Bipolar Disorder Flashcards
1
Q
What are the main characteristics of bipolar disorder (BD)?
A
BD is a mood disorder involving abnormal shifts in mood, energy, activity, sleep, and cognition. It often begins around age 20 and includes depressive and manic/hypomanic episodes. Early onset is linked to worse prognosis, longer delays in treatment, and higher rates of comorbid anxiety and substance use disorders.
2
Q
What are the types of bipolar disorder in DSM-5?
A
- Bipolar I Disorder: Manic episodes, often with psychotic symptoms (75% of manic episodes).
- Bipolar II Disorder: Alternating depressive and hypomanic episodes, with no full mania.
- Cyclothymic Disorder: Recurrent depressive and hypomanic symptoms over two years, but not meeting criteria for a major affective episode.
3
Q
What is the global burden and prevalence of bipolar disorder?
A
BD is the 17th leading source of disability worldwide.
* Prevalence: 1.5–2.4%.
Bipolar I prevalence is equal across sexes; Bipolar II is more common in females.
4
Q
What comorbidities are common in BD?
A
- Psychiatric comorbidities: Anxiety disorders, ADHD, and substance use disorders.
- Medical comorbidities: Metabolic syndrome, obesity, type 2 diabetes, and migraine.
- Suicide risk: 6–7% of people with BD commit suicide, and overall mortality is twice that of the general population.
5
Q
How heritable is bipolar disorder, and what are the key genetic findings?
A
Heritability is 70–90%, with genes related to insulin regulation, serotonin, and endocannabinoid signaling implicated. However, genetic variants explain only ~25% of the heritability.
6
Q
What is the “kindling” hypothesis in BD?
A
The kindling hypothesis suggests that stress sensitization leads to recurring episodes of mania or depression. Initially, episodes are triggered by stressors, but over time, they may occur independently due to cumulative neurobiological changes.
7
Q
What neurobiological changes are observed in chronic bipolar disorder?
A
- Reduced cortical thickness in regions like the prefrontal cortex.
- Neuroprogression: Involves mitochondrial dysfunction, inflammation, and oxidative stress, contributing to cognitive and functional decline.
- Reduced response to mood-stabilizing medications over time.
8
Q
What should be ruled out during the diagnostic assessment for BD?
A
Medical and psychiatric conditions that mimic affective episodes (e.g., thyroid dysfunction, substance-induced mood changes) should be excluded.
9
Q
What are the first-line treatments for acute mania?
A
Antipsychotic agents combined with mood stabilizers (e.g., risperidone + lithium).
Risperidone is more effective than lithium, valproate, or aripiprazole.
Non-pharmacological treatment: Bifrontal electroconvulsive therapy (ECT) for refractory mania.
10
Q
What are key considerations in treating bipolar depression?
A
- Low initial doses of medication due to sensitivity to side effects.
- Combination therapies (antipsychotic + mood stabilizer) are common.
- Avoid antidepressants in Bipolar I due to the risk of manic switches.
- Non-pharmacological options: ECT for severe or treatment-resistant depression.
11
Q
What psychotherapeutic approaches are used for bipolar depression?
A
- Psychoeducation.
- Cognitive Behavioral Therapy (CBT).
- Family-Focused Therapy.
- Dialectical Behavioral Therapy.
- Mindfulness-Based CBT.
- Interpersonal and Social Rhythm Therapy.
12
Q
What is the role of maintenance treatment in BD?
Uit welke componenten bestaat maintenance treatment?
A
Due to the chronic and recurring nature of BD, maintenance treatment combines:
1. Pharmacological interventions (e.g., lithium, mood stabilizers).
2. Psychological interventions (e.g., CBT, psychoeducation).
3. Lifestyle changes (e.g., regular sleep patterns, avoiding substance use).
13
Q
Why is lithium a cornerstone of maintenance treatment for BD?
A
Lithium prevents both manic and depressive episodes. However, side effects include renal failure and tremors, requiring regular monitoring.
