Dextromethorphan DSM-5 Diagnosis: Recognizing and Addressing DXM-Induced Psychotic Disorder

Introduction

Dextromethorphan (DXM), a synthetic morphinan derivative, is a widely accessible over-the-counter (OTC) antitussive found in numerous cold and cough remedies. Often referred to as “DXM” or “poor man’s PCP,” its accessibility and perceived safety at recommended doses have made it a common household medication. However, when taken at supratherapeutic levels, dextromethorphan can induce a range of psychotropic effects, culminating in a state of psychosis remarkably similar to that induced by phencyclidine (PCP). This article delves into the critical issue of dextromethorphan abuse, focusing on the diagnosis of dextromethorphan-induced psychotic disorder within the DSM-5 framework, and emphasizes the necessity for clinicians to recognize this under-reported condition. We will explore a significant case of a patient presenting with severe DXM use disorder and subsequent psychotic symptoms, highlighting the diagnostic considerations and therapeutic interventions.

Case Presentation: A 40-Year-Old Female with DXM-Induced Psychosis

Ms. J, a 40-year-old Caucasian woman, presented with a complex history of polysubstance abuse initiating in adolescence. Her substance use trajectory began with alcohol and marijuana at age 14, progressing to include opiates and LSD during her teenage years. At 18, following significant LSD and marijuana consumption, she experienced her first episode characterized by hyper-religiosity, auditory hallucinations, and persecutory delusions. Notably, these symptoms spontaneously resolved despite ongoing LSD use. Throughout her twenties, Ms. J continued to misuse alcohol, marijuana, LSD, valium, and amphetamine-type stimulants.

Dextromethorphan entered Ms. J’s substance repertoire at age 29, and she immediately reported a strong affinity for the drug, describing a feeling of spiritual connection. The appeal of DXM was further amplified by its easy availability, low cost, and evasion of standard urine drug screenings. Her typical daily intake involved consuming 12 Corcidin™ Cough and Cold tablets three times daily (totaling 1080 mg of DXM) or 9 Mucinex™ DM Maximum Strength tablets three times daily (totaling 1620 mg of DXM), significantly exceeding the recommended maximum daily dose of 120 mg. For five years, DXM abuse occurred intermittently, averaging 3-4 times per month. Following marital distress, her DXM use escalated to daily consumption for approximately six months, concurrent with marijuana and alcohol abuse, and significantly reduced sleep.

At age 35, a severe DXM binge, estimated at 3000–4000 mg, resulted in a motor vehicle accident, although specific details of this episode remain unclear due to memory impairment. Subsequently, she reverted to her chronic daily DXM use (1080–1620 mg/day) for about a year. Another DXM binge of similar magnitude (3000–4000 mg) occurred around the time of her divorce finalization. This episode was followed by a disturbing dream involving graphic violence from her mother, which transitioned into persistent persecutory delusions and a subsequent assault attempt on her mother. This incident led to arrest and a 14-month period of sobriety in a rehabilitation facility. However, relapse to alcohol abuse occurred within two weeks of discharge, and DXM abuse resumed within four weeks. For the subsequent two years (ages 37-39), her substance use pattern fluctuated between periods of sobriety, weekly, and daily DXM abuse.

In the four months preceding her current presentation, Ms. J reported monthly DXM use at her usual high doses (1080–1620 mg/day), with the most recent use two days prior to hospitalization. She described this last episode as a “dirty high,” attributing it to the concurrent consumption of three beers, which she believed exacerbated her psychiatric decompensation.

Ms. J’s current psychiatric admission was triggered by her discovery sleeping in a stranger’s residence and a subsequent assault on a police officer. Initial assessment was limited by her acute clinical state, but she reported a history of PTSD, depression, and polysubstance abuse. Observations revealed an irritable affect, mood lability, and suspicion towards staff. A urine drug screen was positive only for buprenorphine (non-prescribed). Based on her reported depression, mirtazapine 15 mg nightly was initiated. Despite several days for substance washout, her symptoms of inappropriate behavior, hostility, illogical and disorganized thinking, and delusions of misinterpretation persisted. Following the introduction of an antipsychotic, her behavior became more coherent and appropriate, allowing for a more detailed history revealing her extensive DXM abuse. Her symptoms eventually stabilized with olanzapine 10 mg nightly and divalproex extended-release 1,000 mg nightly. She remained hospitalized for twenty days until symptom resolution and was discharged on mirtazapine, olanzapine, and divalproex ER.

