Somatic Symptom Disorder

Somatic Symptom Disorder (SSD) is a condition in which a person experiences one or more physical symptoms that are genuinely distressing and disruptive to daily life, accompanied by disproportionate thoughts, feelings, or behaviors related to those symptoms. Introduced in DSM-5 in 2013, SSD replaced a fragmented set of DSM-IV diagnoses and made a landmark shift: the diagnosis no longer requires that symptoms be medically unexplained. The biology is real, the distress is real, and the path forward involves understanding the science of how the mind and body interact.

Table of Contents

1. Overview and DSM-5 2013 Renaming
2. DSM-5 Diagnostic Criteria (SSD vs Illness Anxiety Disorder)
3. The Mind-Body Connection: Allostatic Load and Central Sensitization
4. Functional Neurological Disorder Overlap
5. Causes and Risk Factors
6. Symptoms, Presentations, and Subtypes
7. Assessment and Diagnosis
8. Treatment: CBT and ACT Evidence
9. Pharmacotherapy and Integrative Approaches
10. Healthcare Navigation and Working with Providers
11. Recovery and Prognosis
12. Key Research Papers
13. Featured Videos

1. Overview and DSM-5 2013 Renaming

Somatic Symptom Disorder was formally introduced in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) in 2013. It replaced a collection of DSM-IV diagnoses that were widely criticized as stigmatizing, overly fragmented, and diagnostically unreliable:

• Somatization disorder — required a complex checklist of multiple unexplained symptoms
• Hypochondriasis — fear of having a serious disease despite medical reassurance
• Pain disorder — chronic pain where psychological factors played a role
• Undifferentiated somatoform disorder — a catch-all for symptoms that didn't fully meet other criteria

The most important conceptual shift in DSM-5 was the elimination of the requirement for symptoms to be medically unexplained. A person with a confirmed medical diagnosis — cancer, irritable bowel syndrome, coronary artery disease — can still meet criteria for SSD if their thoughts, feelings, or behaviors about that condition are disproportionate and persistently disabling. This change acknowledged that distress and dysfunction related to real illness are clinically significant and deserve treatment in their own right.

The former "hypochondria" category was split cleanly into two diagnoses:

1. Somatic Symptom Disorder with prominent health anxiety — significant somatic symptoms plus high illness preoccupation
2. Illness Anxiety Disorder (IAD) — high illness preoccupation with little or no somatic symptoms

Population prevalence of SSD is estimated at 5–7% in the general adult population, with higher rates in primary care settings (up to 10–15%). The condition causes substantial disability, high healthcare utilization, and is frequently misdiagnosed or under-recognized.

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2. DSM-5 Diagnostic Criteria (SSD vs Illness Anxiety Disorder)

Somatic Symptom Disorder (DSM-5 Criteria)

Criterion A: One or more somatic symptoms that are distressing or result in significant disruption of daily life. These symptoms may or may not have a clear medical explanation — the presence of a medical diagnosis does not exclude SSD.

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:

1. Disproportionate and persistent thoughts about the seriousness of one's symptoms
2. Persistently high level of anxiety about health or symptoms
3. 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 lasting more than 6 months.

Specifiers:

• With predominant pain (previously called pain disorder) — somatic symptoms primarily involve pain
• Persistent — severe symptom burden, marked functional impairment, and long duration

Illness Anxiety Disorder (IAD) — Contrast with SSD

IAD (the successor to hypochondriasis) is characterized by preoccupation with having or acquiring a serious illness, with little or no somatic symptoms. Key features:

• Somatic symptoms are absent or mild — preoccupation is about what might be wrong, not current symptoms
• Illness preoccupation is easily triggered and difficult to reassure
• Excessive health-related behaviors (repeated medical visits, internet searches, body checking) or maladaptive avoidance
• Duration of at least 6 months

Prevalence of IAD is estimated at approximately 1.3–10% of the general population. Like SSD, it responds to CBT and SSRIs, though the primary target is health anxiety rather than somatic distress. Patients with IAD often feel profoundly misunderstood and may resist the diagnosis — careful, validating communication is essential.

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3. The Mind-Body Connection: Allostatic Load and Central Sensitization

Understanding SSD requires understanding the genuine neurobiology linking psychological experience to physical symptoms. This is not metaphor — it is measurable physiology.

