Somatic symptom disorder


Somatic symptom disorder is a mental health condition characterised by an excessive focus on physical symptoms—such as pain or shortness of breath—that cause significant distress or impairment. Individuals with SSD experience disproportionate thoughts, emotions, and behaviors related to their symptoms. The symptoms themselves are not deliberately produced or feigned, and their underlying cause—whether organic, psychogenic or unexplained—is irrelevant to the diagnosis.
Manifestations of somatic symptom disorder are variable; symptoms can be widespread, specific, and often fluctuate. Somatic symptom disorder corresponds to how an individual views and reacts to symptoms rather than the symptoms themselves, and it can develop in the setting of existing chronic illness or newly onset conditions.
Several studies have found a high frequency of comorbidity with major depressive disorder, generalized anxiety disorder, and phobias. Somatic symptom disorder is frequently associated with functional pain syndromes, such as fibromyalgia and irritable bowel syndrome. Somatic symptom disorder typically leads to poor overall functioning, interpersonal issues, unemployment or problems at work, and financial strain as a result.
The etiology of somatic symptom disorder is unknown. Symptoms may result from a heightened awareness of specific physical sensations alongside health anxiety. There is some controversy surrounding the diagnosis, since symptom perception and response are inherently subjective, and may depend on the clinician's interpretation. Additionally, people with known physical illnesses can sometimes be misdiagnosed with it.

Signs and symptoms

Somatic symptom disorder is characterized by unclear and inconsistent symptom histories that seldom improve with medical treatments. Key signs include misinterpreting normal sensations as abnormal, avoiding physical activity, heightened sensitivity to medication side effects, and seeking care from multiple providers for the same issues.
Manifestations of somatic symptom disorder are highly variable. Recurrent ailments usually begin before age 30; most patients have many somatic symptoms, while others only experience one. The severity may fluctuate, but symptoms rarely go away completely for long periods. Symptoms might be specific, such as regional pain and localized sensations, or general, such as fatigue, myalgia, and malaise.
Individuals with somatic symptom disorder have obsessive worries about their health. They often misinterpret normal sensations as severe illnesses, believe their symptoms are serious despite no medical basis, feel medical evaluations are inadequate, fear physical activity will harm them, and spend excessive time focused on their symptoms.
Somatic symptom disorder pertains to how an individual interprets and responds to symptoms instead of the symptoms themselves. Somatic symptom disorder can occur even in those who have an underlying chronic illness or medical condition. When somatic symptom disorder is comorbid with another ailment, individuals may hyperreact to the presence of the other condition's features. They may be unresponsive to treatment or unusually sensitive to drug side effects. Those with somatic symptom disorder who also have another physical ailment may experience significant impairment that is not expected from the condition.

Comorbidities

Research on comorbid mental disorders and self-reported psychopathology in individuals with somatic symptom disorder has revealed a substantial frequency of comorbidity with depression and anxiety; however, other psychiatric comorbidities have often been overlooked. Major depressive disorder, generalized anxiety disorder, and phobias were the most commonly concurrent conditions.
In studies evaluating physical ailments, 41.5% of those with semantic dementia, 11.2% of those with Alzheimer's disease, 25% of female patients with non-HIV lipodystrophy, and 18.5% of patients with congestive heart failure fulfilled somatic symptom disorder criteria. Among those with fibromyalgia, 25.6% met somatic symptom disorder criteria and exhibited higher rates of depression than those who did not meet the criteria. In one study, 28.8% of those with somatic symptom disorder had asthma, 23.1% had cardiovascular disease, and 13.5% had gout, rheumatoid arthritis, or osteoarthritis.

Complications

and other substance abuse are frequently observed, sometimes being used to alleviate symptoms but simultaneously increasing individuals' risk of substance dependence over baseline. Other complications include poor overall functioning, problems with relationships, unemployment or difficulties at work, and financial stress due to excessive clinical visits.

