Early EEG monitoring for detecting postanoxic status epilepticus during therapeutic hypothermia: a pilot study.

OBJECTIVE: To determine whether routine electroencephalography (EEG) detected electrical status epilepticus (ESE), masked by neuromuscular blockade, in comatose cardiac-arrest survivors receiving therapeutic hypothermia. DESIGN: Prospective 3-year study. SETTING: Medical ICU. PATIENTS: Fifty-one consecutive comatose cardiac-arrest patients treated between May 2005 and May 2008 using a standardized protocol of hypothermia with neuromuscular blockade. INTERVENTION: EEG was performed routinely as soon as possible after starting therapeutic hypothermia. EEG recordings were read by an independent neurophysiologist who was blinded to patient data. MEASUREMENTS AND MAIN RESULTS: Median body temperature at EEG recording was 33.0°C (range 32.4-33.8). ESE was found on 5 (10%) of the 51 EEG recordings: three patients had continuous rhythmic generalized spikes and two patients had continuous rhythmic focal spike-waves. Of the 17 (33%) patients who were discharged alive, 8 (8/51, 16%) had a CPC score of 1, 4 (8%) of 2, and 5 (10%) of 3. All patients with ESE died during their ICU stay. CONCLUSION: These preliminary results indicate that postanoxic status epilepticus can be masked by neuromuscular blockade during our protocol of therapeutic hypothermia. Routine EEG monitoring might be helpful in cardiac-arrest survivors receiving therapeutic hypothermia. Further studies including continuous EEG monitoring are needed to determine whether early diagnosis and treatment of ESE during therapeutic hypothermia improves the outcome.

Therapeutic hypothermia for coma after cardiorespiratory arrest caused by hanging.

We report a case in which mild therapeutic hypothermia was used successfully in a patient with coma after cardiorespiratory arrest induced by hanging.

Lysergic acid amide-induced posterior reversible encephalopathy syndrome with status epilepticus.

INTRODUCTION: Posterior reversible encephalopathy syndrome (PRES) is known to occur in association with several substances. However, lysergic acid amide (LSA) is not among the previously reported causes of PRES. METHODS: We report on a patient with PRES presenting as convulsive status epilepticus associated with hypertensive encephalopathy after LSA ingestion. Magnetic resonance imaging was performed and catecholamine metabolites assayed. RESULTS: The patient achieved a full recovery after aggressive antihypertensive therapy and intravenous anticonvulsivant therapy. The clinical history, blood and urinary catecholamine levels, and response to treatment strongly suggest that PRES was induced by LSA. CONCLUSION: LSA, a hallucinogenic agent chiefly used for recreational purposes, should be added to the list of causes of PRES.

Recurrent takotsubo cardiomyopathy triggered by convulsive status epilepticus.

INTRODUCTION: Takotsubo cardiomyopathy can complicate several conditions including neurological emergencies. A few recurrent cases associated with seizures have been reported, but none of the patients had status epilepticus. The pathophysiology of takotsubo syndrome, although debated, may involve stunning of the myocardium by a catecholamine storm triggered by stress. Patients with epilepsy may be at increased risk for takotsubo syndrome, which may occur repeatedly. METHODS: We report on a postmenopausal woman with symptomatic epilepsy who experienced recurrent takotsubo cardiomyopathy triggered by convulsive status epilepticus. Brief seizures were not associated with takotsubo syndrome. The relevant literature was reviewed. RESULTS: Over a 1-year period, she experienced two episodes of convulsive status epilepticus with complete neurological recovery after treatment. Echocardiography showed latero-septo-apical hypokinesia and apical ballooning. The cardiac abnormalities resolved fully and she recovered her baseline level of self-sufficiency. During the same period, she experienced several brief seizures, with no cardiac manifestations. CONCLUSION: The occurrence of takotsubo cardiomyopathy in association with convulsive status epilepticus, but not with brief seizures, supports neurogenically mediated myocardial stunning related to direct toxicity of endogenous catecholamines. Neuro-intensivists must be aware of this potentially fatal but fully reversible cardiac complication, which may be among the causes of death in patients with status epilepticus.