Somatic Symptom Disorder — Viva

Q1: First principles — the DSM-5-TR cluster and the conceptual revolution (3 min)

Examiner: DSM-5 substantially restructured the somatoform disorders. Take me through the new cluster, and tell me why the change matters clinically.

Expected answer:

• The DSM-5-TR cluster is Somatic Symptom and Related Disorders, comprising: Somatic Symptom Disorder (SSD), Illness Anxiety Disorder (IAD), Conversion / Functional Neurological Symptom Disorder (FND), Psychological Factors Affecting Medical Condition (PFAMC), Factitious Disorder, plus Other Specified and Unspecified categories. Malingering is NOT a mental disorder — it is a behaviour motivated by external gain.
• The pivotal conceptual change is that DSM-5 dropped the requirement that symptoms be 'medically unexplained.' DSM-IV somatoform disorders required absence of medical disease; DSM-5-TR defines the disorder by the positive B-criterion — the maladaptive cognitive-affective-behavioural response.
• Why it matters clinically: (a) theoretically sound — you cannot prove a negative; (b) reframes the disorder from exclusion to positive diagnosis; (c) reduces the impulse to chase ever-more tests to prove absence of disease; (d) allows SSD to be diagnosed in a patient WITH active medical disease (e.g. stable IHD with disproportionate concern). The disorder is about the response, not the absence.
• ICD-11 uses the equivalent term Bodily Distress Disorder (BDD), and the Lancet 2024 review by Löwe advocates the broader term persistent physical symptoms.

Follow-up: Define each member in one line. SSD: somatic symptoms + excessive thoughts/feelings/behaviours, 6+ months. IAD: preoccupation with having/acquiring serious illness; symptoms absent/mild; 6+ months. Conversion/FND: motor/sensory symptom incompatible with disease; not consciously produced. PFAMC: psychological factors worsen a diagnosed medical condition. Factitious: falsification/induction with intent to deceive; internal motive (sick role). Malingering: feigning for external gain.

Q2: Differentiating the cluster — the deception axis and the FND signs (3 min)

Examiner: A 26-year-old presents with right-leg paralysis and midline-split sensory loss. The MRI is normal. How do you tell conversion from factitious disorder from malingering, and what clinical signs support a positive FND diagnosis?

Expected answer:

• The cardinal discriminator is conscious production. In conversion/FND, symptoms are not consciously produced — the patient genuinely experiences the deficit. In factitious disorder, symptoms are consciously falsified or induced; the motive is internal (assumption of the sick role; no external reward). In malingering, symptoms are consciously feigned for external incentive (money, drugs, leave, avoiding prosecution); malingering is NOT a mental disorder.
• Positive FND signs (not just exclusion): Hoover sign (hip extension in the 'weak' leg returns when testing contralateral hip flexion — the complementary limb movement); collapse/give-way weakness on initial testing that becomes strong with sustained effort; tremor entrainment (functional tremor entrains to the rhythm of contralateral repetitive tapping); midline-split sensory loss that does not respect dermatomes; tubular/tunnel vision (concentric, physiologically impossible in organic disease); functional gait (knee-buckling without falls); abductor sign.
• La Belle Indifférence — the apparent lack of distress about a severe deficit described by Charcot — is present in only ~30% of cases and is neither universal nor diagnostic.
• The diagnosis is now made positively by an FND-trained neurologist using these signs, not by exclusion alone.

Follow-up: How would you investigate suspected dissociative (non-epileptic) seizures? Capture an event on video-EEG monitoring — the absence of epileptiform activity during a typical event is diagnostic. Prolactin rises transiently after a generalised tonic-clonic epileptic seizure but not after a dissociative seizure (a supportive but imperfect discriminator). The PNES phenotype — eyes closed, asynchronous out-of-phase thrashing, pelvic thrusting, side-to-side head, recall, no postictal confusion — distinguishes from epileptic seizures.

Q3: Pathophysiology and formulation — the vicious cycle (3 min)

Examiner: A colleague dismisses a patient with SSD as 'all in her head.' Correct them, and walk me through the pathophysiology.

Expected answer:

• Correct the framing: SSD is a recognised neuropsychiatric disorder with measurable neurobiology — not 'all in the head.' The symptoms are real, the distress is real, and the disorder is treatable. Stigma damages care.
• The cognitive-behavioural model (Salkovskis/Warwick): bodily sensation → catastrophic misinterpretation ('this twinge is a heart attack') → anxiety → autonomic arousal → amplifies the sensation (palpitations, sweating, hyperventilation generate more symptoms) → safety behaviours (checking, reassurance-seeking, internet, avoidance) → reduce anxiety only transiently and reinforce the illness belief → the cycle tightens.
• The neurobiology: functional MRI shows hyperactivity of the anterior insula and anterior cingulate cortex — the brain's interoceptive (body-state mapping) and salience networks. Normal sensations are detected and amplified — the somatic spotlight. Somatosensory amplification is the perceptual correlate: the patient genuinely experiences the signal as louder.
• The 3 Ps formulation: Predisposing (childhood adversity, alexithymia, family modelling, genetic loading) → Precipitating (life stressor, illness, health scare) → Perpetuating (iatrogenic reinforcement from unnecessary tests, avoidance, secondary gain, comorbid mood/anxiety, substance use).
• For conversion/FND, modern models emphasise functional disconnection between motor-programming and conscious-awareness circuits, with a top-down Bayesian inference failure (the brain predicts the deficit and enacts it).

