Week 10: Mental Illness

This week was about mental health and the brain. This is a rather interesting topic, as it explains some common experiences of people with physical phenomena in the brain. I have usually thought that mental disorders would be mostly caused by repeated disturbed thinking and less by purely physical properties of the brain. However, the book switched this view a lot, with a contrary view that mental disorders should be called brain disorders due to their strong physical nature.

The chapter discussed anxiety disorders, affective (mood) disorders and schizophrenia. Anxiety is often characterized with increased activity in the hypothalamic-pituitary-adrenal gland axis (HPA-axis), which is regulated by the amylgada and the hippocampus. Amylgada increases the stress response by releasing corticotropin-releasing hormone (CRH) and hippocampus decreases it via the response of CRH. It was surprising that the amount of CRH receptors in hippocampus could be increased with SSRI treatment (serotonin selective reuptake inhibitor), as the link between them is unclear. Anxiety could somehow be seen from hippocampus, as high amounts of blood cortisol causes there death of neurons. This somehow confirms that anxiety is not cowardly fear but suffering from an excessive stress response of the body.

Mood disorders are also affected with these similar mechanisms in the brain, and it was said that it is rather a rule than exception that anxiety disorders correlate with mood disorders. However, the excessive activity of the anterior cingulate cortex does correlate with depression, and it is intuitive that repeating unpleasant thoughts and the feeling of emptiness would somehow originate from the cortex. The treatments for depression were also a bit surprising, as many of those were a bit unconventional (like electroconvulsive therapy and lithium medication).

I also wonder how does anxiety and depression relate to memory, as long-term memory is assumed to be functioned via hippocampus. Hippocampus has also 2% annual neurogenesis rate, some studies say that mood disorders could decrease the hippocampal neurogenesis. Wikipedia page on adult neurogenesis actually points out that it is assumed that the mood improving effect of SSRIs is related to the increased neurogenesis in the hippocampus.

I heard from a lecture on another course that one cause for schizophrenia is a different distribution of neural connectivity: there is less short connections and more long connections between neurons in schizophrenic patients. This seems like there would be “jumps in logic” in schizophrenic brain, but I can’t say if that is actually the case. In general, it is inspiring that there are many hypotheses but still no clear understanding how different brain disorders work. Those would be interesting and rewarding research topics.