Early EEG Detection of Treatable Non-Convulsive Status Epilepticus in Severe COVID-19-Associated Encephalopathy: A Case Report

Introduction

Neurological complications of COVID-19 include encephalopathy, cerebrovascular events, seizures, and status epilepticus. In critically ill patients, impaired consciousness is often multifactorial and may reflect hypoxemia, sepsis, systemic inflammation, metabolic derangement, or sedative exposure. EEG abnormalities are common in patients with COVID-19-associated encephalopathy, but most findings are nonspecific, including diffuse slowing, focal slowing, rhythmic activity, and periodic patterns.^1,2

NCSE is a clinically important and potentially treatable cause of coma because it may occur without overt motor convulsions. EEG is therefore essential when bedside examination and systemic evaluation do not sufficiently explain persistent depressed consciousness. This principle is not limited to COVID-19; EEG should be considered in persistent unexplained encephalopathy or coma in general when impaired consciousness is disproportionate to systemic illness. We report an older patient with severe COVID-19-associated encephalopathy in whom early EEG identified treatable NCSE and serial EEG documented treatment response.

Case Report

An 85-year-old woman with Parkinsonism, type 2 diabetes mellitus, and prior cerebrovascular disease presented with severe COVID-19 pneumonia and progressive impairment of consciousness. Severe acute respiratory syndrome coronavirus 2 infection was confirmed by polymerase chain reaction, with a cycle threshold value of 17.8. Chest radiography showed right lung consolidation, and brain computed tomography demonstrated mild cerebral atrophy and periventricular lucency without acute hemorrhage, infarction, or mass effect.

She received remdesivir and dexamethasone for severe COVID-19 pneumonia. Respiratory failure progressed, and endotracheal intubation was required on hospital day 7. Tocilizumab was subsequently administered. Despite treatment of pneumonia and supportive intensive care, her neurological status deteriorated to coma.

Laboratory evaluation showed elevated inflammatory markers and mild hypomagnesemia but no major hepatic, renal, thyroid, or cerebrospinal fluid abnormality sufficient to explain the depth of coma. Cerebrospinal fluid showed no pleocytosis. Because persistent coma appeared disproportionate to systemic factors alone, EEG was obtained on hospital day 10.

On the day of EEG evaluation, arterial blood gas analysis showed pH 7.601, PaCO₂ 24.8 mm Hg, PaO₂ 212.0 mm Hg, HCO₃⁻ 23.9 mmol/L, base excess 2.2 mmol/L, and oxygen saturation 99.6%. These findings indicated marked alkalemia with hypocapnia under ventilatory support, without persistent hypoxemia or hypercapnia sufficient to explain the depth of coma. Arterial blood gas, laboratory, and cerebrospinal fluid results relevant to systemic contributors to coma are summarized in Supplementary Table S1.

The initial EEG demonstrated abundant rhythmic/periodic discharges lateralized to the right hemisphere at approximately 2 Hz. Sequential EEG epochs then showed early right temporal ictal activity and subsequent spatiotemporal evolution in rhythmicity, amplitude, and field distribution, consistent with focal electrographic seizures and NCSE (Figure 1A–C).

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Figure 1.

Initial EEG on hospital day 10 demonstrating non-convulsive status epilepticus.

Levetiracetam and lacosamide were administered, followed by midazolam infusion under EEG monitoring. Midazolam infusion was continued for approximately 48 h. During midazolam treatment, there was no immediate improvement in consciousness, as expected in the setting of sedative infusion; however, the EEG background became suppressed and the epileptiform/electrographic seizure pattern resolved. Follow-up EEG on hospital day 13 showed resolution of NCSE, with residual diffuse background slowing at 5 to 6 Hz, superimposed 1 to 2 Hz slow waves, and a sporadic right-hemispheric spike maximal at C4 (Figure 2). Approximately 4 days after midazolam treatment, the patient developed spontaneous eye opening, with improvement from E1M1VT to E4M1VT, with verbal response not testable because of endotracheal intubation. The patient was later transferred for ventilator weaning before hospital discharge.

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Figure 2.

Follow-up EEG after midazolam treatment on hospital day 13.

Discussion

This case emphasizes that persistent coma in severe COVID-19 should not automatically be attributed to systemic illness alone. The clinical message is broader than COVID-19: persistent unexplained encephalopathy or coma should prompt consideration of EEG when impaired consciousness persists after stabilization of cardiopulmonary factors or remains disproportionate to systemic illness.

Published EEG studies in COVID-19 show that most abnormalities are nonspecific markers of encephalopathy, including diffuse slowing, focal slowing, rhythmic delta activity, and periodic patterns.^1,2 Although acute symptomatic seizures appear uncommon among unselected hospitalized COVID-19 patients, with a pooled frequency of 0.71%, seizure risk is higher among patients selected for EEG evaluation, reaching 8.49% in one meta-analysis. ³ This supports targeted EEG use in critically ill patients with persistent unexplained coma. Status epilepticus and recurrent electrographic seizures have been reported in critically ill COVID-19 patients, but they represent a clinically important subset rather than the usual explanation for coma. ⁴

The clinical value of EEG in this case was twofold. First, it established a treatable diagnosis by demonstrating right temporal electrographic seizures and right-lateralized rhythmic/periodic discharges. Second, serial EEG documented treatment response, showing seizure resolution after antiseizure therapy and midazolam infusion. This before-and-after neurophysiological sequence is important because bedside examination alone could not distinguish NCSE from toxic-metabolic or inflammatory encephalopathy.

The arterial blood gas results on the day of EEG also clarify the clinical context. Although severe systemic infection and mechanical ventilation likely contributed to encephalopathy, the patient had adequate oxygenation and no hypercapnia when EEG was performed. Therefore, persistent depressed consciousness could not be fully attributed to hypoxemia or hypercapnia, and EEG was clinically justified to evaluate for an additional treatable neurological contributor.

The mechanisms linking COVID-19 and NCSE are likely multifactorial. Systemic inflammation, endothelial dysfunction, hypoxemia, metabolic stress, and blood-brain barrier disruption may lower seizure threshold.^4,5 In this patient, advanced age, prior cerebrovascular disease, and Parkinsonism may have further reduced cerebral reserve.

Critical care EEG reporting should use standardized terminology. The 2021 American Clinical Neurophysiology Society terminology supports precise description of rhythmic and periodic patterns, distribution, frequency, and evolution. ⁶ In the present case, right temporal electrographic seizures with evolution supported NCSE rather than nonspecific encephalopathy alone. This interpretation is also consistent with consensus recommendations emphasizing prompt recognition and treatment of NCSE. ⁷ Similar COVID-19 presentations mimicking NCSE have also been described. ⁸

The absence of immediate clinical awakening during midazolam infusion does not argue against NCSE, because the sedative itself suppresses arousal. In this case, the most objective immediate treatment response was electrographic resolution, whereas clinical improvement was delayed and became evident after the sedative effect had subsided.

This report has limitations. Brain magnetic resonance imaging and long-term cognitive follow-up were unavailable, and sedative exposure and systemic inflammation may have contributed to encephalopathy. Nevertheless, the temporal relationship between EEG-confirmed NCSE, treatment, electrographic resolution, and delayed clinical improvement supports the diagnostic relevance of early EEG in this setting.

Conclusion

Early EEG should be considered when severe COVID-19-associated encephalopathy presents with persistent or disproportionate coma. Identification of NCSE can alter treatment and allow objective monitoring of neurological recovery. The same approach should be generalized to persistent unexplained encephalopathy or coma more broadly, particularly after oxygenation and ventilation have been stabilized.

Supplemental Material