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The prevalence of bipolar disorder is inconsistent across different countries.
False
Patients from black and ethnic minority groups in the UK are less likely to present with a first episode of mania than the white population.
False
Social exclusion may influence the differences in bipolar disorder presentations among various ethnic groups.
True
The DSM-5 and ICD-10 classify hypomania and mania based on the presence of psychotic features.
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Patients from minority groups have easier access to mental health services compared to the white population.
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The lifetime risk for bipolar disorder is approximately 2-3%.
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The 6-month prevalence of bipolar disorder is significantly lower than the lifetime prevalence.
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Bipolar disorder affects men more than women.
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The mean age of onset for bipolar disorder is around 30 years in community studies.
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Bipolar disorder is often comorbid with anxiety disorders and cardiovascular disease.
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Distinguishing bipolar disorder from recurrent unipolar depression is easy and straightforward.
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Bipolar II disorder can be diagnosed solely based on the presence of hypomania without requiring a major depressive episode.
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In DSM-5, a manic episode is equivalent to a hypomanic episode in ICD-10.
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The presence of mild hypomanic episodes may influence treatment response in patients with recurrent major depression.
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The distinction between unipolar and bipolar depression is always clear and straightforward for clinicians.
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The term 'bipolar spectrum' refers specifically to bipolar I and II disorders only.
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According to DSM-5, a current mixed episode is categorized as a depressive episode.
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In the DSM-5 classification, mania with psychosis is classified as severe.
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Cyclothymia is included under bipolar I and II disorders in DSM-5.
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Manic disorders cannot be easily distinguished from schizophrenia due to overlapping symptoms.
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Patients with bipolar II disorder typically regard spells of hypomania as an illness.
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Extreme social disinhibition in older patients is a strong indicator of bipolar disorder.
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The symptoms of mania typically change quickly in content but can outlast the phase of over-activity.
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Schizoaffective disorder is used when there is a mixture of features from both manic disorders and schizophrenia.
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A family history of borderline personality disorder can help distinguish it from rapid cycling bipolar disorder.
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In younger adults, head injury or HIV may not lead to the manifestation of mania.
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Drug-induced states of excitement can last for a prolonged period even after treatment starts.
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Mood disturbances in borderline personality disorder are often linked to interpersonal issues.
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Diagnosis of recurrent unipolar depression is straightforward compared to bipolar disorder.
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The concordance rate for mood disorders in monozygotic twins of a proband with bipolar disorder is about 40%.
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Family studies indicate that first-degree relatives of bipolar probands have an increased risk of schizoaffective disorder.
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Bipolar disorder has a heritability estimate of approximately 85%.
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Molecular linkage studies have consistently identified specific genes associated with mood disorders.
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The familial segregation of bipolar disorder follows a simple Mendelian inheritance pattern.
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Genome-wide association studies (GWAS) have identified several risk loci for bipolar disorder.
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The genetic risk for bipolar disorder is primarily due to a few high-effect individual genes.
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There is currently a reliable diagnostic biomarker identified for bipolar disorder.
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Epistasis refers to the genetic interactions that contribute to the risk of bipolar disorder.
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Advancements in imaging have clearly distinguished bipolar disorder from recurrent unipolar depression.
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Childhood sexual abuse is specifically linked to the development of bipolar disorder.
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Life events have no impact on the episodes of depression and mania in bipolar patients.
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A high level of expressed emotion in a family can worsen the symptoms of bipolar disorder.
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Dopamine overactivity has been definitively proven as a cause of mania in bipolar patients.
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Anticonvulsants used in bipolar disorder management alter brain glutamate levels.
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The hypothalamic-pituitary-adrenal (HPA) axis is unaffected in patients with bipolar disorder.
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Increased levels of glutamate in bipolar patients have been a reliable diagnostic marker.
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Goal attainment can trigger manic episodes in bipolar patients.
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Cortisol levels are typically lower in individuals with bipolar disorder compared to healthy controls.
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The 'kindling' effect suggests that negative life events have a diminishing influence over time.
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In patients with bipolar disorder not taking lithium, hippocampal volumes are higher than in recurrent depression.
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Cerebral volume reduction over the course of bipolar illness may indicate a degenerative process in some patients.
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Functional imaging studies show a narrower range of neural dysregulation in bipolar disorder compared to unipolar depression.
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Bipolar depressed patients show reduced neural responses in the amygdala when exposed to negative emotional cues.
