East Asian Arch Psychiatry 2023;33:3-14 | https://doi.org/10.12809/eaap2237

REVIEW ARTICLE

Psychosis Related to Baclofen Withdrawal or Overdose: A Systematic ReviewCME
Poh Jan Jane Phu, Jeffrey CL Looi, Pramod C Nair, Stephen Allison, Sherry Kit Wa Chan, Tarun Bastiampillai

Poh Jan Jane Phu, College of Medicine and Public Health, Flinders University, Adelaide, Australia
Jeffrey CL Looi, Academic Unit of Psychiatry and Addiction Medicine, The Australian National University Medical School, Canberra Hospital, Canberra, Australia; Consortium of Australian-Academic Psychiatrists for Independent Policy Research and Analysis (CAPIPRA), Canberra, Australia
Pramod C Nair, College of Medicine and Public Health, Flinders University, Adelaide, Australia; Discipline of Clinical Pharmacology, Flinders Health and Medical Research Institute, Flinders University, Adelaide, Australia
Stephen Allison, College of Medicine and Public Health, Flinders University, Adelaide, Australia; Consortium of Australian-Academic Psychiatrists for Independent Policy Research and Analysis (CAPIPRA), Canberra, Australia
Sherry Kit Wa Chan, Department of Psychiatry, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China; State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong Special Administrative Region, China Tarun Bastiampillai, College of Medicine and Public Health, Flinders University, Adelaide, Australia; Consortium of Australian-Academic Psychiatrists for Independent Policy Research and Analysis (CAPIPRA), Canberra, Australia; Department of Psychiatry, Monash University, Australia

Address for correspondence: Dr Poh Jan Jane Phu, Department of Psychiatry, Flinders University, Flinders Drive, Bedford Park, Adelaide, Australia. Email: jane-phu@outlook.com

Submitted: 15 August 2022; Accepted: 17 November 2022


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Abstract

Objective: To systematically review case reports of psychosis related to withdrawal or overdose of baclofen, which is a gamma-aminobutyric acid (GABA) B agonist.

Methods: PubMed, MEDLINE, CINAHL, and PsychINFO were searched to identify articles related to psychosis secondary to withdrawal or overdose of baclofen using the terms ‘baclofen’ and ‘ psychosis’. Comparisons were made between cases in terms of concomitant antipsychotic use, diagnosis of delirium, and evidence of association. Quality of case reports was assessed using the CARE Case Report Guidelines checklist.

Results: In total, 34 patients from 28 case reports were reviewed. Twenty-three patients experienced psychosis upon baclofen withdrawal; among them, 18 had resolution of psychosis upon reinitiation of baclofen, whereas antipsychotic monotherapy was less successful (only four of eight patients responded). An additional baclofen withdrawal period led to recurrence of psychotic symptoms in four of seven patients. Eleven patients had psychosis on induction or after overdose of baclofen; among them, four patients had resolution of psychosis upon cessation of baclofen. The mean quality of the case reports was 6.4 of 13.

Conclusion: Considering its GABAergic agonism, along with evidence of psychosis on induction or withdrawal, baclofen may have some antipsychotic and pro-psychotic properties.

Key words: Baclofen; GABA-B receptor agonists; Psychotic disorders; Schizophrenia

Introduction

Baclofen is a gamma-aminobutyric acid (GABA) B agonist commonly used to treat muscle spasms and dystonia (eg, in  multiple sclerosis).1 In the 1970s, clinical trials of baclofen treatment for schizophrenia demonstrated mixed results.2-4

Currently, the most widely used treatments for schizophrenia involve antipsychotic agents, which are primarily dopamine blockers. Approximately 15% to 30% of patients who do not respond to these antipsychotic medications are considered to have treatment-resistant schizophrenia.5,6 Clozapine, the only effective medication for treatment- resistant schizophrenia, targets multiple receptor pathways (eg, dopaminergic, cholinergic, glutamatergic, and GABAergic).5 Its efficacy may be mediated by the GABAB pathway,7 and abrupt clozapine cessation can lead to withdrawal psychosis.8,9 Considering the pharmacological modes of action of baclofen and clozapine,7 as well as their association with withdrawal psychosis,9,10 GABAB receptor signalling may be involved in the pathophysiology of psychosis. Research of GABA involvement in the pathophysiology of psychosis is needed to determine how baclofen may cause psychosis on induction.

