3.9.8 Bipolar affective disorder
Bipolar Affective Disorder
Extreme mood swings and devastating depressions are symptoms of the mental disease that is bipolar affective disorder (BPAD). Manias can be extremely intense and endure for extended periods of time. Even more severe and lasting for weeks or even months are the lows, or depression. Although depressive episodes are frequent, at least one-lifetime manic episode must occur for bipolar disorder type 1 to be present. A minimum of one hypomanic episode and one severe depressive episode are required for bipolar 2 disorder to be diagnosed (Grande et al., 2016).
Symptoms:
Mania: When someone goes through this, their mood can become excessively high and linger for several days or even weeks. They might need very little sleep at this point and might be overly energised and confident. Mania is more frequently linked to dangerous actions including spending binges, snap judgements, and reckless sex.
Depression: Low mood, weariness, and loss of interest in activities are signs of depression. Additionally, emptiness, remorse, and feelings of worthlessness can be experienced by those who have bipolar disorder. Oversleeping, poor appetite and difficulties concentrating are more frequently linked to it. Suicidal ideas and actions may result from this.
DSM vs ICD
Here’s a comparison of DSM-5 and ICD-11 diagnostic criteria for Bipolar Disorder in table format:
| Criteria: | DSM-5: | ICD-11: |
|---|---|---|
| Presence of manic/hypomanic episodes | ✓ | ✓ |
| Presence of depressive episodes | ✓ | ✓ |
| Exclusion of Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified (for manic/hypomanic episodes) | ✓ | ✓ |
| Exclusion of Schizophrenia, Schizophreniform Disorder, Delusional Disorder, Psychotic Disorder Not Otherwise Specified, or Psychotic Disorder Due to a General Medical Condition (for depressive episodes) | ✓ | – |
| Causation of clinically significant distress or impairment in social, occupational, or other important areas of functioning | – | ✓ |
It’s important to note that both the DSM-5 and ICD-11 provide specific criteria for the diagnosis of Bipolar Disorder and that the specific criteria may vary based on the severity and type of the disorder.
Neurobiology of BPAD
Even with significant advances we still lack an understanding of the underlying neurobiology of bipolar disorder. Our current diagnostic schema for bipolar disorder is based upon descriptive terms as opposed to clear causal mechanisms.
MRI imaging has demonstrated that the lateral ventricles of patients suffering from an episode were significantly larger. The increased volume of the lateral ventricles directly correlated with the number of manic episodes the patient had suffered. Studies suggest that bipolar illness may be progressive and deleterious, thus contributing to brain tissue deterioration with recurrent relapses (Maletic, 2014).
Functional brain changes in BPAD:
- Increased responsiveness of limbic brain regions involving emotional regulation.
- The dorsolateral and dorsomedial prefrontal cortex and anterior cingulate cortex both show reduced responsiveness.
- The amygdala, ventrolateral prefrontal cortex and ventral anterior cingulate cortex all show increased responsiveness.
(Langan, 2009)
Hypothalamic-pituitary axis dysfunction:
ACTH and cortisol response dysregulation following CRH stimulation has been described in bipolar patients. Changes in CRH secretion appear clinically prior to manic or hypomanic symptoms.
In bipolar patients, pituitary hypoactivity has been found. The degree of neuroendocrine disruption is substantially associated with the intensity of the manic episode.
References:
(1) Grande, I., Berk, M., Birmaher, B., & Vieta, E. (2016). Bipolar disorder. The Lancet, 387(10027), 1561-1572.
(2) Langan C, McDonald C. Neurobiological trait abnormalities in bipolar disorder. Mol Psychiatry (2009) 14:833–46 10.1038/mp.2009.39
(3) Maletic, V. and Raison, C. (2014). Integrated Neurobiology of Bipolar Disorder. Frontiers in Psychiatry, [online] 5. doi:10.3389/fpsyt.2014.00098.