Theories of depression Flashcards
The amygdala
Part of the limbic system appears to be a crucial way station for processing novel stimuli of emotional significance and coordinating or organizing cortical responses
The hippocampus
Adjacent to the amygdala, the hippocampus is most associated with learning and memory. Emotional or contextual learning appears to involve a direct connection between the hippocampus and the amygdala. Also, the hippocampus regulates the HPA axis by inhibiting activity.
The Prefrontal Cortex (PFC).
We think of the PFC as the structure that holds representations of goals and appropriate responses to obtaining these goals. There are areas of specialization. For example, whereas left-sided activation of regions of the PFC is more involved in goal-directed or appetitive behaviors, regions of the right PFC are implicated in avoidance behaviors and inhibition of appetitive pursuits. Subregions in the PFC appear to localize representations of behaviors related to reward and punishment.
The anterior cingulate cortex (ACC).
The ACC is involved in attention, motivation, and environmental exploration and appears to help integrate attentional and emotional inputs. The more rostral and ventral region has an affective subdivision that connects extensively with limbic regions of the brain. Activation of the ACC may facilitate control of emotional arousal, particularly when thwarting goal when attainment encountering novel problems.
Two categories that attempt to integrate various pathologic findings into an understanding of the etiology of depression
neurogenesis hypotheses and neuroplastic hypotheses.
Neurogenesis Hypotheses
Neurogenesis hypotheses suppose that brain abnormalities lead to depression, Some versions attempt to link the role of stress, particularly chronic stress, in causing depression. Stress can cause increased activity in the HPA axis, which results in increased glucocorticoid production. Glucocorticoids are known to decrease neurogenesis. As neurogenesis continues in the adult hippocampus, this may be an area preferentially affected by stress. The hippocampus is then unable to adequately regulate the HPA axis, leading to continued elevated glucocorticoid levels in the brain and further inhibition of neurogenesis.
Neuroplasticity Hypotheses.
Neuroplasticity hypotheses propose that the atrophy of already developed neurons causes depression. In this version, rather than a deficit of nerve growth, atrophy occurs in already mature neurons. As noted, chronic stress can increase glucocorticoid levels, which can cause atrophy. It can also decrease the expression of BDNF, which is essential for the survival, growth, and differentiation of neurons in the brain; the result is atrophy. As this preferentially happens in the hippocampus, this can account for the finding of decreased hippocampal volume in depressed patients.
Biologic Theories
- The Monoamine Hypothesis.
- Brain Dysfunction.
- Neurogenesis Hypotheses.
- Neuroplasticity Hypotheses.
Psychosocial Theories
- Life Events and Environmental Stress.
- Psychodynamic Theories of Depression.
- Cognitive Theory.
- Learned Helplessness.
- Evolutionary Theory.
Life Events and Environmental Stress.
A long-standing clinical observation is that stressful life events more often precede first, rather than subsequent, episodes of mood disorders. One theory proposed to explain this observation is that the stress accompanying the first episode results in long-lasting changes in the brain’s biology. As a result, a person has a high risk of undergoing subsequent episodes of a mood disorder, even without an external stressor.
Psychodynamic Theories of Depression.
The psychodynamic understanding of depression defined by Sigmund Freud and expanded by Karl Abraham is known as the classic view of depression. That theory involves four key points: (1) disturbances in the infant-mother relationship during the oral phase (the first 10 to 18 months of life) predispose to subsequent vulnerability to depression; (2) depression can be linked to real or imagined object loss; (3) introjection of the departed objects is a defense mechanism invoked to deal with the distress connected with the object’s loss; and (4) because the lost object is regarded with a mixture of love and hate, feelings of anger are directed inward at the self.
Cognitive Theory.
According to cognitive theory, depression results from specific cognitive distortions present in persons susceptible to depression. These distortions, referred to as depressogenic schemata, are cognitive templates that perceive both internal and external data in ways that are altered by early experiences. Aaron Beck postulated a cognitive triad of depression that consists of (1) views about the self—a negative self-precept, (2) about the environment—a tendency to experience the world as hostile and demanding, and (3) about the future—the expectation of suffering and failure. Therapy consists of modifying these distortions.
Elements of cognitive theory
Element
Definition
Cognitive triad
Beliefs about oneself, the world, and the future
Schemas
Ways of organizing and interpreting experiences
Cognitive distortions
Persistent ways of thinking that are inaccurate and usually negatively biased
Arbitrary inference
Drawing a specific conclusion without sufficient evidence
Specific abstraction
Focus on a single detail while ignoring other, more important aspects of an experience
Overgeneralization
Forming conclusions based on too little and too narrow experience
Magnification and minimization
Over- or undervaluing the significance of a particular event
Personalization
Tendency to self-reference external events without basis
Absolutist, dichotomous thinking
Tendency to place experience into all-or-none categories
Learned Helplessness.
The learned helplessness theory of depression connects depressive phenomena to the experience of uncontrollable events. For example, when dogs in a laboratory are exposed to electrical shocks from which they cannot escape, they showed behaviors that differentiate them from dogs not exposed to such uncontrollable events. The dogs exposed to the shocks would not cross a barrier to stop the flow of electric shock when put in a new learning situation. They remained passive and did not move. According to the learned helplessness theory, the shocked dogs learned that outcomes were independent of responses, so they had both cognitive motivational deficits (i.e., they would not attempt to escape the shock) and emotional deficits (indicating decreased reactivity to the shock). In the reformulated view of learned helplessness as applied to human depression, internal causal explanations may produce a loss of self-esteem after adverse external events. Behaviorists who subscribe to this theory often stress that improvement of depression is contingent on the patient’s learning a sense of control and mastery of the environment.
Evolutionary Theory.
Some theorists take an evolutionary perspective toward depression. From this perspective, depression is an adaptive response to perceived threats in the environment. From this perspective, depression is an adaptive response to perceived threats in the environment, and the tendency for depressed persons to withdraw from the environment in the face of possible threats could be protective. Beyond threats of bodily harm, social threats (e.g.,of exclusion or defeat) could also be considered threats in that such social threats can reduce one’s perceived fitness, and hence, the desirability of a mate. The depressive response in which one decreases activity, withdraws from social situations, and approaches novel situations with a negative bias (“that person will think I am a loser”) could be interpreted as adaptive ways to reduce risk and avoid further social failures. There are many varieties of evolutionary theory, some of which stress the adaptive benefit of depression, others which see it as an outmoded response which may have had a benefit in ancient societies, but is counterproductive in our modern world. Other versions see the basic ability to vary mood as adaptive but suggest depression is a dysregulation of that normal function. These theories are difficult to test, as it is challenging to test the fitness of a particular trait that is very common in a population.
