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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 1  |  Issue : 4  |  Page : 301-303

Multifactorial organic etiological agents causing catatonia: A learning experience


1 Department of Psychiatry, Institute of Post Graduate Medical Education and Research Hospital, Kolkata, West Bengal, India
2 Department of General Medicine, ESI Hospital, Belur, West Bengal, India

Date of Web Publication31-Aug-2015

Correspondence Address:
Dr. Ajay Halder
Puspak Apartment, GR-FR, FL-A, 14/17A, East Mall Road, Kolkata - 700 080, West Bengal
India
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Source of Support: Nil., Conflict of Interest: There are no conflicts of interest.


DOI: 10.4103/2395-2296.163939

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  Abstract 

Catatonia is a well-known neuropsychiatric clinical condition. The most common cause of catatonia is psychiatric illnesses like schizophrenia and depression. The important clinical features of catatonia are ambitendency, automatic obedience, catalepsy, echolalia, echopraxia, rigidity, posturing, etc., Several organic causes are also responsible for catatonic symptoms, which we don't keep in our mind in our day-to-day practice. Here, we described case series of catatonia that are related to organic etiological factor.

Keywords: Catatonia, investigation, posturing, rigidity


How to cite this article:
Halder A, Biswas A. Multifactorial organic etiological agents causing catatonia: A learning experience. Int J Educ Psychol Res 2015;1:301-3

How to cite this URL:
Halder A, Biswas A. Multifactorial organic etiological agents causing catatonia: A learning experience. Int J Educ Psychol Res [serial online] 2015 [cited 2019 Jul 21];1:301-3. Available from: http://www.ijeprjournal.org/text.asp?2015/1/4/301/163939


  Introduction Top


The concept of catatonia was first described by Kahlbaum (1874). Catatonia is a well-known neuropsychiatric syndrome, and it's important clinical features are mutism, stupor, refusal to eat or drink, posturing and excitement or hypokinesia.[1] However, it has been suggested that catatonia is underrecognized and underdiagnosed.[2] Nowadays, the introduction of antipsychotics has reduced significantly the incidence of catatonia but it is still not uncommon.[3] The exact cause of catatonia has not been detected till now, but some hypotheses have been offered. A "topdown modulation" of basal ganglia due to deficiency of cortical gamma amino butyric acid, the primary inhibitory neurotransmitter of the brain, may explain the motor symptoms of catatonia.[4] Catatonia is also caused by a sudden and massive blockade of dopamine.[5] In chronic catatonia with prominent speech abnormalities, positron emission tomography has identified abnormalities in metabolism bilaterally in the thalamus and frontal lobes.[6] Identification of the underlying organic causes, if any, should be a priority in the management of catatonia. Prompt treatment in the early phases of catatonia is crucial to obtain a lasting abatement of symptoms. We present four cases to highlight the organic causation of catatonia and the importance of early recognition of such cases.


  Case Reports Top


Case 1

N.S, a 40-year-old housewife, admitted in Institute of Postgraduate Education and Research (IPGME and R) Hospital, Kolkata with complaints of weakness and lethargy followed by gradual withdrawal from household activities for last 8 months. Eventually, she became mute and showed some kind of unusual posturing. Physical examination was grossly normal except pallor. Mental state examination revealed some catatonic features including of waxy flexibility, mutism, posturing and rigidity. Blood examination showed hemoglobin 9 g/dl with significant raised mean corpuscular volume (MCV). Other laboratory investigations including thyroid function tests, liver function tests, serum electrolytes, renal function tests, C-reactive protein and cranial computed tomography (CT) were normal. She was not responded at all with adequate important treatment varieties such as a course of antipsychotic like risperidone, intramuscular lorazepam injection, modified electroconvulsive therapy, and psychotherapy. As her blood parameter was very much suggestive of folate and Vitamin B12 deficiency, we started hydroxycobalamine 1 mg intramuscular injection on every alternate day and tablet folic acid orally 5 mg daily. After continuous 2 weeks of treatment with this regime, she showed marked improvement in all aspects of catatonia. Her hemoglobin level was measured subsequently, and it was 12.5 mg/dl with normal MCV.

Case 2

A.S, a 68-year-old Hindu married depressive male was on treatment with 40 mg fluoxetine daily. After 2 weeks of treatment, he developed some catatonic features such as stupor, rigidity, cataplexy, and posturing. He was not febrile at all. His serum sodium level was 112 meq/L, and potassium level was 4.1 meq/L. Other important investigations such as liver function tests, serum creatinine level, complete blood count, chest X-ray, and thyroid function tests were within normal range. Fluoxetine was suspected as the offending agent to cause hyponatremia. Therefore, it was discontinued, and the patient was on supplementary sodium therapy. Miraculous improvement of catatonic symptoms was noted after correction of hyponatremia. Subsequently, the patient was discharged with tablet mirtazapine as an antidepressive agent.

Case 3

An 18-year-old school girl, T.D, admitted in IPGME and R, Hospital due to sudden onset mutism, posturing and negativism. She had a history of fever for 5 days and then she rapidly developed all these catatonic features. She also had an episode of seizure on the day of admission to the psychiatry unit. She was febrile, but the rest of the physical examination was normal except for catatonic symptoms. Electroencephalography showed slow waves and CT of the brain was normal. Cerebrospinal fluid analysis for polymerase chain reaction was confirmed a positive infection with herpes simplex virus type 1. She was on intravenous infusion of acyclovir 10 mg/kg body weight in every 8 h interval for 10 days and oral antiepileptic medication (sodium valproate). Gradually, she made a slow but complete recovery.