Dextromethorphan and DSM-5 Diagnosis: Differentiating DXM-Induced Psychosis

The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), provides a framework for diagnosing substance-induced psychotic disorder. In the context of dextromethorphan, the key diagnostic criteria include:

  • Prominent hallucinations or delusions. As seen in Ms. J’s case, she experienced both hallucinations (auditory and potentially visual, as suggested by the vivid dream) and delusions (persecutory delusions related to her mother).
  • Evidence from history, physical examination, or laboratory findings of both (1) and (2):
    • The symptoms in Criterion A developed during or soon after substance intoxication or withdrawal or after exposure to a medication. Ms. J’s psychotic symptoms were temporally related to her DXM use, escalating with increased dosage and frequency. While other substances were also used, DXM was consistently associated with her psychotic episodes, particularly the severe episodes.
    • The involved substance/medication is capable of producing the mental disorder. The pharmacological properties of DXM, particularly its NMDA receptor antagonism, are well-established to induce PCP-like psychotic symptoms, supporting a causal link.

Differential Diagnosis: It is crucial to differentiate DXM-induced psychosis from primary psychotic disorders such as schizophrenia or schizoaffective disorder. Several factors aid in this differentiation:

  • Temporal Relationship to Substance Use: DXM-induced psychosis typically emerges in close temporal proximity to DXM use and remits with abstinence. In contrast, primary psychotic disorders have a more chronic and enduring course, although substance use can certainly complicate their presentation.
  • Substance Use History: A thorough substance use history is paramount. Identifying a pattern of DXM abuse preceding or coinciding with psychotic symptoms strengthens the likelihood of a substance-induced etiology.
  • Clinical Course: Resolution of psychotic symptoms with cessation of DXM and appropriate pharmacological intervention (as seen in Ms. J’s case) further supports a substance-induced diagnosis. Primary psychotic disorders often require more prolonged and complex treatment.
  • Urine Drug Screening: While standard urine drug screens do not detect DXM, a negative screen for other substances (excluding buprenorphine in Ms. J’s case, which was addressed) can raise suspicion for less commonly screened substances like DXM when psychotic symptoms are present without clear etiology. However, it is important to note that false positives for PCP can occur with high DXM concentrations, necessitating confirmatory testing like mass spectrometry if PCP is suspected.

Discussion: The Under-Recognition of DXM-Induced Psychosis

Data from poison control centers indicate a peak in DXM abuse in the mid-2000s, highlighting a significant public health concern. Despite awareness and some state-level restrictions on DXM sales to minors, federal regulations remain absent, largely due to DXM’s perceived benefits in cough management and potential therapeutic applications in other conditions like depression and neurological disorders.

DXM’s mechanism of action as a noncompetitive NMDA receptor antagonist, similar to ketamine and PCP, elucidates the shared psychotic symptomatology. The fact that routine urine drug screens fail to detect DXM contributes to its under-recognition as a cause of substance-induced psychosis. Clinicians may not routinely consider DXM intoxication in the differential diagnosis of acute psychosis, particularly in the absence of positive findings on standard drug screens.

The dose-dependent nature of DXM’s effects, ranging from mild perceptual alterations to severe psychophysical dissociation and violent behavior, further complicates diagnosis. The lack of a prominent withdrawal syndrome in Ms. J’s case, possibly due to her intermittent binging pattern, also underscores the variability in clinical presentation.

Therapeutic Implications and Management

Management of DXM-induced psychosis primarily focuses on symptomatic treatment. Pharmacological interventions reported in the literature include benzodiazepines for acute agitation and low-dose antipsychotics (haloperidol, risperidone, quetiapine). The successful use of olanzapine has also been documented. In Ms. J’s case, a combination of olanzapine (antipsychotic) and divalproex ER (mood stabilizer) proved effective in controlling severe psychotic symptoms. This combination may be particularly beneficial in cases with mood lability or agitation alongside psychosis.

The case underscores the critical need for clinicians to:

  • Maintain a high index of suspicion for DXM abuse in patients presenting with acute-onset psychosis, especially in adolescents and young adults.
  • Obtain a thorough substance use history, specifically inquiring about OTC cough medicine use.
  • Consider DXM intoxication in the differential diagnosis, even when standard urine drug screens are negative.
  • Educate patients and the public about the risks of DXM abuse and its potential psychiatric sequelae.

Conclusion

This case of severe dextromethorphan use disorder and DXM-induced psychotic disorder highlights the clinical significance of recognizing and appropriately diagnosing this condition. Dextromethorphan, readily available and inexpensive, poses a significant abuse potential and represents a likely underdiagnosed cause of substance-induced psychosis. Increased awareness among clinicians regarding the psychiatric manifestations of DXM abuse, coupled with thorough diagnostic evaluation and targeted treatment strategies, is crucial to mitigating the adverse consequences of this often-overlooked substance use disorder. Further research into the prevalence, diagnostic markers, and optimal treatment approaches for DXM-induced psychotic disorder is warranted.

References

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