Causes

Somatic symptoms can stem from heightened awareness of normal body sensations alongside a tendency to interpret those sensations as abnormal. Studies suggest that risk factors of somatic symptoms include childhood neglect, sexual abuse, and substance abuse. Psychosocial stressors, such as unemployment and poor job performance, may also be risk factors. There could also be a genetic element: A 2010 study of monozygotic and dizygotic twins found that genetics explained 7% to 21% of participants' risk for somatic symptoms, with the remainder related to environmental factors. In another study, various single-nucleotide polymorphisms were linked to somatic symptoms.

Psychological

Evidence suggests that along with more broad factors such as early childhood trauma or insecure attachment, negative psychological factors including catastrophizing, negative affectivity, rumination, avoidance, health anxiety, or a poor physical self-concept have a significant impact on the shift from unproblematic somatic symptoms to a severely debilitating somatic symptom disorder. Those who experience more negative psychological characteristics may regard medically unexplained symptoms to be more threatening and, therefore, exhibit stronger cognitive, emotional, and behavioral awareness of such symptoms. In addition, evidence suggests that negative psychological factors have a significant impact on the impairments and behaviors of people suffering from somatic symptom disorder, as well as the long-term stability of such symptoms.

Psychosocial

stresses and cultural norms influence how patients present to their physicians. American and Koreans engaged in a study to measure somatization within the cultural context. It was discovered that Korean participants used more body-related phrases while discussing their connections with stressful events and experienced more sympathy when asked to read texts using somatic expressions when discussing their emotions.
Those raised in environments where expressing emotions during stages of development is discouraged face the highest risk of somatization. In primary care settings, studies indicated that somaticizing patients had much greater rates of unemployment and decreased occupational functioning than non-somaticizing patients.
Traumatic life events may cause the development of somatic symptom disorder. Most people with somatic symptom disorder originate from dysfunctional homes. A meta-analysis study revealed a connection between sexual abuse and functional gastrointestinal syndromes, chronic pain, non-epileptic seizures, and chronic pelvic pain.

Physiological

The hypothalamo pituitary adrenal axis has a crucial role in stress response. While the HPA axis may become more active with depression, there is evidence of hypocortisolism in somatization. In somatic disorder, there is a negative connection between elevated pain scores and 5-hydroxy indol acetic acid and tryptophan levels.
It has been suggested that proinflammatory processes may have a role in somatic symptom disorder, such as an increase of non-specific somatic symptoms and sensitivity to painful stimuli. Proinflammatory activation and anterior cingulate cortex activity have been shown to be linked in those who experienced stressful life events for an extended period of time. It is further claimed that increased activity of the anterior cingulate cortex, which acts as a bridge between attention and emotion, leads to increased sensitivity of unwanted stimuli and bodily sensations.
Pain is a multifaceted experience, not just a sensation. While nociception refers to afferent neural activity that transmits sensory information in response to stimuli that may cause tissue damage, pain is a conscious experience requiring cortical activity and can occur in the absence of nociception. Those with somatic symptom disorder are thought to exaggerate their symptoms through choice perception and perceive them in accordance with an ailment. This idea has been identified as a cognitive style known as "somatosensorial amplification". The term "central sensitization" has been created to describe the neurobiological notion that those predisposed to somatization have an overly sensitive neural network. Harmless and mild stimuli stimulate the nociceptive specific dorsal horn cells after central sensitization. As a result, pain is felt in response to stimuli that would not typically cause pain.

Neuroimaging evidence

Some literature reviews of cognitive–affective neuroscience on somatic symptom disorder suggested that catastrophization in patients with somatic symptom disorders tends to present a greater vulnerability to pain. The relevant brain regions include the dorsolateral prefrontal, insular, rostral anterior cingulate, premotor, and parietal cortices.

Genetic

Genetic investigations have suggested modifications connected to the monoaminergic system, in particular, may be relevant while a shared genetic source remains unknown. Researchers take into account the various processes involved in the development of somatic symptom disorder as well as the interactions between various biological and psychosocial factors. Given the high occurrence of trauma, particularly throughout childhood, it has been suggested that the epigenetic changes could be explanatory. Another study found that the glucocorticoid receptor gene is hypomethylated in those with somatic symptom disorder and in those with depression.