Nonconvulsive status epilepticus has traditionally been thought of as a rare condition.
There is little data regarding its true incidence, but evidence suggests it is far more common than once believed. Nonconvulsive status epilepticus can have an array of presentations and can be a diagnostic enigma for those unaware of its existence or those who believe, as it was once taught, that this condition is isolated to critically ill patients in the intensive care unit. Herein, we discuss the case of a patient with a focal traumatic brain injury who was found to be in nonconvulsive status epilepticus. This condition is one that physicians need to consider, especially those physicians caring for patients with traumatic brain injuries.
Nonconvulsive status epilepticus (NCSE) is defined as a period of ongoing seizure activity which may present as an alteration in behavior or mental status, albeit in the absence of motor activity.1 There are two recognized classifications of NCSE including absence status epilepticus (primary generalized) and complex partial (secondary generalized). NCSE has, in years past, been considered a rare condition. This is in large part the result of the fact that there have been very limited data from which to accurately describe the incidence of NCSE. Historically, most data have been drawn from single center studies with small sample sizes.2 Nevertheless, the incidence has been estimated to be 15-20/100,000 cases per year.3 These values may underestimate the true incidence. In one study of patients who presented to the ED with altered mental status (AMS) and without convulsions who received EEG studies, 37% were found to have NCSE.4 Notably, nearly half of patients with NCSE will not have any history of epilepsy.5 While in years past NCSE was thought to have an incidence of 3%, subsequent studies have shown it to be more common ranging from 16-43% of all status epilepticus cases.6-9 This is notable as the morbidity and mortality of NCSE is estimated to be 39 and 18% respectively.1
A 49-year-old male was brought to the ED by emergency medical services (EMS) after being found down outside. The patient was intoxicated (ethanol level of 459 mg/dL) and was unable to recall the preceding events but alleges he was struck in the head with a bottle. The patient’s chief complaint was rib pain and headache. GCS was 15 and vitals were blood pressures of 116/74, heart rate of 60/min, temperature 97.4℉, respiratory rate 14/minute, SPO2 100% on room air. The patient had no significant medical history and specifically no history of seizures. He reported drinking alcohol and smoking tobacco and marijuana daily. On physical examination, there was tenderness to palpation of the left chest wall and generalized abdominal tenderness. The patient underwent computed tomography (CT) imaging of his head, cervical spine, chest, abdomen, and pelvis, with findings of a traumatic subarachnoid hemorrhage in the right frontotemporal region (Hess and Hunt 3, modified Fischer grade 1) with a hyper-density along the temporal operculum in a gyral pattern.
Given these findings and concern for acute alcohol withdrawal, the patient was admitted to the intensive care unit (ICU) for continued monitoring. He was started on levetiracetam 500 mg po every 12 hrs for 7 days. A follow-up CT brain was stable in appearance, and on hospital day (HD) 2 the patient developed multiple intermittent and random episodes of sinus tachycardia with a rate of 130s-150s. These episodes lasted seconds to minutes, during which the patient was without any hemodynamic compromise and he remained asymptomatic. A 12-lead ECG was obtained just after an episode, which showed a sinus rhythm at a rate of 92 beats/min, with normal axis and without any acute changes. The QT-corrected was noted to be prolonged at 497 msec, and 2 g IV magnesium sulfate was given. After an unremarkable workup for causes of sinus tachycardia, Cardiology recommended metoprolol tartrate 12.5 mg PO every 12 hrs.
On the evening of HD 2, the patient had repeated episodes of sinus tachycardia now associated with upward gaze and tonic-clonic hand motions concerning for seizures. Surprisingly, throughout these episodes the patient was interactive and cooperative, without any confusion or postictal state. The patient was placed on long term monitoring for epilepsy (LTME). 21 EEG electrodes were placed according to the International 10/20 System. A single EKG electrode was also placed. Video recording was time-locked with EEG recording.
