorbid
substance use disorders and anxiety disorders worsen the prognosis of the illness and
markedly increase the risk of suicide among patients who are unipolar major
depressive and bipolar.
ETIOLOGY
Biological Factors
Many studies have reported biological abnormalities in patients with mood
disorders. Until recently, the monoamine neurotransmittersnorepinephrine,
dopamine, serotonin, and histaminewere the main focus of theories and research
about the etiology of these disorders. A progressive shift has occurred from focusing
on disturbances of single neurotransmitter systems in favor of studying
neurobehavioral systems, neural circuits, and more intricate neuroregulatory
mechanisms. The monoaminergic systems, thus, are now viewed as broader,
neuromodulatory systems, and disturbances are as likely to be secondary or
PROLACTIN.
Prolactin is released from the pituitary by serotonin stimulation and inhibited by
DA. Most studies have not found significant abnormalities of basal or circadian
prolactin secretion in depression, although a blunted prolactin response to various
serotonin agonists has been described. This response is uncommon among
premenopausal women, suggesting that estrogen has a moderating effect.
Alterations of Sleep Neurophysiology.
Depression is associated with a premature loss of deep (slow wave) sleep and an
increase in nocturnal arousal. The latter is reflected by four types of disturbance: (1)
an increase in nocturnal awakenings, (2) a reduction in total sleep time, (3) increased
phasic rapid eye movement (REM) sleep, and (4) increased core body temperature.
The combination of increased REM drive and decreased slow wave sleep results in a
significant reduction in the first period of non-REM (NREM) sleep, a phenomenon
referred to as reduced REM latency. Reduced REM latency and deficits of slow wave
sleep typically persist after recovery of a depressive episode. Blunted secretion of GH
after sleep onset is associated with decreased slow wave sleep and shows similar
state-independent or trait-like behavior. The combination of reduced REM latency,
increased REM density, and decreased sleep maintenance identifies approximately
40 percent of depressed outpatients and 80 percent of depressed inpatients. Falsenegative findings are commonly seen in younger, hypersomnolent patients, who may
actually experience an increase in slow wave sleep during episodes of depression.
Approximately 10 percent of otherwise healthy individuals have abnormal sleep
profiles, and, as with dexamethasone nonsuppression, false-positive cases are not
uncommonly seen in other psychiatric disorders.
Patients manifesting a characteristically abnormal sleep profile have been found to
be less responsive to psychotherapy and to have a greater risk of relapse or
recurrence and may benefit preferentially from pharmacotherapy.
Immunological Disturbance.
Depressive disorders are associated with several immunological abnormalities,
including decreased lymphocyte proliferation in response to mitogens and other
forms of impaired cellular immunity. These lymphocytes produce neuromodulators,
such as corticotropin-releasing factor, and cytokines, peptides known as interleukins.
There appears to be an association with clinical severity, hypercortisolism, and
immune dysfunction, and the cytokine interleukin-1 may induce gene activity for
glucocorticoid synthesis.
Structural and Functional Brain Imaging.
Computed axial tomography and magnetic