Background Therapeutic hypothermia (TH) improves outcomes in comatose patients resuscitated from cardiac arrest. However, nonconvulsive status epilepticus (NCSE) may cause persistent coma. The frequency and timing of NCSE after cardiac arrest is unknown. Methods Review of consecutive subjects treated with TH and receiving continuous EEG (cEEG) monitoring between 8/1/2009 and 11/16/2010. Demographic data, survival, and functional outcome were prospectively recorded. Each cEEG file was analyzed using standard definitions to define NCSE. Data were analyzed using descriptive and non-parametric statistics. Results Mean age of the 101 subjects was 57 years (SD 15) with most subjects being male (N = 55, 54%) and experiencing out-of-hospital cardiac arrest (N = 78; 77%). Ventricular fibrillation was the initial cardiac rhythm in 39 (38%). All subjects received TH. Thirty subjects (30%) awoke at a median of 41 h (IQR 30, 61) after cardiac arrest. A total of 29/30 (97%) subjects surviving to hospital discharge were awake. Median interval from arrest to placement of cEEG was 9 h (IQR 6, 12), at which time the mean temperature was 33.9°C. NCSE occurred in 12 (12%) subjects. In 3/12 (25%) subjects, NCSE was present when the cEEG recording began. In 4 subjects, NCSE occurred within 8 h of cEEG recording. One (8%) subject with NCSE survived in a vegetative state. Conclusions NCSE is common in comatose post-cardiac arrest subjects receiving TH. Most seizures occur within the first 8 h of cEEG recording and within the first 12 h after resuscitation from cardiac arrest. Outcomes are poor in those who experience NCSE.

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Summary:Nonconvulsive status epilepticus (NCSE) is difficult to diagnose in the obtunded/comatose patient. Such patients often have other serious medical conditions, and the diagnosis is frequently delayed. We review criteria for diagnosis, treatment, and prognosis of NCSE in this setting. Terms that have been used to describe SE in obtunded/comatose patients without tonic-clonic convulsions include subtle generalized SE, electrographic SE, SE in comatose patients, generalized electrographic SE, non-tonic-clonic SE, subclinical SE, and NCSE. Sometimes the same term has been used when describing different disorders, and different terms are often applied for the same entity. The incidence of NCSE in obtunded/comatose patients is uncertain. Clinically they may display subtle, intermittent focal or multifocal rhythmic movements suggestive of seizures; there may not be movements. NCSE can occur in a variety of disorders, including hypoxia, metabolic disturbances, and after convulsive seizures. A number of EEG patterns have been described in NCSE, and many of these are controversial, particularly as to whether they are ictal. These include periodic lateralized epileptiform discharges (PLEDS), bilateral independent PLEDS (BIPLEDS), periodic epileptiform discharges (PEDS), which can be either focal or generalized, and generalized triphasic waves (TWs). The diagnostic criteria for NCSE also are controversial, and there are no agreed-on criteria to diagnose NCSE in obtunded/comatose patients, nor is there consensus on how it should it be treated. Furthermore, outcome is poor, and several studies suggest that treatment may not be helpful.

We reviewed the long-term outcome of 39 adults whose electroencephalograms (EEGs) showed acute periodic lateralized epileptiform discharges (PLEDs). Parameters studied included outcome, presence or absence of a seizure disorder (both prior to and subsequent to the PLEDs), seizure type and frequency, and etiology of the PLEDs. The mortality rate was 41%, as 16 of 39 patients died during their hospitalization or within 2 months of discharge. Of the 23 survivors, 7 (30%) had a significant decline in their ability to provide self-care. A recent stroke (13 patients, 33%) was the most frequent cause of PLEDs. In this subgroup particularly, poor outcome, i.e., death or functional decline, was common (10 of 13 patients). Thirty-six patients had seizures just prior to or during the hospitalization when PLEDs were observed; focal motor seizures were the most common type (n = 22). Patients with a history of seizures prior to the occurrence of PLEDs continued to have seizures following discharge. In addition, 4 of 9 patients with new onset seizures associated with PLEDs had subsequent seizures.

This review discusses a variety of causes of stupor and coma and associated electroencephalographic (EEG) findings. These include metabolic disturbances such as hepatic or renal dysfunction, which are often characterized by slowing of background rhythms and triphasic waves. Hypoxia and drug intoxications can produce a number of abnormal EEG patterns such as burst suppression, alpha coma, and spindle coma. Structural lesions, either supra- or infratentorial, are reviewed. EEGs in the former may show focal disturbances such as delta and theta activity, epileptiform abnormalities, and attenuation of faster frequencies. In infratentorial lesions, the EEG may appear normal, particularly with a pontine lesion. Some patients may be encephalopathic because of ongoing epileptic activity with minimal or no motor movements. This entity, nonconvulsive status epilepticus (NCSE), is difficult to diagnose in obtunded/comatose patients, and an EEG is required to verify the diagnosis and to monitor treatment. Several EEG patterns and their interpretation in suspected cases of NCSE such as periodic lateralized epileptiform discharges (PLEDs), bilateral independent periodic lateralized epileptiform discharges (BIPLEDs), generalized periodic epileptiform discharges (GPEDs), and triphasic waves are reviewed. Other entities discussed include the locked-in syndrome, neocortical death, persistent vegetative state, brainstem death, and brain death.

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