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Disease/ Disorder

Definition

Somatic Symptom Disorder (SSD) is a new diagnosis listed in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) 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 changed in such a way as to simplify and re-conceptualize the criteria to be easier for non-psychiatrists to diagnose.1 The focus has shifted towards positive diagnostic signs and symptoms, rather than on the absence of a medical explanation for the signs and symptoms. The new positive diagnostic criteria focus on symptoms that significantly impact the individual for an extended time period. The diagnosis of SSD under the DSM-V is 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 states that you should specify if the diagnosis is:1

  1. With Predominant Pain (previously pain disorder): The specifier is for individuals whose somatic symptoms predominantly involve pain.
  2. Persistent: A persistent course is characterized by severe symptoms, marked impairment, and long duration (more than 6 months).

And the DSM asks that you specify the current severity:1

  1. Mild: Only one of the symptoms specified in Criterion B is fulfilled.
  2. Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
  3. 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).

Etiology

No published research accounts for the etiology of SSD.

Epidemiology including risk factors and primary prevention

The prevalence of SSD is difficult to establish as the new diagnostic criteria under the DSM-V subsumes other somatoform disorders such as hypochondriasis and panic disorder. Extrapolating data from the prior diagnoses that contribute to SSD would be theoretical at best as not all patients with the former diagnoses will qualify for the SSD diagnoses under the DSM-V, particularly in those with unexplained symptoms.2 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 of SSD. There is some concern that these patients with known medical diseases will start to be labeled as mentally ill if they also now qualify for the SSD diagnosis.3,4  Despite all of this, some have still hypothesized from the previously published literature that the prevalence of SSD may be 4-6% of the general population, but as discussed, this is theoretical at best.1,5 Prevalence rates of SSD are suspected to be higher,  up to 25 to 60%, in patients with functional somatic syndromes such as fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome.6

Risk factors/primary prevention:

  1. There is no published research as yet regarding risk factors or primary prevention of SSD. However, there has been research published regarding correlations involving SSD. One study shows that for patients suffering from psychogenic non-epileptic seizures, the patients that also qualify for an SSD diagnosis are more likely to report polyallergy.7 Another study stated that for patients being worked up for multiple sclerosis, if they brought a list of symptoms, there was a high incidence of SSD.8
  2. 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 so as to not mislabel women or undereducated, socioeconomically disadvantaged patients who are more likely to be casually dismissed as “catastrophizers” when presenting with physical symptoms.3

Patho-anatomy/physiology

There is not a 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. Childhood experiences of parental neglect and sexual abuse may be associated with somatization.10,11

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. They define nociplastic pain 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 as they felt that not all forms of nociplastic pain are of purely central origin. Patients with 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, which is why persistently 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 also some 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 some evidence that suggests prodromal symptoms of SSD appear in childhood and adolescence.10 There is limited data published on the course of SSD, but one study suggests that in elderly individuals with SSD rated as severe, they display lower cognition 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, suggesting 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:

  1. Dyaesthetic Penoscrotodynia (burning pain in the genital skin) has been found in a retrospective study to be a type of SSD.18
  2. The DSM-V states that SSD is associated with high rates of comorbid depression and anxiety but most of the studies that support the correlation utilize data regarding somatoform disorders defined prior to the new DSM-V diagnostic criteria.1
  3. A 2018 study demonstrates that CRPS is associated with a history of psychological problems or somatization and that patients involved in litigation are even more likely to suffer from multiple previous psychiatric vulnerabilities. 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 from SSD.20

No complications have been clearly established for SSD. However, one paper that 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..21 However, they note that their criteria for somatic symptom burden differs from the DSM-V criteria for SSD, and that while the connection to SSD is noteworthy, it is premature to draw 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 some similar symptoms.17

Essentials of Assessment

History

History and interview are 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
  • Neurologic 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 is also a new diagnosis under the DSM-V where a patient has no or only very mild symptoms, but has great anxiety and preoccupation that they have a serious disease. Another disorder that it is important to distinguish from SSD is generalized anxiety disorder which could be confused with the B criteria, but it is not due solely to somatic symptoms. Rather, it is anxiety due to multiple events, situations, or activities.1

Physical examination

There is no physical examination component that is necessary for the diagnosis of SSD. Under the new DSM-V criteria, there is no need to rule out medical causes of the symptoms because they can have the diagnosis of SSD whether or not their symptoms can be medically explained.1 However, a thorough physical exam can be helpful to 1) rule out serious underlying medical issue, 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 need to be evaluated like any other new symptoms, including a physical exam.

