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The presentation of catatonia can vary, making its management challenging, particularly in resource-limited settings in South Africa.
CLINICAL REFLECTIONS
Catatonia is a neuropsychiatric syndrome characterized by motor, behavioral, and autonomic abnormalities, often associated with psychiatric and medical conditions.1 Despite its rarity, catatonia is a psychiatric emergency that necessitates prompt diagnosis and treatment to prevent significant morbidity. However, the presentation of catatonia can vary, making its management challenging, particularly in resource-limited settings.2-6
This case report discusses the management of “John,” a 26-year-old man with catatonia at a rural district hospital in Mpumalanga, South Africa. It is a notable case due to the limited resources and lack of electroconvulsive therapy (ECT), which is often recommended, and treatment by junior doctors. The case exemplifies how, in South Africa, junior doctors are frequently tasked with treating complex conditions like catatonia, often with little supervision. It highlights the effective use of Lorazepam, the first line pharmaceutical treatment, in the absence of ECT. The report underscores the importance of adaptability and utilizing available resources to treat psychiatric emergencies.
Case Report
“John,” a 26-year-old African man, was referred to our facility after a 2-month stay at another district hospital. He had been brought to the initial hospital by the police after being found wandering the streets, unable to communicate or identify himself. His psychiatric history was initially unknown. For the first 6 weeks, no psychiatric intervention was provided (as the patient was being treated as a social case) until a fall resulting in a fractured capitulum raised suspicion of an underlying psychiatric condition. Risperidone 2 mg and fluoxetine 20 mg were started, but no benzodiazepines or psychiatric rating scales were utilized.
Upon transfer to our hospital in April 2024, John exhibited classic catatonic symptoms: mutism, waxy flexibility and negativism, with a Bush Francis Catatonia Rating Scale (BFCRS) score of 23. An intravenous dose of 5 mg midazolam led to improvements in symptoms, though BFCRS was not reassessed.
Laboratory tests revealed elevated inflammatory markers (C-reactive protein 76mg/L, erythrocyte sedimentation rate: 100mm/hr), but no source of infection was identified, and other test results were normal. The medical team (also junior doctors) hypothesized that the raised inflammatory markers could be related to the fracture.
Under the supervision of a visiting psychiatrist, treatment with risperidone 2 mg nocte, biperiden 2 mg twice a day, and lorazepam was initiated. Despite minimal verbal communication, John once spoke, requesting a cigarette, indicating slight improvement.
Two weeks post-admission, John’s father was identified by the police, and provided a history of previous psychiatric treatment with antipsychotics, mentioned a family history of mental illness, and linked the onset to cannabis use. His father also provided context regarding John’s recent disappearance, linking it to a financial conflict and subsequent threats from a neighbor, whom John believed had placed a curse on him, leading to his inability to speak. Soon after, John developed scrotal swelling, diagnosed as a scrotal abscess, and once this was treated, septic markers normalized.
One month later, John began communicating with his father but remained mute with hospital staff. Approximately 2 weeks later, he was discharged and continued to improve. At 1 month follow up, John was fully communicative and showed no further signs of catatonia or psychosis and remained stable foe 3 months postdischarge.
Discussion
Catatonia is a psychomotor syndrome that can be associated with psychiatric conditions like schizophrenia and mood disorders or medical conditions, including infections and metabolic disturbances. The diagnosis is based on clinical observation, supported by tools such as the BFCRS.
This case illustrates the challenges of diagnosing catatonia in resource limited settings, where psychiatric conditions are often misdiagnosed and mental health services are limited. In this instance, the patient was misclassified as a “social case” for 6 weeks before appropriate treatment was initiated. This delay underscores the importance of junior doctors being able to recognize such a wide array of clinical presentations.
The use of risperidone and lorazepam, once catatonia was suspected, aligns with established treatment guidelines. Benzodiazepines, particularly lorazepam, are considered the first-line treatment for catatonia due to their rapid and often dramatic effect on symptoms. In cases where benzodiazepines are ineffective, or ECT is unavailable, antipsychotics like risperidone can be considered, although caution is required due to the risk of worsening catatonia, particularly in cases associated with neuroleptic malignant syndrome. The patient’s improvement on this regimen highlights the effectiveness of pharmacological treatment.
The patient’s psychiatric history, cannabis use, and social stressors may have precipitated the catatonic episode, though sepsis secondary to the scrotal abscess cannot be excluded as a contributing factor.
Concluding Thoughts
This case report illustrates the challenges of diagnosing and managing catatonia in a resource-limited rural hospital setting. Despite the initial misclassification and delayed treatment, the patient's successful management with lorazepam and risperidone emphasizes the importance of adaptability in resource-limited settings. Increased awareness of catatonia and its treatment among health care providers, especially in underresourced areas, is essential for improving patient outcomes.
Dr Lehnerdt is a community service medical doctor working at Tintswalo Hospital in Mpumalanga, South Africa.
References
1. Fink M, Taylor MA. Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge University Press; 2003.
2. Oldham MA, Lee HB. Catatonia vis-à-vis delirium: the significance of recognizing catatonia in altered mental status. Gen Hosp Psychiatry. 2015;37(6):554-559.
3. Daniels J. Catatonia: clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci. 2009;21(4):371-380.
4. Bhati MT, Datto CJ, O’Reardon JP. Clinical manifestations, diagnosis, and empirical treatments for catatonia. Psychiatry (Edgmont). 2007;4(3):46-52.
5. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391-398.
6. Walther S, Stegmayer K, Wilson JE, Heckers S. Structure and neural mechanisms of catatonia. Lancet Psychiatry. 2019;6(7):610-619.