Abstract
Trollor and Sachdev [1] found a high frequency of catatonia in cases of neuroleptic malignant syndrome (NMS) in which electroconvulsive therapy (ECT) was used (76%, 42/55). Electroconvulsive therapy was considered a preferred primary treatment for NMS when, among other indications, catatonia is a major feature and when lethal catatonia cannot be ruled out. Their findings raise two related questions for discussion: (i) Is NMS a heterogenous condition with catatonic and non-catatonic NMS being two major subgroups? and (ii) Does catatonia merit a place as a specifier or modifier in the diagnosis of NMS?
The relationship between catatonia and NMS remains a moot point. There is considerable overlap in symptomatology between NMS and lethal (malignant) catatonia. It has been argued that NMS is a malignant variant of catatonia [2]. However, the catatonic syndrome, defined by a constellation of predominantly motor signs, is not described in many single case reports and case series studies of NMS. It would appear that while some cases of NMS may be neuroleptic-related catatonic states, many others are not.
It has been suggested that NMS is an aetiologically heterogenous condition which includes catatonic variants and non-catatonic pathological reactions to neuroleptics [3]. Several catatonic variants have been described in the literature. Neuroleptics may cause a catatonic-parkinsonian syndrome. The malignant form of this neuroleptic-induced catatonia is an NMS-variant often reported [4]. Various authors have described the conversion of antecedent catatonia, particularly the malignant type, into NMS following exposure to neuroleptics [3]. Moreover, catatonia, a non-specific syndrome, may develop secondarily during the course of NMS. More studies are needed to examine if NMS with catatonia and NMS without catatonia constitute two distinct subgroups with different clinical courses and responses to treatments.
Catatonia in NMS is probably underrecognised. Case reports of NMS with catatonia often provide no clear description of the catatonic symptoms present. Some make no attempt to separate NMS and catatonic features. Such diagnostic imprecision and confusion make it difficult to study the course of catatonia in NMS. In some of Troller and Sachdev's nine reported cases, the persistence of catatonic features was taken as signs of continuation of NMS (it was not clear if NMS core features persisted). In one patient (Patient 3) catatonic symptoms developed after a previous NMS episode. This was regarded as a relapse of NMS, although core features of NMS were absent.
It is argued that catatonia deserves a proper place in the diagnosis of NMS. The heterogeneity of NMS with catatonic and non-catatonic NMS being two major subgroups merits more research attention. Catatonia is a specifier of mania and depression in DSM-IV [5]. The catatonia specifier provides an opportunity to define a more homogeneous sub-grouping of individuals with the mood disorders. It is worth exploring the use of catatonia as a specifier in the diagnosis of NMS.