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Year : 2013  |  Volume : 22  |  Issue : 1  |  Page : 32-36  Table of Contents     

Catatonia: Etiopathological diagnoses and treatment response in a tertiary care setting: A clinical study

1 Department of Psychiatry, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India
2 Department of Psychiatry, Nalanda medical College, Patna, India
3 Department of Psychiatry, IHBAS Institute of Human Behaviour and Allied Sciences, Delhi, India

Date of Web Publication24-Dec-2013

Correspondence Address:
Santosh Ramdurg
Department of Psychiatry, SDM College of Medical Sciences and Hospital, Dharwad 580 009, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-6748.123612

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Aim: Catatonia is caused by a variety of psychiatric and organic conditions. The onset, clinical profile, and response to treatment may vary depending on the underlying cause. The study is an attempt to explore clinical profile, possible etiological correlates with neurotic/psychotic spectrum illnesses, and response to treatment and outcome in patients of catatonia. Materials and Methods: Retrospective chart analysis by using semistructured data sheet for the analysis of sociodemographic data, clinical profile, precipitating event, and response to treatment in patients with catatonic symptoms admitted to IHBAS (Institute of Human Behaviour and Allied Sciences, New Delhi, India) from January 2009 to December 2010 was undertaken. Results: Catatonia was commonly observed in patients with the following profile - late twenties, female, Hindu religion, urban background, and housewives. Psychotic spectrum disorder (57%, N=35) was the most commonly entertained diagnosis and affective disorder (18%, N=11) being the second common. Thirty four percent of the subjects responded to lorazepam treatment and rest required modified electroconvulsive therapy (MECT). Conclusion: Catatonia is more likely to be associated with Schizophrenia and Other Psychotic Disorders in Indian settings. Majority of patients responded to therapy either by lorazepam alone or to its augmentation with modified ECT. The study being a retrospective one, the sample being representative of the treatment seeking group only, and unavailability of the follow up data were the limitations of the study

Keywords: Catatonia, etiopathogenesis, response to treatment

How to cite this article:
Ramdurg S, Kumar S, Kumar M, Singh V, Kumar D, Desai NG. Catatonia: Etiopathological diagnoses and treatment response in a tertiary care setting: A clinical study. Ind Psychiatry J 2013;22:32-6

How to cite this URL:
Ramdurg S, Kumar S, Kumar M, Singh V, Kumar D, Desai NG. Catatonia: Etiopathological diagnoses and treatment response in a tertiary care setting: A clinical study. Ind Psychiatry J [serial online] 2013 [cited 2022 Nov 30];22:32-6. Available from: https://www.industrialpsychiatry.org/text.asp?2013/22/1/32/123612

Catatonia is observed in psychiatric patients in both acute and chronic settings. Despite its common occurrence, catatonia remains a poorly understood, poorly studied, and poorly recognized syndrome, which will continue to challenge clinician's diagnostic and management skills. Difficulties in the clinical conceptualization and management of catatonia have been called 'the catatonic dilemma'. [1] Theoretical organization of approach to a case of catatonia remains disputed. [2] Many areas of overlap make the presentation unclear.

Various authors have classified Catatonia as chronic or acute, isolated acute episodes versus chronic recurrent or periodic catatonia retarded or excited forms, independent syndrome versus those occurring in association with other psychiatric, neurological, and medical illnesses. [3],[4] Various classifications for catatonia have been proposed. Catatonia as a separate diagnostic entity is being proposed in upcoming ICD 11 and DSM-V. [5],[6]

Its management with benzodiazepines, especially lorazepam has been widely studied and it has been employed in the treatment of the various forms of catatonia, but the effect size of most studies employing benzodiazepines for management of catatonia is small and they have methodological shortcomings. [2],[7],[8],[9],[10],[11],[12] Though lorazepam has been proven to be a treatment with fair results, the degree of symptom response in different patients may vary. ECT is considered the next modality of treatment, especially for resistant cases. ECT has been shown to be effective in the management of prolonged catatonia, and the cases that have shown partial response to pharmacologic treatments. [13],[14]

