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. 2026 Feb 2;33(1):e70224. doi: 10.1002/cpp.70224

Goal Pursuit‐Focused CBT for Bipolar Disorder: A Four‐Case Series

Andrea Gragnani 1,2,, Allison Uvelli 1,3,, Marco Saettoni 1,
PMCID: PMC12865336  PMID: 41630512

ABSTRACT

Background

BD is a chronic, cyclical condition marked by severe mood instability and significant impairment. Although pharmacological and psychotherapeutic interventions have demonstrated efficacy, challenges remain in preventing relapse and sustaining long‐term euthymia. This study evaluates a CBT‐based intervention designed to reduce symptom severity and recurrence by targeting three core maintenance factors: intolerance of anergic states, addiction to mania, and meta‐emotional problems.

Method

Four individuals diagnosed with BD participated in a one‐year CBT intervention tailored to address these key vulnerabilities. Assessments were conducted at baseline, post‐treatment, and at 18‐ and 24‐month follow‐ups, measuring depression, mania, quality of life, and personality functioning. Changes were evaluated with RCI and repeated measures ANOVA.

Results

All four patients showed a marked reduction in depressive symptoms at the end of treatment and at the 24‐month follow‐up, with a large effect size (η2 = 0.83). Improvements were also observed in the quality of life and maladaptive personality traits over time. Notably, euthymia was maintained throughout the follow‐up period, with no recurrence of manic episodes or new affective cycles.

Conclusion

Despite limitations, these preliminary findings suggest that this three‐goal CBT intervention targeting core maintenance factors in bipolar disorder may promote sustained clinical improvements, increase long‐term stability, and reduce reliance on medication.

Keywords: bipolar disorder, case series, cognitive behavioural therapy, euthymia maintenance, treatment adherence

Summary

  • A CBT intervention specifically tailored to bipolar disorder can effectively target core vulnerability mechanisms, intolerance of anergy, reinforcement of manic states, and meta‐emotional problem.

  • Focusing on the maintenance of euthymia, rather than solely on symptom reduction, may enhance long‐term stability and reduce relapse frequency.

  • Clinicians may benefit from integrating psychoeducation, acceptance‐based strategies, and cognitive techniques that reduce activation‐driven coping and increase tolerance of low‐energy states.

  • Detailed case trajectories suggest that sustained therapeutic engagement and early discussion of treatment rationale support adherence in long‐term CBT protocols for bipolar disorder.

  • This treatment model offers clinicians a structured yet flexible framework to address both depressive and expansive vulnerabilities within a unified cognitive‐behavioural formulation.

1. Introduction

Bipolar disorder (BD) is a chronic psychiatric condition characterized by recurrent depressive, hypomanic, and manic episodes with substantial functional impairment (APA 2013; Grande et al. 2016). Although traditionally conceptualized as an illness primarily managed through pharmacological treatment (Miklowitz and Goldstein 1990; Goodwin and Jamison 2007), recent evidence emphasizes the importance of integrating structured psychological interventions to improve long‐term stability and reduce relapse risk (Miklowitz et al. 2020; Valdivieso‐Jiménez 2023). Randomized clinical trials have shown that CBT, family‐focused therapy, interpersonal and social rhythm therapy, and psychoeducation can significantly enhance outcomes when combined with medication (Colom and Vieta 2006; Miklowitz et al. 2007).

Despite these findings, most CBT protocols for BD originate from treatments for unipolar depression and anxiety, which limits their effectiveness in addressing bipolar‐specific mechanisms such as mood cycling, reward hypersensitivity, emotional hyper‐reactivity, and the reinforcing properties of expansive states. Moreover, although psychotherapy contributes to relapse prevention, evidence regarding its capacity to sustain long‐term euthymia remains mixed (Oud et al. 2018; Novick and Swartz 2019), and recent reviews underscore the need for interventions guided by clearer explanatory models of BD's distinct affective states (Oliva et al. 2025).

To address these limitations, the present study adopts a CBT model specifically adapted for BD (Saettoni et al. 2021), integrating clinical observation (Akiskal and Pinto 1999; Akiskal et al. 2003) with contemporary theories of reward sensitivity, goal dysregulation, and emotional reactivity (Johnson 2005a, 2005b; Fletcher and Johnson 2011). Within this framework, BD is maintained by three core mechanisms: (a) the ‘addiction to mania’ (Gruber 2011a, 2011b; Maremmani et al. 2012); (b) the intolerance of anergy, abulia, and anhedonia (Goodwin and Jamison 2007; Saettoni et al. 2021); and (c) the meta‐emotional problem (Ellis 1980; Rainone and Mancini 2018). Targeting these processes may offer a more precise, mechanism‐focused approach to relapse prevention, beyond stabilizing acute symptoms.