Allostatic Load

Allostatic load refers to the cumulative physiological burden imposed on the body by chronic stress. When the stress response is chronically activated, the body's regulatory systems — the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system, the immune system — are pushed outside their optimal range over time. The consequences include:

• Dysregulated cortisol patterns (elevated basal cortisol or blunted diurnal rhythm)
• Sympathetic nervous system hyperactivation with reduced parasympathetic tone
• Elevated inflammatory markers (IL-6, CRP, TNF-alpha)
• Altered HPA axis feedback sensitivity

High allostatic load reliably predicts greater somatic symptom severity. Among the strongest contributors to allostatic load are Adverse Childhood Experiences (ACEs) — trauma, neglect, and household dysfunction in the first 18 years of life — which show a clear dose-response relationship with SSD in adults. The ACE Study (Felitti et al., 1998) demonstrated that individuals with 4 or more ACEs had dramatically higher rates of somatic symptoms, unexplained medical conditions, and healthcare utilization throughout adult life.

Central Sensitization

Central sensitization describes a state of amplified neural signaling within the central nervous system in which normal stimuli produce exaggerated or prolonged sensory responses. The mechanisms include:

• NMDA receptor hypersensitivity at dorsal horn synapses, lowering the pain threshold and widening the receptive field of pain neurons
• Reduced descending inhibitory control — the serotoninergic and noradrenergic pathways from the brainstem that normally suppress pain signals are underactive
• Altered thalamic gating — the thalamus normally acts as a filter for sensory input; in central sensitization, this filtering is impaired
• Neuroinflammation — microglial activation in the dorsal horn and brain can amplify nociceptive signaling

Neuroimaging studies in SSD patients have identified consistent patterns of altered activation in the insula (interoceptive processing), anterior cingulate cortex (emotional salience and pain evaluation), and somatosensory cortex. These are measurable, reproducible findings — not artifacts.

The Symptom Is Real

This point is clinically and ethically critical. SSD is not "all in your head" in the dismissive sense that phrase is used. The distress is genuine, the dysfunction is genuine, the neurobiological alterations are genuine, and the interaction between mind and body is a feature of normal human physiology operating under extraordinary pressure. Patients with SSD have often been told their symptoms are fabricated or that there is "nothing wrong" — this framing is inaccurate, harmful, and predictive of poor treatment engagement. Accurate psychoeducation acknowledges the reality of the symptom experience while introducing the neuroscience of amplification.

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4. Functional Neurological Disorder Overlap

Functional Neurological Disorder (FND), formerly called conversion disorder, involves neurological symptoms that are not accounted for by structural neurological disease and are associated with positive neurological signs on examination. Common FND presentations include:

• Non-epileptic seizures (functional seizures, previously called psychogenic non-epileptic seizures or PNES)
• Functional weakness or paralysis (often with positive Hoover sign — hip extension returns when attention is distracted)
• Functional tremor (shows entrainment — changes frequency to match an externally imposed rhythm)
• Functional sensory loss and functional vision changes
• Functional gait disturbance

FND and SSD share overlapping mechanisms. Both involve predictive processing errors — the brain generates strong top-down predictions about bodily state that override or distort bottom-up sensory signals. Both involve altered interoception — the perception of signals arising from within the body. Research by neurologist Jon Stone (University of Edinburgh) and the FND Action network has transformed the understanding of FND from a diagnosis of exclusion to a diagnosis with its own positive clinical findings and its own neuroscience.

FND and SSD frequently co-occur in the same individual. A patient may have functional seizures (FND) alongside chronic abdominal pain and health anxiety (SSD). Treatment for FND typically includes:

• Physiotherapy — movement retraining targeting the dysfunctional movement pattern, not the underlying "psychological cause"
• CBT adapted for FND, addressing the beliefs and behaviors that maintain symptoms
• Psychoeducation about the mechanism — explaining the software versus hardware analogy (the brain's programming is disrupted, not the hardware/structure)
• Multidisciplinary coordination between neurology, psychiatry, physiotherapy, and psychology

Patients with FND report significant diagnostic delays (average 7 years in some surveys) and profound invalidation from healthcare providers. Patient-facing resources such as FND Hope and Jon Stone's neurosymptoms.org provide accessible, accurate psychoeducation.