14
Q
Why is bipolar disorder often misdiagnosed as major depressive disorder (MDD)?
A
- Depressive episodes are usually the first symptom.
- These episodes last longer than manic/hypomanic episodes.
- 1/3 of patients remain undiagnosed until 10 years after onset.
15
Q
What are the risks of untreated or poorly managed BD?
A
- Increased neuroprogression (cognitive and functional decline).
- Higher rates of suicide and physical comorbidities.
- Reduced response to treatment over time.
16
Q
What is ADHD, and how does it present in children?
A
ADHD is a neurodevelopmental disorder with an onset before age 12, lasting at least 6 months. It features persistent inattention and/or hyperactivity and impulsivity that impair functioning in at least two settings (e.g., home and school). ADHD is the most common childhood disorder, with a prevalence of 75% in males. –> van de mensen die ADHD heeft is 75% man.
17
Q
What is bipolar disorder (BD), and how does it differ from ADHD?
A
BD is a mood disorder characterized by episodes of mania (elevated mood, grandiosity, decreased sleep need) and depression. Unlike ADHD, BD presents with prominent mood changes, aggressive behaviors, and alterations in sleep and circadian rhythms.
18
Q
What are the shared characteristics of ADHD and BD?
A
- Early onset in childhood or adolescence.
- Persistence into adulthood.
- Frequent underdiagnosis, overdiagnosis, or misdiagnosis.
19
Q
What are the heritability rates for ADHD and BD?
A
- ADHD: 60–80% heritability, reflecting polygenic risk.
- BD: 58–85% heritability, with a strong family history (90%) being the most significant risk factor.
20
Q
How do hyperactivity symptoms differ in ADHD and BD?
A
- ADHD: Hyperactivity is stable and situational, worsened by classroom demands.
- BD: Hyperactivity fluctuates with mood episodes, often accompanied by impulsivity, aggression, and grandiosity.
21
Q
How do sleep disturbances differ in ADHD and BD?
A
- ADHD: Normal circadian rhythms; no reduced sleep need.
- BD: Altered circadian rhythms with parasomnia, reduced total sleep, and bed-wetting. Hyperactivity disrupts sleep and contributes to “eveningness.”
22
Q
How do mood symptoms in ADHD differ from BD?
A
- ADHD: Mood symptoms are secondary to academic or social difficulties.
- BD: Mood symptoms involve rapid and random shifts, often dysphoric and irritable, with higher suicidality and psychosis risk.
23
Q
How do aggressive behaviors differ in ADHD and BD?
A
- ADHD: Verbal and physical aggression arises from irritability and impulsivity, with unintentional property damage.
- BD: Aggression involves property destruction, verbal outbursts, and violent behavior linked to failure to control anger.
24
Q
What distinguishes hypersexual behavior in ADHD and BD?
A
- BD: Early sexual interest or increased sexual behaviors are common.
- ADHD: Hypersexuality is not typically observed.
25
How do academic difficulties differ in ADHD and BD?
* ADHD: Poor concentration, inattention, and resistance to homework completion interfere with achievement.
* BD: Academic performance is variable, with cognitive giftedness and verbal advances sometimes observed.
26
What complicates the differential diagnosis of ADHD and BD?
1. Overlapping symptoms (e.g., hyperactivity, impulsivity).
2. High comorbidity with disorders like conduct disorder (CD) and oppositional defiant disorder (ODD).
3. Misdiagnosis due to complex presentations.
27
How does the course of ADHD and BD differ?
* ADHD: Symptoms like hyperactivity may improve over time, but inattention persists into adulthood (⅔ of cases).
* BD: Chronic, alternating mood episodes (mania and depression), often misdiagnosed as ADHD in early stages.
28
What are the first-line treatments (medication) for ADHD and BD?
* ADHD: Stimulants (e.g., methylphenidate) for inattention and hyperactivity.
* BD: Mood stabilizers and atypical antipsychotics, especially for early-onset BD.
