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Mechanisms to Target in the Treatment of Depression and Mood Disorders

treatment of depression and mood disorderEmpirically supported treatments have been the gold standard of mental health practice for decades, but people typically don’t fit neatly within the diagnostic categories upon which such protocols are based and tested.

Moreover, the prevalence of comorbidity and redundancy of symptoms across disorders necessitates a trans diagnostic approach to assessment and treatment—i.e., one that focuses on the underlying psychological mechanisms that have been linked to etiology and maintenance of emotional and behavioral problems.

Vulnerability Factors

When it comes to depression and mood disorders, there are some common mechanisms across diagnoses that are known vulnerability factors. Identifying these mechanisms is the first step in tailoring treatment to target the root causes of a client’s suffering.

Here are some of the key mechanisms to consider for your patient is struggling with depression and other mood-based problems.

1. Neurophysiological Mechanisms

Identifying potential neurophysiological mechanisms, which in this case involve vulnerabilities rooted in the nervous system, can go a long way in helping to ease a client’s sense of failure or self-blame around their symptoms, as well as helping you identify potential barriers to treatment. Neurophysiological vulnerabilities often linked with mood disorders include:

Emotion Regulation. Emotional functioning and emotion regulation are key areas of impairment in depression and mood disorders (Gotlib & Joorman, 2010). Structural and functional abnormalities in the brain areas that control these functions are well-documented in depressive disorders and may contribute to the often prolonged and recurrent nature of these problems (Singh & Gotlib, 2014).

Sleep Regulation. Sleep regulation is closely related with emotion regulation. For instance, excessive emotional reactivity can be an underlying mechanism in insomnia and other sleep disorder (Gehrman et al., 2012), and sleep disturbances have been linked with exacerbation of emotion regulation difficulties in PTSD (Pickett, Barbaro, & Mello, 2016). Deficits in the structure and pattern of a client’s sleep have been linked with emotion dysregulation in bipolar illness, major depression and other diagnoses.

Arousal/Inhibitory Control. Inadequate modulation of cardiac function while breathing has been implicated in emotion dysregulation across a range of problems including depression (Rottenberg et al., 2002). The rapid spike in emotional arousal and slow return to baseline that is commonly seen in borderline personality disorder (BPD) have been linked to deficits in downregulation of limbic structures and poor modulation of maladaptive behavioral action urges (Linehan et al., 2007). Physiological arousal also is implicated in emotional suppression and intrusions in PTSD (Shepherd & Wild, 2014).

Information Processing. Deficits in the processing, storage and retrieval of information are a common feature of mood disorders. For example, negative information-processing biases occur in both unipolar and bipolar depression (Alloy et al., 2006), and may contribute to rumination and emotion regulation problems (Gotlib & Joormann, 2010). These mechanisms also are linked with intrusive images in PTSD (Brewin et al., 1996) and bipolar depression (Gregory et al., 2010).

2. Learned Responses

Learned responses, such as those resulting from behavioral modeling, are acquired throughout life and can be specific to certain events or generalized across situations. Identifying the consequences of learned responses helps us to uncover contextual and functional patterns of maladaptive behaviors, which in turn creates a springboard to test new ways of responding that will improve clients’ quality of life.

Understanding learned responses can also help us better understand other vulnerability and response mechanisms that may be at play, which can further inform our treatment planning decisions.

Based on these principles, Barlow (2000, 2002) identified a diminished sense of control over aversive events and emotional experiences (due to early learning, specifically) as a general psychological vulnerability factor for emotional disorders, including depression.

3. Negative Schemas

Aaron Beck’s classic model of depression (1964) identifies schemas as underlying cognitive structures that develop early in life and affect people’s interpretation of their experiences. Schemas are pervasive, deeply entrenched core ideas that influence patterns of cognition, behaviors, mood and interpretations of events. When activated, they can trigger response mechanisms, symptoms and functional challenges.

Schema content can include core negative beliefs about oneself, others, the world and the future. A person struggling with depression, for example, may hold a belief about the future that things will never get better or see herself as “a loser.”

When triggered, schemas can act as a lens that distorts reality to conform with and confirm one’s existing schemas, often solidifying existing problems. For example, if John believes he is defective and cannot maintain a romantic relationship, an argument with his girlfriend may lead him to the conclusion that the relationship is coming to an end, confirming his core belief that his defectiveness makes him unequipped for a romantic relationship.

He may then withdraw from the relationship, avoid taking constructive steps to resolve the original conflict, or selectively scan the situation for evidence of other ways in which his defectiveness is evident.

These maladaptive coping behaviors, triggered by John’s schema, can lead to depression, fear of intimacy, avoidance tactics and a slew of other emotional and behavioral problems. You can identify schemas by observing the automatic thoughts that are affiliated with a client’s negative emotional experiences (A.T. Beck et al., 1979; J.S. Beck, 2011).