2. Methods

2.1. Participants

A sample group of three males and one female participated in a treatment program at the Center of Cognitive Psychotherapy for bipolar disorder. The average age was 44.75 (SD = 14.86); the males were married, while the female was unmarried. All participants received pharmacotherapy throughout the entire treatment duration. Inclusion criteria involved being Italian and having a diagnosis of either type 1 or type 2 bipolar disorder in the depressive or mixed phase. Exclusion criteria included a diagnosis of borderline or antisocial personality disorder, cyclothymia, substance use disorder (as a primary diagnosis), and debilitating chronic diseases.

2.2. Cases Presentation

The clinical vignettes of the four cases considered are presented below.

  1. Matthew, a 43‐year‐old man with BD type I, had experienced recurrent depressive and manic episodes with periods of psychosis requiring hospitalization. Before entering treatment, he reported a prolonged depressive phase (HAM‐D = 29), persistent dysregulation around achievement goals, and significant intolerance of anergy. His illness course showed marked summer seasonality and abrupt polarity shifts linked to overactivation and work‐related stress. Despite good adherence to pharmacotherapy, he continued to experience severe mood instability. His main goals were to reduce depressive symptoms and prevent new manic recurrences.

  2. Henry, aged 62, presented with BD type II characterized by decades of alternating depressive, hypomanic, and mixed episodes, often associated with financial stressors and interpersonal shame. His father also had BD, and Henry's onset occurred at age 20. Despite periods of functional remission, he experienced frequent polarity shifts and significant impulsivity. At intake, he was in a depressive episode with mixed features (HAM‐D = 22). Comorbid obsessive‐compulsive personality traits and generalized anxiety were identified. Henry sought treatment to stabilize mood fluctuations and reduce recurrent cycles of overactivation and collapse.

  3. Alicia, a 26‐year‐old woman with BD type I, had experienced multiple manic, depressive, and mixed episodes since age 22, often associated with reduced pharmacological adherence and intense emotional reactivity. Her functioning oscillated between ambitious goal pursuit in artistic work and profound aversion to anergy and apathy, states she associated with parental vulnerability. At intake, she presented with a severe depressive episode (HAM‐D = 30) and high interpersonal sensitivity. She sought therapy to stabilize her mood, improve adherence, and develop more flexible responses to internal states.

  4. Alfred, aged 48, had a 30‐year history of BD type II with a stable yearly pattern of depressive and hypomanic episodes. His functioning was strongly tied to performance, competitiveness, and avoidance of perceived incompetence. Depressive episodes typically emerged during the summer months. Despite several previous therapies, he continued to experience recurrent polarity shifts and difficulty tolerating low‐energy states. At intake, he presented with mild depression (HAM‐D = 13) and the goal of reducing episode frequency and stabilizing daily functioning.

Table 1 below summarizes the patients' disorder characteristics. A complete description of each clinical case is provided in the Supplementary Materials (Text S1).

TABLE 1.

Characteristics of patients' diseases.

Participants Bipolar disorder Age Age of first episode Life theme
Matthew Type 1 43 38 Social upliftment, pleasure‐seeking, building a family
Henry Type 2 62 30 Social upliftment
Alicia Type 1 26 24 Fame and success
Alfred Type 2 48 18 Feel confident and skilled

2.3. Measures

Depressive symptoms were assessed monthly with the Hamilton Depression Rating Scale (HAM‐D; Hamilton 1960), using the standard 17‐item total score (ranging from 0 to 66). Manic symptoms were assessed with the Young Mania Rating Scale (YMRS; Young et al. 1978), administered monthly following the guidelines of the original validation studies (ranging from 0 to 56). Quality of life was evaluated at baseline, post‐treatment, and follow‐ups with the QL‐Index (Spitzer et al. 1981), a brief 5‐item measure assessing functioning and subjective well‐being. Personality functioning was assessed at the same time points using the PID‐5‐BF (Fossati et al. 2021), which evaluates five maladaptive personality domains.

2.4. Procedures

The treatment was provided by psychotherapists who specialize in CBT and have solid experience with bipolar disorder, and who supervised each other throughout the process. They are recognized for their work in both clinical settings and research and are affiliated with the schools and clinical centers of the School of Cognitive Psychotherapy (SPC).

AG is a psychologist and psychotherapist, while MS is a medical doctor, psychiatrist, and psychotherapist.

The first four individuals who requested CBT for BD in March 2023 and met the inclusion and exclusion criteria were enrolled in the program. No eligible patients declined treatment during this period. Engagement was facilitated through an initial psycho‐educational session, during which therapists introduced the psychological mechanism underlying BD and provided a concise explanation of the treatment model and its objectives. This allowed patients to develop a clear understanding of the rationale for the intervention and to commit to the year‐long program.

