PMC7284455_01
Imaging evaluation of an ischemic stroke patient with concomitant
COVID-19.. This 53-year-old man presented in the emergency department of a
comprehensive stroke centre on March 18, 2020. The patient was aphasic
with right hemiplegia. The National Institute of Health Stroke Scale
(NIHSS) score was 16. He was afebrile and his family members denied any
symptoms attributable to COVID-19. Neurological symptoms'
onset-to-presentation time was 1 h. A non-contrast brain computed
tomography (CT)-scan was performed, intracranial haemorrhage was
excluded and early hyperacute signs of left middle cerebral artery
ischemia were disclosed (loss of grey-white matter differentiation (A).
No other contraindications existed and intravenous thrombolysis with
alteplase was administered. Door-to-needle time was relatively prolonged
(70 min), since the CT-scan was occupied at that time with chest
examinations of patients with possible SARS-CoV-2 infection. There was
no availability for mechanical thrombectomy in this institution
(after-hours presentation of the patient and limited personnel in the
catheter laboratory). Diagnostic work-up revealed two possible stroke
mechanisms: atrial fibrillation of unknown duration with subsequent
cardio-embolism, and concomitant atherothrombotic disease, causing
haemodynamically significant (>70%) stenosis of the internal carotid
arteries bilaterally. During the next 48 h, the patient presented
neurological deterioration (NIHSS-score of 22) and follow-up brain CT
showed an extensive infarction in the distribution of the left middle
cerebral artery (B). At that time, the patient developed a low-grade
fever, most probably due to aspiration. Chest CT-scan was indicative of
bilateral aspiration pneumonia (C). Oropharyngeal swabs were also
examined for SARS-CoV-2 on RT-PCR assay, but the virus was not detected.
Three days later, the patient was intubated and transferred to the
general intensive care unit. The second oropharyngeal swab test was
positive for SARS-CoV-2 RNA. The patient expired on March 24, 2020 due
to further neurological deterioration from cerebral oedema.
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We present the case reports of two stroke patients with clearly identified underlying aetiopathogenic stroke mechanisms, who also suffered from COVID-19 manifestations (Figures 1 and 2). For example, early cerebral imaging should be preserved in order to avoid unnecessary delays, noted in our patient presented in the case report (Figure 1).
Imaging evaluation of a patient with intracerebral haemorrhage with
concomitant COVID-19.. A 67-year-old man with a history of hypertension, diabetes,
hypercholesterolemia and coronary artery disease presented to the
emergency department of a comprehensive stroke centre on April 6, 2020
after waking up with slurred speech, left-sided weakness and numbness.
Admission systolic and diastolic blood pressure levels were
178/106 mmHg. The patient was afebrile with no respiratory symptoms.
However, history provided by his wife suggested that earlier in the
morning, prior to his admission, he had an increased body temperature of
38.5 C. Brain computed tomography scan uncovered right thalamic
intracerebral haemorrhage with mass effect and intraventricular
extension (A). The patient was admitted in the stroke unit. Due to the
history of fever, a nasopharyngeal swab was performed on the day of
admission and was negative for SARS-CoV-2. However, on the following day
the patient redeveloped fever, so work-up with blood cultures, chest
X-ray (B) and urinalysis was performed but did not uncover any obvious
source of infection. A second nasopharyngeal swab was ordered and came
back positive for SARS-CoV-2 RNA. Despite SARS-CoV-2 infection, the
patient never experienced any symptoms of dyspnoea, cough, chest pain or
diarrhoea during his hospitalization. He only reported the presence of
mild generalized headache and nausea, which could have been attributable
to the intracerebral haemorrhage. A certain causal association between
COVID-19 and intracerebral haemorrhage cannot be established based on
the evidence in this case, especially since the patient had a medical
history of three common risk factors of manifesting both the diseases
(Table
3). However, it may be postulated that blood pressure
dysregulation due to angiotensin converting enzyme 2 (ACE2) inactivation
by SARS-CoV-2 could have been at least partially involved in the
development of intracerebral haemorrhage.
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We present the case reports of two stroke patients with clearly identified underlying aetiopathogenic stroke mechanisms, who also suffered from COVID-19 manifestations (Figures 1 and 2).
Imaging evaluation of a left facial palsy patient with concomitant
COVID-19.. A 27-year-old man was admitted to the isolation ward of a tertiary centre
on March 16, 2020, presenting with myalgia, cough, fever and left-sided
headache for 4 days. He had just returned from Spain the day before
admission. On examination his lungs were clear and neurological
examination was unremarkable. Reverse-transcription
polymerase-chain-reaction (PCR) performed on the nasopharyngeal swab was
positive for SARS-CoV-2. On day 3 of hospitalization, he developed left
retro-auricular pain, dysgeusia and left facial weakness. Neurological
examination showed a left facial nerve palsy. There was no associated
neck stiffness, vesicles in the outer ear, or parotid swelling.
Cerebrospinal fluid (CSF) studies showed no cells, and protein and
glucose levels were normal. CSF PCR was negative for herpes simplex
virus, varicella zoster virus and SARS-CoV-2. His magnetic resonance
imaging of the brain showed contrast enhancement of the left facial
nerve (Figure). He was treated with lopinavir/ritonavir for reducing
SARS-CoV-2 viral replication. He received a 1-week course of
prednisolone and valacyclovir for treatment of facial palsy. Upon review
1 week later, his headache had resolved, and improvement was noted in
facial weakness.
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In the spectrum of PNS involvement in COVID-19, we present the case report of a patient with confirmed SARS-CoV-2 infection who developed facial nerve palsy during hospitalization (Figure 3).