key: cord-0708450-lohm82qu
authors: Gaughan, Maria; Connolly, Sean; Direkze, Shamindra; Kinsella, Justin A.
title: Acute new-onset symptomatic seizures in the context of mild COVID-19 infection
date: 2020-09-10
journal: J Neurol
DOI: 10.1007/s00415-020-10214-w
sha: 9f7b721b0aacc84cdca84146eb5ec4138fc81f76
doc_id: 708450
cord_uid: lohm82qu

nan

In the midst of the COVID-19 global pandemic, two patients with no previous history of seizures presented to our institution with acute symptomatic seizures in the context of mild respiratory SARS-CoV-2 infection.

An 87-year-old male presented to the Emergency Department (ED) at our hospital following a generalised tonic-clonic seizure, with another 30-s convulsion witnessed in ED.

During a recent admission at another hospital for treatment of cellulitis, hoarseness prompted COVID-19 testing. RT-PCR amplification of SARS-Cov-2 nucleic acid from a nasopharyngeal swab was positive. He had remained otherwise asymptomatic and tested negative for SARS-CoV-2 prior to discharge. He had a history of traumatic brain injury, 32 years previously, from which he made a full recovery.

Examination in ED revealed drowsiness and disorientation with no lateralising clinical signs. Urgent brain CT revealed encephalomalacia involving the inferior frontal and bilateral anterior temporal lobes consistent with previous trauma. CXR was normal. Laboratory investigations are outlined in Table 1 . RT-PCR amplification of SARS-Cov-2 nucleic acid from a nasopharyngeal swab was positive. CSF was not performed due to rapid clinical recovery. The patient remained clinically well with no respiratory symptoms throughout admission.

EEG was performed following discharge. This demonstrated intermittent fronto-temporal dysfunction maximal on the right side, compatible with the known imaging abnormalities.

A 77-year-old female presented to ED following a prolonged first generalized tonic-clonic seizure. A further generalised convulsion in the ambulance was terminated with 4 mg intravenous (IV) Lorazepam after 3 min.

Collateral history revealed malaise for two days prior to presentation, but no respiratory symptoms. She had no relevant past medical history. She was high functioning at baseline, working in higher education as a course director.

Urgent noncontrast CT brain and CT angiography was normal. CXR demonstrated bibasal infiltrates. RT-PCR amplification of SARS-Cov-2 nucleic acid from a nasopharyngeal swab was positive. CSF constituents were normal (Table 1) and SARS-CoV-2 in CSF was not detected. MRI Brain was normal.

The patient had a prolonged encephalopathy with disorientation and bradyphrenia resulting in a protracted admission. EEG was performed three weeks following initial presentation and demonstrated significant bilateral cerebral dysfunction without any epileptiform abnormalities (Fig. 1) . Montreal Cognitive Assessment (MOCA) performed four months post hospitalization was 24/30, suggesting persistent cognitive deficit.

We describe two patients presenting acutely with newonset seizures in the context of COVID-19 infection. While one patient had a history of traumatic brain injury 32 years previously, this was not accompanied by or followed by seizures and the second patient had no known risk factors for seizures. In this case, severity of COVID 19 infection-in terms of hypoxia, multi-organ failure or marked metabolic derangement, suggested as potential confounders [1] , did not appear to be a causative factor. The severe and prolonged cognitive deficit in the second patient was notable given the relatively mild clinical course of her COVID-19 infection. We presume she developed a form of COVID-19-related encephalopathy with persistent EEG abnormalities noted. We note that neither patient had radiological or biochemical evidence of direct CNS COVID-19 involvement.

While initial reporting suggested that neurological complications were uncommon in COVID-19 infection, seizures as the presenting complaint are increasingly reported [2, 3] . Rarely, severe neurological presentations manifest in those with mild infection [4, 5] .

The pathological mechanism underlying multisystem involvement in SARS-Co-V2 is unclear. The possibility of direct invasion of the neural parenchyma via the olfactory bulb, resulting in neuronal death without widespread inflammation has been postulated [6] . The second pathogenic theory of a proinflammatory cascade in the context of a cytokine storm seems less likely here in the context of mild COVID-19 infection. The pathophysiological mechanisms involved remain elusive, particularly given the rarity of SARS-CoV-2 detection in the CSF [7] . Lack of access to detailed investigations due to resource restrictions will limit data available in retrospective reporting. 

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