Though, we realize that catatonia is a condition caused by a variety of metabolic, neurological, psychiatric, and toxic conditions including neuroleptic malignant syndrome (NMS) and extra pyramidal syndrome (EPS), and our understanding about the etiopathogenesis of the illness has improved in last three decades it still poses difficulties in diagnosis and treatment, and has guarded outcome in some cases. [15],[16]

There are very few studies that have assessed the etiopathogenesis and phenomenology of catatonia in India. [9],[10],[11],[12] Most of the data are in the form of case reports, in which catatonia due to various causes has been reported and some have reported the use of electroconvulsive therapy (ECT) and lorazepam.

There are only a few studies that have been conducted in India with the aim to explore the etiopathogenesis and treatment response in patients presenting with catatonia in inpatient treatment settings. Findings from most of these differ from rest of the world in terms of occurrence of catatonia in association with different psychiatric illnesses and response to treatment. There are only a few studies available that have evaluated precipitating event(s) prior to catatonia. With these lacunae in mind, we attempted exploring the etiopathogenesis of catatonia, clinical profile of these individuals, precipitating event(s) prior to catatonia, and duration required for achieving response to treatment with Lorazepam and MECTs. We have also attempted to explore the possible association of catatonic syndrome to neurotic/psychotic spectrum illnesses and find possible etiological correlates to it.

   Materials and Methods Top


Institute of Human Behaviour and Allied Sciences (IHBAS) is an exclusive mental-health-related service providing tertiary care institute situated in northern India with inpatient and outpatient facilities. All patients admitted in the inpatient were routinely assessed using a detailed semistructured data sheet that was recorded systematically by both junior and senior resident (trained psychiatrist). The diagnosis of catatonia was made if the patient presents with following symptoms for more than 24 hours: [1] motoric immobility or stupor, [2] excessive motor activity, [3] extreme negativism or mutism, [4] peculiarities of voluntary movement as evidenced by posturing stereotyped movements, prominent mannerisms, or prominent grimacing, [5] echolalia or echopraxia and other catatonic symptoms. In some cases, Brush Francis catatonic rating scale was applied for evaluation to monitor the response of treatment in majority of the cases. [17]

After detailed evaluation, all patients presenting with catatonia are initially given a trial of parental or oral lorazepam (through Ryles Tube) for 3-4 days at doses ranging from 4-12 mg/day. Patients who do not respond to lorazepam trial or relapse even after receiving adequate trial of lorazepam are applied modified electroconvulsive therapy (MECT). Once they recover from catatonia they are evaluated for lifetime psychiatric illness. Depending on the diagnosis, majority of the subjects were routinely rated on various instruments (e.g., PANSS, HAM-D, YMRS, BFCRS, AIMS etc.).

It was a cross-sectional study of all patients who were admitted to the inpatient psychiatry unit of IHBAS, New Delhi with catatonic symptoms between January 2009 and December 2010.

   Results Top

During the given period (of two years) a total of 61 patients were admitted with provisional diagnosis of catatonia. Sociodemographic data suggests that the mean age of presentation of catatonia was 28 years. Prevalence was more in females, with education less than matriculation, Hindu religion, married persons, from urban background, housewives and students by occupation [Table 1].
Table 1: Clinical diagnosis

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Family history of psychiatric illness was present in 16% of patients with the equal prevalence of affective and psychotic disorders among the family members [Table 1]. Substance use disorder was present in 20% of patients with nicotine being the most common substance abused. Mean duration of catatonic symptoms at presentation was 26 days with the median of 7 days and minimum duration of 1 day and maximum of 8 months (240 days). The mean duration of psychiatric illness prior to the current presentation was 3.3 years with the median of 1 year. In 49% of patients, catatonia had its onset in association with some precipitating event, among which fever and interpersonal problems were found to be the most common.