Participants were involved in a 12‐month CBT program, attending weekly sessions (about 45 per patient). Before starting therapy, each patient went through a thorough psychological assessment. The tests measuring depression and mania were administered monthly by A.U. (psychologist) as well as at the two follow‐ups, while the other scales were administered at pre‐ and post‐intervention and at the two follow‐ups. The therapy began in March 2023 and ended in March 2024. Follow‐up assessments are planned for September 2024 and March 2025. All patients gave their informed consent to participate, and the study received approval from the Ethics Committee of the Scuola di Psicoterapia Cognitiva (protocol number 5/25).

2.5. Treatment

The intervention followed a flexible CBT approach tailored to the patient's affective state to achieve and maintain euthymia. Treatment began with a standard cognitive‐behavioural assessment consistent with NICE guidelines (2006, 2014), including longitudinal reconstruction of the disorder and identification of cognitive and behavioural correlates (e.g., Genogram, and the Life Chart Retrospective; Bowen 1979).

During acute phases, the focus was on safety, reduction of dysregulated behaviours, and initial affective stabilization. Techniques included behavioural activation for depressive phases (Ferster 1973; Lewinsohn 1974; Beck et al. 1979), behavioural inhibition strategies for manic or hypomanic hyperactivity (Saettoni et al. 2021), DBT‐derived skills to reduce distress intolerance and impulsivity (Van Dijk et al. 2013; Linehan and Wilks 2015), mindfulness exercises (Burgos‐Julián et al. 2022; Musket et al. 2021), and cognitive restructuring targeting excessive goal pursuit. Psychoeducation and self‐monitoring supported awareness of prodromal signs and lifestyle regularity (Colom and Vieta 2006; Colom et al. 2009).

The core and most extensive phase of the intervention was dedicated to reducing vulnerability to polarity shifts. This process targeted three mechanisms central to bipolar disorder: craving for activation (‘addiction to mania’), intolerance of anergy, abulia, and anhedonia, and addressing meta‐emotional problems, in particular, the evaluations of depressive states. Patients were guided to reinterpret low‐energy states as normative, reduce catastrophic appraisals, and develop a more flexible relationship with internal experiences (Mancini and Gragnani 2004; Perdighe and Mancini 2012). Cognitive acceptance procedures, reappraisal of personal values and goals, and exploration of the developmental origins of rigid success‐oriented beliefs supported this process. Techniques used included belief and goal history reconstruction, chairwork‐based cognitive restructuring (Pugh 2020), values clarification (Hayes 2004; LeJeune and Luoma 2019), imagery rescripting (Arntz and Weertman 1999), and acceptance‐based interventions for anergy and abulia (Saettoni et al. 2021). A detailed version of the full treatment protocol is included in the Supplementary Materials (Text S2).

2.6. Statistical Analysis

Initially, we planned to analyse the pre‐ and post‐assessment differences for each case across all measures used, employing the Reliable Change Index (RCI; Jacobson and Truax 1991). This index calculates the ratio between the observed differences and the standard error of measurement. A score that exceeds 1.96 indicates a statistically significant change. Next, we estimated trends in symptom means over time using Kendall's Tau and Pearson's r correlation tests, which align with standard single‐case study methodologies (Bulté and Onghena 2013). In this context, negative correlations indicate a decrease in variables, while positive correlations suggest an increase. Finally, we conducted a repeated measures ANOVA for the entire group, focusing solely on the 15 measurements of depression and mania. This analysis was intended to assess the treatment's effectiveness by examining within‐group differences over time. A post hoc power analysis with an effect size of 0.05, a probability of a type I error of 0.05, a sample size of 4, 15 measurements, and a correlation among repeated measures of 0.50 revealed a power of 90%.

3. Result

3.1. Qualitative Description

As summarized in Table 2, all four patients exhibited significant improvements in both depressive and manic symptoms from baseline (T0) to the end of treatment (T12), with stability or further gains observed at 18‐ and 24‐month follow‐ups. Three patients (Cases 1, 2, and 3) began treatment with severe depressive symptoms (HAM‐D ≥ 25), while Case 4 had mild depression. By T12, all had scores below the clinical threshold (HAM‐D < 8), indicating full remission, which was maintained over time. Manic symptoms were below clinical relevance at baseline for all cases (YMRS < 20) and remained stable post‐treatment and during follow‐ups. Quality of life improved progressively, with particularly notable gains for Cases 1 and 3 between T12 and FU24. In terms of personality functioning, all patients showed a reduction in overall trait dysfunction (PID‐5‐BF total scores), most markedly in Cases 1 and 3, with changes generally consolidating by the 12‐month mark and remaining stable thereafter.

