Electroconvulsive therapy for catatonia secondary to neuroleptic malignant syndrome in a patient with multiple sclerosis

To the Editor

A 41-year-old woman in rural New Zealand who had experienced relapsing-remitting multiple sclerosis (MS) from age 16, with visual impairment, ataxia, dysarthria and impaired mobility, presented to the hospital in an agitated state following 3 days of insomnia with pressured speech and hallucinations. Her change in mental state coincided with the use of cannabis from a new supplier. Olanzapine 10 mg given intramuscularly resulted in only brief sedation.

Due to the ongoing agitation, intravenous access, brain imaging and lumbar puncture were not possible and in an attempt to sedate her she was given repeated doses of haloperidol intramuscularly to a total of 15 mg. Following this, she developed limb rigidity and her agitation increased. Her symptoms continued over 48 h and she was transported to a tertiary hospital.

On arrival, she was ‘agitated, writhing, muttering’ with a new global increase in tone. Her temperature and heart rate were elevated and labile. Cerebrospinal fluid, magnetic resonance imaging with contrast and electroencephalogram were unremarkable. Her creatine kinase (CK) was 6736 U/L (normal less than 180 U/L).

Catatonia was noted with a Bush–Francis Catatonia Rating Scale (BFCRS; Bush et al., 1996) score of 28 out of 66. A diagnosis of catatonia secondary to neuroleptic malignant syndrome was made. Her neuroleptics were stopped.

Lorazepam was started and increased to 16 mg/day. Her catatonia symptoms reduced; however, core features, namely, excitement, echopraxia, rigidity, a positive grasp reflex and autonomic instability persisted (BFCRS = 8).

Electroconvulsive therapy (ECT) was delivered with bitemporal placement at 104 mC calculated by stimulus dose titration. Rocuronium was used as the muscle relaxant. ECT was delivered twice weekly for six treatments at the same dose. Her agitation and rigidity decreased and her grasp reflex was lost after the first treatment (BFCRS = 5). Her symptoms decreased with each treatment until no indication of catatonia remained (BFCRS = 0); there was no deterioration of her MS symptoms.

In the subsequent 12 months, there were no relapses of MS or catatonia. Her husband noted that she has new difficulty forming new memories, although this has not been quantified.

Discussion

While MS is not a contraindication for ECT, caution around the use of anaesthesia is required: (1) Hyperthermia or hyperkalaemia related to suxamethonium use can be circumvented using rocuronium or similar agents. (2) Challenging airways and diminished physiological reserve can be managed with careful anaesthetic assessment and post-anaesthetic nursing care (Makris et al., 2014). (3) There are historical reports of anaesthesia leading to relapse in MS. A review of neurostimulation in MS identified 21 case reports of ECT being used for patients with MS (Palma et al., 2014). Of these 19 improved. Three of these cases featured catatonia, and all improved. One, from 1951, developed left hemiparesis.

It is unclear whether MS increased the risk of catatonia. The consequences of the administration of haloperidol would suggest cautious use of neuroleptics in agitated patients with MS. Using the BFCRS allowed replicable assessment of the catatonia and set it apart from her underlying MS. Before ECT, cognition would normally be assessed to distinguish the effect of ECT from cognitive disorder related to MS. However, in medical emergencies such as catatonia, assessment of cognition is not possible. This adds to the sparse but positive literature related to ECT for catatonia in MS patients.