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Cognitive deficits in bipolar disorder can be observed even in first-episode patients.
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The genetic predisposition to bipolar disorder may involve hundreds to thousands of relevant genes.
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There is substantial evidence that cognitive deficits in bipolar disorder increase throughout the course of the illness.
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Similarities in neuropathological changes exist between patients with bipolar disorder and patients with schizophrenia.
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Euthymic bipolar patients display decreased activity in cortical regions when presented with positive emotional stimuli.
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Adverse early experiences, including abuse, have no impact on the predisposition to bipolar disorder.
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Study Notes
Epidemiology of Bipolar Disorder
- Lifetime risk for bipolar disorder: 0.3-1.5%
- 6-month prevalence similar to lifetime prevalence, indicating chronic nature of disorder
- Equal prevalence in men and women
- Mean age of onset: 18 years in community studies
- Highly comorbid with other disorders, including anxiety, substance misuse, and general medical conditions
Transcultural Factors
- Rates of bipolar disorder consistent across countries
- Increased prevalence in certain minority groups within countries, such as black and ethnic minority groups in the UK
- Patients from these minority groups more likely to present with first episode of mania and prominent psychotic features
Classification
- DSM-5 and ICD-10 distinguish hypomania from mania based on duration of symptoms, absence of psychotic features, and lesser degree of social and occupational impairment
Differential Diagnosis of Bipolar Disorder
Mania
- Distinguished from:
- Schizophrenia
- Organic brain disease (e.g. brain tumor, HIV infection)
- Amphetamine-induced excitement
Schizophrenia
- Distinguished from mania by:
- Auditory hallucinations and delusions
- More equal mixture of features of both syndromes (schizoaffective disorder)
Organic Brain Disorder and Drug Misuse
- Consider organic brain lesion, especially in middle-aged or older patients with expansive behavior and no past history of affective disorder
- Drug misuse can cause manic-like symptoms, distinguishable by history and urine drug screening
Bipolar Disorder and Recurrent Depression
- Distinguished by:
- Symptoms of mania or hypomania in past history
- Brief periods of hypomania may be difficult to identify or remember
Classification of Bipolar Disorder
- ICD-10 and DSM-5 classification systems:
- Manic episode
- Hypomanic episode
- Bipolar affective disorder (ICD-10) / Bipolar I and II disorders (DSM-5)
Aetiology
Overview
- Aetiological overlap between recurrent unipolar depression and bipolar disorder
- High heritability of bipolar disorder
- Molecular genetic techniques used to identify genetic loci relevant to pathophysiology
Genetic Causes
- Family and twin studies:
- Increased risk of both bipolar and unipolar mood disorders in first-degree relatives of bipolar probands
- High heritability (around 85%)
- Mode of inheritance:
- Polygenic inheritance with multiple genes of modest effect
- Rare structural chromosomal abnormalities and gene-gene interactions may contribute to genetic risk
- Molecular genetics:
- Genome-wide association studies (GWAS) have identified risk loci with some robustness to replication
- Identified genes cluster around biologically meaningful processes (e.g. voltage-gated calcium channels)
Brain Imaging
Structural Brain Imaging
- Changes in brain volume measured by MRI inconclusive due to confounding factors
- Hippocampal volumes lower in bipolar patients not taking lithium, reversed in patients taking lithium
- Reduction in cerebral volume over course of illness, suggesting possible degenerative process
Functional Imaging
- Bipolar depressed patients show elevated neural responses in amygdala and abnormal activity in prefrontal cortical regions
- Euthymic bipolar patients show elevated amygdala responses and decreased activity in cortical regions to positive emotional stimuli
- Abnormalities in neural responses to negative and positive emotional stimuli, including reward processing
Neuropsychological Changes
- Cognitive deficits present in bipolar disorder during both acute illness and periods of euthymia
- Modest but widespread deficits in executive function, verbal memory, attention, and processing speed
Conclusions
- Major genetic contribution to predisposition to develop bipolar disorder
- Environmental factors, including adverse early experiences, may also contribute to pathophysiology
- Brain imaging studies show functional abnormalities consistent with disordered emotional regulation and reward processes
- Modest but widespread neuropsychological deficits present in bipolar disorder
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Description
Test your knowledge on the epidemiology of bipolar disorder, including its lifetime risk, prevalence, and comorbidities. This quiz covers transcultural factors and more.