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5. Causes and Risk Factors

SSD arises from the interaction of biological vulnerability, psychological factors, and social context. No single cause is sufficient or necessary, and the model is biopsychosocial rather than reductively psychological.

Biological Factors

• Sex — SSD is approximately twice as common in women (2:1 female-to-male ratio), consistent across cultures and study designs; this likely reflects both hormonal influences on pain processing and social factors in symptom expression
• Genetic predisposition — twin studies estimate heritability of somatic symptom severity at approximately 30–40%; specific genes are not yet characterized but may involve serotonin transporter, HPA axis regulation, and inflammatory pathways
• Autonomic nervous system dysregulation — altered heart rate variability, reduced baroreflex sensitivity, and sympathetic hyperactivation are common findings

Psychological Factors

• Adverse Childhood Experiences (ACEs) — one of the strongest and most consistently replicated risk factors; sexual abuse and emotional neglect are particularly strongly associated with adult SSD; ACEs alter HPA axis development and inflammatory set-points
• Alexithymia — difficulty identifying and describing emotional states; when emotions cannot be processed in the usual ways, they may be expressed through the body (somatization in the psychoanalytic sense); alexithymia predicts poor response to insight-oriented therapies
• Anxiety and depression — comorbidity rates of 30–60%; anxiety amplifies interoceptive attention and catastrophic interpretation of body signals; depression reduces descending inhibitory pain pathways
• Childhood illness modeling — growing up with an ill parent or experiencing significant childhood illness oneself can establish illness as an organizing framework for distress

Social Factors

• Low socioeconomic status — increases chronic stress load and reduces access to mental healthcare
• Medical trauma and iatrogenic harm — invasive procedures, poorly communicated diagnoses, and dismissive medical encounters contribute to ongoing symptom amplification
• The diagnostic odyssey — years of undiagnosed symptoms and repeated medical testing can paradoxically reinforce somatic vigilance and illness identity
• Secondary gain — not fabrication, but the real social consequences of illness (disability benefits, reduced demands, increased care from others) can inadvertently maintain symptoms in some cases

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6. Symptoms, Presentations, and Subtypes

Common Somatic Symptom Domains

Pain is the most common presenting symptom cluster in SSD and includes:

• Headache (tension-type, migraine-pattern, or diffuse)
• Back and neck pain (often without structural correlate on imaging)
• Abdominal and pelvic pain
• Diffuse musculoskeletal pain (overlap with fibromyalgia)
• Chest pain (often evaluated extensively for cardiac causes before SSD is considered)

Fatigue is nearly universal in SSD — chronic, not relieved by rest, often described as bone-deep exhaustion that makes normal activities feel impossible. Overlap with chronic fatigue syndrome (myalgic encephalomyelitis) is substantial.

Gastrointestinal symptoms — nausea, bloating, alternating constipation and diarrhea, early satiety — overlap substantially with irritable bowel syndrome (IBS), which shares central sensitization mechanisms with SSD.

Neurological symptoms — dizziness, vertigo, cognitive difficulties ("brain fog"), non-epileptic spells, weakness, and sensory disturbances — shade into FND territory and are among the most frightening presentations for patients.

Cardiovascular symptoms — palpitations, chest tightness, dyspnea — are among the most common drivers of emergency department visits and extensive cardiac workups.

The Behavioral Dimension: Health Anxiety

In SSD with prominent health anxiety, the behavioral consequences of symptom preoccupation are as disabling as the symptoms themselves:

• Reassurance-seeking — repeated visits to doctors, ER, or urgent care; multiple specialist opinions; requesting repeated tests. Paradoxically, reassurance provides only brief relief before anxiety returns, driving further reassurance-seeking in a self-maintaining cycle.
• Body checking — repeated self-examination (palpating for lumps, checking skin changes, monitoring heart rate)
• Internet symptom-checking — the "Dr. Google spiral" in which each searched symptom generates a new list of serious diagnoses to worry about
• Avoidance — restricting activities out of fear they will worsen symptoms or trigger a medical crisis; can lead to profound deconditioning that reinforces fatigue and pain
• Provider-shopping — seeking a new doctor who will find the "real" medical explanation; this creates fragmented care and increases the risk of unnecessary interventions

These behaviors are not manipulative or consciously chosen — they are understandable responses to frightening, unexplained physical experiences. Effective treatment acknowledges this while gently introducing the concept that these behaviors maintain rather than resolve the cycle.