29
Can stimulants be used for comorbid ADHD and BD?
No, stimulants are avoided in BD as they can worsen sleep and circadian disturbances, and potentially exacerbate mood episodes.
30
What treatments are recommended for ADHD-BD comorbidity?
Mood stabilizers or atypical antipsychotics to manage BD.
Adjunctive therapy for ADHD symptoms, with careful monitoring of side effects and mood stabilization.
31
What is the prevalence and impact of pediatric MDD?
Pediatric MDD affects ~25% of youth.
Associated with high morbidity, distress, and suicide risk (2nd leading cause of death in youth).
Early differentiation of unipolar and bipolar MDD is critical to prevent treatment complications, such as manic switches with antidepressants.
32
Why is distinguishing unipolar MDD from bipolar MDD important in pediatric populations?
Antidepressants can induce manic symptoms or increase the risk of suicidal behaviors in children with bipolar MDD.
Accurate diagnosis ensures effective and safe treatment.
33
What were the inclusion criteria for the literature review conducted by Uchida et al.?
* Original studies assessing both MDD and BD.
* Comparison between unipolar and bipolar MDD.
* Participants under 18 years old.
* Cross-sectional study design.
34
What are the four clinical factors over-represented in bipolar MDD compared to unipolar MDD?
1. High rates of psychiatric comorbidities.
2. High rates of family history of psychiatric illness.
3. Greater severity of depression.
4. Higher levels of impairment.
35
What psychiatric comorbidities are more common in children with bipolar MDD?
* Behavioral disorders (e.g., ODD, CD).
* Anxiety disorders.
* Adolescents with bipolar MDD are more likely to have a comorbid substance use disorder.
36
How does family history differ between bipolar and unipolar MDD?
Children with bipolar MDD are more likely to have first-degree relatives with:
* Bipolar disorder (BD).
* MDD.
* Behavioral disorders (ODD, anxiety).
Bipolar MDD is also linked to a family history of mania/hypomania.
37
What distinguishes the severity of depression in bipolar MDD?
More depressive episodes and severe symptoms, including:
* Hopelessness, sadness, irritability.
* Sleep problems, loss of interest, suicidal/self-harm behaviors.
More frequent hospitalizations.
38
What types of impairments are more severe in bipolar MDD compared to unipolar MDD?
* Peer and family difficulties.
* Behavioral problems in school.
* Severe disturbances in major life roles.
39
How do behavioral difficulties manifest in children with bipolar MDD?
* Aggression is more severe in bipolar MDD than unipolar MDD.
* Bipolar MDD is also associated with severe behavioral disturbances.
40
How do irritability and age of onset differ between bipolar and unipolar MDD?
Bipolar MDD: Extreme irritability and earlier onset (~1.5 years earlier than unipolar MDD).
Unipolar MDD: Persistent irritability.
41
What conclusions did Uchida et al. draw about distinguishing bipolar from unipolar MDD?
* Bipolar MDD has greater severity and impairment.
* Differences exist in psychiatric comorbidities and family history.
* Results are preliminary and based on only four cross-sectional studies. Further research is needed.
42
What is the prevalence of bipolar disorder (BD) across different age groups?
Adults: 2.1%
Adolescents: 2.3%
Youth (7-21 years): 1.8%
Symptoms often start between 15-19 years.
43
What are the diagnostic criteria for Bipolar I Disorder in children?
Manic episode lasting at least 1 week, with elevated or irritable mood or increased energy most of the day.
At least 3 symptoms: grandiosity, decreased need for sleep, talkativeness, racing thoughts, distractibility, increased goal-directed activity, risky behavior.
Manic symptoms cause marked impairment, such as hospitalization or inability to function.
44
How is Bipolar II Disorder diagnosed in children?
At least 1 hypomanic episode and 1 major depressive episode.
Hypomanic episode lasts at least 4 days; depressive episode lasts at least 2 weeks.
No history of manic episodes.
45
What is Cyclothymic Disorder?
