Etiology - Mood Disorders

ETIOLOGY

Various theories for the etiology of mood disorders exist. The most recent research focuses on chemical biologic imbalances as the cause. Nevertheless, psychosocial stres-sors and interpersonal events appear to trigger certain physiologic and chemical changes in the brain, which sig-nificantly alter the balance of neurotransmitters (Akiskal, 2005). Effective treatment addresses both the biologic and psychosocial components of mood disorders. Thus, nurses need a basic knowledge of both perspectives when work-ing with clients experiencing these disorders.

Biologic Theories

Genetic Theories

Genetic studies implicate the transmission of major depres-sion in first-degree relatives, who are at twice the risk for developing depression compared with the general popula-tion (APA, 2000). First-degree relatives of people with bipo-lar disorder have a 3% to 8% risk for developing bipolar disorder compared with a 1% risk in the general population. For all mood disorders, monozygotic (identical) twins have a concordance rate (both twins having the disorder) two to four times higher than that of dizygotic (fraternal) twins. Although heredity is a significant factor, the concordance rate for monozygotic twins is not 100%, so genetics alone do not account for all mood disorders (Kelsoe, 2005).

Markowitz and Milrod (2005) discussed indications of a genetic overlap between early-onset bipolar disorder and early-onset alcoholism. They noted that people with both problems have a higher rate of mixed and rapid cycling, poorer response to lithium, slower rate of recovery, and more hospital admissions. Mania displayed by these cli-ents involves more agitation than elation; clients may respond better to anticonvulsants than to lithium.

Neurochemical Theories

Neurochemical influences of neurotransmitters (chemical messengers) focus on serotonin and norepinephrine as the two major biogenic amines implicated in mood disorders. Serotonin has many roles in behavior: mood, activity, aggressiveness and irritability, cognition, pain, biorhythms, and neuroendocrine processes (i.e., growth hormone, cor-tisol, and prolactin levels are abnormal in depression). Deficits of serotonin, its precursor tryptophan, or a meta-bolite (5-hydroxyindole acetic acid, or 5-HIAA) of serotonin found in the blood or cerebrospinal fluid occur in people with depression. Positron emission tomography demon-strates reduced metabolism in the prefrontal cortex, which may promote depression (Tecott & Smart, 2005).

Norepinephrine levels may be deficient in depression and increased in mania. This catecholamine energizes the body to mobilize during stress and inhibits kindling. Kindling is the process by which seizure activity in a spe-cific area of the brain is initially stimulated by reaching a threshold of the cumulative effects of stress, low amounts of electric impulses, or chemicals such as cocaine that sen-sitize nerve cells and pathways. These highly sensitized pathways respond by no longer needing the stimulus to induce seizure activity, which now occurs spontaneously. It is theorized that kindling may underlie the cycling of mood disorders as well as addiction. Anticonvulsants inhibit kindling; this may explain their efficacy in the treatment of bipolar disorder (Akiskal, 2005).

Dysregulation of acetylcholine and dopamine also is being studied in relation to mood disorders. Cholinergic drugs alter mood, sleep, neuroendocrine function, and the electroencephalographic pattern; therefore, acetyl-choline seems to be implicated in depression and mania. The neurotransmitter problem may not be as simple as underproduction or depletion through overuse during stress. Changes in the sensitivity as well as the number of receptors are being evaluated for their roles in mood disorders (Tecott & Smart, 2005).

Neuroendocrine Influences

Hormonal fluctuations are being studied in relation to depression. Mood disturbances have been documented in people with endocrine disorders such as those of the thy-roid, adrenal, parathyroid, and pituitary glands. Elevated glucocorticoid activity is associated with the stress response, and evidence of increased cortisol secretion is apparent in about 40% of clients with depression, with the highest rates found among older clients. Postpartum hor-mone alterations precipitate mood disorders such as post-partum depression and psychosis. About 5% to 10% of people with depression have thyroid dysfunction, notably an elevated thyroid-stimulating hormone. This problem must be corrected with thyroid treatment, or treatment for the mood disorder is affected adversely (Thase, 2005).

Psychodynamic Theories

Many psychodynamic theories about the cause of mood disorders seemed to “blame the victim” and his or her family (Markowitz & Milrod, 2005):

·    Freud looked at the self-depreciation of people with depression and attributed that self-reproach to anger turned inward related to either a real or perceived loss. Feeling abandoned by this loss, people became angry while both loving and hating the lost object.

·    Bibring believed that one’s ego (or self) aspired to be ideal (i.e., good and loving, superior or strong) and that to be loved and worthy, one must achieve these high standards. Depression results when, in reality, the per-son was not able to achieve these ideals all the time.

·    Jacobson compared the state of depression with a situa-tion in which the ego is a powerless, helpless child vic-timized by the superego, much like a powerful and sadistic mother who takes delight in torturing the child.

·    Most psychoanalytical theories of mania view manic episodes as a “defense” against underlying depression, with the id taking over the ego and acting as an undis-ciplined hedonistic being (child).

·    Meyer viewed depression as a reaction to a distressing life experience such as an event with psychic causality.

·    Horney believed that children raised by rejecting or un-loving parents were prone to feelings of insecurity and loneliness, making them susceptible to depression and helplessness.

·    Beck saw depression as resulting from specific cognitive distortions in susceptible people. Early experiences shaped distorted ways of thinking about one’s self, the world, and the future; these distortions involve magni-fication of negative events, traits, and expectations and simultaneous minimization of anything positive.