Writing in Psychopharmacology Bulletin, authors Chinenye Okoro, Kaye Homer, Marlene Kelbrick, Jonny Walker, Mary Sam, Justine Burge, Rosie Richards, Gabriela Paduret, and Feras Ali Mustafa examined a 53-year-old Caucasian female who had been under the care of the early intervention for psychosis (EIP) service following a first episode psychosis. At the time of first presentation an incidental finding of a small meningioma was diagnosed through contrast MRI brain scan. The psychotic episode appeared unrelated to this following acute liaison psychiatric and neurology review and was thought to be stress-related at the time. There was no history of substance misuse, other significant medical illness or family psychiatric history. The patient had in recent months reported symptoms suggestive of being in the perimenopausal phase that include changes in menstrual cycle. Although not formally diagnosed, the patient also presented with possible features of autistic spectrum disorder. Following a first episode psychosis, the patient was briefly treated with aripiprazole (antipsychotic) up to a dose of 10 mg in the morning. The patient stopped medication 3 months later. She remained well and stable following medication cessation.

After 18 months under the care of the EIP service, the healthcare team was alerted of a sudden change in presentation with predominant confusion (reported to have been her usual self the previous day although report of a possible stressful incident at work earlier that week). The team attended the home address the same day (day 1). She presented with mutism, immobility (lying on her bed) and had not eaten or drunk any fluids for the duration of that day. The Bush-Francis catatonia rating scale score was 14. She was taken to A&E the same evening and admitted to the general hospital.

The next day (day 2) she was reviewed by the EIP consultant psychiatrist and acute liaison consultant psychiatrist attached to the general hospital. She presented with immobility, mutism, staring (vacant perplexed appearance with gaze, and reduced blinking) and rigidity. Catatonia was diagnosed. The Bush-Francis catatonia rating scale score was 16. She was given a lorazepam ‘challenge test’ at the time of 2 mg intravenous lorazepam. Response was rapid, with change in eye contact, verbal response and some movement, however brief, followed shortly by the onset of sedation and falling asleep.

The next morning when she awoke (day 3), there was no evidence of catatonia. She presented with normal movement and eye contact, engaging, conversant and coherent. There was no evidence of acute psychiatric disturbance. Physical health investigations completed during the admission revealed nil significant, and neurological advice was sought from the neurosurgical specialist centre following brain imaging. Once all investigations had been completed, she was discharged home with a brief period of support from the psychiatric crisis and home treatment team for additional monitoring catatonia has been adequately treated.15,18 There is a lack of evidence of frequency of lorazepam administration and related outcomes.20

In this patient case, the response to a single dose of 2 mg intravenous lorazepam provided an initial brief response, followed by sedation and a period of sleep, after which there were no longer features of catatonia present. Therapeutic response appears most effective in acute catatonia, with longer duration of symptoms a predictor for poor response.17,20–22 Here, the condition was identified and treated early (identified on day 1, and treated on day 2), which may have contributed to the outcome following a single dose of intravenous lorazepam. The relatively quick onset of sedation (that is often only later seen in the course of treatment) may be related to the dosage, where a lower dose (such as 1 mg) may have been sufficient for a positive response in this particular individual. A practical learning point may also be the way the test is done, such as when intravenous infusion of lorazepam is started, to consider pausing after 1 mg has been given and allow re-evaluation of catatonic features before proceeding with the full 2 mg dose unless the patient has fallen asleep or the response to 1 mg was not adequate.

The presence of what has been reported as an incidental finding of a meningioma during the patient’s first presentation to health services, is thought to be unlikely to have contributed to the presentation of acute catatonia. A CT and MRI brain scan with contrast completed at the time of admission to the general hospital, found no change in lesion size and no mass or oedematous effect on surrounding structures. The lorazepam ‘challenge test’ not only confirms the diagnosis, but often will make the underlying pathology become more evident.17 In this case, all physical health investigations found no specific underlying cause, and there was no evidence of an underlying acute psychotic or other psychiatric condition. Whilst there are no case reports of stress-induced catatonia to the authors’ knowledge, acute stress may be associated with GABAergic neurotransmission receptor attenuation.23 There are however case reports of catatonia in post-traumatic stress disorder with reference to Shorter and Fink (2018)24 postulating that catatonia is associated with fear and alarm triggered by trauma, being an overwhelming psychic response, and a proposed link to the animal defence of tonic immobility in a predatory environment.25,26 Psychogenic theories on vulnerability and overwhelming anxiety due to perceived trauma or danger may be more applicable in certain patient populations for example autistic spectrum disorder.27 The presence of autistic spectrum disorder features (although not formally diagnosed), a previous stress-induced psychotic episode, and likely perimenopausal oestradiol fluctuation increasing sensitivity to psychosocial stress all highlight the potential relevance of a stress-vulnerability model in this case, especially in the context of reported stress at work preceding the onset of catatonia.

Conclusion

Clinicians, both in medical and psychiatric settings need to be familiar with the symptoms of catatonia in order to be able to detect and effectively treat early, with less severe symptoms and early treatment related to better outcomes, and likely reduced need for more invasive treatment such as ECT.29 Untreated catatonia is associated with significant morbidity and mortality. Rating scales such as the Buch-Francis Catatonic rating scale may be a helpful aid for diagnosis and determination of severity and evaluating response,30 with the lorazepam ‘challenge test’ serving as both treatment and confirmation of diagnosis. Underlying physical and or psychiatric causes need to be identified and treated where present.

References not included