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7. Assessment and Diagnosis

Validated Screening Tools

The PHQ-15 (Patient Health Questionnaire-15) is the most widely used brief measure of somatic symptom burden. It assesses 15 common somatic symptoms (stomach pain, back pain, pain in arms/legs/joints, headaches, chest pain, dizziness, fainting spells, palpitations, shortness of breath, pain during sex, constipation/diarrhea, nausea/gas/indigestion, fatigue, sleep problems, and feeling weak). Scoring: 0–4 minimal, 5–9 low, 10–14 medium, 15–30 high somatic symptom burden.

The PHQ-9 and GAD-7 assess comorbid depression and generalized anxiety, which are present in 30–60% of SSD patients and require parallel treatment.

The Whiteley Index (WI) measures health anxiety, including disease conviction, bodily preoccupation, and disease phobia. Useful for characterizing the IAD spectrum.

Medical Workup Principles

A focused, thoughtful medical workup is appropriate — the goal is to rule out conditions that genuinely require medical treatment, not to exhaustively exclude every remote possibility. Standard considerations include:

• Thyroid function (TSH, free T4) — hypothyroidism and hyperthyroidism both cause somatic symptoms
• Complete blood count, metabolic panel, inflammatory markers (ESR, CRP)
• Autoimmune screening (ANA, rheumatoid factor) if symptom pattern suggests
• Neurological examination; neuroimaging if clinically indicated by focal neurological findings
• Gastrointestinal evaluation proportionate to symptom severity

A critical principle: avoid over-testing. Each negative test provides only brief reassurance in SSD — within days or weeks, doubt returns and may drive demands for further testing. Repeated normal tests can paradoxically deepen the conviction that "something must be wrong that they haven't found yet." The goal is to complete a reasonable workup, communicate results clearly, and transition from a purely diagnostic frame to a management frame.

Communicating the Diagnosis

The way SSD is explained to patients significantly affects treatment engagement. Helpful framing:

• Acknowledge that the symptoms are real, distressing, and disabling — never use the phrase "there's nothing wrong"
• Explain the neuroscience of central sensitization in accessible language ("the volume dial for pain signals in your nervous system is turned up too high")
• Avoid any framing that implies the patient is inventing or exaggerating symptoms
• Present the mind-body connection as normal biology, not a character flaw
• Frame treatment as addressing the whole person, not as psychiatric dismissal

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8. Treatment: CBT and ACT Evidence

Cognitive Behavioral Therapy (CBT)

CBT is the most extensively studied psychological treatment for SSD and its predecessor diagnoses. It targets three interlocking domains:

1. Cognitive targets — catastrophic interpretation of symptoms ("this pain means something serious is wrong"), health anxiety cognitions, selective attention to body signals, and negative illness representations
2. Behavioral targets — safety behaviors such as reassurance-seeking, avoidance, body checking, and excessive rest; graded activity scheduling to counter deconditioning; behavioral activation
3. Physiological targets — diaphragmatic breathing, progressive muscle relaxation, and techniques to down-regulate autonomic hyperactivation

A course of CBT for SSD typically involves 10–20 individual sessions, though shorter formats (6–8 sessions) have also shown benefit. Meta-analytic reviews report effect sizes of d = 0.6–0.8 versus usual care for somatic symptom reduction, with additional benefits for anxiety, depression, and functional impairment. Gains are generally maintained at 12-month follow-up.

An important goal clarification for patients entering CBT: the aim is not symptom elimination but rather reducing the degree to which symptoms interfere with life. Symptom improvement often occurs as a secondary result of changing the relationship with symptoms — but when patients enter CBT expecting the therapist to "cure" their pain, early treatment dropout is common.

Acceptance and Commitment Therapy (ACT)

ACT represents a distinct approach that does not target symptom reduction as the primary goal. Instead, ACT focuses on:

• Psychological flexibility — the ability to maintain contact with difficult thoughts and feelings without being controlled by them
• Acceptance — allowing symptoms to exist without fighting them or letting them define the person
• Values clarification — identifying what matters most and pursuing that life despite symptoms
• Defusion — changing one's relationship to catastrophic thoughts rather than trying to change their content

Multiple RCTs have demonstrated ACT equivalent or superior to CBT for chronic pain with somatic symptom comorbidity. ACT is particularly well-suited for patients who have already undergone CBT without full benefit, or those who are resistant to the idea of "thinking differently" about their symptoms.