TABLE 2.

Initial, final, and follow‐up scores of the measures.

HAM‐D YMRS QL‐Index PID‐5‐BF
T0‐T12‐FU18‐FU24 T0‐T12‐FU18‐FU24 T0‐T12‐FU18‐FU24 T0‐T12‐FU18‐FU24
Case 1 29‐7‐7‐6 4‐4‐2‐2 4‐5‐10‐10 38‐20‐12‐9
Case 2 22‐6—6‐6 16‐4—4‐4 3‐9—9‐9 26‐16‐15‐15
Case 3 30‐7‐3‐3 5‐2—2‐2 2‐6‐8‐8 41‐21‐20‐20
Case 4 13‐2‐1‐1 5‐5‐4‐2 6‐9‐9‐10 31‐24‐20‐18

As shown in Table 3, all four cases exhibited a marked reduction in the frequency of mood episodes from pre‐treatment to the end of treatment, with complete remission maintained at follow‐up. The most striking changes were observed in Cases 2 and 4, which moved from high episode frequency to full stabilization.

TABLE 3.

Affective manifestations.

Pre‐treatment 12‐months treatment Follow up (18–24)
Case 1 4 (2 depressive phases, 2 manic phases) 1 (manic phase) 0
Case 2 35 (17 depressive phases, 16 hypomanic phases, 2 mixed phases) 2 (1 depressive phase and 1 hypomanic phase) 0
Case 3 6 (4 depressive phases, 2 manic phases) 2 (1 depressive phase and 1 hypomanic phase) 0
Case 4 49 (27 depressive phases, 22 hypomanic phases) 1 (depressive phase) 0

Finally, no patients were hospitalized during or after treatment. These qualitative results suggest that the integrated treatment protocol was effective in reducing affective symptoms and improving subjective quality of life, with benefits persisting up to 2 years post‐treatment.

3.2. Quantitative Outcomes

The patients reported reliable and significant change, as defined by the RCI ≥ 1.96 cut‐off, in depression, mania, quality of life, and personality characteristics at the end of the treatment, and changes were maintained at the follow‐up of 18 and 24 months. Depression and personality pathology consistently decreased over time, and quality of life increased, confirmed by findings at Pearson's r, and Kendall's tau (Table 4), and visually observable from the graphic (Figures 1, 2; Figures S1S2).

TABLE 4.

Time series of depression, mania, quality of life, and personality pathology over time.

Depression
RCI Kendall's Tau (p) Pearson's r (p)
Case 1 6.44 −0.20 (0.15) −0.46 (< 0.05)
Case 2 4.48 −0.50 (< 0.05) −0.56 (< 0.05)
Case 3 4.81 −0.71 (< 0.001) −0.77 (< 0.001)
Case 4 7.56 −0.77 (< 0.001) −0.89 (< 0.001)
Mania
Case 1 0.65 −0.44 (0.83) 0.20 (0.46)
Case 2 2.37 −0.42 (< 0.05) −0.50 (< 0.05)
Case 3 0.97 −0.43 (< 0.05) −0.54 (< 0.05)
Case 4 0.97 −0.16 (0.42) −0.24 (0.38)
Quality of life
Case 1 −3.24 0.91 (< 0.05) 0.94 (< 0.05)
Case 2 −3.24 0.70 (< 0.05) 0.87 (< 0.05)
Case 3 −3.24 0.91 (< 0.05) 0.94 (< 0.05)
Case 4 −2.16 0.91 (< 0.05) 0.94 (< 0.05)
Personality
Case 1 5.59 −1.00 (< 0.05) −1.00 (< 0.05)
Case 2 2.12 −0.91 (< 0.05) −0.94 (< 0.05)
Case 3 4.05 −0.91 (< 0.05) −0.94 (< 0.05)
Case 4 2.51 −1.00 (< 0.05) −1.00 (< 0.05)

FIGURE 1.

FIGURE 1

Time series of depression. Changes in total scores of HAM‐D (12 monthly measurements and 2 follow‐ups). Legend: total score ranges from 0 to 66, with ≤ 25 indicating severe depression; 18–24 moderate depression; 8–17 mild depression; and ≥ 7 absence of depression.

FIGURE 2.

FIGURE 2

Time series of mania. Changes in total scores of YMRS (12 monthly measurements and 2 follow‐ups). Legend: total score ranges from 0 to 56, with a cut‐off of 12 for hypomania and 20 for mania.

In the case of mania, the results differ from the previous findings, as only one case (Case 2) showed a significant improvement. This can be explained by the fact that, according to the inclusion criteria, patients could not be in an acute manic phase at the start of treatment. Notably, Case 2 was the only one presenting with the highest level of manic symptoms at intake. In any case, euthymia was maintained across all participants, and manic episodes were successfully prevented throughout the treatment and follow‐up periods.

