Clinical Analysis: Ms. Palaniyamal, 47F

ECG Interpretation

• T-wave inversions/flattening visible in V1–V4 (anterior distribution)
• The machine flags "ST & T wave abnormality, consider anterior ischemia"
• QTc 462 ms — borderline prolonged (cutoff for females is 450–460 ms)
• No LBBB, no STEMI pattern

Critical Clinical Concern: This is NOT a straightforward Conversion Disorder episode

Differential Diagnosis

• Cardiac syncope from arrhythmia or ischemia can cause anoxic convulsions with bilateral limb stiffness — mimicking a seizure or conversion episode
• Anterior ST-T changes suggest possible LAD territory ischemia/demand ischemia
• QTc 462 ms: borderline prolonged QTc can predispose to Torsades de Pointes → syncope → convulsive movements
• No eye rolling and no mouth deviation actually favor cardiac/anoxic syncope over true epilepsy

• Bilateral tonic stiffness can be tonic seizure (frontal lobe, tonic-clonic tonic phase)
• However, absence of eye rolling and post-ictal features would be unusual
• 5 prior episodes — needs EEG review

• Prior label of conversion disorder does NOT preclude a new organic cause
• Absence of eye deviation and mouth deviation does point toward functional, but cardiac cause must be ruled out first
• Harrison's (p. 714): "patients with psychiatric disorders rarely have hemodynamic changes concurrent with these episodes" — but this ECG shows objective cardiac abnormality

• Can cause tetany (bilateral stiffness), LOC, prolonged QT
• Must check electrolytes

Immediate Workup Required

1. Troponin I/T (high sensitivity) — now and repeat at 3 hours → rule out NSTEMI/demand ischemia
2. Serum electrolytes — Ca²⁺, Mg²⁺, K⁺, Na⁺ (hypocalcemia causes tetany + QT prolongation)
3. Blood glucose — hypoglycemia causes LOC + stiffness
4. 12-lead ECG serial — compare with any prior ECGs
5. Echo — wall motion abnormality if troponin rises

• EEG (if cardiac/metabolic causes ruled out)
• Neuroimaging (MRI brain) if new neurological signs
• Holter/prolonged cardiac monitoring — arrhythmia during episodes

Key Management Points

• Do NOT simply reassure as conversion disorder given the ECG abnormality
• Admit for cardiac monitoring given anterior ST-T changes and borderline QTc
• Avoid QT-prolonging drugs (avoid haloperidol, certain antiemetics) given QTc 462 ms
• If troponin rises → cardiology consult, ACS protocol
• If electrolytes abnormal (especially ↓Ca²⁺) → correct and observe for resolution of symptoms
• If all cardiac/metabolic workup negative → neurology review, EEG, reconsider functional neurological disorder diagnosis

Bottom Line

The anterior ST-T changes on this ECG in a patient presenting with LOC and bilateral limb stiffness must be taken seriously. Cardiac syncope with anoxic convulsions (from arrhythmia, ischemia, or QTc-related arrhythmia) is a life-threatening cause that must be excluded before this is labelled a conversion episode. The prior diagnosis of conversion disorder can create anchoring bias — this ECG warrants urgent troponin, electrolytes, and continuous cardiac monitoring.

Medication Review in Context

The Compounding Problem: Double QT Prolongation

• Escitalopram 20mg (higher dose — FDA dose-dependent QT warning)
• Clomipramine (TCA — direct cardiac sodium/potassium channel blockade)

Reinterpreting the ECG

Clinical Correlation: Drug Effect + LOC Episodes

• Lowered seizure threshold → lowers the threshold for convulsive episodes (both epileptic and functional)
• Orthostatic hypotension → syncope with secondary convulsive movements
• QTc prolongation → risk of Torsades de Pointes → LOC + stiffness

• At this dose, QT prolongation is clinically significant
• Combined with clomipramine — additive risk for arrhythmia

Revised Priority Workup

1. Troponin — still needed to exclude true ACS, but lower pre-test probability now
2. Serum electrolytes — K⁺, Ca²⁺, Mg²⁺ (hypokalemia + hypomagnesemia worsen drug-induced QTc prolongation significantly)
3. Drug levels if available (clomipramine/nortriptyline levels)
4. EEG — clomipramine lowers seizure threshold; rule out epileptiform activity
5. Holter monitor — capture arrhythmia during episodes

Immediate Management Recommendations

1. Do not add any further QT-prolonging drug — avoid metoclopramide, haloperidol, ondansetron, azithromycin
2. Discuss with psychiatrist — consider:
   • Reducing or switching escitalopram (escitalopram has the highest QT risk among SSRIs)
   • Clomipramine dose review — even at 10mg, the combination is concerning
3. Correct electrolytes aggressively if K⁺ <4.0 or Mg²⁺ low
4. Continuous cardiac monitoring during admission given QTc 462 ms on dual QT-prolonging agents
5. Propranolol (Betacap) — interestingly, beta-blockers are actually used to treat congenital long QT syndrome, so this is not contributing to QTc prolongation; however watch for bradycardia

Bottom Line

The anterior ST-T changes and QTc 462 ms are most likely drug-induced — escitalopram 20mg + clomipramine is a well-recognized QT-prolonging combination. More critically, clomipramine lowers seizure threshold and can cause orthostatic syncope, both of which may be contributing to her recurrent LOC episodes. The prior "conversion disorder" label needs reassessment — these episodes may be drug-facilitated rather than purely functional. Psychiatry review for medication rationalization is essential.

Revised Clinical Synthesis

What We Now Know

Working Diagnosis: Drug-Facilitated Functional/Convulsive Episodes

• Lowers seizure threshold dose-dependently
• Causes orthostatic hypotension → syncope → anoxic convulsions (bilateral stiffness without eye rolling — classic anoxic posturing)
• Directly responsible for ST-T changes and QTc prolongation on this ECG

• Additive QTc prolongation
• At 20mg, FDA recommends caution specifically due to cardiac effects

The Episode Explained

Clomipramine → ↓seizure threshold + orthostatic hypotension
                        ↓
              Syncope / cerebral hypoperfusion
                        ↓
         Bilateral tonic stiffening (anoxic convulsion)
         — No eye rolling
         — No mouth deviation
         — No post-ictal confusion (likely brief)
                        ↓
              Labelled "conversion disorder"
              (5 similar episodes = pattern)

Pending — Still Recommended

Management Plan

• Continuous cardiac monitoring (QTc 462 ms on dual QT drugs)
• Check and aggressively correct K⁺ ≥4.0 mmol/L and Mg²⁺ ≥0.8 mmol/L
• Avoid all QT-prolonging co-medications

• Escitalopram — consider switching to sertraline or fluoxetine (lower QT risk among SSRIs)
• Clomipramine — review necessity; if needed for OCD/depression, consider switching to a safer TCA or alternative
• Propranolol — continue (not contributing to QTc; may actually be mildly protective)

• Formal reconsideration of the "conversion disorder" diagnosis
• EEG to exclude subclinical epileptiform activity (drug-lowered threshold)
• If EEG normal + orthostatic hypotension confirmed → episodes are convulsive syncope, not conversion disorder

Bottom Line

Negative troponin and normal bloods make this a drug-induced problem. Clomipramine + escitalopram together are causing QTc prolongation, lowering the seizure threshold, and likely causing orthostatic syncope with anoxic bilateral stiffening. These episodes have probably been misattributed to conversion disorder for years. Psychiatric medication review is the single most important intervention here, alongside an EEG and orthostatic BP measurement.