Participants with bipolar disorder showed thinner cortical gray matter in the frontal, temporal and parietal regions of both cerebral hemispheres. Bipolar disorder had the greatest effect on the left pars opercularis, the left fusiform gyrus, and the left rostral median frontal cortex. Bipolar brain function is also associated with the hippocampus. The hippocampus plays a role in learning, consolidating and recovering memory.
It also participates in the functions of verbal memory, stress responses, emotions, goal-directed activity and sensorimotor integration. A recent study found that patients with bipolar disorder showed reductions in the hippocampus compared to people without mood disorders. 3 When this happens, memory is severely affected. The right side of the hippocampus helps to associate places with specific memories, while the left side regulates verbal and visual memory.
This region of the brain helps you regulate your emotional responses. Bipolar disorder is widely believed to result from chemical imbalances in the brain. There are three characteristic mood episodes associated with bipolar disorder (depression, mania, and hypomania), as well as stable periods called euthymia. Bipolar disorder is characterized by a combination of state-related changes in psychological function that are restricted to episodes of illness, along with trait-related changes that persist during periods of remission, regardless of symptom status.
Bipolar I disorder is characterized by changes in mood that can go from a high-energy manic state to a low-energy depressive state. Stressful life events, or alcohol or drug abuse, can make bipolar disorder more difficult to treat. The limited number of imaging studies in bipolar depression has also highlighted changes in prefrontal and subcortical activity. A resting state positron emission tomography (PET) study in a remarkably large group (n %3D4) of patients with bipolar depression reported decreases in prefrontal cortical metabolism, and increased subcortical metabolism, compared to healthy controls.
First, it has become apparent that, in bipolar disorder, there is a combination of status-related changes during episodes of illness and longer-lasting trait-related changes that persist, during periods of symptom remission. In addition, functional imaging studies, which allow researchers to see how the brain works during episodes, suggest that bipolar disorder can cause functional abnormalities. Identifying disease markers for bipolar disorder will facilitate early detection of bipolar episodes, which can save patients and their families considerable distress. These studies have employed a variety of designs, either comparing bipolar patients with and without lithium medication90, comparing euthymic patients treated with lithium91, or studying the effects of lithium versus placebo in healthy volunteers.
Ongoing research in high-risk populations, such as unaffected first-degree relatives of those tested bipolar, can identify neurocognitive markers associated with bipolar vulnerability, but studies so far have not been conclusive and are limited by small sample sizes. In people with bipolar disorder, some parts of the hippocampus may be smaller than in people without a mood disorder, although research results have not always been consistent. Compared to healthy controls, the bipolar depression group showed improved subcortical activation in the amygdala, thalamus, and basal ganglia. Cao hopes that the study, which was funded in part by the National Institute of Mental Health (NIMH), will pioneer future research into details within the hippocampus as a marker for accurate diagnosis and positive response to treatment of bipolar disorder.
It is difficult to determine if these changes are restricted to manic status (perhaps indicative of an “orbitofrontal injury syndrome”), or if they occur in both mania and bipolar depression, given the small number of studies examining these processes in bipolar depression. Finally, the current literature on bipolar disorder has failed to consistently control a number of clinical factors that supposedly may affect, in neurocognition, including medication status, 9 comorbidities, including substance use disorders10 and specific dimensions of symptoms, such as suicide11 or insomnia. . .
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