Heart Mind

: 2018  |  Volume : 2  |  Issue : 4  |  Page : 119--121

Overlooking catatonia: Can't see the forest for the trees

Steven A Svoboda1, Gurjot K Malhi2, Anita S Kablinger2,  
1 Virginia Tech Carilion School of Medicine, Carilion Clinic, Roanoke, VA, USA
2 Department of Psychiatry and Behavioral Medicine, Carilion Clinic, Roanoke, VA, USA

Correspondence Address:
Mr. Steven A Svoboda
Department of Psychiatry and Behavioral Medicine, Carilion Clinic, 2017 S Jefferson St 2nd Floor, Roanoke, VA 24014


Catatonia is a psychomotor syndrome with poorly understood pathophysiology that frequently occurs concurrently with acute psychiatric and medical illnesses. Its prevalence among psychiatric inpatients has been reported to be as high as 38% and is primarily observed in those with mood disorders. Diagnosis requires the presence of at least three of the following signs: mutism, negativism, immobility, agitation, waxy flexibility, catalepsy, posturing, grimacing, stereotypies, mannerisms, echopraxia, and echolalia. Although the most commonly observed signs are immobility and mutism, the presentation of catatonia is often highly variable and shares significant overlap with other neurological conditions. Consequently, diagnosing this complex clinical syndrome remains a challenge. Here, we present a case of catatonia initially unrecognized in a patient with major depressive disorder with psychotic features. The patient's catatonia was perceived incidentally after administration of a one-time dose of a benzodiazepine while on the inpatient psychiatry ward. Subsequent daily treatment with a benzodiazepine resulted in a drastic improvement in the patient's functioning over the following week. This case underscores the importance of performing a detailed psychiatric examination to avoid missing the diagnosis of catatonia, especially for patients with affective and psychotic disorders as more subtle catatonic signs may be masked. Therefore, being proficient at recognizing all the features and patterns of catatonia is essential for early detection and treatment.

How to cite this article:
Svoboda SA, Malhi GK, Kablinger AS. Overlooking catatonia: Can't see the forest for the trees.Heart Mind 2018;2:119-121

How to cite this URL:
Svoboda SA, Malhi GK, Kablinger AS. Overlooking catatonia: Can't see the forest for the trees. Heart Mind [serial online] 2018 [cited 2022 Sep 26 ];2:119-121
Available from: http://www.heartmindjournal.org/text.asp?2018/2/4/119/270068

Full Text


Catatonia is a psychomotor syndrome with poorly understood pathophysiology that frequently occurs concurrently with acute psychiatric and medical illnesses.[1] Its reported prevalence among psychiatric inpatients ranges anywhere from 7% to 38% and is primarily observed in those with affective and psychotic disorders.[1],[2] In a retrospective study of 220 patients with catatonia, 46% had an underlying affective disorder, 26% had a psychotic disorder, and only 16% had an underlying medical/neurological illness.[1] The diagnosis of catatonia according to the diagnostic and statistical manual-V requires the presence of at least three of the following signs: mutism, negativism, immobility, agitation, waxy flexibility, catalepsy, posturing, grimacing, stereotypies, mannerisms, echopraxia, and echolalia.[3] The most commonly observed signs include immobility and mutism which are present in over 90% of patients.[1] Due to the highly variable presentation of catatonia and similarities it shares with other neurological conditions, this complex clinical syndrome often poses a diagnostic challenge for clinicians.

The literature suggests that the diagnosis of catatonia is often delayed and failure to treat in a timely manner is associated with significant morbidity.[1],[2],[3],[4],[5],[6],[7] A retrospective study of 34 patients found that the meantime to the diagnosis of catatonia was 15 days.[4] Many of the complications associated with catatonia are a result of prolonged immobilization and refusal to eat or drink such as pneumonia, decubitus ulcers, muscle contractures, thrombosis, malnutrition, and dehydration.[4],[5],[6],[7] Furthermore, catatonia increases the risk of developing neuroleptic malignant syndrome which can be life-threatening.[4],[5],[6],[7] Therefore, early recognition and treatment is crucial to reduce these potential adverse outcomes.