Sensory gating in schizophrenia can be studied using the P50 wave on electroencephalography, which occurs early during stimulus processing.11 Cholinergic neurons are modulated by GABA interneurons in the context of a second stimulus, which reduces second stimulus amplitude in healthy individuals. However, in schizophrenia, the stimulus is not effectively diminished with a P50 ratio >50%, whereas healthy individuals exhibit a P50 ratio of <40%.12 The absence of sensory gating and presence of stimulus misperception13,14 may be influenced by GABA receptor modulation of cholinergic neurons in schizophrenia. The use of clozapine reduces this lack of P50 gating in patients with schizophrenia,12 in a manner modulated by the GABA system. Molecular modelling studies have demonstrated that clozapine directly binds to the GABAB receptor7, indicating a possible mechanism of action.7 Autoradiography findings of lower pre-pulse inhibition have been demonstrated in baclofen- and clozapine-treated schizophrenia mouse models, suggesting similar effects at a neurobiological level.15

Baclofen has been used in epilepsy, but it is now mainly used to treat muscle spasticity1 and alcohol withdrawal.16 Its use requires caution because it has been associated with toxicity leading to life-threatening symptoms (eg, arrhythmias, respiratory failure, and coma).17 Its dosing for neuropsychiatric disorders is challenging because it cannot easily pass the blood-brain barrier via passive diffusion and its plasma-to–cerebrospinal fluid concentrations are poorly correlated.18 Although baclofen targets GABAB agonism to dampen neuronal signalling in skeletal muscle, GABA interneurons affect multiple neuromodulators including dopamine, which may affect the pathophysiology of psychosis.19

Here, we explored the association between baclofen and psychosis by conducting a narrative review of case reports of psychosis related to baclofen withdrawal or overdose.

Methods

This systematic review was registered in PROSPERO (reference: CRD42022371450). In September 2021, databases of PubMed, MEDLINE, CINAHL, and PsychINFO were searched using terms ‘baclofen’ and ‘psychosis’ to identify case series and case reports related to psychosis secondary to baclofen withdrawal/induction/overdose (Figure). The reference lists of selected articles were also screened to identify additional case reports regarding baclofen-related psychosis. All articles were manually retrieved by one reviewer; each article’s relevance to baclofen-related psychosis was confirmed by another reviewer.10,20-61

All selected articles were manually categorised. Baclofen withdrawal cases were those with a history of baclofen use, no overdose event, and a period of baclofen cessation or dose reduction prior to psychosis symptom onset. Baclofen overdose to withdrawal cases were those with an overdose event (>200 mg orally or >1300 μg intrathecally) and a period of cessation prior to symptom onset. Baclofen overdose or induction cases were those with either an overdose or usual dosage that resulted in psychosis symptom onset. A maximum oral dose of ≥200 mg has been associated with an increased incidence of adverse events,17 and an intrathecal dose of 1300 μg/day is the recommended maximum daily dose.20

Relevant clinical information was retrieved by one reviewer and then confirmed by another reviewer. This information included psychosis history, antipsychotics use, psychosis treatment, and delirium status. Delirium was considered present if a diagnosis of delirium was recorded; otherwise, symptoms suggesting or refuting a diagnosis of delirium were noted. Other recorded data included any further trials of baclofen and responses to those trials, any changes in symptoms, specific antipsychotics used, and relevant history. The Naranjo Probability Scale was noted to be used in some case reports to determine the association of baclofen with psychosis in overdose and induction cases.62 Quality of case reports was assessed using the 13-item CARE Case Report Guidelines.63

Results

In total, 34 patients from 28 case reports were analysed: 18 patients had baclofen withdrawal psychosis,10,42-52 five patients had baclofen overdose followed by withdrawal psychosis,21-23,53,54 and 11 patients had baclofen overdose or induction psychosis (two with higher than usual dose and nine with normal dose).24-26,34,55-61

Baclofen withdrawal psychosis

Eighteen patients exhibited some form of psychotic symptoms after baclofen withdrawal (Table 110,42-52). The mean duration of prior baclofen use was 2.4 (range, 0.5-5) years, and the mean duration of withdrawal was 43 (range, 12-144) hours. Most common psychosis-related symptoms were hallucinations including visual (75%), auditory (50%), both (37.5%), or unspecified (12.5%). Delusions were present in five (28%) patients, three of whom experienced both delusions and hallucinations. None of the reports used a formal schizophrenia rating scale for symptom assessment. The maximum daily baclofen dose was 160 mg (oral) or 800 μg (intrathecal), and the mean oral dose was 83 mg/day. One patient had prior antipsychotic use for schizophrenia, 11 patients did not have, and the remaining six patients had no such data.

