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Somatic Symptom Disorder (SSD) is a diagnosis listed in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) released in 2013. SSD loosely replaces several old diagnoses, namely Somatization Disorder, Undifferentiated Somatoform Disorder, Pain Disorder, and also includes a portion of the old diagnosis Hypochondriasis.

The diagnostic criteria were revised to simplify and re-conceptualize the diagnostic process for non-psychiatrists.1 The focus has shifted towards diagnosis of SSD based on positive diagnostic signs and symptoms, rather than on the absence of a medical explanation preceding a diagnosis. The new positive diagnostic criteria focus on symptoms that significantly impact the individual’s functioning for an extended time period. The diagnosis of SSD under the DSM-V has previously been considered controversial due to the concern that it is overly inclusive and creates a large potential for false positives; however, it is a slightly more restrictive diagnosis than the previous DSM-IV criteria which allowed for many patients with “medically unexplained” symptoms to be diagnosed with somatoform disorder.2

Somatic Symptom Disorder Diagnostic Criteria per DSM V1

Criterion A: One or more somatic symptoms that are distressing or result in significant disruption of daily life.

Criterion B: Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following

  • Disproportionate and persistent thoughts about the seriousness of one’s symptoms
  • Persistently high level of anxiety about health or symptoms
  • Excessive time and energy devoted to these symptoms or health concerns

Criterion C: Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months)

Further, the DSM-V states that the following specifications should be made1

  • With Predominant Pain (previously pain disorder): for individuals whose somatic symptoms predominantly involve pain.
  • Persistent: characterized by severe symptoms, marked impairment, and long duration (more than 6 months).

 Severity specifications are outlined as1

  • Mild: Only one of the symptoms specified in Criterion B is fulfilled.
  • Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
  • Severe: Two or more of the symptoms specified in Criterion B are fulfilled, plus there are multiple somatic complaints (or one very severe somatic symptom).


No published research accounts for the etiology of SSD.

Epidemiology, including risk factors and primary prevention

Historically, the prevalence of SSD was difficult to establish as the diagnostic criteria under the DSM-V subsumed other somatoform disorders such as hypochondriasis and panic disorder. An article by Kurlansik and Maffei estimates the prevalence of SSD as between 5 and 7% in the general population and 17% in the primary care population.17 Onset of SSD can begin in adolescence or childhood, and is considered more common in females than in males, with female to male ratios being estimated at 10:1. 37 Further studies examined the incidence of SSD in the general population via self-report questionnaires and found that mean frequencies of SSD in the population were as high as 12.9% (CI 12.5-13.3 95%).38 When compared to previous somatic symptom disorders (i.e., somatization disorder, undifferentiated somatoform disorder, pain disorder, etc.) SSD was found to exhibit both reliability and validity, as well as good clinical utility.38

Extrapolating data from the prior diagnoses that contribute to SSD to determine prevalence was considered but rejected because not all patients with the former diagnoses would qualify for the SSD diagnoses under the DSM-V, particularly in those with unexplained symptoms.3 Also, there are additional patients with explained medical conditions that can now be diagnosed with SSD if they suffer from the B and C criteria. This leads to concern for the risk of those with known medical disease having their symptoms attributed to psychological distress if they also qualify for the SSD diagnosis.3,4 With suspected prevalence rates of SSD at up to 25 to 60% in patients with functional somatic syndromes (i.e., fibromyalgia, chronic fatigue syndrome irritable bowel syndrome) it is important to avoid ascribing all somatic symptoms to SSD despite any overlap.6

Risk factors/primary prevention

  •  Substance use, and childhood sexual abuse and neglect have been identified as potential risk factors for SSD or somatization.17 There is also published research regarding correlations involving SSD. One study shows that for patients suffering from psychogenic non-epileptic seizures, patients who also qualify for an SSD diagnosis are more likely to report polyallergy.7 Another study stated that for patients being evaluated for multiple sclerosis, if they brought a list of symptoms, there was a high incidence of SSD.8 The aforementioned studies suggest a potential behavioral or personality based component that may indicate risk of SSD symptoms.
  • Risk factors that have been historically associated with somatoform disorders and somatization include female sex, fewer years of education, lower socioeconomic status, history of childhood chronic illness, history of sexual abuse or other trauma, and concurrent general medical or psychiatric disorders.9 It is important to note that this data is based on previous studies of multiple types of somatoform disorders and not on the newer diagnostic criteria for SSD under the DSM-V. It is possible that many of these risk factors also apply to SSD; however, caution should be taken to avoid the mislabeling of women and those who are undereducated or socioeconomically disadvantaged as “catastrophizers” when presenting with physical symptoms.3
  • A prospective study in patients with vertigo and dizziness found that those who developed SSD within the 1-year study period had higher baseline levels of health anxiety, were more likely to exhibit catastrophic thinking, had a stronger self-concept of bodily weakness, participated in more frequent illness-related behaviors (e.g., taking medication), and had higher levels of depression and anxiety.39


