A woman is visiting her primary doctor, complaining of constant headaches, joint pain, and fatigue. Her doctor does the preliminary check-up and asks some questions but is unable to pinpoint why. He may suggest bloodwork or other tests, both of which will still not reveal the problem. Later, it is revealed that she has been frequently going to various doctors, all of which have found nothing. With all of that in mind, it is likely that she has a somatoform disorder (1), specifically Somatic Symptom Disorder.
Somatic Symptom Disorder, formerly known as Somatization Disorder, is under the overarching label of somatoform disorders. To be diagnosed with Somatic Symptom Disorder (SSD), a person must experience at least one or more somatic, or relating to the body, complaint, high anxiety about one’s health, and feeling symptoms regardless of whether there is an actual problem or not (2). This what makes SSD different from Hypochondriasis, a more well-known somatoform disorder. Hypochondriasis patients typically do not have physical manifestations of symptoms while SSD patients do (3).
Expressed symptoms of SSD are not figments of the imagination like one would believe. Some studies say that it is likely that these symptoms are caused by hyperactive chemicals in the brain that do not lower after stressful situations. A study performed by Rief and Auer compared a healthy control group to a group with SSD and were tasked to perform activities with frequent distractions to raise stress levels and then take a break between each activity. The healthy group and SSD group experienced increased levels of cortisol (hormone relating to stress) and decreased levels of serotonin (regulator of anxiety) during the task. However, during rest periods only the healthy group experienced a stabilization of the chemicals resulting in lower heart rates and stress levels (4).
Chemical release is not the only piece of the puzzle. Imaging has been successful in locating several changes in brain activity relating to the presence of somatoform symptoms, however the findings have not been specific enough to directly attribute to SSD. Changes included decreased blood flow to the thalamus (5) and lowered glucose metabolism rates, both of which can also be attributed to dysmorphia, depression, and other anxiety disorders. “Brain research on somatoform disorders is at its earliest inception. Although differences…have been described in some studies, the specificity of these findings is unclear” states Bantick, who conducted several studies using PET scans and fMRI scans to locate the differences in brain activity of people with SSD (6).
Unfortunately, due to the complication of diagnosing a specific somatoform disorder, it is difficult to study individual disorders to find a link in neural imaging, measures of chemical releases, and relation to other mental disorders such as anxiety and depression, which also alters imaging and chemical release. According to an analysis of treatment protocols for somatoform disorders, the above issues make “somatoform disorders… one of the most controversial and mind boggling areas of modern psychiatry.” (7). This inability to diagnose has left professionals struggling to adapt and treat these disorders, leaving patients to wonder why their brain is literally making them sick.
(1) Somatoform disorders are disorders that cause unexplained bodily symptoms and extreme anxiety about the bodily health
(2) “Somatic Symptom Disorder.” Mental Help James Marcia and SelfIdentity Comments, Sober Media Group, 15 Oct. 2015, http://www.mentalhelp.net/articles/somatic-symptom-disorder/.
(3) Dimsdale, Joel E., and Robert Dantzer. “A Biological Substrate for Somatoform Disorders: Importance of Pathophysiology.” Psychosomatic Medicine, vol. 69, no. 9, 2007, pp. 850–854., doi:10.1097/psy.0b013e31815b00e7.
(4) Rief, Winfried, and Arthur J. Barsky. “Psychobiological Perspectives on Somatoform Disorders.” Psychoneuroendocrinology, vol. 30, no. 10, 2005, pp. 996–1002., doi:10.1016/j.psyneuen.2005.03.018.
(5) The thalamus is responsible for accurately directing signals from the body to the brain and vice versa
(6) Rief, Winfried, and Arthur J. Barsky. “Psychobiological Perspectives on Somatoform Disorders.” Psychoneuroendocrinology, vol. 30, no. 10, 2005, pp. 996–1002., doi:10.1016/j.psyneuen.2005.03.018.
(7) Khare, Shrayash. “Validity of Current Treatment Protocols to Overcome Hypochondriasis.” Journal Of Clinical And Diagnostic Research, 2017, doi:10.7860/jcdr/2017/22509.9262.