Fourteen of the 18 patients restarted or increased the original baclofen dose and exhibited a positive response. Seven patients had another period of baclofen withdrawal: four had symptom recurrence (and responded to subsequent reinitiation of baclofen) and three did not. Four of the 18 patients received antipsychotic treatment for their psychotic symptoms: one patient responded to antipsychotics with concomitant benzodiazepines, two patients responded to adjunctive antipsychotics along with reinitiation of baclofen, and one patient exhibited an equivocal response to antipsychotic monotherapy.

Only one patient had fluctuating orientation and confusion consistent with delirium. Five patients had possible delirium, with terms such as ‘confused’ being recorded. Others did not have comments on specific delirium symptoms.

The mean quality of these case reports was poor: 6.16 of 13 (range, 3-9), as determined by the CARE Case Report Guidelines checklist. No standardised diagnostic scales for psychosis or delirium were used. Although patient identification, clinical findings, and therapeutic intervention were generally reported, detailed patient histories were absent.

Baclofen overdose followed by withdrawal psychosis

Five patients overdosed on baclofen and then developed withdrawal psychosis (Table 221-23,53,54). The duration of withdrawal after baclofen overdose ranged from 24 hours to 4 days. Psychotic symptoms were reported in a descriptive manner, without assessments by standardised symptom rating scales. Most symptoms were hallucinations: both visual and auditory (in three patients), visual only (in one patient), and auditory only (in one patient). Four patients also experienced accompanying delusions. The rates of auditory hallucinations and delusions were higher in these patients than in patients with baclofen withdrawal psychosis. Of the five patients, four responded to reinitiation of baclofen (one of them required concomitant antipsychotics) and one recovered with antipsychotics and benzodiazepines alone. Delirium was identified in three of the five patients via clinical assessment, whereas delirium was ruled out in the remaining two patients. Only one case report23 included Naranjo Probability Scale results, which indicated that the adverse reaction had a probable association with the use of baclofen. The mean quality of these case reports was poor: 6.6 of 13 (range, 4-8).

Baclofen overdose or induction psychosis

Two patients with baclofen overdose psychosis had particularly high doses of baclofen (300 mg orally and 1400 μg intrathecally) [Table 324-26,34,55-61]. Reported symptoms included both hallucinations and delusions. The first patient did not experience delirium and had no history of psychosis or prior antipsychotic use.24 Her psychotic symptoms resolved when the baclofen dose was reduced to 50 μg. Although the Naranjo Probability Scale was not used to evaluate the association of psychosis with baclofen, baclofen dose increases led to the recurrence of similar symptoms, which resolved with dose reduction. The second patient had a history of binge-eating disorder and received supratherapeutic levels of baclofen. He experienced visual hallucinations, delusions, and psychomotor agitation.25 Reinitiation of baclofen at a lower dose led to psychosis resolution. Notably, signs of confusion were reported, but no other delirium criteria were specified. The Naranjo Probability Scale results indicated a possible causal relationship between baclofen overdose and psychosis. The quality of the two case reports was low: 6 and 8 of 13, respectively.

Nine patients exhibited psychosis while receiving therapeutic doses of baclofen. The mean oral dose was 47 mg/day, and the treatment duration ranged from 1 day to 4 months. Eight patients experienced auditory (n = 6), visual (n = 4), and both (n = 3) hallucinations. Seven patients experienced delusions. Three patients were diagnosed with delirium and the remaining six patients were ruled out or did not suggest having delirium. One patient had prior antipsychotic use for severe idiopathic dystonia, six patients had no history of psychotic disorder, and three patients had no specifically reported history of psychosis.