The EEG was interpreted by a board-certified epileptologist. Upon EEG initiation, the background was noted to demonstrate a continuous slow rhythm largely in the delta frequency of 1-3Hz, ranging between 10-50uV. There was no posterior dominant rhythm and no eye opening/closing artifacts. Spontaneous variability was present. The interictal rhythm was continuous, slow, generalized, and lateralized to right. At times there was evidence of asymmetry, there were faster and slower activities on the right, particularly in the right frontal/temporal region when compared to the left side. During the patient’s continuous video EEG monitoring, EEG evidence of seizures in the right hemisphere were captured from the beginning of the recording without any clear clinical signs. There was also evidence of diffuse encephalopathy and structural abnormality of the right hemisphere, consistent with the patient's known right SAH and hemorrhagic contusion. The patient was in focal EEG status since the initiation of the recording while the patient exhibited no clinical signs of seizure. Hyperventilation and photic stimulation were not performed. Single lead EKG showed regular, heart rate at 60 per minute. As a result of these findings, 3 g levetiracetam and 1 mg lorazepam IV were given followed by 1 g levetiracetam PO every 12 hrs. Following the initial bolus, there was no recurrence of seizure.
There are a variety of known etiologies of NCSE including electrolyte abnormalities, hypoxic-ischemic encephalopathy, traumatic brain injury (TBI) and acute hormonal disturbances.10-11 Nearly 75% of patients with NCSE have no identifiable changes on physical examination other than a decrease in responsiveness,12-13 which can often readily be attributed to another etiology. NCSE can present with negative symptoms including confusion and lethargy or subtle and often overlooked positive symptoms including blinking, nystagmus, facial twitching or tremulousness. In a small study of 48 patients, abnormal ocular movements were shown to be a specific clinical finding in NCSE as compared with patients without NCSE.14 While much of the data on NCSE is drawn from populations of patients who are acutely ill or comatose, these data suggest that patients with NCSE may have a worse prognosis as compared with convulsive status epilepticus.15,16 Similarly, it has been demonstrated that up to 14 percent of patients treated for convulsive status epilepticus persist in NCSE upon initiation of EEG monitoring.15 In contrast to critically ill patients in the ICU setting, NCSE outside the ICU can present with a plethora of subtle clinical manifestations.17 NCSE can be difficult to distinguish from absence seizure,18 with EEG being critical to the diagnosis where 50% of nonconvulsive seizures are identified within the first hour of EEG initiation.19
The scarcity of data regarding NCSE extends to treatment with very little literature being available regarding the most efficacious treatment modalities and without any randomized trials providing evidence to support treatment recommendations.20 NCSE management is not addressed in the status epilepticus guidelines published by the Neurocritical Care Society,21 resulting in much variation in care and even recognition of this condition amongst clinicians.
NCSE and Traumatic Brain Injury
Among TBI patients, seizures are not uncommon and are an important component of prognosis. Nearly 25% of patients with traumatic brain injuries who have a seizure in the first week after injury, will progress to have subsequent seizures.22 The development of epilepsy after TBI has a broad incidence ranging from 4.4-53% depending on the population studied.23 In a retrospective analysis of 451 adult TBI patients 9.3% had EEG evidence of electrographic status epilepticus with 19% being associated with intracerebral hemorrhage including trauma.24-25 NCSE may be particularly harmful among patients with TBI. As animal data suggests, the acutely injured brain has greater sensitivity to damage posed by NCSE.26-27
This case exemplifies an anomalous cause of sinus tachycardia. As described, patients with TBI are at high risk for seizures, including those who may present without typical clinical motor findings. This unique case of focal status epilepticus related to acute head trauma highlights the need for physicians to be cognizant of this condition and to have a high clinical suspicion for NCSE in patients with TBI who are presenting with disparate signs and symptoms.
- Shneker, B. F., & Fountain, N. B. (2003). Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Neurology, 61(8), 1066-1073. https://doi.org/10.1212/01.wnl.0000082653.40257.0b
- Rudin, D., Grize, L., Schindler, C., Marsch, S., Ruegg, S., & Sutter, R. (2011). High prevalence of nonconvulsive and subtle status epilepticus in an ICU of a tertiary care center: a three-year observational cohort study. Epilepsy Res, 96(1-2), 140-150. https://doi.org/10.1016/j.eplepsyres.2011.05.018
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- Coeytaux, A., Jallon, P., Galobardes, B., & Morabia, A. (2000). Incidence of status epilepticus in French-speaking Switzerland: (EPISTAR). Neurology, 55(5), 693-697. https://doi.org/10.1212/wnl.55.5.693
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