There is no known anatomical or physiological explanation for SSD. Because the DSM-V definition of SSD was established in 2013, most of the hypotheses regarding the pathogenesis of SSD is informed by studies on illness anxiety disorder and functional somatic syndromes such as fibromyalgia and irritable bowel disorder.

In 2017, the International Association for the Study of Pain (IASP) developed a new descriptor of pain distinct from nociceptive and neuropathic pain called nociplastic pain. Nociplastic pain is defined as “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.” This new descriptor was chosen as a response to the literature supporting decreased connectivity of the medial prefrontal cortex to the posterior constituents of the default mode network and increased connectivity to the insular cortex in patients with functional somatic syndromes. Some pain experts prefer the term centralized somatization, but that term was ultimately rejected by the IASP due to the fact that all forms of nociplastic pain are considered purely of central origin. Symptoms of SSD would be categorized under nociplastic or mixed pain, with many benign somatic sensations or physical symptoms becoming overly amplified by patients who have become overly sensitized to pain.12 High levels of health anxiety also contribute to the perpetuation or worsening of SSD, as patients tend to vigilantly monitor their bodies for any symptoms or changes. Because of this, high levels of anxiety about health have now been incorporated into the diagnostic criterion B of SSD.1

Some evidence supports a genetic component in the pathogenesis of SSD. A national study (n>28,000 individuals) found that genetic factors contribute anywhere between 7 to 21% to somatic symptoms with the remaining contribution likely attributable to environmental factors.13 There is evidence to suggest a genetic component in the co-occurrence of anxiety and depression with somatic symptoms.14

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

There is evidence that suggests prodromal symptoms of SSD appear in childhood and adolescence.10 There are limited data published on the course of SSD, but one study suggests that in elderly individuals with SSD rated as severe, lower cognition was observed as measured by the Mini Mental-State Examination.15 Another publication states that old data referring to somatoform disorders in general is applicable to SSD and suggests that self-reports of bodily weakness is a predictor of symptom severity.16

Multiple studies have associated high somatic symptom burden to greater health care utilization and functional impairment, independent of age, anxiety disorders, depressive disorders, and general medical disorders. Based on the data that is available regarding the course of illness in somatization disorders, the course is thought to be chronic, with waxing and waning of symptoms. There is no clear evidence regarding the rate of recovery or recurrence of SSD.17

Specific secondary or associated conditions and complications

Associated conditions include

  • Dysaesthetic Penoscrotodynia (burning pain in the genital skin) has been found in a retrospective study to be related to SSD.18
  • The DSM-V states that SSD is associated with high rates of comorbid depression and anxiety.1
  • A 2018 study demonstrated that CRPS was associated with a history of psychological distress or somatization. This association is important to consider as patients with undiagnosed SSD may be prematurely or incorrectly diagnosed with CRPS due to the amplification of their symptoms due to SSD.20

No complications have been clearly established for SSD. However, an article focused on the somatic symptom burden reports that patients with a high somatic symptom burden were more likely to score high on self-reported measures of health care utilization as well as have high scores on measures of psychological distress.2 It was noted that their criteria for somatic symptom burden differs from the DSM-V criteria for SSD, and that while the connection to SSD is noteworthy, caution is advised when drawing definitive conclusions about SSD utilizing their data. Other diagnoses to consider when suspecting SSD include mental health disorders such as depression, panic disorder, generalized anxiety disorder, substance use disorder, and chronic fatigue syndrome which may present with similar symptoms.17

Essentials of Assessment


Conducting a history and interview is essential to diagnose SSD, and patients should fulfill all three diagnostic criteria as mentioned above.

