Acute
catatonia is a non-specific, relatively frequent syndrome, which manifests itself through characteristic motor signs that enables its diagnosis. It occurs in association with
mood disorders, psychotic disorders and several somatic or toxic diseases. Its short-term prognosis is of paramount importance. Without effective treatment, it is associated with high mortality. Despite the vital risk inherent in this disorder, it is not recognized as an independent diagnostic category by international rankings, which makes its diagnostic detection difficult and consequently does not allow adequate therapeutic care. However, if
benzodiazepines and electroconvulsive therapy have proved effective in the treatment of acute
catatonia, the role of atypical
antipsychotics remains controversial. In fact, despite the progress made by the DSM-IV-TR and CIM 10 by the recognition of the etiologic diversity of
catatonia, we deplore the absence to date of a consensus on clinical management and
therapy of
catatonia, which constitutes a source of
confusion for practitioners in their approach to catatonic patients. To illustrate the difficulty in supporting these patients, we report here a clinical vignette.
CLINICAL FEATURES: Mr. M. aged 21, without psychiatric history, has shown a functional acute psychotic episode involving a delirious and hallucinatory syndrome associated with a marked catatonic dimension.
Olanzapine was initiated at a dose of 10mg/d on the nineth day of hospitalization; the clinical picture was complicated by a
malignant catatonia justifying the halt of
olanzapine and the institution, in intensive units, of 15mg per day of
lorazepam. After 72hours, the patient has not responded to this treatment. ECT was expected, but the patient died on the 12th day.
DISCUSSION: This case raises a threefold question: the crucial issue of immediate vital prognosis, that of the truthfulness of the positive diagnosis of this psychotic table and finally the issue of therapeutic care, primarily the well-founded or otherwise use of an atypical
antipsychotic for the treatment of this type of
psychotic disorder. For Mr. M., the clinical diagnosis that he has shown, according to the DSM IV-TR, is brief
psychotic disorder "temporary diagnosis". This diagnosis - brief
psychotic disorder - does not actually allow for a specific clinical approach to this type of psychotic table. The immediate vital prognosis inherent in the catatonic dimension may not be properly evaluated and the therapeutic conduct may miss the application of the specific treatment of the catatonic syndrome. The proper diagnosis for this type of
psychotic disorder would be "
catatonia" as proposed by Taylor and Fink, instead of "brief
psychotic disorder" if the international rankings have included this disorder as a separate and independent diagnosis. The identification by international rankings of the catatonic syndrome as an independent diagnostic category seems essential for clinicians to allow: its clinical detection, the establishment of a syndromic diagnosis of catatonic disorder, appropriate prognostic evaluation and finally, the application of a suitable therapeutic strategy. Conventional treatment,
benzodiazepine- and/or ECT-based, can solve the catatonic episode in a few days, irrespective of its etiology and its severity. Moreover, while all authors agree that conventional
antipsychotics may induce a catatonic state or worsen a preexisting
catatonia into a
malignant catatonia and should thus be avoided for catatonic patients or with prior catatonic episodes, recent data from the literature emphasize the frequent and successful use of atypical
antipsychotics, including
olanzapine, in various clinical forms of benign
catatonia. However, our patient did not respond to treatment with
olanzapine and got even more complicated. Was the
malignant catatonia that this patient has shown induced by olanzapine ? The answer to this question seems difficult since some authors report the efficacy of
olanzapine in
malignant catatonia. We wonder if we should have kept
olanzapine and strengthen its dosage like Cassidy et al. in 2001 and Suzuki et al. in 2010 for the treatment of the malignant form constituted in this patient rather than having stopped it and used
lorazepam as indicated by Taylor and Fink in 2003.
IN CONCLUSION: