What is the role of EEG in the workup of status epilepticus (SE)?

Updated: Feb 13, 2018
  • Author: Julie L Roth, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
  • Print
Answer

EEG is the criterion standard for diagnosing EEG, and some authors believe that EEG should be a routine part of management of SE. [3, 4] Nevertheless, EEG is rarely available in the acute-care setting; normally, it is obtained through neurologic consultation. When EEG is unavailable for the acute workup, presumptive treatment strategies must occasionally be started before EEG confirmation becomes available.

Because of the possibility of subtle SE, an EEG should be strongly considered if the patient is not starting to awaken within 20-30 minutes after seizure cessation. High clinical suspicion for continued unresponsiveness from this subtle SE is necessary, along with timely consultations and occasional insistence on obtaining EEG.

Several groups have shown that electrical SE often persists when clinical seizure activity has ceased. [41, 60] DeLorenzo et al prospectively examined 64 patients who clinically appeared to have controlled SE. These patients were comatose and had no overt clinical signs of convulsive activity. However, EEG demonstrated persistent seizures in 48%, and 14% of these patients had nonconvulsive SE (predominantly of the complex partial type). [60]

EEG is often helpful in solidifying the diagnosis of focal SE, and it may be crucial in differentiating focal SE from some of the other mimics. Simple partial seizure activity occasionally lacks an EEG correlate. The absence of ongoing epileptiform activity does not completely exclude simple partial SE. However, absence of an EEG correlate should at least call the diagnosis of focal SE into question. Many patients with EPC have a repetitive discharge on EEG that is time-locked to the motor activity.

Because recurring complex partial seizures without interval neurologic recovery constitutes CPSE, a single EEG lacking ongoing partial seizure activity does not entirely preclude the diagnosis; the study may have been performed between seizures. Repeated or prolonged EEG recordings may be crucial in confirming CPSE

Although not always required for the diagnosis of status, EEG can be extremely useful to validate the diagnosis and often helps in categorizing the type of status. See the images below.

Focal status epilepticus. Electroencephalograph (E Focal status epilepticus. Electroencephalograph (EEG) in a patient with epilepsia partialis continua caused by Rasmussen encephalitis before hemispherectomy. The patient had long-standing, intractable partial epilepsy since the first decade of life. Seizures included complex partial with occasional secondary generalization and repetitive myoclonus involving the left side of the body. Note the frequent epileptiform discharges at 1-2 Hz involving the right frontocentral channels. These were evident on many of the patient's routine EEGs. Clinical myoclonus is often correlated with high-voltage bursts of such activity.
Focal status epilepticus. Electroencephalograph (E Focal status epilepticus. Electroencephalograph (EEG) in a 35-year-old patient with a history of intractable partial epilepsy, in complex partial status epilepticus. The patient underwent a rapid antiepileptic drug taper as an inpatient for long-term video/EEG monitoring as a presurgical candidate. On clinical observation, the patient abruptly stopped and stared, exhibiting automatisms. This first of 2 EEG fragments covers approximately 30 seconds and illustrates the start and evolution of a seizure in the right temporal lobe. The onset appears to be at Sp2 and T4. Note the time of the event, 18:35 on May 9.
Focal status epilepticus. This electroencephalogra Focal status epilepticus. This electroencephalographic (EEG) fragment was obtained at approximately 12:39 on May 10, 18 hours after the onset of complex partial status epilepticus originating in the right temporal lobe, in a 35-year-old patient with a history of intractable partial epilepsy. Other EEG acquisitions over the interval were identical. On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners. Note the persistent epileptiform discharges at 1.5-2.5 Hz with phase reversal mainly at Sp2 though infrequently shifting to Sp1 and F7. The bulk of the discharges are maximal at Sp2, reflecting their mesial temporal origin, with rare, subtle, and low-amplitude reflection from lateral neocortical channels (F8). Background activities are slow with admixed beta frequencies. This finding corresponds to complex partial status epilepticus.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!