Abstract
Neuroleptic malignant syndrome and catatonia in a patient with dementia
Catatonia and neuroleptic malignant syndrome (NMS) occur in conditions other than schizophrenia and affective disorders [1]. The concept of NMS and catatonia being part of a continuum arising from dopamine blockade rather than two separate disorders has been examined by several authors [2], [3]. In reports in which catatonia was followed by NMS it has been suggested that the presence of catatonia increases patient vulnerability to NMS [4]. We report a case of what initially appeared to be the sequential development of NMS and catatonia in a patient with dementia.
A 66-year-old woman initially presented with cognitive impairment, persecutory delusions and behavioural disturbance. She was admitted to an inpatient psycho-geriatric service where a diagnosis of dementia of mixed Alzheimer's and vascular type was made. The patient was commenced on donepezil 5 mg, increasing to 10 mg daily and risperidone 2 mg daily. The patient was discharged to the care of her family after symptomatic improvement.
One year later the patient re-presented following further cognitive decline and relapse of persecutory delusions. Assessment findings were consistent with progression of dementia.
Risperidone was gradually increased to 4 mg day−1. Although the delusions decreased in intensity the patient developed prominent parkinsonism that did not resolve with benztropine. Olanzapine was started and risperidone slowly withdrawn. The parkinsonism improved but over the next 10 days the persecutory delusions returned.
Despite olanzapine 15 mg day−1 the patient remained fearful and agitated. She paced and engaged in semi-purposeful activity. She developed insomnia unresponsive to hypnotics. Chlorpromazine 50 mg nocte was added. In the first 24 h the patient appeared less distressed and insomnia resolved, but over the next 48 h the patient became febrile, displayed increased muscle tone and disturbance of consciousness. Full blood examination indicated a mild increase in total white cells; creatine kinase (CK) was 370 U L−1 and rose to 1134 U L−1 over the next 12 h. A diagnosis of NMS was made and neuroleptics were ceased.
After 36 h the patient was alert, muscle rigidity had resolved and CK had started to return to normal. Persecutory delusions and behavioural disturbance had abated. Cognitive impairment remained unchanged.
Approximately 12 days after all neuroleptics had been ceased the patient displayed waxy flexibility and posturing. She became mute and uncooperative. The patient was afebrile and CK remained within normal range. A diagnosis of catatonia was made.
Treatment options, including electroconvulsive therapy (ECT) were considered. Given the already severe cognitive impairment, the decision to utilize ECT was deferred and lorazepam 1 mg three times per day was commenced. It was noted that the patient became more amenable to directions in the hour after lorazepam. Over the next week the patient became less resistive, posturing was less marked and she was able to speak. The persecutory delusions and agitation did not recur. The patient remained stable on 1 mg lorazepam three times per day and was discharged to a psycho-geriatric nursing home.
It has been noted that catatonia may go unrecognized in the elderly and may be confused with the behavioural disturbance of dementia [5]. On reflection, the sequence of events in the present case raises the possibility that the initial agitation and restlessness signalled the onset of catatonia rather than distress related to persecutory delusions. In retrospect the use of lorazepam, rather than increasing doses of olanzapine and addition of chlorpromazine, may have better managed the symptoms and averted NMS.
The present case highlights that catatonia may occur in dementia. Furthermore in rare cases one should be aware that behavioural disturbance in dementia may mask catatonia. In addition it is a reminder that clinicians should remain vigilant for the occurrence of NMS whenever prescribing neuroleptics.