Somatic symptoms that are common in SSD include:1,22

  • Pain symptoms: joint pain, back pain, headache, chest pain, abdominal pain, dysuria
  • Nonspecific symptoms: fatigue, syncope, dizziness
  • Gastrointestinal symptoms: nausea, vomiting, abdominal pain, bloating, gas, diarrhea
  • Cardiopulmonary symptoms: shortness of breath, chest pain, palpitations
  • Neurological symptoms: movement disorders, sensory loss, weakness, paralysis
  • Reproductive organ symptoms: dyspareunia, dysmenorrhea, erectile dysfunction

The most common somatic symptoms in children and adolescents with SSD include abdominal pain, nausea, back pain, blurry vision, fatigue, and headache.23

It is important to differentiate SSD from Illness Anxiety Disorder which consists of a patient who has either no symptoms or very mild symptoms accompanied by significant anxiety and preoccupation on the risk of serious disease.  Generalized anxiety disorder can also present with somatic symptoms that align with the B criteria of SSD. The key distinction from SSD is that feelings of anxiety in Generalized Anxiety Disorder are related to multiple events, situations, or activities as opposed to solely somatic symptoms.1

Physical examination

There is no physical examination component that is necessary for the diagnosis of SSD. Under the DSM-V criteria, there is no need to rule out medical cause of the symptoms because a diagnosis of SSD can be made with or without a medically explained presentation.1 However, a thorough physical exam can be helpful to 1) rule out serious underlying medical issues, 2) ease patient’s anxieties and assure patients that their complaints are taken seriously, and 3) establish a baseline to detect changes over time. It should also be noted that as new symptoms develop, they cannot be merely lumped into a prior SSD diagnosis but should be evaluated through a physical exam.

Functional assessment

There may be a tendency amongst those with SSD to avoid physical activity. An aforementioned study on somatic symptom burden and health anxiety found that patients with high somatic symptom burden have increased functional impairment as measured by the Sheehan Disability Scale. It was noted that the study does not match directly with DSM-V criteria of SSD but that there are significant similarities.21

Laboratory studies

There is no laboratory study to confirm the diagnosis of SSD, as it is not necessary to rule out medical causes of symptoms to have the diagnosis of SSD. Due diligence and concern should be exercised to all new presenting symptoms in a patient regardless of their diagnosis of SSD. However, excessive diagnostic testing in the presence of low clinical suspicion in a patient with SSD can be detrimental as it could lead to false positive results, which exacerbate health anxiety and/or could lead to unnecessary treatments/procedures.24


There are no imaging studies that confirm the diagnosis of SSD. There is, however, research stating that there are brain regions associated with a greater vulnerability to pain and catastrophizing of symptoms such as the dorsolateral prefrontal, insular, rostral anterior cingulate, and premotor and parietal cortices.25 However, imaging to assess for irregularities of these areas is neither inclusive nor exclusive of the diagnosis, and no research has shown any correlation with SSD in particular.

Supplemental assessment tools

Several questionnaires have been developed and can be helpful in the assessment of SSD.

  • Somatic Symptom Disorder-B Criteria Scale (SSD-12) is a self-report questionnaire, which assesses excessive thoughts, worrying, or behaviors related to somatic symptoms. SSD-12 was developed specifically for the diagnosis of SSD.26
  • The Patient Health Questionnaire -15 item (PHQ-15) is the most widely used instrument to assess the number of distressful somatic symptoms.27
  • The Somatic Symptom Scale 8 (SS-8) was derived from the PHQ-15 and is used to quantify the burden of somatic symptoms.28

The combination of the SSD-12 with either the PHQ-15 or the SS-8 considerably improves identification of people at risk for somatic symptom disorder.29

Early predictions of outcomes

Data from nine population-based studies (n = 28,377) using various instruments (PHQ-15, Zerssen 14, Lifetime Composite International Diagnostic Interview [Lifetime CIDI], Symptom Checklist-90-Revised [SCL-90-R], and Somatic Symptom Inventory Score [SSI score]) found that higher scores were significantly correlated with health status and healthcare use, even after adjustment for confounders such as age, gender, anxiety/depression, and general medical illness.22 However, as the diagnosis of SSD was established in 2013, there are limited publications evaluating outcomes of SSD and none on early predictors of outcomes.

