Symptom dimensions to address heterogeneity in tinnitus

This chapter provides a critical review of recent behavioral and neuroimaging evidence of reward processing abnormalities in mood disorders. The primary focus is on the neural mechanisms underlying disruption in approach motivation, reward learning, and reward-based decision-making in major depression and bipolar disorder. Efforts focused on understanding how reward-related impairments contribute to psychiatric symptomatology have grown substantially in recent years. This has been driven by significant advances in the understanding of the neurobiology of reward processing and a growing recognition that disturbances in motivation and hedonic capacity are poorly targeted by current pharmacological and psychotherapeutic interventions. As a result, numerous studies have sought to test the presence of reward circuit dysfunction in psychiatric disorders that are marked by anhedonia, amotivation, mania, and impulsivity. Moreover, as the field has increasingly eschewed categorical diagnostic boundaries in favor of symptom dimensions, there has been a parallel rise in studies seeking to identify transdiagnostic neural markers of reward processing dysfunction that may transcend disorders. The thesis of this chapter is twofold: First, evidence indicates that specific subcomponents of reward processing map onto partially distinct neurobiological pathways. Second, specific subcomponents of reward processing, including reward learning and effort-based decision-making, are impaired across different mood disorder diagnoses and may point to dimensions in symptom presentation that possess more reliable behavioral and neural correlates. The potential for these findings to inform the development of prevention and treatment strategies is discussed.

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Symptom dimensions of major depression in a large community-based cohort

Psychological Medicine ◽

10.1017/s0033291721001707 ◽

2021 ◽

pp. 1-8

Author(s):

Michael Wainberg ◽

Peter Zhukovsky ◽

Sean L. Hill ◽

Daniel Felsky ◽

Aristotle Voineskos ◽

...

Keyword(s):

Primary Care ◽

Major Depression ◽

Risk Scores ◽

Polygenic Risk Score ◽

Psychiatric Diagnoses ◽

Uk Biobank ◽

Community Based ◽

Symptom Dimensions ◽

Polygenic Risk ◽

Large Community

Abstract Background Our understanding of major depression is complicated by substantial heterogeneity in disease presentation, which can be disentangled by data-driven analyses of depressive symptom dimensions. We aimed to determine the clinical portrait of such symptom dimensions among individuals in the community. Methods This cross-sectional study consisted of 25 261 self-reported White UK Biobank participants with major depression. Nine questions from the UK Biobank Mental Health Questionnaire encompassing depressive symptoms were decomposed into underlying factors or ‘symptom dimensions’ via factor analysis, which were then tested for association with psychiatric diagnoses and polygenic risk scores for major depressive disorder (MDD), bipolar disorder and schizophrenia. Replication was performed among 655 self-reported non-White participants, across sexes, and among 7190 individuals with an ICD-10 code for MDD from linked inpatient or primary care records. Results Four broad symptom dimensions were identified, encompassing negative cognition, functional impairment, insomnia and atypical symptoms. These dimensions replicated across ancestries, sexes and individuals with inpatient or primary care MDD diagnoses, and were also consistent among 43 090 self-reported White participants with undiagnosed self-reported depression. Every dimension was associated with increased risk of nearly every psychiatric diagnosis and polygenic risk score. However, while certain psychiatric diagnoses were disproportionately associated with specific symptom dimensions, the three polygenic risk scores did not show the same specificity of associations. Conclusions An analysis of questionnaire data from a large community-based cohort reveals four replicable symptom dimensions of depression with distinct clinical, but not genetic, correlates.

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