A chronic, fluctuating mood disturbance lasting at least 2 years.
Symptoms of hypomania and depression do not meet full criteria for a hypomanic, manic, or major depressive episode.
46
What are red flag symptoms for pediatric bipolar disorder?
1. Aggression several times a day with little provocation.
2. Decreased need for sleep (episodic).
3. Spontaneous mood shifts out of context.
4. High-risk behaviors inappropriate for the situation.
5. Family history of mood disorders, especially BD.
47
What is the difference between bipolar disorder (BD) and ADHD?
BD: Manic symptoms (e.g., grandiosity, decreased need for sleep, mood changes) are more prevalent and episodic.
ADHD: Symptoms are persistent and stable, with no episodic nature.
48
How does oppositional defiant disorder (ODD) differ from bipolar disorder (BD)?
ODD: Chronic angry/irritable mood and defiant behavior for at least 6 months.
Unlike BD, ODD does not include manic symptoms.
49
What comorbid disorders are common in pediatric bipolar disorder (BD)?
ADHD: 60%-90% of cases.
ODD: 47%-88% of cases.
Anxiety disorders are more common in BD than non-BD pediatric patients.
Adolescents with BD have a 5x higher risk of substance use disorder.
50
What is the difference between BD and anxiety disorders?
BD: Manic symptoms (e.g., grandiosity, risky behaviors) are key distinguishing factors.
Anxiety: Mood swings and irritability may occur but lack manic behavior.
51
What is rapid cycling in bipolar disorder?
Defined as 4 or more mood episodes (manic, hypomanic, or depressive) within 1 year.
Indicates greater mood dysregulation.
52
How should clinicians approach the diagnosis of pediatric bipolar disorder?
Assess for episodes of mania, hypomania, and depression.
Rule out comorbid disorders like ADHD, ODD, and anxiety.
Interview both parents and children to identify episodic symptom changes.
53
Why is distinguishing bipolar disorder from other conditions critical?
Misdiagnosis can lead to inappropriate treatments, such as stimulants for ADHD that may worsen BD symptoms.
Proper diagnosis guides effective treatment strategies for mood stabilization.
54
What is the Zeitgeber hypothesis in relation to IPSRT?
Unstable or disturbed daily routines lead to instability in the circadian rhythm. For sensitive individuals, this can result in affective episodes.
55
What are the main focuses of interpersonal and social rhythm therapy (IPSRT)?
1. Links between mood symptoms and social relationships and roles.
2. Maintaining regular daily routines.
3. Identifying and managing causes of rhythm disturbances.
56
How does IPSRT compare to intensive clinical management (ICM) in session structure?
IPSRT: Sessions last 45-55 minutes, focus on social rhythm regularity and interpersonal relationships.
ICM: Sessions last 20-25 minutes, focus on somatic symptoms, medication education, sleep hygiene, and general support.
57
What were the four treatment strategies used in the study?
1. Acute and maintenance IPSRT (IPSRT/IPSRT).
2. Acute and maintenance ICM (ICM/ICM).
3. Acute IPSRT followed by maintenance ICM (IPSRT/ICM).
4. Acute ICM followed by maintenance IPSRT (ICM/IPSRT).
58
What were the key findings regarding IPSRT’s effectiveness?
1. Participants who received IPSRT during the acute phase had fewer mood episodes.
2. IPSRT increased regularity of social rhythms by the end of acute treatment.
3. No difference between treatment types in time to remission.
4. Overall return rate after 2 years was 43.2%, with the highest return rate in the ICM/IPSRT group (63%).
59
What variables affected long-term outcomes in the study?
1. Physical health: Participants in good physical health had better outcomes with acute IPSRT.
2. Medical conditions or anxiety disorders: Benefited more from acute ICM, likely due to its focus on somatic symptoms.
3. Marital status: Married participants had better outcomes, likely due to stable support from their partner.
60
How does IPSRT reflect the Zeitgeber hypothesis?
IPSRT helps stabilize social rhythms, reducing the risk of affective episodes. Participants were most motivated to establish stable routines immediately after an acute episode.
61
What limitations were identified in this study?
Variables strongly associated with outcomes were not equally distributed across the maintenance study conditions. This makes initial interpretations more challenging.
62
Why might IPSRT sessions be more effective than ICM sessions?
IPSRT sessions are longer (45-55 minutes), providing more focus on regularity and interpersonal stability. ICM sessions are shorter (20-25 minutes) and focus more on somatic symptoms and general support.
63
What challenges do anxious patients face in IPSRT?
Anxious patients may struggle to focus on social stability and interpersonal relationships, as IPSRT avoids somatic complaints. Such patients may benefit more from ICM, which addresses somatic symptoms.
64
How does marital status influence outcomes in IPSRT and ICM?
Married participants had significantly better outcomes, likely due to stable support from their partner.
65
What is the primary aim of cognitive therapy (CT) in bipolar disorder treatment?
To help patients regulate, examine, and change dysfunctional thinking and behaviors associated with mood states.
To teach strategies for recognizing and coping with prodromes to prevent full-blown episodes.
To emphasize daily routine maintenance and prevent episodes caused by disruptions in social rhythms.
66
What were the four new elements added to traditional cognitive therapy in this study?
1. Emphasis on the diathesis-stress model (combined medication and psychological therapies).
2. Monitoring mood and prodromes to adjust behavior and prevent episodes.
3. Highlighting the importance of sleep and routine to avoid insomnia-triggered episodes.
4. Identifying and compensating for time lost due to previous episodes.
67
What were the four primary hypotheses of the study? - Lam et al.
1. CT will reduce the frequency and duration of bipolar episodes.
2. CT will improve social functioning.
3. CT will enhance coping strategies for bipolar prodromes.
4. CT will lower dysfunctional attitudes related to high goal attainment.
68
What were the four secondary hypotheses of the study?
1. CT will reduce bipolar depressive episodes.
2. CT will reduce manic or hypomanic episodes.
3. CT will lower mood scores (depression/mania) and reduce mood fluctuations.
4. CT will improve medication compliance.
69
What were the main results of the study regarding relapse rates?
Relapse rate in the first 6 months: 28.3% (CT group) vs. 50% (control group).
Relapse rate in the second 6 months: 43.8% (CT group) vs. 75% (control group).
CT group experienced fewer depressive, manic, and mixed episodes.
70
How did cognitive therapy impact hospitalization rates and time in bipolar episodes?
Fewer hospitalizations in the CT group (15% vs. 33%).
CT group had fewer hospital days for bipolar episodes and depression.
CT group spent 27 days in bipolar episodes compared to 88 days in the control group.
71
What did depression scores (BDI) reveal about the effectiveness of CT?
BDI scores in the CT group decreased over time, while scores in the control group increased.
CT reduced feelings of hopelessness and improved coping with depressive and manic prodromes.
72
What improvements in coping strategies were observed in the CT group?
Better coping with depressive symptoms after 6 months.
Improved coping with mania prodromes at 12 months.
73
What was the impact of CT on medication compliance?
CT group showed significantly better medication compliance: 88.4% vs. 66.7% (control group) after 6 months.
74
What were the limitations of the study?
1. No measurement of sleep hygiene or daily routine.
2. No control for the effect of attention from prescribed medication.
75
What is the main conclusion about the effectiveness of combining CT and mood stabilizers?
CT combined with mood stabilizers effectively prevents relapses, reduces hospital admissions, and improves social functioning.
It also regulates manic mood swings and reduces symptoms of both bipolar depression and mania.
76
What are the two main challenges in conducting randomized controlled trials (RCTs) for bipolar disorder?
1. Unstable symptomatic presentations make research on bipolar disorder difficult.
2. Patients often deny illness or reject treatment, affecting study participation and outcomes.
77
Why is the generalizability of findings from maintenance RCTs in bipolar disorder limited?