Case 4

A 15-year-old girl, S.S, attended IPGME and R outpatient department with behavioral changes. She was smiling to self and had been withdrawn from social activities over the previous 3 months. She also exhibited posturing and catalepsy. Her physical examination was normal except for a facial butterfly rash and catatonic features. She was treated with risperidone at the district hospital with poor response. Investigations revealed a high erythrocyte sedimentation rate of 120 mm/1st hour. Anti-Smith and anti-double-stranded DNA antibodies were positive. Hence oral prednisolone was started. Her catatonic symptoms resolved after adding prednisolone to the treatment regime.


  Discussion Top


Several medical, neurological and metabolic disorders are associated with or etiologically related to the clinical syndrome of catatonia.[1],[7],[8] Pernicious anemia is associated with psychiatric conditions such as mood disorder, psychosis and dementia and catatonia.[9],[10] Vitamin B12 deficiency as a causative factor of catatonic symptoms has also been established.[11] Our first case supports the view that there is an association between catatonia and Vitamin B12/folic acid deficiency.

Metabolic abnormalities such as hyponatremia may cause catatonia also.[12] Our second patient's catatonic symptoms are likely to have been due to hyponatremia. The importance of performing serum electrolytes in such patients is highlighted here.

Viral encephalitis and meningitis are not uncommon conditions in our country, India. The presentation may vary from mild symptoms such as headaches to severe presentation such as delirium and seizures. Our third patient developed catatonic symptoms due to viral encephalitis and catatonic symptoms resolved following anti-viral treatment. This case illustrates the importance of considering the possibility of central nervous system infections in the assessment of catatonia.

Patients with systemic lupus erythematosus (SLE) may commonly present with psychiatric and neurological symptoms. Although rarely seen, patients with SLE presenting with catatonia.[13] Our fourth patient presented with catatonic symptoms following SLE and the catatonic symptoms improved with steroids. This case again illustrates the importance of excluding autoimmune disorders such as SLE and the need to perform relevant investigations in the assessment of catatonia, particularly in young female patients.


  Conclusions Top


Although many catatonic presentations are due to psychiatric conditions, it is mandatory to look for organic causes, as early detection and treatment of them will certainly improve the prognosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Daniels J. Catatonia: Clinical aspects and neurobiological correlates. J Neuropsychiatry Clin Neurosci 2009;21:371-80.  Back to cited text no. 1
    
2.
van der Heijden FM, Tuinier S, Arts NJ, Hoogendoorn ML, Kahn RS, Verhoeven WM. Catatonia: Disappeared or under-diagnosed? Psychopathology 2005;38:3-8.  Back to cited text no. 2
    
3.
Stompe T, Ortwein-Swoboda G, Ritter K, Schanda H, Friedmann A. Are we witnessing the disappearance of catatonic schizophrenia? Compr Psychiatry 2002;43:167-74.  Back to cited text no. 3
    
4.
Northoff G. What catatonia can tell us about "top-down modulation": A neuropsychiatric hypothesis. Behav Brain Sci 2002;25:555-77.  Back to cited text no. 4
    
5.
Osman AA, Khurasani MH. Lethal catatonia and neuroleptic malignant syndrome. A dopamine receptor shut-down hypothesis. Br J Psychiatry 1994;165:548-50.  Back to cited text no. 5
    
6.
Lauer M, Schirrmeister H, Gerhard A, Ellitok E, Beckmann H, Reske SN, et al. Disturbed neural circuits in a subtype of chronic catatonic schizophrenia demonstrated by F-18-FDG-PET and F-18-DOPA-PET. J Neural Transm 2001;108:661-70.  Back to cited text no. 6
    
7.
Fink M, Shorter E, Taylor MA. Catatonia is not schizophrenia: Kraepelin's error and the need to recognize catatonia as an independent syndrome in medical nomenclature. Schizophr Bull 2010;36:314-20.  Back to cited text no. 7
    
8.
Fink M. Rediscovering catatonia: The biography of a treatable syndrome. Acta Psychiatrica Scandinavia suppl 2013;441:1-47.  Back to cited text no. 8
    
9.
David AS, Fleminger S, Kopelman MD, Lovestone S, Mellers JD. Lishman's Organic Psychiatry. Oxford: Wiley-Blackwell; 2009.  Back to cited text no. 9
    
10.
Jauhar S, Blackett A, Srireddy P, McKenna PJ. Pernicious anaemia presenting as catatonia without signs of anaemia or macrocytosis. Br J Psychiatry 2010;197:244-5.  Back to cited text no. 10
    
11.
Berry N, Sagar R, Tripathi BM. Catatonia and other psychiatric symptoms with vitamin B12 deficiency. Acta Psychiatr Scand 2003;108:156-9.  Back to cited text no. 11
    
12.
Lee JW, Schwartz DL. Catatonia associated with hyponatremia. Neuropsychiatry Neuropsychol Behav Neurol 1997;10:63-4.  Back to cited text no. 12
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13.
Pustilnik S, Trutia A. Catatonia as the presenting symptom in systemic lupus erythematosus. J Psychiatr Pract 2011;17:217-21.  Back to cited text no. 13
    




 

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