TL;DR: It is concluded that lorazepam and ECT are effective treatments for catatonia and the rating scale has predictive value and displays sensitivity to change in clinical status.
Abstract: Case material and retrospective studies support the use of both lorazepam and ECT in treating catatonia, but few prospective investigations exist and none employ quantitative monitoring of response. In this study we test their efficacy in an open, prospective protocol, and define a "lorazepam test' with predictive value for treatment. Twenty-eight patients with catatonia were treated systematically with parenteral and/or oral lorazepam for up to 5 days, and with ECT if lorazepam failed. Outcome was monitored quantitatively during the treatment phase with the Bush-Francis Catatonia Rating Scale (BFCRS). In 16 of 21 patients (76%) who received a complete trial of lorazepam (11 with initial intravenous challenge), catatonic signs resolved. A positive response to an initial parenteral challenge predicted final lorazepam response, as did length of catatonic symptoms prior to treatment. Neither demographic variables nor severity of catatonia predicted response to lorazepam. Four patients failing lorazepam responded promptly to ECT. It is concluded that lorazepam and ECT are effective treatments for catatonia. The rating scale has predictive value and displays sensitivity to change in clinical status.
TL;DR: The prompt recognition and treatment of catatonia may reduce morbidity in and length of stay for hospitalized psychiatric patients, suggesting that a beneficial response to lorazepam is not limited to patients with pure psychogenic cat atonia.
Abstract: In a prospective open trial conducted on a general psychiatric ward, the authors diagnosed catatonic syndrome 15 times in 12 patients over a 1-year period. These 12 patients represented 9% of all admissions. The following signs were present in two thirds or more of the episodes studied: immobility (100%), staring (92%), mutism (85%), withdrawal/refusal to eat (78%), posturing/grimacing (73%), and rigidity (66%). Other signs of catatonia were seen less frequently. Lorazepam 1 to 2 mg was administered in every case, and patients were evaluated at hourly intervals. Of the 15 episodes, 12 responded completely and dramatically to lorazepam treatment within 2 hours, 1 responded partially, and 2 had no response. Adverse effects were infrequent. A CNS abnormality or dysfunction was evident in 8 of the 12 responders, suggesting that a beneficial response to lorazepam is not limited to patients with pure psychogenic catatonia. The prompt recognition and treatment of catatonia may reduce morbidity in and length of stay for hospitalized psychiatric patients.
TL;DR: This paper proposes that catatonia be considered as a syndrome with various possible causes, and Physicians are advised to be aware of potentially serious organic illnesses which may underlie the catatonic syndrome.
TL;DR: A favorable treatment response was shown for the entireCatatonic sample, with two thirds markedly improved or in remission at the time of discharge, consistent with those of other investigators of the catatonic syndrome for the past 100 years.
Abstract: • We studied 55 patients admitted during 14 months to two inpatient psychiatric units of a municipal hospital who exhibited one or more of the catatonic signs of mutism, stereotypy, posturing, catalepsy, automatic obedience, negativism, echolalia/ echopraxia, or stupor. Only four of the 55 patients satisfied our research criteria for schizophrenia, whereas over two thirds had diagnosable affective disorders, usually mania. The eight catatonic motor signs were nonspecific and homogeneously distributed among the various research diagnostic groups, with the number and type of individual signs unrelated to short-term treatment outcome. A favorable treatment response was shown for the entire catatonic sample, with two thirds markedly improved or in remission at the time of discharge. These findings are consistent with those of other investigators of the catatonic syndrome for the past 100 years.
TL;DR: Evidence from brain imaging studies of patients with psychotic disorders indicates increased neural activity in premotor areas in patients with hypokinetic catatonia, but whether this localised hyperactivity is due to corticocortical inhibition or excess activity of inhibitory corticobasal ganglia loops is unclear.