Functional assessment

There may be a tendency amongst SSD patients to avoid physical activity. There is one study that states that patients with high somatic symptom burden have increased functional impairment as measured by the Sheehan Disability Scale, although they note that their study doesn’t match directly with DSM-V criteria of SSD, but is somewhat similar.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 under DSM-V. Due diligence and concern should be given to all new presenting symptoms in a patient regardless of their diagnosis of SSD. However, excessive diagnostic testing in the setting 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

Imaging

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 catastrophization of symptoms including 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.

  1. Somatic Symptom Disorder-B Criteria Scale (SSD-12) is a self-report questionnaire, which assesses excessive thoughts, worrying, or behaviors related to somatic symptoms. It was developed specifically for the diagnosis of SSD.26
  2. The Patient Health Questionnaire -15 item (PHQ-15) is the most widely used instrument to assess the number of distressful somatic symptoms.27
  3. 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.

Environmental

It is unclear if environmental influences impact the development, progression, or treatment of SSD. However, the DSM-V reapplies research pre-dating the DSM-V, which suggests that SSD is more frequent in patients with low socioeconomic status, few years of education, and those who have recently experience stressful life events.1

Social role and social support system

There is no published data regarding the assessment of SSD specifically in regards to social role or support system. However, organic illnesses, stressful working conditions, and adverse life events have been identified as precipitating factors for bodily distress which may play a role in the development of SSD.1,30

Rehabilitation Management and Treatments

Available or current treatment guidelines

There are no guidelines regarding the treatment of SSD. Much of the evidence regarding pharmacotherapy, cognitive behavior therapy, and mindfulness-based therapy for somatic symptom disorder is based on research that pre-dates the existence of the SSD diagnosis as it stands in DSM-V. With that being said, 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

  1. 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.
  2. 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.
  3. Good communication with the patient is essential which 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 to explain basic concepts on 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
  4. Set realistic treatment goals based on functional attitudes and behaviors.
  5. Consider antidepressant medication or psychological referral for evaluation and treatment of possible depression, anxiety, or traumatic history.
  6. If appropriate, schedule outpatient visits at regular intervals that are not contingent on active symptoms.

There is some limited research published specifically on treatment of SSD based on the new DSM-V diagnostic criteria. 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

Rehabilitation guidelines

There are no treatment guidelines when it comes to the physical rehabilitation of patients with SSD. However, developing a close collaboration between the patient and the mental health practitioner would likely be useful in coping with the B criteria. And it is important to note that SSD patients tend to engage in less physical activity and score higher on disability rating systems, thus an explicitly set goal of functional improvement rather than complete resolution of somatic symptom(s) is crucial.17,31

Coordination of care

Early recognition of SSD and involving psychology/psychiatry to help manage symptoms is important. It may also be important to educate ancillary staff such as nursing and physical, occupational, and speech therapists regarding SSD.

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 regarding what somatic symptom disorder is, and an explanation that it is a medically recognized diagnosis that significantly impacts the patient’s quality of life and can be associated with increased disability.

