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Published online by Cambridge University Press:  02 January 2018

Rosemary Baker
Affiliation:
Learning Disability Service, The Hollies, Parklands Hospital, Aldermaston Road, Basingstoke, Hampshire RG24 9RH
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Abstract

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Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
Copyright © 2002. The Royal College of Psychiatrists

Sir: We read with interest Carey et al's description (Psychiatric Bulletin, February 2002, 26, 68-70) of a patient with catatonia and neuroleptic malignant syndrome (NMS). We have also recently treated a patient for both conditions.

Our patient was a 48-year-old woman who had suffered an intracranial bleed at birth resulting in left-sided hemiplegia and mild learning disability. Diagnosis of schizoaffective disorder, manic type, was made at the age of 16 years. She had only four previous admissions, most recent in 1983, and had been effectively treated with thioridazine.

She developed a florid psychosis following the change from thioridazine to quetiapine (as per Committee on Safety of Medicines guidelines) and the treatment of menopausal hot flushes with clonidine. Treatment was again changed, this time to chlorpromazine. Four days later, she developed NMS. When the NMS symptoms resolved, she remained mute, akinetic, doubly incontinent and had poor fluid intake for 4 weeks, with no evidence of psychosis. Resolution occurred spontaneously after listening to her favourite tape, Beatles. Since the resolution of the catatonia, she has suffered repeated epileptic seizures of all types. However, there is a history of falls in the months prior to admission.

Our case raised several important diagnostic and management issues. The general psychiatric staff (nursing and doctors) attributed the early signs of NMS to a combination of this patient's learning disability, mental illness and hemiplegia. The medical team believed her symptoms were ‘behavioural’ and attributed the raised creatine-phosphokinase to a fall 1 month earlier. Once they accepted the diagnosis of NMS, diagnosed by the learning disability team, she was transferred back to the psychiatric unit and care was by the in-patient staff and community learning disability team.

Management was purely supportive while there was no evidence of a disturbed mental state or deterioration in physical health, since there appeared to be no clear consensus in the literature about the treatment of catatonia and the family had concerns about the use of medication and electroconvulsive therapy. The thioridazine was restarted slowly after a normal electrocardiogram at the request of the family, when the psychosis re-emerged. A literature search also suggested this was a suitable drug following NMS. Sodium valproate was added for treatment of the epilepsy but has also been a very effective mood stabiliser.

Interestingly, when the patient emerged from her catatonic state, she used the hemiplegic arm without any difficulties for a few days before it returned to a spastic premorbid position. Finally, the family are extremely pleased with the patient's progress, believing her mental state to be the best they have ever seen it and this is echoed by all staff who have known this woman.

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