This paper surveys four psychiatric conditions — depression, mania, anxiety disorders, and Tourette syndrome — examining the major theoretical frameworks proposed to explain each and the pharmacological treatments developed in response. For each condition, the paper reviews psychoanalytic, behavioral, cognitive, humanistic, biopsychosocial, and biological models, noting where research has lent greater support to certain explanations. It then outlines the classes of medications used clinically, their mechanisms of action, and their side-effect profiles. The paper draws on peer-reviewed sources to contextualize these treatments within broader debates about the validity of competing etiological models.
According to the DSM-IV-TR, a person must exhibit at least five of nine specified symptoms for a minimum of two weeks to receive a diagnosis of depression. Numerous theoretical frameworks have been proposed to explain the causes of this disorder:
1. Psychoanalytic theories — internal conflicts and a low self-image lead to anger turned inward.
2. Behavioral theories — stressors disrupt normal reinforcement patterns.
3. Cognitive theories — cognitive distortions, cognitive errors, and mistaken underlying assumptions drive depressive thinking.
4. Humanistic theories — an excessive concern with the expectations and values of others leads a person away from genuineness and wholeness.
5. Biopsychosocial models — psychological, biological, and social factors all play a role. An important outgrowth is the diathesis–stress model, which asserts that depression occurs when a preexisting vulnerability (diathesis) is triggered by stressful life events. That vulnerability may be biological, psychological, or both.
6. Biological models — an imbalance of neurotransmitters — specifically serotonin, norepinephrine, and dopamine — is implicated in depression.
Research has generally favored cognitive and biological theories, although this does not substantiate them as the only valid explanations (Lauber, Falcato, Nordt, & Rossler, 2003). The growth of biological models has in turn driven the development of numerous pharmaceutical treatments.
Medications for depression generally fall into three classes:
1. MAO inhibitors work by reducing monoamine oxidase, the enzyme that breaks down the neurotransmitters believed to be deficient in the brains of depressed people. Potentially fatal side effects can occur when patients eat foods containing the amino acid tyrosine, such as liver, fermented beverages, and aged cheese. These drugs are rarely used today.
2. Tricyclic antidepressants work by inhibiting the reuptake of serotonin and norepinephrine. Side effects include dry mouth, blurry vision, constipation, cognitive impairment, drowsiness, anxiety, emotional blunting, and sexual dysfunction.
3. SSRIs (selective serotonin reuptake inhibitors) selectively block the reuptake of serotonin and are the most commonly prescribed medications for depression today. Potential side effects include reduced blood-clotting capacity, anxiety, hypomania, sexual effects, and an increased risk of suicide.
The mechanism of all antidepressants is such that therapeutic effects are not typically seen for two to six weeks after treatment begins. Although many people assume that SSRIs such as Paxil are more effective than older drug classes, research indicates that all classes are equally effective; SSRIs are preferred largely because they produce fewer side effects. These medications work best for patients whose symptoms are more vegetative or biologically based — such as fatigue and insomnia. While different drugs within the same class may work better for different individuals, approximately 10–20% of patients do not respond to treatment.
Mania is a state of prolonged elevated mood, heightened arousal, and increased energy. It is often considered the opposite of depression and represents the "high" pole of bipolar disorder. Psychological theories of mania are not as well developed as those for depression, and mania resulting from medications or illicit drug use should always be ruled out before other explanations are pursued. Relevant theoretical frameworks include:
1. Psychoanalytic theories — similar to those for depression; internal conflicts regarding a low self-concept produce mania as a reaction-formation.
2. Biopsychosocial models — diathesis–stress models are thought to account for mania better than purely psychological models, and they are currently the most widely accepted, given that a large number of manic episodes appear to be triggered by stress (Barrios, Chaudhry, & Goodnick, 2001).
3. Biological models — an overabundance of neurotransmitters in the brain is thought to produce mania. Several neurotransmitters have been implicated, including dopamine, serotonin, glutamate, and norepinephrine.
Although biologically based theories are favored, the exact cause of mania has not yet been determined. Medications used to treat mania include Lithium (often the first-line choice), anticonvulsants (e.g., Depakote and Tegretol), antipsychotic medications (e.g., Risperdal), and some antihypertensive drugs such as Verapamil. These medications reduce manic symptoms but carry a wide range of side effects, including tremor, nausea, cognitive difficulties, allergic reactions, and risk of overdose. Side effects are often severe enough that patients discontinue the medication — a common challenge with many psychotropic drugs.
There are several distinct anxiety disorders, all of which share the experience of heightened arousal and a pervasive sense of fear. The major theoretical frameworks proposed to explain anxiety disorders include:
"Anxiety models and three medication categories reviewed"
"Genetic and neurological causes; neuroleptic treatments"
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