Methylphenidate for Refractory Catatonia in a Patient With Schizophrenia When Electroconvulsive Therapy Was Unavailable: A Case Report

Introduction

Catatonia is a clinical syndrome characterized commonly by mutism and immobility but also by automatic obedience, gegenhalten, ambitendency, posturing, rigidity, stereotypy, echolalia, and echopraxia, among other symptoms. It can occur in psychiatric and medical conditions and is increasingly conceptualized as a transdiagnostic neuropsychiatric syndrome rather than a manifestation restricted to schizophrenia.¹,³ The Bush-Francis Catatonia Rating Scale (BFCRS) is commonly used to quantify symptom severity; the 23-item scale ranges from 0 to 69, with higher scores indicating greater severity.²

The biological basis of catatonia remains incompletely understood, but converging evidence implicates dysregulation of GABAergic, dopaminergic, and glutamatergic signaling within distributed frontoparietal and cortico-striatal networks.¹⁰,¹¹ Reduced GABAergic activity and altered dopaminergic transmission have been proposed to contribute to the motor and behavioral manifestations of catatonia, while glutamatergic/NMDA signaling may also be dysregulated.¹⁰,¹¹ These models provide a conceptual basis for the established efficacy of GABA-enhancing benzodiazepines and for investigation of agents that modulate dopaminergic or glutamatergic signaling. Benzodiazepines are among the best-studied pharmacologic treatments, but response is not universal, and ECT remains an important treatment for patients who do not respond adequately to benzodiazepines.¹³,¹⁴

Methylphenidate is a psychostimulant that inhibits the dopamine and norepinephrine transporters, thereby decreasing reuptake and prolonging the action of these neurotransmitters within the synaptic cleft.¹² This increases dopaminergic and noradrenergic signaling rather than directly increasing dopamine synthesis. Because diminished dopaminergic transmission has been hypothesized to contribute to catatonic symptoms, enhanced dopaminergic signaling provides a theoretical rationale for methylphenidate as a treatment option.¹²

Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist approved for the treatment of moderate-to-severe Alzheimer disease and has also been studied off-label as an alternative or adjunctive treatment for catatonia.¹⁶ Its use in catatonia is based on the hypothesis that excessive glutamatergic/NMDA signaling may contribute to the syndrome; published case reports and reviews describe rapid responses in some patients.¹⁶ In the present case, memantine was selected after lorazepam produced oversedation without adequate improvement in core catatonic features. Although methylphenidate has been described in several case reports of refractory catatonia, the existing literature remains limited and heterogeneous.⁴⁻⁹ Prior reports have included patients with major depressive disorder, bipolar disorder, mania with psychosis, and schizophrenia, with methylphenidate used at varying doses and sometimes in combination with other agents or ECT.⁴⁻⁹

The present case extends that literature by describing an older adult with chronic schizophrenia who received low-dose methylphenidate without subsequent ECT after ECT was not feasible. The case therefore provides an additional example of stimulant responsiveness in a population and treatment context that differ from several prior reports, while also illustrating the difficulty of determining causality when methylphenidate is added to ongoing memantine.

Case Presentation

A disheveled 68-year-old male with schizophrenia, most recently treated with clozapine and ziprasidone, presented with rigid posturing, poor eye contact, reduced blinking, and waxy flexibility, with his legs maintained in elevated positions for prolonged periods. He mirrored movements and repeated phrases. The patient was unable to communicate his subjective mood, while his observed affect was restricted; his speech was garbled. Vital signs were within normal limits.

A trial of lorazepam (2mg IV each day) was initiated and continued for several days, but the patient developed oversedation with minimal improvement in catatonic symptoms. BFCRS at that time was calculated to be 14. Memantine was then initiated and improved alertness but did not improve posturing, rigidity, or stereotypy. ECT was considered but was not feasible because the patient was not medically cleared for treatment at the available outpatient facility.

Methylphenidate 5 mg twice daily was started based on prior reports of benefit in catatonia (Table 1).4-9 Within days of adding methylphenidate to ongoing memantine, the patient’s symptoms improved, with a decrease in BFCRS to 2. Residual symptoms subsequently resolved. Paranoid delusions and auditory hallucinations emerged during the period of clinical improvement but resolved within 48 hours without intervention. Because the hallucinations emerged after the patient’s mutism and other catatonic symptoms had begun to improve, and because they resolved without discontinuation of methylphenidate or other intervention, a direct stimulant-induced psychotic reaction could not be established.

