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Three reports in this number of the Acta Psychiatrica Scandinavica reflect on catatonia in children and adolescents. The medical historian Edward Shorter finds catatonia recognized in children and adolescents under many names. It appears as catalepsy and stupor in the older literature, then as schizophrenia, autism, and hysteria, and only recently as catatonia. The change in labels explains the frequent opinion that catatonia has disappeared (1).

Much childhood psychopathology is ascribed to abuse and trauma. Dirk Dhossche asks whether catatonia can result from the same experiences and finds that catatonia is associated with deprivation, abuse, and trauma and that relief is obtained by applying catatonia treatment protocols (2).

At an academic medical center, Neera Ghaziuddin and her colleagues examined the charts of 101 patients admitted to a pediatric psychiatry facility seeking the presence of 3 or more catatonia signs. Eighteen charts (17%) documented catatonia but in only two had the referring physicians recognized the syndrome (3).

Catatonia is a motor dysregulation syndrome that is increasingly recognized among adult patients but is hardly recognized in child medicine or child psychiatry texts. Life-threatening, catatonia is often quickly treatable to remission, a rare opportunity in clinical psychiatry. It is not that the catatonia syndrome is uncommon, but it is hidden under many guises. Labeled mainly as a type of schizophrenia it often appears within bipolar and major depression, within autism spectrum disorders especially in those patients with self-injurious behaviors, and as elective mutism, persistent refusal syndrome, Tourette syndrome, or anti-N-methyl D-aspartate (NMDA) receptor encephalitis (4).

Catatonia was delineated among psychiatric and medically ill patients in 1874 by Karl Kahlbaum in a small monograph of 104 pages (5). Mutism, posturing, motor rigidity, verbigeration, stupor, and excited states were its main signs. He described the condition so well that within a few years catatonia was widely recognized. In the late 1890s, Emil Kraepelin incorporated catatonia within his concept of dementia praecox. When Eugen Bleuler changed the concept to ‘schizophrenia,’ catatonia lost its independence, and in succeeding decades, catatonia remained hidden within schizophrenia in evolving psychiatric classifications.

The search for predictors of outcome to select treatments from among the cornucopia of new medicines found catatonia among patients with manic depression and as a neurotoxic response to the more potent neuroleptic drugs. When a neuroleptic malignant syndrome (NMS) was delineated in the 1980s, its similarity to ‘malignant catatonia’ (MC) was slowly recognized. Both syndromes are marked by fever, motor rigidity, torpor or excitement, and vegetative abnormalities. Based on the belief that the neuroleptic drugs acted on brain dopamine, the recommended prescription for NMS was dopamine agonists and the muscle relaxant dantrolene. These were poorly effective, however, and when the treatments for MC were applied, resolution was prompt. Our recognition that NMS was better treated as a form of MC rather than as dysfunction in dopamine metabolism encouraged greater recognition of catatonia (6).

The efficacy of known treatments fosters interest in catatonia. The report in 1930 by the American William Bleckwenn that the stupor, posturing, mutism, and rigidity of catatonia were relieved by high doses of sodium amobarbital was the first shot of the psychopharmacology era. In 1934, the Hungarian Ladislas Meduna, seeking examples of schizophrenia for his experiments with the chemical induction of grand mal seizures, selected patients with catatonia in the belief that they were bona fide examples of schizophrenia (7). Of the recognized varieties of schizophrenia, his best results were achieved with catatonia. By the 1940s, the much more facile induction of seizures by electric currents established ECT as a second effective relief of catatonia.

In the 1980s, newly developed benzodiazepines were trumpeted as ‘safer’ replacements for amobarbital and reports quickly supported diazepam and lorazepam in catatonia. Treatment protocols today call for test doses of diazepam or lorazepam, and if the motor signs are relieved, treatment is instituted with very high doses. When these fail, ECT is the definitive treatment. Such treatment protocols are effective for the inhibited, delirious, and malignant forms of catatonia (8).

The variety of names for the syndrome reminds us that catatonia is mainly recognized within the Kraepelin/Bleuler rubric of ‘schizophrenia.’ This label carries with it the treatment algorithm of neuroleptic drugs and not the prescription of benzodiazepines and ECT. To assure the benefits of effective treatment that follows proper diagnosis, it is necessary that catatonia be recognized as an identifiable syndrome within the classification of psychiatric disorders (9).

The psychiatric classification is the principal text used to teach physicians how to recognize psychiatric syndromes. The DSM classifications in 1952, 1968, and 1980 recognized catatonia only as a type of schizophrenia. The efficacy of treatments for NMS and MC led the DSM-IV commission in 1994 to add a new class of ‘catatonia secondary to a medical disorder (293.89).’ Interest in catatonia remained small, however, as the belief that catatonia was necessarily a sign of schizophrenia persisted. Indeed, the case literature finds examples of catatonia treated poorly as schizophrenia; applying neuroleptic drugs not only fails to relieve catatonia but often worsens the illness by precipitating NMS.

The APA DSM5 commission published its recommendations for catatonia online in January 2011. http://www.dsm5.org/proposedrevision/pages/proposedrevision.aspx?rid=445 Reviewed June 15, 2011. Schizophrenia catatonic type (295.2) is to be deleted; catatonia secondary to a medical condition is to be continued (293.89); and a new class of catatonia ‘not otherwise specified’ (298.99) is to be created for temporary use in those cases in which no primary condition is identified because of mutism or lack of history. Catatonia may also be added as a specifier to at least ten primary diagnoses, denoted as xxx,x5. This multi-faceted resolution seeks to satisfy many opinions and disregards the science and experience of numerous catatonia scholars in the past two decades (10).

As the ICD commission is undertaking a revision of ICD-11, the members should consider a simpler recognition of catatonia as an independent syndrome (similar to the recognition of delirium) in pediatric and adult cases; that it is recognized by the presence of motor signs listed in catatonia rating scales; that the diagnosis is verified by the relief offered by an injected benzodiazepine or barbiturate; and that the diagnosis is validated by effective treatment with benzodiazepines and ECT.

Catatonia is a motor syndrome relevant to the practices of physicians, pediatricians, neurologists, and psychiatrists. It warrants a home of its own in the psychiatric classification and texts.

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