• RCT durations are less than 2 years, while bipolar disorder is lifelong.
• Some patients are treatment-resistant.
• Trials are designed around acute episode treatments, not long-term maintenance.
• Many studies compare active treatments due to industry sponsorship.
• Real-world efficacy is often much lower.
• Few RCTs have large sample sizes.
78
What were the two main aims of this systematic review?
1. To compare the effectiveness of lithium monotherapy with other mood stabilizers (e.g., anticonvulsants, antipsychotics) in maintenance therapy for bipolar disorder.
2. To evaluate the efficacy of lithium combined with other mood stabilizers compared to lithium monotherapy.
79
What were the outcome variables considered in this review?
• Hospitalizations and re-hospitalizations.
• Treatment failures.
• Re-admissions.
• Composite measures of treatment effectiveness.
80
What did the studies show about the effectiveness of lithium monotherapy compared to other mood stabilizers?
• 8 out of 9 studies showed that lithium monotherapy had better outcomes (e.g., fewer hospitalizations, treatment failures) compared to other mood stabilizers.
• Lithium was found to be more effective than valproate, lamotrigine, olanzapine, and quetiapine in most studies.
81
What were the findings on combination therapy (lithium + other mood stabilizers) compared to lithium monotherapy?
• Swedish study: Lithium + olanzapine reduced hospitalizations.
• Italian study: Lithium + quetiapine reduced relapse rates.
• Israeli study: Lithium + atypical antipsychotics reduced hospitalizations.
• US study: No difference between lithium/valproate monotherapy and combinations with antipsychotics.
82
What is the overall conclusion about lithium treatment for bipolar disorder?
• Lithium monotherapy is generally more effective than other mood stabilizer monotherapies.
• Some combination therapies (e.g., lithium + olanzapine or quetiapine) were effective, but most combinations showed no added benefit over lithium monotherapy.
• Lithium reduces the risk of suicide and may prevent dementia onset.
83
What were the limitations of this systematic review?
• The study could not fully rule out residual confounding, which may have influenced the results.
84
What are some benefits of lithium treatment in bipolar disorder beyond mood stabilization?
• Reduces the risk of suicide.
• May help prevent the onset of dementia.
85
What were the two main goals of the Firth et al. (2020) meta-analysis?
1. To investigate causal relationships between modifiable lifestyle behaviors and the prevention of mental disorders.
2. To assess the effectiveness of lifestyle interventions in the treatment of mental disorders.
86
What lifestyle behaviors were analyzed in this meta-analysis?
• Physical activity/exercise
• Smoking
• Sleep
• Dietary patterns
87
How is physical activity linked to the prevention of mental disorders?
Physical activity lowers the risk of:
• Depression and depressive symptoms
• Anxiety disorders (e.g., PTSD, agoraphobia)
• Psychosis and bipolar disorder
• No strong evidence for schizophrenia prevention.
88
What are the risks associated with smoking and mental health?
Increases the risk of:
• Depression and depressive symptoms
• Psychotic disorders and schizophrenia
• Bipolar disorder
• ADHD (though ADHD also influences smoking initiation)
• Prenatal smoking is associated with a 3x higher risk of postpartum depression.
89
What dietary patterns are associated with a reduced risk of depression?
* Mediterranean diet
* Low dietary inflammatory index
* Vitamins
* No evidence that poor diet causes a higher risk of depression. --> drinken van veel suikerhoudende dranken verhoogt risico op depressie!
90
How do sleep disturbances influence mental health?
Sleep disturbances (e.g., insomnia) increase the risk of:
• Depression and depressive symptoms
• ADHD (with short sleep duration)
• Suicidal behaviors
• Both short sleep (<6 hours) and long sleep (>8 hours) increase the risk of depression.
91
Which lifestyle interventions are effective in treating mental disorders?
1. Physical activity
• Reduces depressive symptoms.
• At least 90 minutes of moderate exercise per week helps overall symptoms, especially in MDD.
