DEPRESSION

Depression Sign…

Depression (major depression) is defined as depressed mood on a daily basis for a minimum duration of 2 weeks. An episode may be characterized by sadness, indifference or apathy, or irritability and is usually associated with change in neurovegetative functions, including sleep patterns, appetite and weight, motor agitation or retardation, fatigue, impairment in concentration and decision making, feelings of shame or guilt, thoughts of death, dying or suicide. Patients with depression have a profound loss of pleasure in all enjoyable activities, exhibit early morning awakening, feel that the dysphoric mood state is qualitatively different from sadness, and often notice a diurnal variation in mood (worse in morning hours). Paradoxically, these more severe features predict a good response to antidepressant treatment.

Factors That Can Make Someone Depression

The incidence of depression increases with age; the disorder is approximately twice as prevalent in women as in men, regardless of age. These gender differences were previously believed to reflect sociocultural factors, but recent longitudinal twin studies indicate that the liability to major depression in adult women is largely genetic in origin, and that the effect of environmental factors is transitory and does not affect lifetime prevalence. The relationship between psychological stress, negative life events, and the onset of depressive episodes is complex. Negative life events can precipitate and contribute to depression, but recent data indicate that genetic factors influence the sensitivity of individuals to these stressful events. In most cases, both biologic and psychosocial factors are involved in the precipitation and unfolding of depressive episodes. The most potent stressors appear to involve death of a relative, assault, or severe marital or relationship problems.

Some Agent That Can Induce Depression

• Antihypertensive drugs (b-adrenergic blockers, calcium channel blockers)
• Anticholesterolemic agents
• Antiarrhythmic agents
• Glucocorticoids
• Antimicrobials
• Systemic analgesics
• Antiparkinsonian medications
• Anticonvulsants

Diseases which associate with depression

• Cardiac diseases about 20 and 30% manifest a depressive disorder.
• Cancer, depend on tumor site, severity of illness, and type of medical or surgical intervention. There is an overall mean prevalence of 25%.
• Neurologic disorders (cerebrovascular disorders, Parkinson's disease, multiple sclerosis, traumatic brain injury, left-hemisphere strokes)
• Diabetes mellitus
• Hypothyroidism

Learn More About Depression Mechanism

The neurobiology of unipolar depression is poorly understood. Although evidence for genetic transmission is not as strong as in bipolar disorder, monozygotic twins have a higher concordance rate (46%) than dizygotic siblings (20%), with little evidence for any effect of a shared family environment. Parallels between the affective, motor, and cognitive dysfunctions seen in unipolar depression and those observed in diseases of the basal ganglia have suggested that neural networks involving prefrontal cortex and the basal ganglia may be involved. This hypothesis is supported by positron emission tomography (PET) studies of brain glucose metabolism that show a decrease in metabolic rate in the caudate nuclei and frontal lobes in depressed patients that returns to normal with recovery. Single-photon emission computed tomography (SPECT) studies show comparable changes in blood flow. Magnetic resonance imaging (MRI) findings in some patients include an increased frequency of subcortical white matter lesions. However, because these findings are more prevalent in patients with late onset of depressive illness, their significance remains unproven. A number of studies document increased ventricle-to-brain ratios in some patients with recurrent depression, but whether this finding is state-dependent or represents true cerebral atrophy is controversial.

Postmortem examination of brains of suicide victims suggest altered noradrenergic activity, including increased binding to a1-, a2-, and b-adrenergic receptors in the cerebral cortex and a decreased total number and density of noradrenergic neurons in the locus coeruleus. Involvement of the serotonin system is suggested by findings of reduced plasma tryptophan levels, a decreased cerebrospinal fluid level of 5-hydroxyindolacetic acid (the principal metabolite of serotonin in brain), and decreased platelet serotonergic transporter binding. An increase in brain serotonin receptors in suicide victims is also reported. Depletion of blood tryptophan, the amino acid precursor of serotonin, rapidly reverses the antidepressant benefit in depressed patients who have been successfully treated. However, a decrement in mood after tryptophan reduction is considerably less robust in untreated patients, indicating that, if presynaptic serotonergic dysfunction occurs in depression, it likely plays a contributing rather than a causal role.

Neuroendocrine abnormalities that reflect the neurovegetative signs and symptoms of depression include (1) increased cortisol and corticotropin-releasing hormone (CRH) secretion, (2) an increase in adrenal size, (3) a decreased inhibitory response of glucocorticoids to dexamethasone, and (4) a blunted response of thyroid-stimulating hormone (TSH) level to infusion of thyroid-releasing hormone (TRH). Antidepressant treatment leads to normalization of these pituitary-adrenal abnormalities.

Diurnal variations in symptom severity and alterations in circadian rhythmicity of a number of neurochemical and neurohumoral factors suggest that biologic differences may be secondary to a primary defect in regulation of biologic rhythms. Patients with major depression show consistent findings of a decrease in rapid eye movement (REM) sleep onset (REM latency), an increase in REM density, and, in some subjects, a decrease in stage IV delta slow-wave sleep.
Although antidepressant drugs result in a blockade of neurotransmitter uptake within hours, their therapeutic effects typically emerge over several weeks, implicating neuroadaptive changes in second messenger systems and transcription factors as possible mechanisms of action.

Depression Treatment

Treatment planning requires coordination of short-term symptom remission with longer term maintenance strategies designed to prevent recurrence. The most effective intervention for achieving remission and preventing relapse is medication, but combined treatment, incorporating psychotherapy to help the patient cope with decreased self-esteem and demoralization, improves outcome.
It is essential to counsel patients about depression and the medications they are receiving. An educational approach is best, describing what is known about the depressive syndrome and how the medications may help. Advice about stress reduction, side effects, and expected length of treatment and cautions that alcohol may exacerbate depressive symptoms and impede drug response are helpful. Patients should be given time to describe their experience and the impact it has had on them, their family, and their outlook. Occasional empathic silence may be as helpful for the treatment alliance as verbal reassurance.