case_images: PMC7284455_01
case_images: 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.
case_images: 10.1177_1756286420932036-fig1.jpg
case_images: PMC7284455_01_10.1177_1756286420932036-fig1.jpg
case_images: fig1-1756286420932036
case_images: 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).
case_images: 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.
case_images: 10.1177_1756286420932036-fig2.jpg
case_images: PMC7284455_01_10.1177_1756286420932036-fig2.jpg
case_images: fig2-1756286420932036
case_images: 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).
case_images: 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.
case_images: 10.1177_1756286420932036-fig3.jpg
case_images: PMC7284455_01_10.1177_1756286420932036-fig3.jpg
case_images: fig3-1756286420932036
case_images: 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).