Catatonia under evaluation was commonly entertained (39.3%) diagnosis at admission followed by psychotic spectrum disorders (32.7%) and affective disorder (16.3%) [Table 2]. At the time of discharge, 35 patients were diagnosed with schizophrenia and other psychotic illness, 11 with affective disorders, and 9 with catatonia under evaluation. Most of the cases with diagnosis of catatonia under evaluation turned out to suffer from psychotic spectrum disorder at discharge.
Table 2: Response to lorazepam treatment

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Initially all subjects received injection lorazepam. While treating with lorazepam when there was no change in the symptoms of catatonia it was considered 'no response' whereas when the patient became at least minimally communicative (no more mute) or started even minimally taking oral feed, he/she was considered to have partial response. If the patient had unassisted activity of daily living (ADL) and had no difficulty in feeding or communicating verbally it was considered good response. When there was prolonged (usually 3 to 5 days) partial response or no response to lorazepam, the modified electroconvulsive therapy (MECT) was then considered and administered after appropriate consent and evaluation. The MECTs were administered on alternate days unless there was any contraindication to the same. The MECTs were discontinued if there clinical response to Lorazepam reached a plateau after three to five consecutive MECTs. A total of 34 patients showed good response to trial of lorazepam. Partial response was seen in seven and no response to lorazepam was observed in 20. Among good responders 40% responded within 48 hours of initiation of therapy [Table 3]. When MECT was added to the no or partially responsive patients group, the catatonic symptoms of 42% of them responded and but 2% showed no response to this modality as well. Six out of eleven patients with affective disorder required MECT. Eighteen out of 35 patients from psychotic spectrum disorder category and three out of nine patients from catatonia under evaluation: Three out of nine category required MECT. Regarding response to lorazepam, there was no statistically significant difference between patients with affective disorder and schizophrenia spectrum disorder. Altogether, nine patients required more than 30 days of treatment for recovering completely from catatonia. Out of these nine, two cases suffered from affective disorder and seven from schizophrenia and psychotic spectrum disorder. Minimum three MECT and maximum 35 MECT were used to treat the group. ANOVA was conducted to find difference in duration of treatment required for complete response among different contextual disorders (e.g., bipolar disorder, psychosis, and catatonia under evaluation) associated with catatonia. There was no statistically significant difference between these two groups. We also subjected the data to correlation statistics to evaluate relationship between existence of any difference in total duration of illness versus total duration of catatonia, total duration of catatonia versus time duration for complete response, and total duration of illness versus time duration for complete response. The result did not show any statistical significance difference among these different groups. Almost all the cases were screened for common organic conditions and had investigated for thyroid function tests, neuroimaging studies (CT/MRI brain) along with routine clinical investigation (hemogram, biochemistry etc). In most of the cases, the investigations were found to be within normal limit except in seven (three had vitamin B12 deficiency, hemorrhagic contusion, granuloma, and lacunar infarct was present in three different patients).
Table 3: Illness and time duration for complete response (ANOVA)

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   Discussion Top

The study showed catatonia to be occurring commonly in young, having its onset in late twenties (28 years) but could it occur at any age, which is in accordance with previous studies. [9] It was found to be common in females, patients with education less than matriculation, Hindu religion, housewives and students, patients from urban background, which again matches with others studies and represented profile of the majority of the patients. Almost equal prevalence in both married and unmarried groups is suggestive of no significant role of marital status. Few patients had a family history of psychiatric illness (16.4%) suggestive of possible genetic etiology that is comparable with other studies. [10] This study has its merits as it was conducted in a developing country at a tertiary care cum training mental health institution that serves the northern part of India. The clinical profile of the sample was matched with rest of that described in world literature regarding the age of onset, sex, education level, occupation, and family history of psychiatric illness. Substance use disorder was found to be less common in our patients, compared to the sample from other studies. This issue requires further in-depth examination.

