The effect of dexmedetomidine on status epilepticus in a patient with anti-NMDA receptor encephalitis A 35-yr-old Caucasian woman was hospitalized in psychiatry, after childbirth, for psychomotor agitation, visual hallucinations, and incoherent speech. On admission, electroencephalography, brain imaging and cerebrospinal fluid examination showed no abnormalities. On day 7, she was found unconscious, and admitted to the intensive care unit (ICU). She developed status epilepticus alternating with periods of agitation. SE persisted despite combined treatment with phenytoin sodium, levetiracetam, and delorazepam. Intravenous dexmedetomidine (0.4 lgkg-1hr-1) was administrated for conscious sedation, and improvement from the SE was observed in 30min,as documented with EEG tracings. Electroencephalography spectral analysis showed a significant increase in beta activity, which is typical of dexmedetomidine. SE relapsed after dexmedetomidine interruption and resolved when the infusion was restarted. Anti-N-methyl-D-aspartate receptor (NMDA-R) antibodies were detected in the CSF. N-methyl-D-aspartate receptor antibodies are a rare cause of autoimmune encephalitis, often misdiagnosed with psychosis, which typically leads to seizures and drugresistant SE. Contradictory results have been reported on the effects of the alpha-2 agonist dexmedetomidine in epilepsy. In animals, dexmedetomidine has been shown both to reduce and increase the seizure threshold in local anestheticinduced epilepsy. Another question is the exact relationship between dexmedetomidine and NMDA-R. N-methyl-Daspartate receptors are ionotropic glutamate receptors that play a key role in excitatory synaptic transmission. Dexmedetomidine can depress NMDA-R-mediated transmission. Dexmedetomidine exerts its activity on G-protein coupled alpha-2 adrenoreceptors through inhibition of cyclic adenosine monophosphate and Our observations suggest a possible role for dexmedetomidine in the management of drug-resistant SE in the ICU. In patients with NMDA-R encephalitis and seizures, dexmedetomidine could be a useful bridge between typical pharmacological approaches and plasmapheresis.
The effect of dexmedetomidine on status epilepticus in a patient with anti-NMDA receptor encephalitis / Coluzzi, Flaminia; Angelini, Albina; Simmaco, Maurizio; Alampi, Daniela; Alessandri, Elisa; Grassi, Eugenio; Grazia Monina, Maria; Rocco, Monica. - In: CANADIAN JOURNAL OF ANAESTHESIA. - ISSN 1496-8975. - (2020), pp. 1677-1679. [10.1007/s12630-020-01753-x]
The effect of dexmedetomidine on status epilepticus in a patient with anti-NMDA receptor encephalitis
Flaminia Coluzzi
Primo
Writing – Original Draft Preparation
;Albina AngeliniSecondo
Investigation
;Maurizio SimmacoInvestigation
;Daniela AlampiMembro del Collaboration Group
;Elisa AlessandriMembro del Collaboration Group
;Eugenio GrassiInvestigation
;Monica RoccoUltimo
Writing – Review & Editing
2020
Abstract
The effect of dexmedetomidine on status epilepticus in a patient with anti-NMDA receptor encephalitis A 35-yr-old Caucasian woman was hospitalized in psychiatry, after childbirth, for psychomotor agitation, visual hallucinations, and incoherent speech. On admission, electroencephalography, brain imaging and cerebrospinal fluid examination showed no abnormalities. On day 7, she was found unconscious, and admitted to the intensive care unit (ICU). She developed status epilepticus alternating with periods of agitation. SE persisted despite combined treatment with phenytoin sodium, levetiracetam, and delorazepam. Intravenous dexmedetomidine (0.4 lgkg-1hr-1) was administrated for conscious sedation, and improvement from the SE was observed in 30min,as documented with EEG tracings. Electroencephalography spectral analysis showed a significant increase in beta activity, which is typical of dexmedetomidine. SE relapsed after dexmedetomidine interruption and resolved when the infusion was restarted. Anti-N-methyl-D-aspartate receptor (NMDA-R) antibodies were detected in the CSF. N-methyl-D-aspartate receptor antibodies are a rare cause of autoimmune encephalitis, often misdiagnosed with psychosis, which typically leads to seizures and drugresistant SE. Contradictory results have been reported on the effects of the alpha-2 agonist dexmedetomidine in epilepsy. In animals, dexmedetomidine has been shown both to reduce and increase the seizure threshold in local anestheticinduced epilepsy. Another question is the exact relationship between dexmedetomidine and NMDA-R. N-methyl-Daspartate receptors are ionotropic glutamate receptors that play a key role in excitatory synaptic transmission. Dexmedetomidine can depress NMDA-R-mediated transmission. Dexmedetomidine exerts its activity on G-protein coupled alpha-2 adrenoreceptors through inhibition of cyclic adenosine monophosphate and Our observations suggest a possible role for dexmedetomidine in the management of drug-resistant SE in the ICU. In patients with NMDA-R encephalitis and seizures, dexmedetomidine could be a useful bridge between typical pharmacological approaches and plasmapheresis.File | Dimensione | Formato | |
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