Lastly, repeated measures ANOVA results showed a significant improvement in depression with an effect size of 0.83 after the cognitive behavioural treatment, as observed at the final FU24 assessment, and a nonsignificant variation for mania (Table 5; see also T12 results in Table S1 in Supplementary materials and Tables S2S5 for the progress of pharmacological treatment).

TABLE 5.

Within‐group comparison of depression and mania between baseline and final assessment.

Sum of squares (residual) df Root‐mean‐square F p η2p
Depression 1534 (299) 14 (42) 109.6 (7.11) 15.4 < 0.001 0.83
Mania 209 (498) 14 (42) 15 (11.9) 1.26 0.27 0.29

4. Discussion

This case series examined a CBT intervention specifically tailored to bipolar disorder and grounded in a process‐focused framework (Saettoni et al. 2021). The treatment targeted three core maintenance mechanisms described in the literature: intolerance of anergy and abulia (Goodwin and Jamison 2007; Rainone and Mancini 2018), reinforcement processes associated with ‘addiction to mania’ (Gruber 2011a, 2011b; Maremmani et al. 2012), and meta‐emotional problems (Mancini and Semerari 1991; De Silvestri 1999). Across the four cases, depressive symptoms decreased substantially, quality of life improved, and maladaptive personality traits declined. Manic symptoms, subclinical at baseline given the inclusion criteria, remained stable throughout treatment and follow‐up. These findings are consistent with previous evidence supporting the role of psychological interventions in enhancing affective stability in bipolar disorder (Colom and Vieta 2006; Salcedo et al. 2016), although the effect size for depression observed here (η2 = 0.83) appears particularly robust. A central contribution of this work lies in emphasizing long‐term maintenance of euthymia as a primary therapeutic objective. All patients remained euthymic during the 12‐month follow‐up, with no recurrent episodes, hospitalizations, or need for pharmacological escalation, an outcome in line with previous findings on integrated psychoeducational and cognitive‐behavioural approaches (Colom and Vieta 2006; Miklowitz et al. 2007). By fostering greater tolerance of low‐energy states and reducing the drive for excessive activation in line with reward‐sensitivity and goal‐dysregulation models (Johnson 2005a, 2005b; Fletcher and Johnson 2011), patients reported increased flexibility and a diminished reliance on high‐arousal states to regulate mood.

4.1. Limitations

This study has several limitations that must be acknowledged. First, the small sample size of four patients limits the generalizability of the findings. Without a control group, it is not possible to definitively attribute the observed improvements to the therapeutic intervention alone, as other confounding variables may have contributed. Moreover, despite the inclusion of a follow‐up period, longer‐term data would be necessary to evaluate the durability of effects beyond 2 years. Finally, while we assessed symptomatology, personality traits, and quality of life, we did not include direct neurobiological or behavioural measures of change, which could provide a more comprehensive understanding of therapeutic impact.

5. Conclusion

Despite the methodological constraints, this study provides preliminary support for a process‐oriented CBT intervention that targets the specific maintenance and exacerbation mechanisms of bipolar disorder. By intervening on the core vulnerabilities and dysfunctional patterns associated with both depressive and expansive phases, meaningful and sustained clinical improvements were achieved. These findings underscore the potential of individualized cognitive‐behavioural approaches to enhance long‐term stability, reduce pharmacological burden, and improve overall functioning in patients with bipolar disorder.

Author Contributions

Andrea Gragnani: writing – review and editing, writing – original draft, project administration, investigation, conceptualization, supervision. Allison Uvelli: writing – review and editing, writing – original draft, methodology, formal analysis, data curation. Marco Saettoni: writing – review and editing, writing – original draft, project administration, investigation, conceptualization, supervision.

Funding

The authors have nothing to report.

Ethics Statement

All patients gave their informed consent to participate, and the study received approval from the Ethics Committee of the Scuola di Psicoterapia Cognitiva (protocol number 5/25).

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Text S1: Cases presentation.

Text S2: The extended treatment protocol.

Figure S1: Time series of personality symptoms. Changes in total scores of PID (T0‐T12 measurements and 2 follow‐ups).

Figure S2: Time series of quality of life. Changes in total scores of QOL (T0‐T12 measurements and 2 follow‐ups).

Table S1: Within‐group comparison of depression and mania between baseline and T12.

Table S2: Pharmacological treatment of case 1: Matthew.

Table S3: Pharmacological treatment of case 2: Henry.

Table S4: Pharmacological treatment of case 3: Alicia.

Table S5: Pharmacological treatment of case 4: Alfred.