The results showed that catatonia occurred in all kind of illnesses ranging from psychotic spectrum to mood disorders, mental retardation, and organic brain syndrome suggestive of catatonia being an illness of multifactorial etiology. [3],[14] We found catatonia to be in common association with more in schizophrenia and other psychotic spectrum disorders while compared to mood disorders with is a comparatively contradictory finding from rest of the world but it matched with many Indian studies. [9],[10],[12] Study by Dutt et al. reported catatonia to be more frequently associated with psychotic disorders rather than mood disorders. [12] A multicentric study on schizophrenia found the highest frequency of catatonic schizophrenia in India (21.8%) while the worldwide reported average was 8.2%. [10] In majority of patients, diagnoses remained catatonia under evaluation at admission and also at discharge, requiring longer follow up for confirming its etiology. These patients presented with exclusively catatonic symptoms without any identifiable causative or associated disorder despite of close observation in the ward. This group of patients require long-term follow up after discharge for finding an etiological diagnosis. In our study, we evaluated diagnosis at admission (provisional diagnosis) and at discharge (final diagnosis after investigation and having the patient evaluated in detail). Apart from the syndromal diagnosis, the provisional contextual diagnosis (e.g. bipolar or psychotic spectrum disorder) that was entertained at the time of admission for management and communication purposes often changed at the time of discharge because of the detailed history, ward observation, and the opportunity of mental status examination after the catatonic symptoms resolved during the management process. At the time of discharge, majority of patients were diagnosed to be having schizophrenia and other psychotic disorders in association with the catatonic symptoms rather than affective disorder. In this study, we also looked into precipitating event prior to the onset of catatonia and we found nearly half of them had some significant (either to patient or the informant/relative) precipitating event prior to catatonia onset and majority of them had events such as death of loved one, love failure or divorce etc., Infection was present in one fourth of patients.

We also analyzed the data on response to treatment. The response to treatment was considered 'no response' when there was no change in mutism/negativism/oral intake, whereas it was considered 'partial response' when the patient became at least minimally communicative (no more mute) or started even minimally taking oral feed. If the patient had unassisted ADL and had no difficulty in feeding or communicating verbally it was considered 'good response'. Regarding the response more than half of them responded to lorazepam and rest required MECT. Existing literature suggests that nearly 80% of them do respond to lorazepam that was not observed in our sample.

Among poor responders to MECTs, nearly half of them had psychotic spectrum disorder and another half had affective disorder. Seven out of nine cases of psychotic spectrum disorder turned out to be refractory requiring more than 1 month of therapy for complete resolution of catatonia that potentiates the fact that psychotic spectrum disorder turning chronic shows poor response to MECTs.

Statistical tests (correlation analysis and ANOVA) could not demonstrate any significant difference between affective and psychotic spectrum mental illnesses associated with catatonia as far as response to treatments is concerned. This is in accordance to earlier findings. This also suggests that catatonia is multifactorial independent syndrome requiring special category in DSM-V and ICD-11.

We are bringing few important issues in to the discussion. First though catatonia is currently considered a multifactorial illness, it responds to specific treatments either in the form of lorazepam or MECT in majority of cases that were seen in our study. Secondly benzodiazepines act by enhancing the GABA activity in the brain. Studies have shown that patients with neurotic spectrum illness especially those having anxiety disorder have low GABA activity in their brains. [8] Patients with affective disorders in general respond well to MECT. The same holds true for patients with catatonia. Many international studies report that catatonia is commonly seen in association with mania rather than psychotic spectrum disorder.