Follow-up: Why does each normal investigation make things worse? The normal result provides transient reassurance that fades, and reinforces the belief that the next test might find something — locking the cycle tighter and increasing healthcare utilisation. This is why structured SSD care explicitly limits reassurance-driven testing.

Q4: Management — the evidence ladder (3 min)

Examiner: Take me through your management of a patient with established SSD — drug, dose, therapy, follow-up structure, and what to avoid.

Expected answer:

• Universal principles (the VALIDATE mnemonic): Validate symptoms (real, not dismissed); therapeutic Alliance (consistent clinician); Limit repeated unnecessary tests; Integrated single medical home; Diary scheduled visits every 2 to 4 weeks regardless of symptoms; Aim for function not disease-finding; Treat comorbidity (depression, anxiety); Empower the patient with a shared model.
• First-line psychological: CBT, 8 to 16 sessions — strongest evidence base; restructures catastrophic cognitions, reduces safety behaviours, graded return to activity, attention retraining. Specialist alternatives: psychodynamic interpersonal therapy, ACT, MBCT.
• Pharmacological: SSRI first-line — sertraline (start 25 to 50 mg, titrate slowly to 100 to 200 mg), citalopram, escitalopram, paroxetine. Start LOW, titrate SLOWLY, expect 6 to 8 weeks for effect, pre-warn about side effects to prevent misinterpretation as new disease. SSRIs work even without comorbid depression (independent analgesic/interoceptive effects). SNRI (duloxetine, venlafaxine) for pain-predominant SSD; TCA (amitriptyline 10 to 25 mg nocte) for chronic pain overlap.
• FND-specific pathway: positive diagnosis by neurology → specialist FND physiotherapy (motor retraining) → CBT → treat comorbidity → graded return to function.
• AVOID: opioids (dependence, hyperalgesia, overdose), long-term benzodiazepines (dependence), repeated unnecessary investigations, multiple specialists, polypharmacy in the elderly.
• Stepped care: Step 1 (primary care self-help + scheduled reviews) → Step 2 (group/individual CBT) → Step 3 (specialist CBT + SSRI + MDT) → Step 4 (combined MDT / pain programme / inpatient for severe functional decline).

Follow-up: How do you frame the consultation when no disease is found? (1) Acknowledge and validate ('your symptoms are real'). (2) Give a positive diagnostic label ('this is functional neurological disorder'). (3) Explain with a shared model ('your nervous system is a faulty alarm — the signal is real, the wiring needs retraining'). (4) Set collaborative functional goals. Resist the impulse to order 'one more test.'

Q5: The acutely changing patient and the law — pitfalls and culture (3 min)

Examiner: A 65-year-old man with known SSD and stable ischaemic heart disease phones with new central chest pain for 40 minutes, diaphoresis, and breathlessness. The GP wants to reassure him at home. What do you do, and why? Then tell me how Indian law and culture intersect with SSD care.

Expected answer:

• Send him in for serial ECG and troponin to exclude acute coronary syndrome. The label of SSD confers no protection against genuine acute illness — this patient has the same lifetime risk of acute MI as anyone else. The single most dangerous pitfall in SSD is missing genuine new organic disease by assuming a symptom is functional. The rule: an acute change in a known SSD patient ALWAYS warrants genuine medical reassessment — vital signs, focused examination, clinically-indicated tests.
• Once ACS is excluded, return to the SSD pathway — but the medical emergency is worked up first. Document the reasoning explicitly.
• Indian law — Mental Healthcare Act 2017: protects the rights of patients with mental illness including SSD. Capacity and consent are decision-specific and time-specific; capacity must be formally assessed (understand, retain, use, weigh, communicate). A patient who lacks capacity for a specific decision may be treated in their best interest; the Act is rights-based and decouples care from coercion. Attempted suicide is decriminalised and presumed to be under severe stress — relevant when comorbid depression raises suicide risk.
• Indian cultural context: Dhat syndrome (semen-loss anxiety, ICD-10 F48.0) is a common idiom of distress in young men; treated with combined sex education, SSRI where depression comorbid, CBT, and family counselling. Use a cultural formulation interview; involve family and culturally-concordant services; avoid pathologising normal cultural expressions of distress. NIMHANS protocols and ICMR/IPS guidance inform culturally-adapted CBT for SSD in India.

Follow-up: How do you manage dissociative (non-epileptic) seizures in the emergency department? ABCDE first; ensure airway safety; place in recovery position; do NOT routinely give IV benzodiazepines (risk of respiratory depression, reinforces illness behaviour, masks the diagnosis). Most episodes self-terminate within minutes. Reassure calmly, reduce stimulation (bystanders, lights, noise). Then arrange specialist FND pathway care. Resist the impulse to load antiepileptic drugs — there is no epilepsy to treat.