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Inhibitor-Free Variant of the Cheung Regimen: Successful Adjunctive Therapy in Long-Standing Hypochondriasis With Prominent Somatic Features

Ngo Cheung

Cureus March 17, 2026 DOI: 10.7759/cureus.105367 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Case study Case report Peer reviewed
Sample size 1
Population 34-year-old woman with hypochondriacal obsessive-compulsive disorder and a two-year history of recurrent fear of serious gastrointestinal and cardiac disease
Interventions Dextromethorphan Piracetam
Dose dextromethorphan 30 mg once daily, piracetam 600 mg once daily
Duration Three weeks (time to reported response)
Key findings Adding dextromethorphan 30 mg once daily and piracetam 600 mg once daily to existing medication was followed within three weeks by the disappearance of nocturnal anxiety, cessation of gastrointestinal preoccupations, and mood normalisation, with only mild sleep disruption. The authors propose that low-dose dextromethorphan (NMDA antagonism) plus piracetam (AMPA potentiation) may produce enough neuroplastic change to quiet refractory hypochondriacal OCD even without CYP2D6 inhibition, but caution that ongoing medications, recent regimen changes, and the lack of CYP2D6 genotyping or structured OCD ratings confound the observation.

Abstract

Hypochondriacal obsessive-compulsive disorder (OCD) combines intrusive health anxieties with compulsive reassurance seeking and often resists high-dose selective serotonin reuptake inhibitors and cognitive-behavioural therapy. Interest has shifted toward glutamatergic agents that mimic ketamine's rapid synaptic effects. A 34-year-old woman endured two years of recurrent fear of serious gastrointestinal and cardiac disease. Escitalopram, later switched to fluoxetine, plus intermittent low-dose atypical antipsychotics and benzodiazepines, produced only partial relief. No psychotic features emerged, yet nightly rumination and repeated medical visits persisted. She agreed to add dextromethorphan 30 mg once daily together with piracetam 600 mg once daily. She declined a cytochrome P450 2D6 (CYP2D6)-inhibiting antidepressant, so no pharmacokinetic booster was used. The combination represents a pared-down variant of the Cheung glutamatergic regimen. Within three weeks, the patient reported the disappearance of nocturnal anxiety, cessation of gastrointestinal preoccupations, and overall mood normalisation; only mild sleep disruption occurred, and no other adverse effects surfaced. Even without CYP2D6 inhibition, the pairing of low-dose dextromethorphan (N-methyl-D-aspartate antagonism) and piracetam (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid potentiation) may trigger enough neuroplastic change to quiet refractory hypochondriacal OCD. Although confounded by ongoing medications, recent changes to the background regimen, and the absence of CYP2D6 genotyping or structured OCD ratings, this single observation encourages further controlled study of low-risk glutamatergic augmentation for anxiety-spectrum disorders that defy conventional care.

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