Dr. Carroll is clinical assistant professor of Psychiatry at Ohio University College of Osteopathic Medicine in Athens, and chief of Psychiatry Service at the Chillicothe VA Medical Center in Ohio. Dr. Appiani is assistant professor of Pharmacology at Universidad de Buenos Aires, Facultad de Medicina, and Director of ACEDEN in Buenos Aires, Argentina.

Disclosures: Dr. Carroll is a consultant to NMSIS; is on the speaker’s bureaus of Abbott, AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Forest Laboratories, Pfizer, and Janssen; and receives grant support from Pfizer. Dr. Appiani reports no affiliation with or financial interest in any organization that may pose a conflict of interest.

Please direct all correspondence to: Brendan T. Carroll, MD, Chief, Psychiatry Service, MHCL, Chillicothe VA Medical Center, 116A, 17273 State Route 104, Chillicothe, OH 45601; Tel: 740-773-1141, x7871; Fax: 740-772-7179; E-mail: btcarroll1@cs.com.


Catatonia is currently viewed as a neuropsychiatric syndrome of diverse etiology.1 However, there has been a steady decline in the diagnosis of catatonic schizophrenia over the last 50 years.2 Recent studies, however, showed that catatonia was diagnosed in ~10% of patients admitted to acute psychiatric facilities.3,4 When methodically assessed, catatonic signs and symptoms are prevalent in schizophrenia (18% of newly admitted patients with psychoses3 and 38% of patients with chronic schizophrenia).4 There are different types of catatonia (eg, acute and chronic) that show different responses to treatment. Catatonia in children and adolescents occurs frequently and may benefit from established treatments with electroconvulsive therapy (ECT) and benzodiazepines. Catatonia may present with psychogenic polydipsia or ingestion of foreign bodies with medical complications. Some patients with catatonia may be resistant to treatments with ECT and benzodiazepines, and alternative pharmacotherapy must be considered. This issue of Primary Psychiatry addresses the treatment of catatonia in these populations.

Catatonia is a clinical syndrome characterized by a range of psychomotor abnormalities that occur in the context of a wide variety of both psychiatric and medical conditions. In children and adolescents it occurs in affective, psychotic, autistic, developmental, and medical disorders. Catatonia may present with unusual stereotypies and medical comorbidities. Consequently, it is under-recognized and under-diagnosed. This issue offers a collection of several articles to help readers understand more about the unique presentations and varied treatment approaches to catatonia. Each article includes case vignettes to aid the clinician in the recognition of catatonia in daily practice. The diagnosis and treatment recommendations are still undergoing modification with the development of new rating scales and new treatments.

William W. McDaniel, MD, MS, and David R. Spiegel, MD, present case vignettes of patients who required treatment for low sodium and catatonia. The definition of stereotypy from the KANNER scale is repetitive, non-goal-directed movements.5 The scale range is from 0 (absent) to 8 (present, with severe self-injury). The ingestion of non-food items and polydipsia would be included as catatonic signs. The basic tenants for the treatment of medical catatonias are to: treat the underlying medical condition, treat medical catatonia with treatments used for psychiatric catatonias, and treat the comorbid diagnoses to improve the patient’s outcome. In their study, hyponatremia is the co-occurring medical condition.

In their article on catatonia in children and adolescents, Dirk M. Dhossche, MD, PhD, and colleagues present data to support the use of benzodiazepines and ECT. They provide a treatment algorithm that includes careful assessment and judicious use of a lorazepam challenge test. The case vignettes support this approach. They also discuss the importance of the classification of catatonia in the upcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition.6 They emphasize the need for greater independence of the diagnosis of catatonia “for the sake of the children”.

Finally, Brendan T. Carroll, MD, and colleagues, demonstrate the wide variety of pharmacologic treatments. It is difficult to construct a pharmacologic algorithm for the treatment of catatonia. This literature is extensive and the clinician may be distracted by the latest case report. This attempt is to organize the pharmacotherapy along neurochemistry and the known mechanisms of action of the medications. The case vignettes were included to show the presentation of catatonia in the hospital setting. They also underscore the need to use a combination of medications to treat these patients with catatonia. Perhaps the great divide in catatonia is that between g-aminobutyric acid (GABA) and glutamate mechanisms in catatonia. This has been discussed by Northoff7 and has been investigated, usually when benzodiazepines and ECT are not available or not effective.7