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 as well as sexual trauma. Psychologists and psychiatrists can also help to reinforce focus on improved function 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

The entire diagnosis is still considered cutting edge as patients transition from previous DSM-IV diagnoses to DSM-V diagnoses such as SSD. While there is limited research addressing treatment., blonanserin, an atypical antipsychotic, is a cutting edge treatment that has been shown to be effective but has not yet received FDA approval.33 The 2017 IASP inclusion of nociplastic pain is also a new and unique concept that may contribute to a better understanding of and management of SSD in the future.12

Gaps in the Evidence- Based Knowledge

SSD is a new DSM-V diagnosis, therefore there is a large gap of evidence-based knowledge. As mentioned, 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 some criticism that it either over- or under-diagnoses some patients. There have been some publications that 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

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA: American Psychiatric Publishing, 2013.
  2. Claassen-van Dessel N, Van Der Wouden JC, Dekker J, Van De Horst, HE. Clinical value of DSM IV and DSM 5 criteria for diagnosing the most prevalent somatoform disorders in patients with medically unexplained physical symptoms (MUPS) Journal of Psychosomatic Research 2016;82:4-10.
  3. Frances A. The new somatic symptom disorder in DSM-5 risks mislabeling many people as mentally ill. BMJ. 2013;346:f1580.
  4. Hauser W. The somatic symptom disorder in DSM 5 risks mislabeling people with major medical diseases as mentally ill.J Psychosom Res. 2013;75:586-587.
  5. Rosic T, Kalra S, Samaan Z. Somatic symptom disorder, a new DSM-5 diagnosis of an old clinical challenge. BMJ. 2016. doi:10.1136/bcr-2015-212553
  6. Hüsing P, Löwe B, Toussaint A. Comparing the diagnostic concepts of ICD-10 somatoform disorders and DSM-5 somatic symptom disorders in patients from a psychosomatic outpatient clinic. J Psychosom Res. 2018; 113:74.
  7. Robbins NM, Larimer P, Bourgeois JA, Lowenstein DH. Number of patient-reported allergies helps distinguish epilepsy from psychogenic nonepileptic seizures. Epilepsy & Behavior. 2016;55:174-177.
  8. Anbarasan D, Campion G, Campion P, Howard J. Clinical utility of the list sign as a predictor of non-demyelinating disorders in a multiple sclerosis (MS) practice. CNS Spectr. 2016;3:1-6.
  9. Creed FH, Davies I, Jackson J, et al. The epidemiology of multiple somatic symptoms. J Psychosom Res. 2012; 72:311.
  10. Gilleland J, Suveg C, Jacob ML, Thomassin K. Understanding the medically unexplained: emotional and familial influences on children’s somatic functioning. Child Care Health Dev. 2009; 35:383.
  11. Paras ML, Murad MH, Chen LP, et al. Sexual abuse and lifetime diagnosis of somatic disorders: a systematic review and meta-analysis. JAMA. 2009; 302:550.
  12. Trouvin AP, Perrot S. New concepts of pain. Best Practice and Research Clinical Rheumatology. 2019;33:101415
  13. Kato K, Sullivan PF, Pedersen NL. Latent class analysis of functional somatic symptoms in a population-based sample of twins. J Psychosom Res. 2010; 68:447.
  14. Kato K, Sullivan PF, Evengård B, Pedersen NL. A population-based twin study of functional somatic syndromes. Psychol Med. 2009; 39:497.
  15. Inamura K, Shinagawa S, Nagata T, Tagai K, Nukariya K, Nakatama K. Cognitive dysfunction in patients with late-life somatic symptom disorder: a comparison according to disease severity. Psychosomatics. 2015;56:486-494.
  16. Voigt K, Wollburg E, Weinmann N, Herzog A, Meyer B, Langs G, Lowe B. Predictive validity and clinical utility of DSM-5 somatic symptom disorder: Prospective 1-year follow-up study.Journal of Psychosomatic Research. 2013;75:358-361.