Rehabilitation Management and Treatments

Available or current treatment and rehabilitation guidelines

In 2018, a clinical neuroscience journal published recommendations on the management of SSD based on the best available evidence and clinical expertise. Those recommendations include but are not limited to the following practice principles:31

  • Somatic symptoms should be taken seriously even if no well-defined organic pathology is demonstrated. Resist the temptation to concentrate on psychosocial issues too early and too independently of lead complaints.
  • Build an effective, blame-free narrative that incorporates physical and psychosocial mechanisms and addresses contextual factors as amplifiers rather than causes for the patient’s symptoms.
  • Effective communication with the patient is essential and includes reassurance, anticipation of likely outcomes of diagnostic tests, and motivation to actively engage in coping with bodily stress. A 30-minute psychoeducational intervention for patients focused on basic concepts of the neurophysiology of pain and stress in addition to the benefits of exercise and healthy diet was shown to significantly improve somatic symptoms immediately after intervention and at 3 weeks post-intervention.32
  • Set realistic treatment goals based on functional attitudes and behaviors.
  • Consider antidepressant medication or psychological referral for evaluation and treatment of possible depression, anxiety, or traumatic history.
  • If appropriate, schedule outpatient visits at regular intervals that are not contingent on active symptoms.

An article on somatic syndrome disorders recommends that treatment of SSD should be focused on coping with both physical and psychological distress, rather that complete elimination of symptoms.17,31,37 Cognitive Behavioral Therapy has been identified as an effective method of improving functioning and managing somatic complaints.37 Psychopharmacological intervention in the form of SSRIs or SNRIs demonstrated efficacy in improvement of SSD in a study on pharmacological interventions for somatoform disorders in adults.36 Additionally, a two-patient case study found that Blonanserin, an atypical antipsychotic that is not FDA approved, was useful in treating SSD when given with SSRIs.33    

However, caution is advised when prescribing medications to those with SSD, as adverse events may exacerbate concerns related to existing health anxiety.37

Coordination of care

Early recognition of SSD and involving psychology/psychiatry to help manage symptoms is imperative. Collaboration between the patient, medical provider, and the mental health practitioner would likely be useful in promoting adaptive coping and recovery.  Additionally, educating ancillary staff such as nurses, and physical, occupational, and speech therapists regarding SSD is likely beneficial.

Patient & family education

Key patient educational issues include:
Physician acknowledgement of the patient’s symptoms and the impact they have on quality of life.

Family education should include:
Education on somatic symptom disorder and an emphasis on its recognition as a medical diagnosis that can increase disability and significantly impact the patient’s quality of life.38

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Early suspicion and involvement of psychology/psychiatry for evaluation and treatment can be helpful in diagnosing and treating comorbidities such as anxiety and depression and sexual trauma. Psychologists and psychiatrists can also help to reinforce a focus on improved functioning rather than resolution of somatic symptoms.17

Establishing a collaborative, therapeutic alliance with the patient by acknowledging and legitimizing somatic symptoms is essential. This requires a delicate balance between adequately assessing for serious medical issues and limiting diagnostic testing and referrals to specialists when there is a low pretest probability of serious disease.24,31

Cutting Edge/Emerging and Unique Concepts and Practice


Gaps in the Evidence-Based Knowledge

As mentioned above, a gap exists for evidence regarding etiology, epidemiology, pathophysiology, assessment, pharmacological and other forms of treatment, and impact on physical rehabilitation. There is also a need for research regarding specific populations like adolescents and how SSD affects them functionally.34 Since the publication of the DSM-V, there has been criticism that it can lead to over- or under-diagnosis some patient populations. Additional publications attempt to break down SSD into subgroups based on certain characteristics in order to aid in defining treatment goals and choosing treatment options for patients with SSD. Further research on this topic is warranted.35


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Original Version of the Topic

Laurentiu I. Dinescu, MD, Adrian Cristian, MD. Somatization Disorder. 11/27/2012

Previous Revision(s) of the Topic

Jason Hunt, MD, Ankit Patel, MD. Somatic Symptom Disorder. 9/21/2016

Shawn Uraine, MD, Sarah H Yoon, MD. Somatic Symptom Disorder. 12/10/2020

Author Disclosure

Shawn Uraine, MD
Nothing to Disclose

Kristen Sanders, Psy.D
Nothing to Disclose