Here, we present a case of catatonia initially unrecognized in a patient with major depressive disorder with psychotic features. To the best of our knowledge, there has only been one previous case report documenting a missed diagnosis of catatonia in a patient with depression.[2] In our patient, catatonic signs and symptoms were only perceived after several days of thorough evaluation and management on inpatient psychiatry. The key tip-off was when the patient's condition noticeably improved after administration of a low-dose benzodiazepine to ease her anxiety prior to undergoing a magnetic resonance imaging (MRI). Consequently, the patient was prescribed a twice-daily dose of a benzodiazepine, the first-line treatment for catatonia, with the patient exhibiting gradual but marked improvement in function over the next week. This case underscores the importance of performing a detailed psychiatric examination to prevent the overlooking of catatonia. This is especially true for patients who suffer from depression with psychotic features, as more subtle catatonic signs and symptoms may be masked.

 Case Report

A 32-year-old Caucasian female with no past psychiatric history was brought to the emergency department with a complaint of generalized weakness secondary to voluntary starvation. The patient reported not eating for approximately 3 weeks and not drinking for at least several days. She was found to have severe electrolyte abnormalities and metabolic derangements, all of which resolved with appropriate medical treatment. Once the patient was medically stable, psychiatry was consulted due to concerns for anorexia and underlying depression.

During the consultation, the patient was found to have several depressive symptoms, including anhedonia, decreased appetite, sleep disturbance, fatigue, and psychomotor retardation. When asked about the reason for starving herself, she stated that she was observing a religious fast in the hopes that it would lead to a “breakthrough in her life” and reconcile her marriage as “praying was not working.” The patient identified herself as Christian, and her religious preoccupation was evident as she reported “feeling closer to God” and that she “knows him better now” after this experience. She also reluctantly admitted to having auditory hallucinations but was not willing to elaborate on the content of what she was hearing. The patient's insight and judgment were poor, as she did not understand the life-threatening nature of her fasting event. Moreover, the patient demonstrated bizarre behavior that waxed and waned throughout the day such as staring into space, adjusting her clothes repeatedly, and exhibiting severe response latency. However, despite these signs of gazing, stereotypy, and mutism, respectively, catatonia remained unappreciated. A preferred working diagnosis of major depressive disorder with psychotic features and an admission to inpatient psychiatry unit for further evaluation ensued. Treatment with mirtazapine and olanzapine for her depression and hallucinations, respectively, were initiated.

On the inpatient psychiatry unit, significant psychomotor retardation including thought paucity, speech latency, and fixed gaze became more prominent. The patient also displayed signs of withdrawal and negativism as evidenced by a refusal to eat or drink and inability to perform activities of daily living without assistance. Stereotypical behavior was further observed through her repetitive and purposeless adjustment of her clothing. Incidentally, the diagnosis of catatonia was made after the patient received a low dose of diazepam for anxiety prior to undergoing an MRI of the head to exclude an organic etiology. An immediate, although short-lived, improvement in her psychomotor symptoms was observed after this dose. The patient became more conversational and cooperative with the staff and her fidgeting with her clothing had stopped; however, this improvement lasted for only several hours. Consequently, catatonia was suspected and the patient was started on a twice-daily dose of diazepam. Her condition improved gradually but dramatically over the next week. The patient became adherent to medication and diet, was able to perform her activities of daily living without assistance, and had a resolution of her psychomotor symptoms. The magnitude of improvement resulted in discharge home with plans to live with family and to continue treatment in an outpatient setting. She was discharged home on a medication regimen of mirtazapine, olanzapine, and diazepam with a plan to slowly taper the diazepam on an outpatient basis. Follow-up with the patient several months after discharge revealed that she has remained stable without any catatonic relapses.


This case highlights the difficulty in identifying catatonia in patients with concurrent depressive and psychotic symptoms, as they may mask or mimic catatonic symptoms. Despite the patient exhibiting catatonic signs for several days on the psychiatric inpatient unit, the diagnosis only became apparent after the patient's psychomotor retardation immediately improved after receiving a one-time dose of diazepam for anxiety.

