Is the Intensive Anticonvulsant Treatment for Control of Acute Posthypoxic Myoclonic Status Epilepticus Necessary?.
- Author:
Hui Chul CHOI
1
;
Hong Ki SONG
Author Information
1. Department of Neurology, Hallym university College of Medicine, Seoul, Korea. hksong@hallym.or.kr
- Publication Type:Original Article
- Keywords:
Hypoxia;
Acute posthypoxic myoclonus;
Status epilepticus
- MeSH:
Aged, 80 and over;
Airway Obstruction;
Anoxia;
Asthma;
Electroencephalography;
Humans;
Hypoxia, Brain;
Myoclonus;
Neurons;
Persistent Vegetative State;
Prognosis;
Pulmonary Edema;
Retrospective Studies;
Seizures;
Status Epilepticus*
- From:Journal of the Korean Neurological Association
2006;24(2):125-130
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Acute posthypoxic myoclonic seizure is not an uncommon presentation in clinical practices. However, there have been only a few reports which include detailed description on the treatment of acute posthypoxic myoclonic status. METHODS: We retrospectively analyzed the etiology, clinical course, nature and duration of myoclonus after hypoxic brain damage during a ten year period from 1992 to 2002. Patients who had possible explanations for myoclonic seizure other than hypoxic-ischemic events were excluded. RESULTS: Eighty-two patients aged 24 to 81 years old were included in this study. All but 3 patients with pulmonary edema had a history of cardiorespiratory arrest caused by probable cardiogenic origin, acute asthma attack and upper airway obstruction. Ictal EEGs demonstrated intermittent generalized spike and polyspike activities or biPLEDs. Most patients died within a week and 6 patients remained in persistent vegetative states. The clinical outcome was not affected by the drug response of myoclonic status epilepticus or etiology of hypoxia. CONCLUSIONS: Posthypoxic myoclonic status reflects severe and diffuse cortical damage, and implies a very poor prognosis. It may be a transient manifestation of severe cortical damage before massive and irreversible neocortical neuronal death, and aggressive anticonvulsant drug treatment would not be necessary in most patients.