• Not effective for non-affective psychotic disorders.
2. Sleep interventions (CBT)
• Reduces depressive symptoms and severity of hallucinations and paranoia in psychotic disorders.
92
Were dietary interventions effective in treating mental disorders?
• No significant benefits for MDD or bipolar disorder were found in dietary interventions.
93
What potential biological mechanisms link lifestyle factors to mental health?
1. Inflammation: Poor lifestyle behaviors increase inflammation, a risk factor for mental illness.
2. Gut microbiome: Influenced by diet and exercise, though more research is needed.
3. Metabolic diseases: Conditions like diabetes, obesity, and heart disease are linked to mental illness.
94
What percentage of patients with bipolar disorder (BD) are initially misdiagnosed with unipolar depression (UD)?
69% of patients with bipolar disorder are initially misdiagnosed with unipolar depression. On average, these patients consult 4 physicians before receiving the correct diagnosis.
95
What are the functional characteristics of bipolar depression (BD)?
1. Dysfunction in fronto-limbic neural circuits of emotion regulation.
2. Hypersensitivity in fronto-striatal neural circuits of reward processing.
3. Abnormally reduced ventrolateral prefrontal cortex (VLPFC) activity during emotion processing.
4. Increased amygdala, striatum, and medial prefrontal cortex (MPFC) activity.
5. Reduced functional connectivity (FC) between the orbitofrontal cortex (OFC) and amygdala during positive emotional stimuli.
96
What are the structural characteristics of bipolar depression (BD)?
1. Reduced gray matter volume and thickness in:
• Prefrontal cortex (PFC) (especially VLPFC and OFC).
• Insula and temporal regions.
2. Reduced amygdala and hippocampal volume.
3. Decreased white matter tract integrity in frontal regions.
97
How do emotion-processing neural circuits differ between BD and UD?
Bipolar depression (BD):
• Lower amygdala activation during negative stimuli.
• Higher amygdala activation during positive stimuli.
Unipolar depression (UD):
• Lower ACC activation toward negative emotional stimuli.
98
How does the reward hypersensitivity model explain BD?
Suggests hypersensitivity in fronto-striatal neural circuit responses to reward-related events. Underlying mechanism for manic or hypomanic episodes. Increased VLPFC activity during reward anticipation.
99
What are the structural MRI findings in bipolar depression (BD)?
1. Reduced gray matter volume in:
• Hippocampus.
• Amygdala.
2. Reduced cortical thickness in:
• Right DLPFC.
• Left inferior parietal gyrus.
• Right precuneus.
3. Reduced white matter integrity in:
• Anterior corpus callosum.
• Posterior cingulum.
100
What differences in functional connectivity (FC) were found in bipolar depression (BD)?
1. Increased fronto-parietal network (FP) connectivity, linked to limited top-down cognitive control.
2. Higher connectivity for win anticipation and thinner connectivity for loss anticipation.
3. Stronger FC networks of the default mode (DM) or fronto-parietal (FP) regions, including the PFC, ACC, and thalamus.
101
What are the key differences in gray matter volume between BD and UD?
1. Bipolar depression (BD): Reduced gray matter in the hippocampus and amygdala.
2. Unipolar depression (UD): Reduced gray matter in the anterior cingulate cortex (ACC).
102
How do cognitive task studies distinguish BD from UD?
BD:
• Increased fronto-striatal activity and failure of deactivation in the default mode network (DMN).
• Increased activity in VLPFC, PCC, anterior insula, middle temporal gyrus, and parahippocampus during positive memory recall.
• Decreased activity in precuneus, amygdala, and DLPFC.
UD:
• Reduced activity in ventral and dorsal ACC.
103
What do white matter studies show about BD?
BD has reduced white matter integrity in:
• Anterior corpus callosum.
• Posterior cingulum.
• Left superior longitudinal fasciculus (SLF) in the inferior temporal cortex.
White matter tracts are crucial for communication within cognition- and emotion-processing neural circuits.
