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Atypical Presentation of Catatonia in a 20-year-old Male with a Traumatic Brain Injury: A Case Study

1Private practice, Arlington Heights, IL, 60005
2Lakeview Specialty Hospital and Rehab, Waterford, WI, 53185
3Rehabilitation Medicine Specialists, Elgin, IL, 60123
*Corresponding Author:  Private practice,



Catatonia is a syndrome that usually presents with disturbed motor functions, mood, and thought.  It is often effectively treated using the benzodiazepine lorazepam.  This article reports on a patient with an atypical presentation of catatonia that responded well to treatment with lorazepam. Case Description: The case described is a 20-year-old male who had suffered a traumatic brain injury after a motor vehicle accident.  While he did not display characteristic features of catatonia, such as mutism, stupor, or posturing, he did present with language processing and social interaction deficits.  His speech did not fit criteria for any subtype of aphasia, and was characterized by fluent expressive speech with mild-moderate paraphasic errors and virtually complete inability to demonstrated language comprehension.  He was treated with lorazepam because it was hypothesized that his symptoms were a result of catatonia. Treatment with a low dose of lorazepam successfully treated the patient’s catatonia, and his inability to respond to questions or execute instructions and general lack of social reciprocity began to resolve within hours of the initial administration. Conclusion: This finding supports the use of lorazepam in treating patients with atypical presentation of catatonia.

Keywords:  Atypical catatonia, traumatic brain injury, lorazepam


Catatonia, a syndrome that usually presents with disturbed motor functions, mood, and thought, was first identified in 1874 by Karl Kahlbaum [1, 2]. Catatonia literally means ‘to stretch tight.

[3].’ Kahlbaum, a German psychiatrist, characterized this syndrome with symptoms such as mutism, negativism, posturing, grimacing, staring, mannerisms, echophenomena [1, 4, 5], catalepsy, waxy flexibility, automatic obedience, and ambitendency [4]. He defined characteristic features as paralysis, repetitive movements, stupor, seizures, and excited states.  As the 20th century progressed, catatonia began to be increasingly conceptualized as a type of schizophrenia.  Other psychiatric and neurological diseases may also have catatonic symptoms [1, 2, 6, 7], including mood disorders, iatrogenic medication effects, and various forms of acquired neurological impairment.  It was not until the DSM-IV that catatonia was added as a specifier of mood disorders as well as schizophrenia [1, 6].

The prevalence of catatonia is unknown, possibly occurring in 7-31% of the psychiatric population [8]. Catatonia is sometimes misdiagnosed because of the stereotype that catatonic patients will be mute and immobile.  However, most catatonic patients can speak and move freely [4]. It occurs most often in patients with mood disorders [8]. Approximately 25-50% of people who demonstrate catatonic symptoms have an affective disorder, with about 15-20% of people with bipolar disorder demonstrating at least one catatonic symptom [4].  Although catatonia is traditionally considered a specifier for schizophrenia, research suggests that only 5-15% of patients with catatonia have an underlying diagnosis of schizophrenia [8, 4].  Among catatonic patients on a psychiatric unit, the prevalence an associated general medical condition is approximately 20-25% [8]. Research has suggested that people with catatonic symptoms are significantly more likely to have had a history of brain injury when compared to manic, depressed, or surgical patients [9].

Catatonia has both a retarded and excited form.  The retarded form includes symptoms such as posturing, rigidity, repetitive actions, mutisms, and lack of response to stimulation.  The excited form is marked by excitement, continuous agitation, and delirium [1]. Cognitive and affective changes are also present in patients with catatonia [8, 4].  Lesions in numerous areas of the brain (including the frontal cortex, basal ganglia, cerebellum-pons, parietal lobe, and corpus callosum) have been linked to catatonia.  Degeneration of the frontal lobe and ruptured anterior artery aneurysms have also been reported to cause catatonic symptoms.  These findings suggest that catatonia due to brain injury is not caused by a focal insult, but rather by pathway dysregulation [8, 4].

First-line treatments for catatonia often include benzodiazepines (usually lorazepam) [10, 3, 11] and electroconvulsive therapy (ECT) [10, 2]. A 1995 study by Hawkins et al. found that lorazepam was effective in resolving catatonic symptoms in 60-80% of reported cases [6].  ECT alone had a higher resolution rate, resolving 85% of cases [10].  However, recent research has suggested that, within one year, there is a high relapse rate with ECT [12]. Antipsychotics were effective in only 7.5% of cases [10] and may risk causing or worsening catatonic symptoms [15].  Benzodiazepines are agonists of the GABA-benzodiazepine-chloride receptor complex, and have anxiolytic, sedative, anticonvulsant, amnestic, and relaxant properties.  They bind adjacently to the receptor and increase the affinity of GABA for the receptor.  This process increases the inhibitory synaptic action of GABA [13]. Dosages of lorazepam for treatment of catatonia vary slightly, but research supports 1-2 mg intravenously every 4-12 hours for effective treatment.  This dosage may need to be increased over the course of a few days [8].


