Ketamine Infusion Associated with Improved Neurology in a Patient with NMDA Receptor Encephalitis

MacMahon, Michael; Naysmith, M. R.; McCallion, Stephanie; Rhodes, Jonathan

doi:10.1155/2013/383125

Cited by 8 publications

(6 citation statements)

References 5 publications

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“…[7,8] There are some interesting observations in which NMDA antagonist including ketamine may improve symptoms of anti-NMDAR encephalitis. [9] However, the administration of NMDA antagonist to anti-NMDAR encephalitis is not consistent with the mechanism of NMDAR hypofunction in the disorder and in our practice there were not obvious improvement after administration of ketamine or memantine to our patients with anti-NMDAR encephalitis. Recently, Heresco-levy et al [10] reported the clinical and electrophysiological effects of D-serine in a schizophrenia patient positive for anti-NMDAR antibodies.…”

Section: Discussioncontrasting

confidence: 54%

D-cycloserin, a NMDA-agonist may be a treatment option for anti-NMDAR encephalitis

Guan¹,

Du²,

Xu³

et al. 2016

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Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is caused by reversible neuron dysfunction associated an autoantibody-mediated decrease of NMDAR in the entire brain. A N-methyl-D-aspartate (NMDA) -agonist treatment for anti-NMDAR encephalitis might have a role considering its specific mechanism. The authors used D-cycloserine, a partial NMDA-agonist in a refractory case with prolonged intensive care unit duration. A 13-year-old female presented with headache, cognitive deterioration, generalized seizures, coma and hypoventilation with required mechanical ventilation. Anti-NMDAR antibodies were identified in cerebrospinal fluid and serum confirming anti-NMDAR encephalitis. The patient was refractory to firstline and second-line immunotherapy and removal of ovary teratoma. D-cycloserine was then administered and her symptoms improved gradually and significantly. This is the first reported case in which D-cycloserine was applied to this disease. D-cycloserine might be a potential option as specific treatment in anti-NMDAR encephalitis.

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Section: Discussioncontrasting

confidence: 54%

D-cycloserin, a NMDA-agonist may be a treatment option for anti-NMDAR encephalitis

Guan¹,

Du²,

Xu³

et al. 2016

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“…Both these medications were effective in suppressing agitation in our cohort, and no symptomatic worsening was noted despite their effect on the NMDAR. One previous report has described a dramatic sustained benefit with ketamine, whereas others have not found it to be useful . Other candidate medications that act on the NMDAR (e.g.…”

Section: Discussionmentioning

confidence: 92%

Symptomatic treatment of children with anti‐NMDAR encephalitis

Mohammad

Jones

Hong

et al. 2015

Develop Med Child Neuro

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IVMPIntravenous methylprednisolone NMDAR N-methyl-D-aspartate receptor AIM We performed the first study on the perceived benefit and adverse effects of symptomatic management in children with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.METHOD A retrospective chart review was undertaken at two tertiary paediatric hospitals in Australia and New Zealand. We included 27 children (12 males, 15 females; mean age at admission 7y 1mo) with anti-NMDAR antibodies in serum or cerebrospinal fluid with a typical clinical syndrome.RESULTS Only two out of 27 patients were white, whereas 16 out of 27 patients were from the Pacific Islands/New Zealand Maori. The mean duration of admission was 69 days (10-224d) and 48% of patients (13/27) needed treatment in an intensive care setting. A mean of eight medications per patient was used for symptomatic management. Symptoms treated were agitation (n=25), seizures (n=24), movement disorders (n=23), sleep disruption (n=17), psychiatric symptoms (n=10), and dysautonomia (n=four). The medications used included five different benzodiazepines (n=25), seven anticonvulsants (n=25), eight sedatives and sleep medications (n=23), five antipsychotics (n=12), and five medications for movement disorders (n=10). Sedative and sleep medications other than benzodiazepines were the most effective, with a mean benefit of 67.4% per medication and a mean adverse effect-benefit ratio of 0.04 per medication. Antipsychotic drugs were used for a short duration (median 9d), and had the poorest mean benefit per medication of 35.4% and an adverse effect-benefit ratio of 2.0 per medication.INTERPRETATION Long-acting benzodiazepines, anticonvulsants, and clonidine can treat multiple symptoms. Patients with anti-NMDAR encephalitis appear vulnerable to antipsychotic-related adverse effects. Pacific Islanders appear to have a vulnerability to anti-NMDAR encephalitis in our region.Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an antibody-mediated diffuse encephalitis that predominantly affects young adults and children. Children often present with behavioural symptoms and then develop distinctive movement disorders combined with seizures, encephalopathy, sleep disturbance, or dysautonomia.

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“…Electroconvulsive therapy was successfully used for the treatment of refractory dyskinesia, which required continuous infusion of a neuromuscular blocker, after long-lasting treatment with various forms of immunotherapy had failed ( 9 ). Ketamine has also been described as a useful treatment for severe dyskinesia in a young woman with anti-NMDAR encephalitis ( 5 ), but reported ineffective in another two cases ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

“…Data regarding the symptomatic treatment of movement disorders secondary to anti-NMDAR encephalitis before the action of immunotherapy are limited ( 5 – 10 ). To the best our knowledge, there have been no reports on the management of severe movement disorders in patients with anti-NMDAR encephalitis using botulinum neurotoxin serotype A (BoNT-A).…”

Section: Introductionmentioning

confidence: 99%

Management of Refractory Orofacial Dyskinesia Caused by Anti-N-methyl-d-aspartate Receptor Encephalitis Using Botulinum Toxin

Zheng

Shi

et al. 2018

Front. Neurol.

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The use of botulinum neurotoxin serotype A (BoNT-A) injections for the treatment of orofacial dyskinesia secondary to anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is rarely reported. Here, we report a case of an urgent, successful management of severe orofacial dyskinesia in an 8-year-old girl with anti-NMDAR encephalitis using BoNT-A injection. The patient presented with de novo unilateral paroxysmal movement disorder progressing to generalized dystonia and repetitive orofacial dyskinesia. Diagnosis was confirmed by the presence of NMDAR antibodies in serum and cerebrospinal fluid. The orofacial dyskinesia worsened despite the aggressive use of first-line immunotherapy and second-line immunotherapy (rituximab), and resulted in a potentially fatal self-inflicted oral injury. We urgently attempted symptomatic management using BoNT-A injections in the masseter, and induced muscle paralysis using vecuronium. The patient’s severe orofacial dyskinesia was controlled. We observed the effects of the BoNT-A injections and a tapering off of the effects of vecuronium 10 days after the treatment. The movement disorder had improved significantly 4 weeks after the first administration of rituximab. The injection of BoNT-A into the masseter may be an effective treatment for medically refractory orofacial dyskinesia in pediatric patients with anti-NMDAR encephalitis. We propose that the use of BoNT-A injections should be considered early to avoid self-inflicted oral injury due to severe refractory orofacial dyskinesia in patients with anti-NMDAR encephalitis.

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Ketamine Infusion Associated with Improved Neurology in a Patient with NMDA Receptor Encephalitis

Cited by 8 publications

References 5 publications

D-cycloserin, a NMDA-agonist may be a treatment option for anti-NMDAR encephalitis

D-cycloserin, a NMDA-agonist may be a treatment option for anti-NMDAR encephalitis

Symptomatic treatment of children with anti‐NMDAR encephalitis

Management of Refractory Orofacial Dyskinesia Caused by Anti-N-methyl-d-aspartate Receptor Encephalitis Using Botulinum Toxin

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