Encephalopathy in COVID-19 Presenting With Acute Aphasia Mimicking Stroke

Abstract

Introduction: Neurological manifestations are emerging as relatively frequent complications of corona virus disease 2019 (COVID-19), including stroke and encephalopathy. Clinical characteristics of the latter are heterogeneous and not yet fully elucidated, while the pathogenesis appears related to neuroinflammation in a subset of patients. Case: A middle-aged man presented with acute language disturbance at the emergency department. Examination revealed expressive aphasia, mild ideomotor slowing, and severe hypocapnic hypoxemia. Multimodal CT assessment and electroencephalogram (EEG) did not reveal any abnormalities. COVID-19 was diagnosed based on chest CT findings and positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reverse transcription PCR (RT-PCR) on nasopharyngeal swab. The following day, neurological symptoms progressed to agitated delirium and respiratory status worsened, requiring admission to the ICU and mechanical ventilation. Brain MRI and cerebrospinal fluid (CSF) studies were unremarkable. RT-PCR for SARS-CoV-2 on CSF was negative. He received supportive treatment and intravenous low-dose steroids. His neurological and respiratory status resolved completely within 2 weeks. Conclusions: We report a patient with reversible COVID-19-related encephalopathy presenting as acute aphasia, mimicking stroke or status epilepticus, eventually evolving into delirium. Although large-vessel stroke is frequently encountered in COVID-19, our case suggests that focal neurological deficits may occur as the earliest feature of encephalopathy. Neurological status reversibility and the absence of abnormalities on brain MRI are consistent with a functional rather than a structural neuronal network impairment.

Cerebrospinal fluid in COVID-19: A systematic review of the literature

“…As is evident by the fact that 303/430 (70%) patients we identified had CSF SARS-CoV-2 PCR testing performed, it is feasible to perform PCR testing for SARS-CoV-2 in CSF [5-10,15,17,22,24,26-38,43-59, 68-71,73,74,76-78,81,84,88,89,95,97,98,101,103,105,108,109,111, 113,116 156,157,161,164,165,169,171,177,178,[180][181][182][184][185][186][187]190,191,193,[195][196][197][198][199][200][201][203][204][205][206][207]209,[212][213][214][215][216][218][219][220][221][224][225][226][227]230,[233]…”

Cognitive and behavioral manifestations in SARS-CoV-2 infection: not specific or distinctive features?

“…Of interest, CSF analysis showed the presence of blood-brain barrier (BBB) dysfunction and a CSF increase in IL-6–IL-8 levels, in parallel with cytokine level increase in serum [ 54 , 62 ]. Patients receiving immunotherapy, intravenous immunoglobulins and/or steroids, plasmapheresis, and tocilizumab [ 54 – 56 , 59 , 61 , 68 , 69 ] improved, but spontaneous recovery cannot be excluded, since COVID-19-related encephalopathy may have a self-limited course even without a specific therapy [ 15 , 37 , 70 ]. Unfortunately, very few studies assessed cytokine levels in both serum and CSF, in order to correlate disease course with cytokine levels following treatment.…”

Cerebrospinal fluid from COVID-19 patients with olfactory/gustatory dysfunction: A review

“…Of 242 publications from December 1, 2019 and November 18, 2020 that described a unique patient diagnosed with COVID-19 via SARS-CoV-2 PCR or serology who had a neurological symptom and had CSF obtained, we identified 51 that met inclusion criteria. After review of the 51 publications, we identified 70 patients reported to have altered olfactory and/or gustatory function (anosmia/cacosmia/hyposmia and/or ageusia/dysgeusia/hypogeusia); 40 (57%) had both olfactory and gustatory dysfunction, 17 (24%) had isolated olfactory dysfunction and 13 (19%) had isolated gustatory dysfunction [8] , [9] , [10] , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] . In addition to altered olfactory and/or gustatory function, 39 (56%) had symptoms that localized to the central nervous system and 31 (44%) had symptoms that localized to the peripheral nervous system.…”

“…In 13/66 (20%) patients, the CSF WBC count was 0 cells/µL or the CSF WBC:RBC ratio was <1:1,000. The majority of patients (38/66; 58%) had a CSF WBC count of 1-5 cells/µL or were noted to have “no pleocytosis” or “normal WBC.” [10] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] , [26] , [27] , [29] , [30] , [33] , [36] , [37] , [38] , [40] , [41] , [42] , [44] , [45] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] There were 11/66 (17%) patients who had a CSF WBC count >5 cells/µL or noted to be “increased.” [8] , [12] , [17] , [28] , [31] , [32] , [33] , [34] , [35] , [39] , [46]

Fig. 3 Cerebrospinal Fluid White Blood Cell Count Results.

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