CPP-33-e70224-s001.docx (283.2KB, docx)

Acknowledgements

This publication was made possible thanks to the specific contribution of the Scuola di Psicoterapia Cognitiva S.R.L.

Gragnani, A. , Uvelli A., and Saettoni M.. 2026. “Goal Pursuit‐Focused CBT for Bipolar Disorder: A Four‐Case Series.” Clinical Psychology & Psychotherapy 33, no. 1: e70224. 10.1002/cpp.70224.

Contributor Information

Andrea Gragnani, Email: gragnani@apc.it.

Allison Uvelli, Email: allison.uvelli@unisi.it.

Marco Saettoni, Email: marcosaettoni@gmail.com.

Data Availability Statement

The data that support the findings of this study are available in the supplementary material of this article.

References

  1. Akiskal, H. S. , Hantouche E. G., and Allilaire J. F.. 2003. “Bipolar II With and Without Cyclothymic Temperament: ‘Dark’ and ‘Sunny’ Expressions of Soft Bipolarity.” Journal of Affective Disorders 73, no. 1–2: 49–57. 10.1016/S0165-0327(02)00320-8. [DOI] [PubMed] [Google Scholar]
  2. Akiskal, H. S. , and Pinto O.. 1999. “The Evolving Bipolar Spectrum. Prototypes I, II, III and IV.” Psychiatric Clinics of North America 22, no. 3: 517–534. 10.1016/s0193-953x(05)70093-9. [DOI] [PubMed] [Google Scholar]
  3. American Psychiatric Association . 2013. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Publishing. [Google Scholar]
  4. Arntz, A. , and Weertman A.. 1999. “Treatment of Childhood Memories: Theory and Practice.” Behaviour Research and Therapy 37, no. 8: 715–740. 10.1016/S0005-7967(98)00173-9. [DOI] [PubMed] [Google Scholar]
  5. Beck, A. T. , Rush A. J., Shaw B. F., and Emery G.. 1979. Cognitive Therapy of Depression. Guilford Press. [Google Scholar]
  6. Bowen, M. 1979. Family Therapy in Clinical Practice. Jason Aronson. [Google Scholar]
  7. Bulté, I. , and Onghena P.. 2013. “The Single‐Case Data Analysis Package: Analysing Single‐Case Experiments With R Software.” Journal of Modern Applied Statistical Methods 12, no. 2: 28. 10.22237/jmasm/1383280020. [DOI] [Google Scholar]
  8. Burgos‐Julián, F. A. , Ruiz‐Íñiguez R., Peña‐Ibáñez F., Montero A. C., and Santed‐Germán M. A.. 2022. “Mindfulness‐Based and Mindfulness‐Informed Interventions in Bipolar Disorder: A meta‐Analysis Based on Becker's Method.” Clinical Psychology & Psychotherapy 29, no. 4: 1172–1185. 10.1002/cpp.2717. [DOI] [PubMed] [Google Scholar]
  9. Colom, F. , and Vieta E.. 2006. Psychoeducation Manual for Bipolar Disorder. Cambridge University Press. [Google Scholar]
  10. Colom, F. , Vieta E., Sánchez‐Moreno J., et al. 2009. “Group Psychoeducation for Stabilised Bipolar Disorders: 5‐Year Outcome of a Randomised Clinical Trial.” British Journal of Psychiatry 194, no. 3: 260–266. 10.1192/bjp.bp.107.040485. [DOI] [PubMed] [Google Scholar]
  11. De Silvestri, C. 1999. ‘Il mestiere di psicoterapeuta: manuale pratico di psicoterapia cognitivo‐comportamentale.’ Astrolabio.
  12. Ellis, A. 1980. “Rational‐Emotive Therapy and Cognitive Behaviour Therapy: Similarities and Differences.” Cognitive Therapy and Research 4, no. 4: 325–340. 10.1007/BF01178369. [DOI] [Google Scholar]
  13. Ferster, C. B. 1973. “A Functional Analysis of Depression.” American Psychologist 28, no. 10: 857–870. 10.1037/h0035605. [DOI] [PubMed] [Google Scholar]
  14. Fletcher, K. , and Johnson S. L.. 2011. “The Behavioral Activation System and Mania.” Clinical Psychology Review 31, no. 1: 1–12. 10.1016/j.cpr.2010.09.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Fossati, A. , Borroni S., Somma A., Krueger R. F., and Markon K. E.. 2021. PID‐5: Manuale e guida all'uso clinico della versione italiana. Raffaello Cortina Editore. [Google Scholar]
  16. Goodwin, F. K. , and Jamison K. R.. 2007. Manic Depressive Illness: Bipolar Disorder and Recurrent Depression. 2nd ed. Oxford University Press. [Google Scholar]
  17. Grande, I. , Berk M., Birmaher B., and Vieta E.. 2016. “Bipolar disorder.” Lancet 387, no. 10027: 1561–1572. 10.1016/S0140-6736(15)00241-X. [DOI] [PubMed] [Google Scholar]