Resolution of psychotic symptoms was achieved by cessation of baclofen, treatment with antipsychotics, or both. Two patients had monotherapy with antipsychotics; one of them responded positively (ie, resolution of symptoms). Five patients were treated by cessation of baclofen; four of them had symptom resolution, although three required concomitant antipsychotic treatment. Two of the three patients who were treated with baclofen cessation and concomitant antipsychotic treatment exhibited recurrence of psychosis upon reinitiation of baclofen and then resolution after cessation of baclofen. One case report did not indicate whether psychosis resolved after baclofen cessation.26 The remaining two patients had symptom resolution after haemodialysis (n = 1) or reduction of baclofen dose with antipsychotic use (n = 1). The mean quality of these case reports was low: 6.4 of 13 (range, 3-8).

Discussion

Most case reports of baclofen-related psychosis involve withdrawal rather than overdose or therapeutic use. Although findings suggesting a causal relationship between baclofen withdrawal and psychosis have been reported, attempts to confirm this relationship (through repeat withdrawal periods, antipsychotics use, and reinitiation of baclofen to ameliorate adverse symptoms) have been inconclusive. The occurrence of withdrawal psychosis implicates baclofen, and therefore GABABR, in the pathophysiology of psychosis. Although cases of baclofen overdose are rare, these cases suggest a psychosis pattern that is consistent with classical positive schizophrenia symptoms (ie, greater tendency for auditory hallucinations and delusions, rather than visual hallucinations associated with baclofen withdrawal in the absence of overdose). Psychosis after therapeutic use of baclofen suggests a complex pathophysiology; they may involve direct GABABR agonism or the effects of baclofen on dopamine network modulation. The likelihood of psychosis appears to be greater after baclofen withdrawal than after baclofen overdose or therapeutic use. However, the strength of these observations is weak considering the low quantity and variable quality of cases in terms of patient history, description of symptoms and signs, quality of diagnostic assessment, and duration of follow-up (Table 410,21-26,34,42-61).

There were 18 cases of baclofen withdrawal psychosis and five cases of overdose followed by withdrawal psychosis; the mean withdrawal durations were 43 hours and 46.5 hours after baclofen cessation, respectively. Overall, the duration of prior baclofen use was poorly reported and ranged from months to years. Other than clozapine, few medications have been associated with withdrawal psychosis.27 Clozapine withdrawal psychosis usually develops within 24 to 48 hours.28 However, pharmacological studies of the effect of the duration of baclofen use on GABAB signalling are ongoing.29-31 A proportion of patients receiving baclofen have tolerance.32 These findings highlight the variability in GABABR subtypes, which may affect baclofen efficacy. Additionally, the wide range in duration of prior use, from months to years, suggests variability in GABABR subtypes, with the potential for greater susceptibility to baclofen withdrawal psychosis.

The mechanism of baclofen-related psychosis is largely unknown. Baclofen may indirectly modulate dopamine.34 Baclofen acts on GABAB receptors within the ventral tegmental area, leading to negative inhibition of dopaminergic projections in the mesolimbic pathway.35 Chronic suppression of these neurons may result in dopamine receptor hypersensitivity and neuronal excitability, predisposing to psychosis upon baclofen withdrawal.36 However, because GABAB signalling is modulated in a complex manner, inhibition or excitation may occur on the basis of specific activation profiles.37-40

One major limitation of this review was the quality of the case reports, as determined by the CARE Case Report Guidelines. None of the included reports used a standardised symptom rating scale to assess psychotic symptoms,41 nor did most reports evaluate the probably of a drug reaction using the Naranjo Probability Scale.62 Additionally, some case details (eg, medical history and follow-up periods) were missing, inconsistent, or poorly reported. There was limited consideration of delirium as a differential diagnosis, rather than as psychosis solely related to baclofen use. Notably, only 34 cases have been reported in the English-language medical literature. Thus, baclofen withdrawal psychosis cases may be underreported because there have been no formal cohort or controlled studies of baclofen withdrawal psychosis.

Conclusion

The pharmacological agonism of baclofen at the GABA receptor suggests that the GABAergic system is involved in the pathophysiology of psychosis. However, the quality of published case reports of baclofen-related psychosis is low.

Contributors

All authors designed the study, acquired the data, analysed the data, drafted the manuscript, and critically revised the manuscript for important intellectual content. All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

Conflicts of interest

As the editor of the journal, SKWC was not involved in the peer review process. Other authors have disclosed no conflicts of interest.

Funding/support

This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Data availability

All data generated or analysed during the present study are available from the corresponding author on reasonable request.

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