A 20-year-old Caucasian male was transferred from a hospital to an acute neurobehavioral rehabilitation unit in August 2010.  The patient was involved in a motor vehicle accident one month prior to admission.  He was the unrestrained driver of the vehicle, and was thrown approximately 50 feet.  He was found unconscious on the scene and was intubated.  Imaging, including head CT, showed a right temporal depressed skull fracture with subarachnoid hemorrhage, right lateral orbital fracture, and right frontal lobe injuries.  CT of the cervical spine revealed right laminar fracture at C3.  Further workup showed fracture of the left scapular body.  He was initially felt to have had a focal seizure.  He sustained a previous traumatic brain injury in a motor vehicle accident in 2006.  His medical history was otherwise unremarkable. 

At the first hospital, the patient required chemical and mechanical restraints to manage physical aggression and elopement.  He was transferred to a psychiatric unit until placement in a neurobehavioral program could be secured.  PATIENT X was disoriented, restless, and difficult to redirect.  He did not have any further seizures. 

Upon admission to this inpatient rehab program, PATIENT X was placed on intensive supervision due to wandering. During the beginning of his rehabilitation, he was on only rare occasions able to provide his name after numerous repetitions of the question. Instead, he would look at the speaker, appearing to be listening to and understanding what was being said, and then either talk about something completely off topic or say, “hm?” or “mm-hm.”  For example, when asked to identify his current location, he responded:  “the wheel was broke yesterday, but now she is gone.”  He had difficulty maintaining eye contact with the speaker.  He was free from overt motor function abnormalities, although he did demonstrate cogwheel rigidity on exam. Although the patient had difficulties with language, he did not fit the criteria for any subtype of aphasia.  His language processing difficulties were characterized by fluent expressive speech with mild to moderate paraphasic errors and virtually complete inability to demonstrate language comprehension.  PATIENT X demonstrated anomia and was unable to carry out written or oral instructions. 

A few weeks into his rehabilitation, the neuropsychologist suggested that PATIENT X was presenting with catatonia because his difficulties with expressive speech (e.g., preservative speech, difficulty shifting topics) did not better fit the criteria for a disorder such as aphasia.  After consulting with the physician and psychiatrist, a low dosage of lorazepam (0.5mg) was administered for a trial of three days.  Within the first day of administration, improvements were noted across disciplines of care.  PATIENT X was able to participate more in therapies as well as communicate with others.  A few hours after the first dose of lorazepam was administered, the patient was able to perform seven consecutive one-step instructions (e.g., “hand me the pen”), to answer questions posed to him, and to initiate eye contact and demonstrate reciprocal smiling during occupational therapy.  He was unable to perform any one-step instructions in previous therapy sessions.  With these positive results, the dosage was adjusted to 1mg in the morning and 0.5mg at night. 

Within a week, PATIENT X no longer needed intensive supervision while awake, and made no further attempts to elope from the unit.  The patient completed one-unit directions 80% of the time without repetitions and repeated three to four words with 100% accuracy.  After two weeks of being on lorazepam, PATIENT X answered yes/no questions with 100% accuracy, performed two-unit directions with 100% accuracy, and performed three-unit directions with 25% accuracy.  He was able to name objects (confrontational naming) with 30% accuracy.  His medical records indicate that, at times, he still needed some cuing, but that his ability to respond to questions greatly improved.  Orientation gradually improved as well.  After four weeks on lorazepam, he was oriented to person, place, and time.  The patient still tended to perseverate when speaking, especially regarding his discharge, and made some paraphasic errors.  For example, he would perseverate that he was leaving on “1-B,” which was clarified to be the “18th.”

He began interacting with other patients.  He made observations about people and things around him, and made socially appropriate conversation with others.  (For instance, during a game of Uno, he purposely lost in order for another patient to win.  He then commented on the side that he had done this to help the other patient feel better.)  PATIENT X also began to initiate conversations about his family, friends, and goals for his life.  His dosage of lorazepam was decreased to 0.5mg bid about a week before his discharge.  He was discharged to a subacute brain injury rehabilitation unit that was closer to his family, and was expected to stay at that facility only a short time before returning home to live with his mother. 


