The mental illnesses covered in chapter 22 are broken into three categories: anxiety disorders, affective disorders, and schizophrenia. Within these sections hypotheses for biological underpinnings are discussed, along with treatment options. This post will summarize key points related to each major type of disorder before going into more depth on questions that arose during reading.
Anxiety disorders involve the sympathetic division of the autonomic nervous system (ANS), activating the norepinephrine system and the flight or fight response during inappropriate circumstances. Post traumatic stress disorder (PTSD) and obsessive-compulsive disorder (OCD) are two mental illnesses that involve heightened anxiety. Appropriate mediation by the hypothalamic-pituitary-adrenal (HPA) axis is impacted by anxiety disorders, and activity in the hippocampus diminishes while activity in the amygdala increases. Elevated activity in the prefrontal cortex is also observed in anxiety disorders.
Psychotherapy is used to treat anxiety disorders, with the premise that fear responses can be both learned and unlearned. Anxiolytic medications including benzodiazepines, which bind to GABA sites to produce inhibition, and serotonin-selective reuptake inhibitors (SSRIs) are drug options.
Affective disorders include major depression and bipolar disorder (types I & II). The biological basis involves a complex mix of feedback interactions in the diffuse modulatory systems, such as the hypothalamic-pituitary-adrenal-axis. The monoamine hypothesis of affective disorders is tied to levels of the monoamines norepinephrine and/or serotonin, and drugs are used to promote long term changes in these systems. The diathesis-stress hypothesis emphasizes environmental and genetic influences.
Treatments for affective disorders range from psychotherapy and antidepressants to electroconvulsive therapy (ECT), lithium, and in the most extreme cases deep brain stimulation.
Schizophrenia comes from the Greek for “divided mind” and may be more than a single disease. Positive symptoms include hallucinations, delusions, and disorganized speech/behavior while negative symptoms may include memory impairment, muted emotional expression, and difficulty with goal directed behavior.
Biological bases can include genes and environment as well as microscopic structural disruptions. Brains of people diagnosed with schizophrenia have larger ventricle-to-brain size on average than those without the disorder. Defects in myelin sheaths, abnormal neuronal lamination, and reduced cortical thickness are also correlated issues. There are two hypotheses for the neurotransmitter basis of the disease: the dopamine hypothesis and the glutamate hypothesis and it has been observed that drugs affecting both of these systems can help to quell psychotic episodes.
Because some aspects of mental diseases have genetic components, this made me wonder if even disorders caused by environmental factors such as PTSD could be heritable. According to the theory of intergenerational trauma, this hunch has some bearing. According to a 2014 study of glucocorticoid receptor genes in holocaust surviving offspring, parental PTSD is associated with changes in HPA axis function (Yehuda et al. 2014).
The levels of specificity reached in the above study also brings to mind the type of individualized medicine that was briefly mentioned in chapter 22. One of the problems that came up repeatedly in this chapter was that underlying causes or drug reactions were not entirely known, and that no single type of treatment would work universally. This is partially because all mental disturbances do not have a known genetic basis and many different genes could be involved to cause similar issues. Induced pluripotent stem cells (iPSCs) is one newer individualized approach, where a patients own skin cells are chemically treated to create stem cells.
Yehuda, R., Daskalakis, N. P., Lehrner, A., Desarnaud, F., Bader, H. N., Makotkine, I., Flory, J. D., Bierer, L. M., & Meaney, M. J. (2014). Influences of Maternal and Paternal PTSD on Epigenetic Regulation of the Glucocorticoid Receptor Gene in Holocaust Survivor Offspring. American Journal of Psychiatry, 171(8), 872–880. https://doi.org/10.1176/appi.ajp.2014.13121571