  17. Kurlansik S, Maffei MS. Somatic Symptom Disorder. Am Fam Physician. 2016;93(1):49-54.
  18. Anyasodor MC, Taylor RE, Bewley A, Goulding JMR. Dyaesthetic penoscrotodynia may be a somatoform disorder: results from a two-centre retrospective case series. Clin Exp Dermatol. 2016 Mar 1. doi: 10.1111/ced.12824
  19. Munechika T, Fujishiro H, Okuda M, Iwamoto K, Toril Y, Iritani S, Ozaki N. Rapid eye movement sleep without atonia may help diagnose Lewy body disease in middle-aged and older patients with somatic symptom disorder. Psychogeriatrics.2016; doi:10.1111/psyg.12181
  20. Bass C, Yates G. Complex regional pain syndrome type I in the medico-legal setting: High rates of somatoform disorders, opiate use, and diagnostic uncertainty. Medicine, Science, and the Law. 2018;58(3):147-155.
  21. Lee S, Creed FH, Ma Y-L, Leung CMC. Somatic symptom burden and health anxiety in the population and their correlates. Journal of Psychosomatic Research. 2015;78:71-76.
  22. Tomenson B, Essau C, Jacobi F, et al. Total somatic symptom score as a predictor of health outcome in somatic symptom disorders. Br J Psychiatry. 2013; 203:373.
  23. Dell ML, Campo JV. Somatoform disorders in children and adolescents. Psychiatr Clin North Am. 2011; 34:643.
  24. Kroenke K. Diagnostic testing and the illusory reassurance of normal results: comment on “Reassurance after diagnostic testing with a low pretest probability of serious disease”. JAMA Intern Med. 2013; 173:416.
  25. Garcia CJ, Payed N, Serrano-Blanco A, Roca M. Brain dysfunction behind functional symptoms: neuroimaging and somatoform, conversive, and dissociative disorders. Curr Opin Psychiatry. 2009;22:224-231.
  26. Toussaint A, Murray AM, Voigt K, Herzog A, Gierk B, Kroenke K, Rief W, Hennigsen P, Lowe B. Development and Validation of the Somatic Symptom Disorder-B Criteria Scale (SSD-12).Psychosomatic Meidicine. 2016;78:5-12.
  27. Kroenke K, Spitzer RL, Williams JB. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med. 2002; 64:258.
  28. Gierk B, Kohlmann S, Kroenke K, et al. The somatic symptom scale-8 (SSS-8): a brief measure of somatic symptom burden. JAMA Intern Med. 2014; 174:399.
  29. Toussaint A, Hüsing P, Kohlmann S, Löwe B. Detecting DSM-5 somatic symptom disorder: criterion validity of the Patient Health Questionnaire-15 (PHQ-15) and the Somatic Symptom Scale-8 (SSS-8) in combination with the Somatic Symptom Disorder – B Criteria Scale (SSD-12). Psychol Med. 2020; 50:324.
  30. Croicu C, Chwastiak L, Katon W. Approach to the patient with multiple somatic symptoms. Med Clin North Am. 2014; 98:1079.
  31. Henningsen P. Management of somatic symptom disorder. Dialogues Clin Neuroscience. 2018;20:23-31.
  32. Johnson KK, Bennett C, Rochani H. Significant improvement of somatic symptom disorder with brief psychoeducational intervention by PMHNP in primary care. J Am Psychiatr Nurses Assoc. 2020 Sept 23. doi: 10.1177/1078390320960524
  33. Nagoshi Y, Tominaga T, Fukui K. Blonanserin augmentation for treatment-resistant somatic symptom disorder: a case series.Clinical Neuropharmacology. 2016;39:2,112-114
  34. Van Geelen SM, Rydelius P-A, Hagquist C. Somatic symptoms and psychological concerns in a general adolescent populations: Exploring the relevance of DSM-5 somatic symptom disorder. Journal of Psychosomatic Research.2015;79:251-258.
  35. Klemm S, van Broeckhuysen-Kloth S, van Vliet S, Oosterhuis L, Geenen R. Personalized treatment outcomes in patients with somatoform disorder: A concept mapping study. J Psychosom Research. 2018; 109:19-24.

Original Version of the Topic

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

Author Disclosure

Shawn Uraine, MD
Nothing to Disclose

Sarah H Yoon, MD
Nothing to Disclose