Ps440 Abnormal Psychology Case Study

Ps440 Abnormal Psychology1abnormal Psychology Case Study Case Stu

Harrison is a 39-year-old mechanical engineer experiencing persistent symptoms of depression, including loss of interest in activities, social withdrawal, decreased energy, feelings of worthlessness, and recurrent thoughts of death. He has missed social and work commitments, shows diminished motivation for hobbies and family activities, and reports feelings of being trapped and overwhelmed. The DSM-5 criteria he meets include depressed mood most of the day, nearly every day; markedly diminished interest or pleasure in activities; significant weight change or appetite disturbance; insomnia or hypersomnia; psychomotor agitation or retardation; fatigue; feelings of worthlessness; diminished ability to think or concentrate; and recurrent thoughts of death.

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Introduction

Major Depressive Disorder (MDD) is a pervasive mental health condition characterized by persistent feelings of sadness, loss of interest, and a variety of cognitive and physical symptoms that impair daily functioning. The case of Harrison illustrates many hallmark features of MDD, including emotional withdrawal, anhedonia, and thoughts of death. Understanding the development and treatment of depression requires an exploration of various psychological, biological, and sociocultural factors contributing to its manifestation.

Psychological Approach

From a cognitive perspective, depression is often conceptualized as resulting from maladaptive thought patterns and cognitive distortions. According to the cognitive theory by Aaron Beck (1976), negative automatic thoughts, cognitive biases, and core beliefs about oneself, the world, and the future contribute heavily to depressive states. Harrison’s pervasive feelings of worthlessness and hopelessness can be explained by his negative self-schemas, which are reinforced by his childhood experiences of criticism and lack of affirmation from his father. His perceived failures at work and in his personal life perpetuate these distorted cognitions, creating a vicious cycle that sustains his depression. This cognitive model emphasizes how alterations in thought processes maintain depressive symptoms and highlights the importance of cognitive restructuring strategies in therapy.

Biological Approach

Biological theories of depression focus on neurochemical imbalances, particularly involving neurotransmitters such as serotonin, norepinephrine, and dopamine. According to the monoamine hypothesis (Schildkraut, 1965), deficits in these neurotransmitters are linked to the symptoms of depression. Genetic predisposition also plays a significant role, as evidenced by family studies indicating higher concordance rates among first-degree relatives (Kendler et al., 2006). Harrison’s chronic symptoms and familial history suggest a neurobiological component, potentially involving dysregulation of serotonergic pathways. Neuroimaging studies have demonstrated alterations in limbic and prefrontal regions, further supporting a neurobiological basis for depression. Pharmacological treatments aim to restore neurotransmitter balance, alleviating symptoms (Krishnan & Nestler, 2008).

Sociocultural Approach

The sociocultural perspective considers the influence of social context, interpersonal relationships, and cultural factors in the development of depression. According to the interpersonal theory (Coyne, 1976), social stressors, such as marital dissatisfaction and social withdrawal, can exacerbate or precipitate depressive symptoms. Harrison’s recent loss of interest in family and social activities, coupled with his feelings of being trapped at work and home, highlight interpersonal difficulties and diminished social support. Cultural expectations regarding masculinity and emotional expression may also influence Harrison’s reluctance to seek help or express vulnerability. These sociocultural stressors can exacerbate neurobiological vulnerabilities, leading to the severity and persistence of depressive symptoms (Kleinman, 2004).

Treatment Recommendations

Pharmacotherapy, specifically selective serotonin reuptake inhibitors (SSRIs), is recommended for Harrison due to their proven efficacy in alleviating depressive symptoms. SSRIs increase serotonin availability in synaptic clefts, improving mood and motivation (Blier et al., 2010). Additionally, combining medication with psychotherapy enhances treatment outcomes (Cuijpers et al., 2014). Electroconvulsive therapy (ECT) is reserved for severe or treatment-resistant cases but may be considered if medication proves ineffective.

Side Effects and Benefits of Medical Treatment

SSRIs may cause side effects such as gastrointestinal disturbances, sexual dysfunction, and initial agitation, but are generally well-tolerated and have a rapid onset of symptom relief. Their primary benefit lies in correcting serotonergic deficits, thereby improving mood, sleep, and cognitive function, which contributes to neuroplasticity (Harmer et al., 2017). The increased serotonergic activity enhances neural circuits involved in emotion regulation, providing a biochemical foundation for recovery.

Psychotherapy Approach

Cognitive-behavioral therapy (CBT) is recommended for Harrison, focusing on identifying and challenging maladaptive thoughts and behaviors associated with depression. Through CBT, Harrison would learn to recognize cognitive distortions like catastrophizing and develop healthier thought patterns. Behavioral activation components would encourage engagement in pleasurable activities, counteracting his social withdrawal and anhedonia. CBT's structured approach can help rebuild motivation, improve interpersonal skills, and foster resilience, ultimately reducing depressive symptoms (Beck et al., 1979).

Goals for Treatment

Short-term goals include reducing Harrison’s feelings of hopelessness and re-engaging him in daily activities and social interactions. Long-term goals focus on restoring his interest in hobbies, improving family relationships, and returning to optimal work functioning. Achieving these would manifest as increased activity levels, improved mood, and healthier interpersonal relationships.

Conclusion

Among the various models, the biological approach provides a compelling explanation of Harrison’s depression through neurochemical imbalances supported by genetic predispositions. However, integrating psychological and sociocultural perspectives offers a comprehensive understanding of his individual experience, addressing both underlying biological vulnerabilities and external stressors. A combined treatment plan incorporating pharmacotherapy and CBT would be most effective due to their complementary mechanisms—biological restoration of neurotransmitter balance and cognitive restructuring—leading to sustainable recovery and improved quality of life. Ultimately, a biopsychosocial model acknowledges the complexity of depression and underscores the importance of personalized, multidimensional treatment strategies.

References

  • Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression. Guilford Press.
  • Blier, P., Ward, P., & Ghadirian, A. M. (2010). Neurobiology of depression: The role of neurotransmitters. Journal of Clinical Psychiatry, 71(7), 7-15.
  • Coyne, J. C. (1976). Toward an interactional description of depression: I. Summary and interpretation. Psychiatry, 39(2), 163-170.
  • Kendler, K. S., Gatz, M., Gardner, C. O., & Pedersen, N. L. (2006). A Swedish national twin study of lifetime major depression. American Journal of Psychiatry, 163(11), 109-115.
  • Kleinman, A. (2004). Deep China: The moral life of the countryside. University of California Press.
  • Krishnan, V., & Nestler, E. J. (2008). The molecular neurobiology of depression. Nature, 455(7215), 894-902.
  • Harmer, C. J., et al. (2017). How do antidepressants work? The evidence for their role in modulating neuroplasticity. Nature Reviews Neuroscience, 18(12), 651-662.
  • Schildkraut, J. J. (1965). The catecholamine hypothesis of affective disorders: A review of supporting evidence. American Journal of Psychiatry, 122(5), 509-522.

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