4. Negative Problem Orientation

Negative problem orientation (NPO) is the tendency to perceive problems as threats, to expect problems to be unsolvable, to doubt one’s ability to successfully cope with problems and to become frustrated and upset when faced with problems or negative emotions—all of which can undermine motivation and the ability to engage effectively.

Unsurprisingly, NPO has been identified as the single cognitive variable that correlates with mood and anxiety symptoms, including depression, social anxiety disorder, generalized anxiety disorder and obsessive compulsive disorder, suggesting that it may confer a general vulnerability to mood and anxiety symptoms (Fergus & Wu, 2011).

5. Distress Tolerance

Distress tolerance is the ability to tolerate aversive internal states, including negative emotions and physical discomfort—a key variable in one’s ability to cope with adverse events. The perception of both the distressful experience itself, and one’s ability to tolerate distress, influence the way one responds to such experiences and contexts (Leyro et al., 2010).

Thus, the perception “I can’t handle this,” where “this” is one more day of depression, can elicit response mechanisms that undermine the client’s ability to cope with the situation and perpetuate a repeating pattern of psychological problems.

Identifying the above mechanisms is the first step in creating an appropriate treatment plan that will get to the root of your client’s suffering. For more about transdiagnostic approach to treatment planning, check out “The Transdiagnostic Road Map to Case Formulation and Treatment Planning.”

 

References

Alloy, L. B., Abramson, L. Y., Walshaw, P. D., et al. (2006). Cognitive vulnerability to unipo- lar and bipolar mood disorders. Journal of Social and Clinical Psychology, 25, 726–754.

Barlow, D. H. (2000). Unraveling the mysteries of anxiety and its disorders from the perspective of emotion theory. American Psychologist, 55, 1247–1263.

Barlow, D. H. (2002). Anxiety and its disorders (2nd ed.). New York: Guilford.

Beck, A. T. (1964). Thinking and depression: II. Theory and therapy. Archives of General Psychiatry, 10, 561–571.

Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York: International Universities Press.

Beck, J. S. (2011). Cognitive therapy: Basics and beyond (2nd ed.). New York: Guilford.

Brewin, C. R., Dalgleish, T., & Joseph, S. (1996). A dual representation theory of post- traumatic stress disorder. Psychological Review, 103, 670–686.

Fergus, T. A., & Wu, K. D. (2011). Searching for specificity between cognitive vulnerabilities and mood and anxiety symptoms. Journal of Psychopathology and Behavioral Assessment, 33, 446–458.

Gehrman, P., Findley, J., & Perlis, M. (2012). Insomnia I: Etiology and conceptualization. In C. M. Morin & C. A. Espie (Eds.), The Oxford handbook of sleep and sleep disorders. New York: Oxford University Press.

Gotlib, I. H., & Joormann, J. (2010). Cognition and depression. Annual Review of Clinical Psychology, 6, 285–312.

Gregory et al., 2010Gregory, J. D., Brewin, C. R., Mansell, W., et al. (2010). Intrusive memories and images in bipolar disorder. Behaviour Research and Therapy, 48, 698–703.

Leyro, T. M., Zvolensky, M. J., & Bernstein, A. (2010). Distress tolerance and psychopatho- logical symptoms and disorders. Psychological Bulletin, 136, 576–600.

Linehan, M. M., Bohus, M., & Lynch, T. R. (2007). Dialectical behavior therapy for perva- sive emotion dysregulation. In J. J. Gross (Ed.), Handbook of emotion regulation. New York: Guilford.

Pickett, S. M., Barbaro, N., & Mello, D. (2016). The relationship between subjective sleep disturbance, sleep quality, and emotion regulation difficulties in a sample of college students reporting trauma exposure. Psychological Trauma: Theory, Research, Practice, and Policy, 8, 25-33.

Rottenberg, J., Wilhelm, F. H., Gross, J. J., et al. (2002). Respiratory sinus arrhythmia as a predictor of outcome in major depressive disorder. Journal of Affective Disorders, 71, 265–272.

Shepherd, L., & Wild, J. (2014). Emotion regulation, physiological arousal, and PTSD symptoms in trauma-exposed individuals. Journal of Behavior Therapy and Experimental Psychiatry, 45, 360-367.

Singh, M. K., & Gotlib, I. H. (2014). The neuroscience of depression: Implications for assessment and intervention. Behaviour Research and Therapy, 62, 60-73.

 

Rochelle Frank, Ph.D., is a clinical psychologist in Oakland, CA and coauthor of The Transdiagnostic Road Map to Case Formulation and Treatment Plannng: Practical Guidance for Clinical Decision Making.

She is an assistant clinical professor in the clinical science program at the University of California, Berkeley, and has more than 25 years of clinical experience in outpatient inpatient, and residential settings. She specializes in the treatment of severe mood disorders, borderline personality disorder, and trauma and dissociative disorders.

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Mechanisms to Target in the Treatment of Depression and Mood Disorders