The study has given some important insights. Catatonia is a frequently diagnosed condition in Indian setup. Catatonia continues to be more likely associated with schizophrenia and other psychotic disorders than mood disorders in this part of the world. Catatonia tends to appear early in age. It is described that catatonia indicates a better prognosis when associated with schizophrenia and other psychotic disorder that holds well in the study sample because almost all patients responded to therapy either with lorazepam alone or to its augmentation with modified ECT. Strengths of study are fair sample size, associated diagnosis being made as per ICD-10 by three different cadres of psychiatrists that increased the reliability of diagnosis. Inpatients follow up of the patients till recovery made the findings stronger.


The retrospective design of the study was the foremost limitation of the study. The sample was representative of treatment seeking group at a tertiary care setting, rather than a community sample. No follow up data were available. Few of the outpatient population of patients with lesser severity of catatonic symptoms and those who were not admitted for various reasons were likely to have been missing in this study inducing bias.

   References Top

1.Brenner I, Rheuban WJ. The catatonic dilemma, Am J Psychiatry 1978;135:1242-3.  Back to cited text no. 1
2.Taylor MA, Fink M. Catatonia in psychiatric classification: A home of its own. Am J Psychiatry 2003;160:1233-41.  Back to cited text no. 2
3.Fink M, Taylor MA. The many varieties of catatonia. Eur Arch Psychiatry Clin Neurosci 2001;251:s8-13.  Back to cited text no. 3
4.Taylor MA, Fink M. Catatonia in psychiatric classification: A home of its own. Am J Psychiatry 2003;160:1233-41.  Back to cited text no. 4
5.Fink M. Catatonia from its creation to DSM-V: Considerations for ICD. Indian J Psychiatry 2011;53:214-7.  Back to cited text no. 5
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6.Verhoeven WM, van der Heijden FM, Pfuhlmann B, Stöber G. Psychomotor Psychoses - The Enigmatic Catatonic Phenotype. Eur Psychiatr Rev 2011;4:78-83.  Back to cited text no. 6
7.Rosebush PI, Hildebrand AM, Furlong BG, Mazurek MF. Catatonic syndrome in a general psychiatric inpatient population: Frequency, clinical presentation, and response to lorazepam. J Clin Psychiatry 1990;51:357-62.  Back to cited text no. 7
8.Ungvari GS, Kau LS, Wai-Kwong T, Shing NF. The pharmacological treatment of catatonia: An overview. Eur Arch Psychiatry Clin Neurosci 2001;251:s31-4.  Back to cited text no. 8
9.Malur C, Pasol E, Francis A. ECT for prolonged catatonia. J ECT 2001;17:55-9.  Back to cited text no. 9
10.Daniels J. Catatonia: Clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci 2009;21:371-80.  Back to cited text no. 10
11.Taylor MA, Fink M. The catatonia syndrome forgotten but not gone. Arch Gen Psychiatry 2009;66:1173-7.  Back to cited text no. 11
12.Fink M. Catatonia: A syndrome appears, disappears, and is rediscovered. Can J Psychiatry 2009;54:437-45.  Back to cited text no. 12
13.Banerjee A, Sharma LN. Catatonia incidence in acute psychiatric admissions. Indian J Psychiatry 1995;37:35-40.  Back to cited text no. 13
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14.Chalasani P, Healy D, Morriss R. Presentation and frequency of catatonia in new admissions to two acute psychiatric admission units in India and Wales. Psychol Med 2005;35:1667-75.  Back to cited text no. 14
15.Thakur A, Jagadheesan K, Dutta S, Sinha VK. Incidence of catatonia in children and adolescents in a paediatric psychiatric clinic. Aust N Z J Psychiatry 2003;37:200-3.  Back to cited text no. 15
16.Dutt A, Grover S, Chakrabarti S, Avasthi A, Kumar S. Phenomenology and treatment of Catatonia: A descriptive study from north India. Indian J Psychiatry 2011;53:36-40.  Back to cited text no. 16
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17.Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand 1996;93:129-36.  Back to cited text no. 17


  [Table 1], [Table 2], [Table 3]

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