The most compelling reason for diagnosing catatonia is its exquisite responsiveness to treatment, particularly to benzodiazepines. During the last 2 decades, other compounds like zolpidem and glutamate antagonists were used with success in the treatment of this syndrome.7 Modern neuroimaging techniques allow findings of cortical involvement in catatonia, but the primary findings come from pharmacology response to treatment.7 Benzodiazepines are effective in 60% to 80% of patients with acute catatonia.8 It has been described that ~75% of patients can achieve sustained improvement with continuous treatment.9 Zolpidem, a non-benzodiazepine GABAA agonist, also relieves catatonia. There are reports of cases of clinical durable improvement in patients with treatment resistance to ECT and benzodiazepines. These facts give clues about GABAA involvement in the pathophysiology of catatonia.8 Moreover, GABAA receptor binding in right lateral orbitofrontal and right posterior parietal cortex is diminished. There is also a report that correlates catatonic stupor with GABAA binding decrease with flumazenil positron emission tomography scan.9 This gabaergic binding normalized after the treatment with diazepam.9 Another research performed with Spect with iodine-123-iomazenil showed lower cerebral perfusion in the right lower prefrontal cortex and parietal cortex in catatonic patients. In this group of patients the decrease of GABAA receptor binding correlated positively with motor and affective symptoms.10 In summary, catatonic reaction to benzodiazepines and GABAA agonists seems to be paradoxical. Patients treated with lorazepam tend to react with activation rather with sedation, even in those with a post-acute catatonic state. Lorazepam and GABAA agonists show that the principal dysfunction in catatonia may be related to GABA depletion.

Glutamate transmission and N-methyl-d-aspartate (NMDA) antagonists may be involved in the pathophysiology of catatonia through NMDA receptors.11 It has been hypothesized that the decrease in gabaergic tone in prefrontal areas released the supplementary motor areas, resulting in glutamate disinhibition. Thus, the glutamatergic hyperfunction in the striatum may be related to the development of catatonic symptoms.10 There are reports of successful treatments with glutamate antagonists: amantadine, topiramate, and memantine in patients who failed to respond to established treatment, including lorazepam and ECT.11 With these compounds, clinical improvement seems to be gradual. This difference in the time response between GABA agonists and glutamatergic antagonists may suggest that glutamate hyperactivity may be a secondary reaction to gabaergic depletion.11 When these findings are connected, catatonic syndromes are in part due to gabaergic hypoactivity and glutamate hyperactivity, and it seems that in this disorder it is necessary to have a balance between GABA and glutamate concentrations. When this balance is broken catatonia may appear. According to current pharmacology, catatonia may be relieved by diminishing glutamate hyperactivity or by augmenting gabaergic tone.  PP



1.    Taylor MA. Catatonia: a review of a behavioral neurologic syndrome. Neuropsych, Neuropsych Behav. 1990;3:48-72.
 2.    Mahendra B. Where have all the catatonics gone? Psychol Med. 1981;11(4):669-671.
 3.    van der Heijden FM, Tuinier S, Arts NJ, et al. Catatonia: disappeared or under-diagnosed? Psychopathology. 2005;38(1):3-8.
 4.    Ungvari GS, Leung SK, Ng FS, et al. Schizophrenia with prominent catatonic features (‘catatonic schizophrenia’): I. Demographic and clinical correlates in the chronic phase. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):27-38.
 5.    Carroll BT, Kirkhart R, Ahuja N,  et al.  Katatonia – a new conceptual understanding of catatonia. Psychiatry (Edgemont). 2008;5(12):42-50.
6.    Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; In press.
7.  Northoff G. What catatonia can tell us about “top down modulation”: a neuropsychiatric hypothesis.  Behav Brain Sci. 2002:25(5):555-577.
8.    Seethalakshmi R, Dhavale S, Suggu K, et al. Catatonic syndrome: importance of detection and treatment with lorazepam. Ann Clin Psychiatry. 2008;20(1):5-8.
9.    Iseki K, Ikeda A, Kihara T, et al. Impairment of the cortical Gabaergic inhibitory system in catatonic stupor: a case report with neurimaging. Epileptic Disord. 2009;11(2):126-131.
10.    Northoff G, Steinke R, Czcervenka C, et al. Decreased density of GABA A receptors in the left sensorimotor cortex in akinetic catatonia: investigation of in vivo benzodiazepine receptor binding. J Neurol Neurosurg Psychiatry. 1999;67(4):445-450.
11.    Carroll BT, Goforth HW, Thomas C, et al. Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes. J Neuropsychiatry Clin Neurosci. 2007;19(4):406-412.