In this case, the initial failure to recognize catatonia was likely due to multiple reasons. First, the patient did not display obvious catatonic signs such as waxy flexibility, rigidity, posturing, grimacing, verbigeration, echolalia, or echopraxia on admission. Second, the catatonic features that the patient did exhibit including partial mutism, negativism, withdrawal, and refusal to eat were difficult to differentiate from her depressive and psychotic symptoms, especially since these behaviors appeared to wax and wane. Therefore, being adept at recognizing the more subtle features and manifestations of catatonia is paramount to arrive at the proper diagnosis and treatment plan.

Given the prevalence of catatonia and its associated morbidity, early identification and treatment is the key to improving outcomes. Catatonia should be considered in all patients that display psychomotor retardation or decreased overall responsiveness, especially in those with affective and psychotic disorders. In addition, validated screening instruments such as the Bush–Francis Catatonia Rating Scale may aid in the detection of catatonic signs and help prevent a missed diagnosis.[8] While, unfortunately, no screening tool was used in this case, it is highly encouraged. The failure to recognize and treat catatonia in a timely manner could result in severe complications related to immobility including deep venous thrombosis, pneumonia, and pressure ulcers.[4],[5],[6],[7] In psychotic patients, making the diagnosis is even more crucial, as treatment with first-generation antipsychotics is generally contraindicated due to the significantly increased risk of neuroleptic malignant syndrome.[9] Although the use of atypical antipsychotics for catatonic patients with underlying psychotic disorders is controversial, evidence from case reports and retrospective studies have demonstrated effectiveness.[9]

Currently, benzodiazepines are the recommended first-line treatment for catatonia, and a partial response may be observed within minutes of administration, as was seen in our patient.[6],[7],[9] Oftentimes, the first sign of improvement will be talking in mute patients.[9] Of the benzodiazepines, lorazepam is the one most commonly used; however, it is still unknown whether it is the most efficacious.[9] Other benzodiazepines that have been used with success include diazepam, oxazepam, and clonazepam.[9] As no randomized clinical trials have been conducted to test the efficacy of this treatment, these recommendations are based on numerous retrospective and case studies.[2],[4],[5],[9] These studies reveal that up to 80% of patients will achieve remission, often within a week of benzodiazepine treatment.[2],[4],[5],[9] Moreover, the patients least likely to respond to benzodiazepines are those with chronic catatonia associated with schizophrenia.[9] This further underscores the necessity of preventing delays in diagnosis. Furthermore, it is recommended to continue treatment for 3–6 months to prevent relapse.[2] Patients who are refractory to treatment or who achieve only a partial response should be recommended to undergo electroconvulsive therapy (ECT) or ECT with a benzodiazepine.[1],[5],[7],[9]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry 2016;6:391-8.
2Jhawer H, Sidhu M, Patel RS. Missed diagnosis of major depressive disorder with catatonia features. Brain Sci 2019;9. pii: E31.
3Tandon R, Heckers S, Bustillo J, Barch DM, Gaebel W, Gur RE, et al. Catatonia in DSM-5. Schizophr Res 2013;150:26-30.
4Tuerlings JH, van Waarde JA, Verwey B. A retrospective study of 34 catatonic patients: Analysis of clinical care and treatment. Gen Hosp Psychiatry 2010;32:631-5.
5van Waarde JA, Tuerlings JH, Verwey B, van der Mast RC. Electroconvulsive therapy for catatonia: Treatment characteristics and outcomes in 27 patients. J ECT 2010;26:248-52.
6Bhati MT, Datto CJ, O'Reardon JP. Clinical manifestations, diagnosis, and empirical treatments for catatonia. Psychiatry (Edgmont) 2007;4:46-52.
7Rosebush PI, Mazurek MF. Catatonia and its treatment. Schizophr Bull 2010;36:239-42.
8Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand 1996;93:129-36.
9Sienaert P, Dhossche DM, Vancampfort D, De Hert M, Gazdag G. A clinical review of the treatment of catatonia. Front Psychiatry 2014;5:181.