Discussion

Six published cases identified in the manuscript’s literature review describe resolution of catatonic symptoms with stimulant treatment, including five involving methylphenidate and one involving armodafinil plus methylphenidate; one patient also received ECT (Table 1).⁴⁻⁹ The prior reports are clinically heterogeneous. Prowler et al. described an elderly woman with major depressive disorder who responded acutely to methylphenidate after lorazepam nonresponse.⁹ Neuhut et al. reported a 64-year-old man with bipolar disorder who improved with methylphenidate.⁵ Bajwa et al. described a patient with mania and psychosis treated with armodafinil and methylphenidate.⁷ Zeshan et al. reported a 25-year-old woman with schizophrenia who improved with methylphenidate.⁶ Sciberras et al. described an older woman with major depressive disorder who received both ECT and methylphenidate, while Zuckerberg et al. described a 29-year-old man with schizophrenia who received methylphenidate and subsequently ECT.⁴,⁸

The present case differs from these reports in several potentially informative respects. First, the patient was an older adult with long-standing schizophrenia, whereas the prior schizophrenia cases in the table involved substantially younger adults.⁴,⁶ Second, methylphenidate was administered at a low dose of 5 mg twice daily and was followed by improvement within days without ECT. Third, memantine was continued during methylphenidate treatment, making this case relevant to the possible interaction between dopaminergic and glutamatergic strategies. Finally, ECT was considered but could not be performed because the patient was not medically cleared at the available facility. Thus, this report does not establish methylphenidate as a substitute for ECT; rather, it adds a clinically distinct example in which a readily available, rapidly acting oral stimulant was associated temporally with improvement when standard options were limited. The mechanism of the observed response is uncertain. Catatonia has been associated with reduced dopaminergic transmission in motor pathways, as well as abnormalities in GABAergic and glutamatergic signaling.¹⁰,¹¹ Methylphenidate blocks dopamine and norepinephrine transporters, decreasing reuptake and prolonging neurotransmitter activity in the synaptic cleft.¹² The resulting increase in dopaminergic signaling provides a theoretical mechanism by which methylphenidate could improve catatonic motor and behavioral symptoms, particularly in mesostriatal circuits. This remains a hypothesis, however, and the response observed in a single patient cannot establish a causal mechanism.

Memantine may also have contributed to the patient’s improvement. As an NMDA receptor antagonist, it can reduce glutamatergic signaling and has been reported to improve catatonia in case reports and case series.¹⁶ In this patient, however, memantine improved alertness without improving the core catatonic features of posturing, rigidity, or stereotypy. The subsequent improvement after methylphenidate was therefore temporally more closely associated with methylphenidate initiation. Nevertheless, because memantine was continued, an additive or synergistic effect cannot be excluded.

The transient emergence of paranoid delusions and auditory hallucinations warrants consideration because psychostimulants can exacerbate psychotic symptoms in susceptible patients. In this case, the hallucinations appeared during recovery from mutism and resolved within 48 hours without intervention while methylphenidate was continued. The timing therefore does not establish methylphenidate as the cause, and the episode should not be interpreted as evidence supporting age-related changes in positive symptoms of schizophrenia. At the same time, the event underscores the need for careful monitoring for psychosis when stimulants are used in patients with schizophrenia. Benzodiazepines remain a first-line pharmacologic treatment for catatonia, but response is incomplete in a subset of patients.¹³ ECT is highly effective and is an important treatment for benzodiazepine-refractory catatonia, yet access can be limited by geographic distribution, institutional resources, medical clearance, anesthesia availability, cost, and other system-level barriers.¹⁴,¹⁵ Recent reports have specifically described prolonged catatonic illness in community settings where ECT was unavailable or transfer to an ECT-capable facility was difficult.¹⁵ This context is directly relevant to the present case, in which ECT was considered but could not be pursued at the available facility.

Methylphenidate is potentially attractive in this setting because it is widely available, orally administered, familiar to clinicians, and capable of producing relatively rapid pharmacologic effects without the procedural infrastructure required for ECT. These characteristics could make it a practical bridge or alternative when standard treatments are ineffective or temporarily inaccessible. However, methylphenidate is not without risk, including cardiovascular effects, insomnia, appetite suppression, misuse potential, and possible exacerbation of psychosis or mania. Accordingly, its use for catatonia should be individualized and closely monitored.

The principal limitation of this report is that methylphenidate was administered concurrently with memantine, preventing attribution of the clinical response to methylphenidate alone. As with other published stimulant reports, the evidence is based on individual clinical observations rather than controlled comparisons. Nevertheless, the case adds to a small body of literature suggesting that dopaminergic stimulation may have therapeutic potential in catatonia and highlights a clinically relevant scenario in which a rapidly acting, widely available medication may be considered when benzodiazepines are ineffective or poorly tolerated and ECT is not feasible.

Conclusion

Methylphenidate may represent a useful adjunctive treatment for catatonia when benzodiazepines are ineffective or poorly tolerated and ECT is unavailable or impractical. This case extends prior reports by describing an older adult with chronic schizophrenia who improved after low-dose methylphenidate without subsequent ECT. Further research is needed to determine which patients are most likely to benefit, optimal dosing, safety, and the neurobiological mechanisms underlying potential treatment response.

Patient Consent Statement

Verbal informed consent was obtained from the patient for publication of this case report on 10/16/24, including the use of any accompanying clinical details. The patient was informed that efforts would be made to maintain anonymity, such as omitting or altering identifying information. However, complete anonymity cannot be guaranteed. The patient was made aware of the potential for recognition by individuals familiar with their case, and they agreed to proceed. No identifiable patient information is disclosed within this report.

Conflicts of Interest/Disclosures

The authors declare no conflicts of interest. No funding was received for this case report.