Mindfulness-Based Stress Reduction (MBSR)

MBSR (Jon Kabat-Zinn's 8-week standardized program) has demonstrated significant reductions in somatic symptom distress, health anxiety, and catastrophizing in multiple controlled trials. Mechanistically, MBSR appears to reduce hyperactivation of the default mode network (involved in rumination and self-focused worry) and improve interoceptive awareness without amplifying symptom focus. It also reduces healthcare utilization — an important outcome for systems-level planning.

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9. Pharmacotherapy and Integrative Approaches

Antidepressants

Serotonin-norepinephrine reuptake inhibitors (SNRIs) — duloxetine (Cymbalta) and venlafaxine (Effexor) — are the preferred pharmacological first line for SSD with significant somatic symptom burden. Their dual-mechanism action is relevant:

• The noradrenergic component activates descending inhibitory pain pathways from the locus coeruleus, directly reducing central sensitization
• The serotonergic component treats comorbid anxiety and depression, indirectly reducing somatic amplification
• Duloxetine (60–120mg/day) has the strongest evidence base for pain in the context of somatic disorders, with FDA approval for fibromyalgia and diabetic neuropathy that extends mechanistically to SSD

Low-dose tricyclic antidepressants (TCAs) — amitriptyline (10–75mg at bedtime) or nortriptyline — are useful for pain-predominant SSD, especially when sleep disturbance and headache are prominent. Side effects (sedation, dry mouth, constipation, cardiac conduction effects) limit use in higher doses and in older adults.

SSRIs are preferred when the clinical picture is dominated by anxiety, OCD-like health preoccupation, or depression with minimal pain component. They have less direct analgesic effect than SNRIs.

Pregabalin and gabapentin — alpha-2-delta calcium channel ligands — reduce central sensitization at the spinal and supraspinal level. Used for pain-predominant SSD, especially when neurological symptoms are present. Risk of dependence and cognitive side effects warrants careful monitoring.

Integrative Approaches

• Regular aerobic exercise — one of the most consistently beneficial non-pharmacological interventions. Exercise activates descending inhibitory pathways (endogenous opioid and serotonin systems), reduces inflammatory markers, and improves mood. Graded exercise is essential — starting gently to avoid post-exertional worsening and building tolerance progressively.
• Diaphragmatic breathing — activates the parasympathetic nervous system, reduces sympathetic hyperactivation, and provides a patient-controlled tool for acute symptom management
• Physical therapy — addresses deconditioning, improves body confidence, and provides graded exposure to feared movements
• Magnesium supplementation — some evidence for benefit in tension headache, chronic pain, and anxiety; well-tolerated; see Magnesium
• Sleep hygiene — restorative sleep is both a treatment target and a treatment tool; poor sleep amplifies central sensitization and reduces pain tolerance

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10. Healthcare Navigation and Working with Providers

The Diagnostic Odyssey

The average time from first symptom onset to SSD diagnosis is 4–6 years in most studies, and substantially longer when FND is involved. During this time, patients typically see multiple specialists, undergo extensive testing, and receive contradictory explanations. This experience is:

• Financially costly — repeated specialist visits, procedures, and diagnostic tests
• Physically risky — each unnecessary investigation carries its own risk (contrast nephropathy, procedural complications, incidental findings that trigger further investigation)
• Psychologically harmful — repeated dismissal, the message that "we can't find anything wrong," and provider frustration all compound the patient's distress and erode trust

Validated Communication Approaches

Providers working with SSD patients can improve engagement significantly by using validated communication frameworks. A useful template: "Your symptoms are real and they are genuinely distressing. Research shows that when the nervous system is under sustained pressure, the way it processes signals from the body can become amplified — this is a change in the nervous system's software, not a sign that you are imagining things or that there is nothing wrong. We want to work with you on approaches that address that amplification."

