The first descriptions of catatonia can be traced back to 1849 when Bell reported on 40 patients presenting with concurrent mania, delirium, psychosis, sleeplessness, and overactivity. In 1874, Kahlbaum described catatonia as an independent psychiatric syndrome characterized by a cyclical course of alternating manic, depressive, and psychotic phases, with eventual deteriorating course. While catatonia has historically been most closely associated with schizophrenia, it has more recently been recognized as a syndrome related to a range of psychiatric and medical disorders.
Catatonia is now defined as a clinical syndrome characterized by the coexistence of psychiatric and motor signs. Criteria for catatonia are presented in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), and summarized in Table 1. Timely recognition of catatonia can be challenging, possibly due to poor awareness among some clinicians, or the longer period of observation often required for some catatonic signs to emerge. Untreated catatonia can lead to a range of recognized complications, including infection, venous thromboembolism, aspiration pneumonia, and even death. Catatonia is, however, very much a treatable condition with a response rate thought to range from 59% in patients with schizophrenia to over 90% in patients with other psychiatric diagnoses.
Benzodiazepines are the mainstay of treatment of catatonia,[4,6] with lorazepam the most used drug at a dose between 2 and 16 mg/day. Indeed, catatonia can be confirmed with a lorazepam challenge test, where the patient is examined before and after a dose of 1–2 mg of lorazepam. A positive response is a swift and marked reduction in catatonic signs, which can be quantified using the Bush–Francis Catatonia Rating Scale. While the precise mechanisms underlying the pathophysiology of catatonia are still poorly understood, it is hypothesized that it may be characterized by gamma-aminobutyric acid (GABA) receptor cortical dysregulation and deficits in the dorsolateral prefrontal cortex. It is therefore postulated that benzodiazepines may act by increasing cerebral GABA signaling. Where treatment with lorazepam is not successful, or when adverse effects prevent use of therapeutic doses, electroconvulsive therapy (ECT) can also be highly effective.
Early recognition and treatment of catatonia generally leads to rapid resolution of symptoms. However, the presentation, management, and prognosis of catatonia in old age is poorly understood, with only a handful of case studies published in this field to date.[11–13] In this report, we describe the case of an elderly catatonic patient who was ultimately refractory to treatment, raising important implications for the management of catatonia in old age.
J Med Case Reports. 2021;15(406) © 2021 BioMed Central, Ltd.