We are grateful to your correspondent for opening the debate on our letter. Neuroleptic malignant syndrome (NMS)—like the encephalopathy that develops in association with the use of antidepressants—indicates that both it and serotonin syndrome are spectrum disorders induced by drugs with both antidopaminergic and serotonergic effects (1). Medications that affect brain dopamine and serotonin levels are occasionally associated with neurtoxic behavioural and autonomic syndromes, variously described as NMS and toxic serotonin syndromes (TSS). Based on the drugs’ presumed brain mechanisms of action, different corrective interventions have been recommended. Moreover, Fink has claimed that NMS and TSS are not specific syndromes but, rather, examples of a nonspecific generalized neurotoxic syndrome and that they are subtypes of catatonia (2).
For these reasons, NMS and TSS may be confused or they may be presentations of different aspects of the same etiologic cause (dopamine–serotonin imbalance). Although NMS is described as having 4 classic signs, no agreed-upon criteria exist for the diagnosis of the syndrome in terms of severity or combination of these signs, and milder or in complete varieties have been detected and included with the full-blown cases (3).
In our patient, there was no autonomic lability, but there was coma, subfebrile fever, and rigidity on admission. In NMS, mental status changes, coma, and catatonia are common (4). Although creatine kinase (CK) is not a specific indicator of NMS, it may be important for the early detection of the syndrome (3). Muscle isoenzyme of CK may be raised by intramuscular injections, hyperactivity, and catatonia (5); it may also be raised in medically ill patients taking neuroleptics (6). In our case, there were no such conditions. No sedation or paralysis agents were used while the patient was ventilated. Therefore, consciousness was not regained as the result of any sedation wearing off. Otherwise, regaining of consciousness was not the part of the clinical course, it was a secondary event to bromocriptine administration.
We observed no change during a 7-day period of supportive treatment, but the clinical course improved completely within 24 hours of bromocriptine administration. In one review, it has been stated that, when compared with supportive measures alone, bromocriptine in particular shortened the time to the resolution of NMS symptoms (7). Since there was neither hyperkinesia nor clonus in our case, we did not suspect serotonin toxicity.