  18. Gruber, J. 2011a. “Can Feeling Too Good Be Bad? Positive Emotion Persistence (PEP) in Bipolar Disorder.” Current Directions in Psychological Science 20, no. 4: 217–221. 10.1177/0963721411414632. [DOI] [Google Scholar]
  19. Gruber, J. 2011b. “A Review and Synthesis of Positive Emotion and Reward Disturbance in Bipolar Disorder.” Clinical Psychology & Psychotherapy 18, no. 5: 356–365. 10.1002/cpp.776. [DOI] [PubMed] [Google Scholar]
  20. Hamilton, M. 1960. “A Rating Scale for Depression.” Journal of Neurology, Neurosurgery, and Psychiatry 23, no. 1: 56–62. 10.1136/jnnp.23.1.56. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Hayes, S. C. 2004. Acceptance and Commitment Therapy: An Experiential Approach to Behavior Change. Guilford Press. [Google Scholar]
  22. Jacobson, N. S. , and Truax P.. 1991. “Clinical Significance: A Statistical Approach to Defining Meaningful Change in Psychotherapy Research.” Journal of Consulting and Clinical Psychology 59, no. 1: 12–19. 10.1037/0022-006X.59.1.12. [DOI] [PubMed] [Google Scholar]
  23. Johnson, S. L. 2005a. “Mania and Dysregulation in Goal Pursuit: A Review.” Clinical Psychology Review 25, no. 2: 241–262. 10.1016/j.cpr.2004.11.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Johnson, S. L. 2005b. “Life Events in Bipolar Disorders: Towards More Specific Models.” Clinical Psychology Review 25, no. 8: 1008–1027. 10.1016/j.cpr.2005.06.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. LeJeune, J. , and Luoma J. B.. 2019. Values in Therapy: A Clinician's Guide to Helping Clients Explore Values, Increase Psychological Flexibility, and Live a More Meaningful Life. Context Press. [Google Scholar]
  26. Lewinsohn, P. M. 1974. “A Behavioral Approach to Depression.” In The Psychology of Depression: Contemporary Theory and Research, edited by Friedman R. J. and Katz M. M., 157–178. Plenum Press. [Google Scholar]
  27. Linehan, M. M. , and Wilks C. R.. 2015. “The Course and Evolution of Dialectical Behavior Therapy.” American Journal of Psychotherapy 69, no. 2: 97–110. 10.1176/appi.psychotherapy.2015.69.2.97. [DOI] [PubMed] [Google Scholar]
  28. Mancini, F. , and Gragnani A.. 2004. “Il trattamento della depressione: Approcci cognitivi e comportamentali.” Franco Angeli.
  29. Mancini, F. , and Semerari A., eds. 1991. Le teorie cognitive dei disturbi emotivi. La Nuova Italia Scientifica. [Google Scholar]
  30. Maremmani, I. , Maremmani A. G. I., Rugani F., et al. 2012. “Clinical Presentations of Substance Abuse in Bipolar Heroin Addicts at Time of Treatment Entry.” Annals of General Psychiatry 11, no. 1: 23. 10.1186/1744-859X-11-23. [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Miklowitz, D. J. , Efthimiou O., Furukawa T. A., et al. 2020. “Adjunctive Psychotherapy for Bipolar Disorder: A Systematic Review and Component Network meta‐Analysis.” JAMA Psychiatry 78, no. 2: 141–150. 10.1001/jamapsychiatry.2020.2993. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Miklowitz, D. J. , and Goldstein M. J.. 1990. “Behavioral Family Treatment for Patients With Bipolar Affective Disorder.” Behavior Modification 14, no. 4: 457–489. 10.1177/01454455900144005. [DOI] [PubMed] [Google Scholar]
  33. Miklowitz, D. J. , Otto M. W., Frank E., et al. 2007. “Psychosocial Treatments for Bipolar Depression: A 1‐Year Randomized Trial From the Systematic Treatment Enhancement Program.” Archives of General Psychiatry 64, no. 4: 419–426. 10.1001/archpsyc.64.4.419. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Musket, C. W. , Hansen N. S., Welker K. M., Gilbert K. E., and Gruber J. A.. 2021. “Pilot Investigation of Emotional Regulation Difficulties and Mindfulness‐Based Strategies in Manic and Remitted Bipolar I Disorder and Major Depressive Disorder.” International Journal of Bipolar Disorder 9, no. 1: 2. 10.1186/s40345-020-00206-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. National Institute for Health and Care Excellence . 2006. “ Bipolar disorder: The assessment and management of bipolar disorder in adults, children and young people in primary and secondary care (NICE Clinical Guideline No. 38).” https://www.nice.org.uk/guidance/cg38.
  36. National Institute for Health and Care Excellence . 2014. “ Bipolar disorder: assessment and management (NICE Guideline No. CG185).” https://www.nice.org.uk/guidance/cg185. [PubMed]
  37. Novick, D. M. , and Swartz H. A.. 2019. “Evidence‐Based Psychotherapies for Bipolar Disorder.” Focus 17, no. 3: 238–248. 10.1176/appi.focus.20190004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  38. Oliva, V. , Fico G., De Prisco M., Gonda X., Rosa R. A., and Vieta E.. 2025. “Bipolar Disorders: An Update on Critical Aspects.” Lancet Regional Health ‐ Europe 48: 101153. 10.1016/j.lanepe.2024.101135. [DOI] [PMC free article] [PubMed] [Google Scholar]
  39. Oud, M. , Mayo‐Wilson E., Braidwood R., et al. 2018. “Psychological Interventions for Adults With Bipolar Disorder: Systematic Review and meta‐Analysis.” British Journal of Psychiatry 208, no. 3: 213–222. 10.1192/bjp.bp.114.157123. [DOI] [PubMed] [Google Scholar]
  40. Perdighe, C. , and Mancini F.. 2012. “Dall'investimento alla rinuncia: Favorire l'accettazione in psicoterapia.” Cognitivismo Clinico 9, no. 2: 116–134. [Google Scholar]
  41. Pugh, M. 2020. Cognitive Behavioural Chairwork: Distinctive Features. Routledge. [Google Scholar]
  42. Rainone, A. , and Mancini F., eds. 2018. La mente depressa. Franco Angeli. [Google Scholar]
  43. Saettoni, M. , Gragnani A., Iazzetta S., and Lari L.. 2021. “Disturbi bipolari.” In Psicoterapia cognitiva. Comprendere e curare i disturbi mentali, edited by Perdighe C. and Gragnani A., 647–694. Raffaello Cortina Editore. [Google Scholar]
  44. Salcedo, S. , Gold A. K., Sheikh S., et al. 2016. “Empirically Supported Psychosocial Interventions for Bipolar Disorder: Current State of the Research.” Journal of Affective Disorders 201: 203–214. 10.1016/j.jad.2016.05.018. [DOI] [PubMed] [Google Scholar]
  45. Spitzer, W. O. , Dobson A. J., Hall J., et al. 1981. “Measuring the Quality of Life of cancer Patients: A Concise QL‐Index for Use by Physicians.” Journal of Chronic Diseases 34, no. 12: 585–597. 10.1016/0021-9681(81)90005-1. [DOI] [PubMed] [Google Scholar]
  46. Valdivieso‐Jiménez, G. . 2023. “Efficacy of Cognitive Behavioural Therapy for Bipolar Disorder: A Systematic Review.” Revista Colombiana de Psiquiatría. Advance online publication. 10.1016/j.rcp.2023.05.001. [DOI] [PubMed] [Google Scholar]
  47. Van Dijk, S. E. , Van der Meer L., and Van der Does W.. 2013. “A Randomized, Controlled, Pilot Study of Dialectical Behavior Therapy Skills in a Psychoeducational Group for Individuals With Bipolar Disorder.” Journal of Affective Disorders 145, no. 3: 386–393. 10.1016/j.jad.2012.05.054. [DOI] [PubMed] [Google Scholar]
  48. Young, R. C. , Biggs J. T., Ziegler V. E., and Meyer D. A.. 1978. “A Rating Scale for Mania: Reliability, Validity and Sensitivity.” British Journal of Psychiatry 133, no. 5: 429–435. 10.1192/bjp.133.5.429. [DOI] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Text S1: Cases presentation.

Text S2: The extended treatment protocol.

Figure S1: Time series of personality symptoms. Changes in total scores of PID (T0‐T12 measurements and 2 follow‐ups).

Figure S2: Time series of quality of life. Changes in total scores of QOL (T0‐T12 measurements and 2 follow‐ups).

Table S1: Within‐group comparison of depression and mania between baseline and T12.

Table S2: Pharmacological treatment of case 1: Matthew.

Table S3: Pharmacological treatment of case 2: Henry.

Table S4: Pharmacological treatment of case 3: Alicia.

Table S5: Pharmacological treatment of case 4: Alfred.

CPP-33-e70224-s001.docx (283.2KB, docx)

Data Availability Statement

The data that support the findings of this study are available in the supplementary material of this article.


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