Key principles:

• Never say "there is nothing wrong" — instead, explain what you have found and what your working explanation is
• Validate distress before introducing the psychological model
• Use the word "functional" (as in "functional pain") as a neutral medical term, and explain what it means
• Schedule regular, brief follow-up appointments (not as-needed) — proactive scheduling reduces crisis-driven over-utilization and communicates that the provider is committed to the patient

Collaborative Care Models

The most effective healthcare delivery model for SSD is collaborative care — embedding mental health professionals (psychologists, social workers, psychiatry consultants) within primary care settings rather than relying on standalone psychiatry referrals. Key advantages:

• Reduces stigma of psychiatric referral ("I'm being sent away to the crazy doctor")
• Enables close coordination between medical and psychological providers
• Provides brief psychological interventions at the point of care
• Studies show collaborative care significantly reduces somatic symptom burden and healthcare costs versus referral-only models

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11. Recovery and Prognosis

SSD is a chronic condition for many patients, but the prognosis with appropriate treatment is substantially better than is often assumed. Key findings:

• Remission rates of 30–50% are reported in CBT trials, with "remission" defined as a clinically meaningful reduction in somatic symptom burden and functional impairment
• Many patients who do not achieve full remission achieve significant functional improvement — returning to work, social engagement, and valued activities despite ongoing symptoms
• The illness course is typically fluctuating rather than steadily progressive; acute exacerbations often correspond to identifiable stressors

Predictors of Better Outcome

• Earlier treatment — longer duration without treatment is associated with more entrenched symptom patterns and illness identity
• Lower ACE burden
• Absence of comorbid personality disorder
• Engagement with psychological treatment model — patients who can accept a biopsychosocial explanation show better outcomes
• Absence of litigation or active disability claims (not because patients are malingering, but because legal processes maintain illness-focused attention)

Predictors of Poorer Outcome

• Untreated comorbid depression or anxiety
• High ACE burden, particularly sexual abuse history
• Exclusively medicalized view of the condition — strong conviction that a biological explanation will be found and "fix" the symptoms
• Long duration before appropriate treatment begins
• Social isolation — peer support and connection substantially buffer symptom severity

Peer Support and Community

Patient communities and peer support normalize the SSD/FND experience in ways that professional treatment alone cannot. Organizations such as FND Hope, IBS patient networks, and chronic pain communities provide lived-experience perspectives, practical coping strategies, and the profound relief of being believed. Peer support does not replace professional treatment but significantly enhances engagement and sustained recovery.

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12. Key Research Papers

1. Dimsdale JE, et al. Somatic symptom disorder: an important change in DSM. J Psychosom Res. 2013;75(3):223-228. PMID: 23972410
2. Creed F, Barsky A. A systematic review of the epidemiology of somatisation disorder and hypochondriasis. J Psychosom Res. 2004;56(4):391-408. PMID: 15094025
3. Allen LA, et al. Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom. 2002;71(5):255-262. PMID: 12203140
4. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom Med. 2007;69(9):881-888. PMID: 18040099
5. van Dessel N, et al. Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults. Cochrane Database Syst Rev. 2014;(11):CD011142. PMID: 25362239
6. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2-15. PMID: 20961685
7. Fink P, et al. Two functional somatic syndromes. Psychosom Med. 2007;69(4):292-297. PMID: 17470560
8. Brown RJ. Multiple care of functional somatic symptoms. Psychosom Med. 2004;66(4):611-618. PMID: 15272108
9. Barsky AJ, et al. Hypochondriasis and somatosensory amplification. Br J Psychiatry. 1990;157:404-409. PMID: 2261058
10. Haller H, et al. Mindfulness-based interventions for women with breast cancer: an updated systematic review and meta-analysis. Acta Oncol. 2017;56(12):1665-1676. PMID: 29124993
11. Stone J, et al. Functional neurological disorder: the diagnosis is now well established. Pract Neurol. 2020;20(1):3-5. PMID: 31843814

PubMed Topic Searches

• Somatic symptom disorder DSM-5
• Somatoform disorder CBT treatment
• Central sensitization somatic symptoms
• Illness anxiety disorder hypochondriasis
• Functional neurological disorder conversion
• Somatic symptom disorder acceptance commitment therapy

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Connections

• Anxiety
• Depression
• PTSD
• OCD
• Eating Disorders
• Insomnia
• Chronic Pain
• Fibromyalgia
• Stress Management
• Breathwork
• Magnesium
• Burnout
• Fatigue
• Conversion Disorder (FND)
• Dissociative Identity Disorder

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