The case study highlights a good treatment response in a patient with an atypical presentation of catatonia.  The patient presented with language processing and social interaction deficits in the absence of overt motor deficits or mutism, typically considered hallmarks of the diagnosis.  The patient presented with a severe receptive language disorder marked by fluent expression, containing some paraphasic errors, with a virtually complete inability to demonstrate comprehension in oral and written modalities.  Overall, his communication impairments were not consistent with any specific subtype of aphasia.  His symptoms were conceptualized instead as deriving from frontal lobe pathology.  This includes an inability to shift from one cognitive function to another, leaving the patient unable to fluidly respond to his environment, including access to receptive language capacity.  This indicates an unusual variant of catatonia with cognitive systems affected and only minor motor effects (i.e., cogwheel rigidity).

The concept of how catatonia linked to organic brain syndrome can be treated was first proposed by Northoff in 2002.  Northoff’s research looked at four neurotransmitters (dopamine, GABA, glutamate, and serotonin), but focused on the central role of GABA-A receptors.  There appears to be a down regulation of GABA-A receptors, and significantly lower GABA-A receptor binding has been found in catatonic patients.  This decrease in GABA-A receptors is successfully treated with the GABA-A receptor agonist lorazepam [14].

There are clear implications for use of lorazepam with patients who present with atypical catatonia.  A one-dose trail administration of the drug can serve as both a diagnostic tool, as well as treatment because the patient’s response will be quick.  Most catatonic patients will respond to treatment with lorazepam within the first 5-10 minutes to twenty-four hours after administration [14].  Future research regarding the efficacy of treating atypical presentations of catatonia with benzodiazepines (specifically lorazepam) would be beneficial in order to further empirical evidence. 


  1.  Fink, M. (2009).  Catatonia:  A Syndrome Appears, Disappears, and Is Rediscovered.  The Canadian Journal of Psychiatry, 54(7), 437-445.
  2.  Fink, M., & Taylor, M.A. (2001).  The many varieties of catatonia.  European Archives of Psychiatry and Clinical Neuroscience¸251, 1/8-1/13.
  3.  Vancaester, E., & Santens, P. (2007).  Catatonia and neuroleptic mailignant syndrome:  two sides of a coin?  ACTA Neurologica Belgica, 107, 47-50.
  4.  Taylor, M.A. (1993).  The Neuropsychiatric Guide to Modern Everyday Psychiatry.  New York:  The Free Press, A Division of Macmillan, Inc.
  5.  Hem, E., Andreassen, O.A., Robasse, J-M., Vatnaland, T., & Opjordsmoen, S. (2005).  Should catatonia be part of the differential diagnosis of coma?  Nordic Journal of  Psychiatry, 59, 528-530.
  6.  Manjunatha, N., Saddichha, S., & Khess, C.R-J. (2007).  Idiopathic recurrent catatonia needs maintenance lorazepam:  case report and review. Australian and New Zealand    Journal of Psychiatry, 41, 625-627.
  7.  Rommel, O., Tegenthoff, M., Widdig, W., Braunig, P., & Malin, J-P. (1998).  Organic catatonia following frontal lobe injury: response to Clozapine. The Journal of    Neuropsychiatry and Clinical Neurosciences, 10, 237-238.
  8.  Daniels, J. (2009).  Catatonia:  Clinical Aspects and Neurobiological Correlates.  The Journal of Neuropsychiatry and Clinical Neurosciences, 21(4), 371-380.
  9.  James, B.O., Omoaregba, J.O., Lawani, A.O., Ikeji, C.O., & Igbinowanhia, N.G. (2009).  Subdural haematoma presenting as catatonia in a 20-year-old male:  a case  report.   Retrieved January 31, 2011, from
  10.  Hawkins, J.M., Archer, K.J., Strakowski, S.M., & Keck, P.E. (1995).  Somatic Treatment of Catatonia.  The International Journal of Psychiatry in Medicine, 25(4), 345-    369).
  11.  Ungvari, G.S., Chiu, H.F.K., Chow, L.Y., Lau, B.S.T., & Tang, W.K. (1999).  Lorazepam for chronic catatonia:  a randomized, double-blind, placebo-controlled cross-over  study.  Psychopharmacology, 142, 393-398.
  12.  Rajagopal, S. (2007).  Catatonia.  Advances in Psychiatric Treatment, 13, 51-59.
  13.  Julien, R.M, Advokat, C.D., & Comaty, J.E. (2008). A Primer of Drug Action:  A comprehensive guide to the actions, uses, and side effects of psychoactive drugs, 11th  edition.  New York:  Worth Publishers
  14.  Northof, G. (2002).  What catatonia can tell us about “top-down modulation”:  A neuropsychiatric hypothesis.  Behavioral and Brain Sciences, 25, 555-604.
  15.  Van Den Eede, F., Van Hecke, J., Van Dalfsen, A., Van den Bossche, B., Cosyns, P., & Sabbe, BG. (2005). The use of atypical antipsychotics in the treatment of catatonia.  European Psychiatry, 20 (5-6), 422-429.