An 80-year-old hospitalised man develops acute confusion, visual hallucinations, sleep-wake cycle reversal, and fluctuating attention 2 days post-hip replacement. He has no prior cognitive complaints. EEG shows diffuse slowing. What EEG finding, when present, most specifically differentiates delirium tremens from other causes of delirium?
- A Diffuse theta/delta slowing
- B Low-voltage fast activity (beta enhancement) with absence of the expected slow waves ✓
- C Triphasic waves
- D Periodic sharp-wave complexes (1–2 Hz)
Explanation
Delirium tremens (DTs — alcohol withdrawal delirium) is characterised by EEG low-voltage fast activity (beta enhancement, alpha acceleration) due to GABA receptor downregulation and NMDA receptor upregulation — essentially CNS hyperexcitability. This contrasts with metabolic/toxic deliria (liver failure, drugs, sepsis) that show diffuse theta/delta slowing or triphasic waves. Triphasic waves are classically associated with hepatic encephalopathy. Periodic sharp-wave complexes (1–2 Hz) are characteristic of Creutzfeldt-Jakob disease. Recognising DTs' EEG pattern has direct management implications (benzodiazepines, not antipsychotics, are the treatment of choice).
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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Written and medically reviewed by the StethoPrep medical team.