ABSTRACT
Cerebral microbleeds (CMB) emerged as a possible complication of COVID-19. We aimed to assess CMB presence, distribution, and potential underlying pathophysiological mechanisms in hospitalised COVID-19 patients. In a cohort of 112 COVID-19 patients with neurological symptoms admitted to the Geneva University Hospital between March 2020 and May 2021, we assessed CMB distribution, and associations with clinical/ radiological variables. Neuroimaging was performed on a 1.5 T MRI with susceptibility-weighted images, 3D time-of-flight angiography, and 3D-contrast-enhanced fat-saturated T1 black blood VISTA sequences. Two neurologists rated CMB using the Microbleed Anatomic Rating Scale and white matter hyperintensities using the Age-Related White Matter Changes score. 53 patients (47.0%) had CMB;in 45.3% of cases, CMB were found in lobar regions with a predilection for temporal (58.3%) and frontal (29.2%) lobes. Deep CMB were present in 18.9%, with corpus callosum CMB found in 15.0%, in 35.9% CMB distribution was mixed. CMB presence was not related to intubation, pulmonary involvement, nor to radiologic signs of endothelitis. Patients with CMB were more likely to have a higher burden of white matter hyperintensities (OR 1.13, p=0.005, 95% CI: 1.03- 1.24), to have hypertension as a comorbidity (OR= 2.34, p= 0.04, 95% CI: 1.04 - 5.30) and to suffer from an acute stroke during hospitalisation (OR: 3.50 p= 0.012, 95% CI:1.31-9.18). In our sample, COVID-19 patients with neurological symptoms had a high burden of CMB. Their distribution suggests that they may be related to cardiovascular risk factors and cerebral amyloid angiopathy. CMB were also associated with an increased risk of acute stroke.
ABSTRACT
Background/aims: Many reports have described pain appearance or an increase of chronic pain concomitant to SARS-CoV-2 infection. Here, we describe the cases of three patients with chronic cancer pain, in which COVID-19 was associated with a dramatic reduction/disappearance of pain. Methods: Descriptive report of three oncological patients with chronic pain hospitalized in the contexte of acute COVID-19. Clinical information was personally retrieved by the authors, who also examined the patients. Brain MRI was performed when deemed necessary by the referring physician. Autopsy, when conducted, was performed at the request of family members. All three patients were hospitalized between October 2020 and January 2021 Results: In this case series we describe, for the first time, a group of patients with chronic oncological pain, in which severe SARS-CoV-2 infection resulted in a temporary decrease of pain perception. It should be noted that despite optimal treatment, pain was insufficiently controlled in all cases prior to the infection. Patient 1 suffered from medullary compression at D2 due to probable perivertebral metastasis associated with bone lysis;patient 2 suffered from painful rib metastases;patient 3 suffered from neoplastic infiltration of the rectum from a bladder adenocarcinoma. None of the patients had impaired cognitive function that could have compromised their evaluation of pain. None of the patients complained of dyspnea at the moment of hospitalization;moreover, the reappearance of pain in patient 3 coincided with recovery from COVID-19 and de novo onset of dyspnea. Conclusions: To our knowledge, thisis the first case series reporting an acute reduction in pain perception in COVID-19. We believe further investigation is mandatory, as it could shed new light on the mechanisms of pain perception and modulation.
ABSTRACT
Objective: This study aims to compare the clinical characteristics of patients with COVID-19 related encephalopathy with and without radiological signs of intracranial gadolinium vessels enhancement. Background: The SARS-CoV-2 has been associated with neurological complications, including an acute encephalopathy. An unusual intracranial gadolinium vessels enhancement has been reported among these patients;however the prevalence, the clinical characteristics and the association with cerebrovascular complications have not been described yet. Design/Methods: Twenty-nine patients (66.9 ± 9.2 years;10% female) performed an MRI (with 3D T1-weighted black blood VISTA sequences) during acute onset of encephalopathy. The acute encephalopathy was defined by a delirium or a subsyndromal delirium with a pathobiological brain process in patients with a positive SARS-CoV-2 real-time reverse transcription polymerase chain reaction from a nasopharyngeal swab. Results: Twenty-three patients (79%) presented an intracranial gadolinium vessels enhancement, mainly in the vertebral arteries without sign of stenosis. Clinical characteristics were similar between patients with and without intracranial gadolinium enhancement, as well as the prevalence of acute stroke (9% versus 33%, respectively;p-value = 0.119) and microbleeds (52% versus 33%, respectively;p-value = 0.411). Among the 23 patients with an intracranial vessel gadolinium enhancement, 7 patients were treated by high-dose steroid (methylprednisolone 0.5g/d iv for 5 days) with a good clinical outcome. Conclusions: Patients with COVID-19 related encephalopathy present an increased prevalence of intracranial gadolinium vessels enhancement, suggestive of an endotheliitis that is not associated with stroke or microbleeds.
ABSTRACT
Acute encephalopathy is one of the most frequent neurological complication in patients hospitalized for COVID-19. Electrolyte imbalance, drugs, and hypoxemia can all affect brain homeostasis, leading to acute cognitive dysfunction and direct implications of the SARS-CoV-2 are not completely understood. Neurological complications of SARS-CoV-2 infection are poorly understood: an inflammatory insult to the endothelium affecting the blood-brain barrier may explain the clinical presentation, but other hypotheses including direct viral damage or an immune-mediated reaction are also suggested. Among these various potential mechanisms, often combined, the controversy remains.