ABSTRACT
Since the very beginning of the COVID-19 pandemic, numerous researchers have made an effort to determine the molecular composition of the SARS-CoV-2 virus, and the exact pathomechanism through which the virus exerts such a devastating effect on the host/infected organism. Recent scientific evidence highlights the affinity of the virus towards ACE2 receptors, which are widespread in multiple human systems, including the central nervous system (CNS) and cerebral vessels. Such an affinity may explain endothelial dysfunction and damage that is observed in COVID-positive patients in histopathological studies, with subsequent dysregulation of the cerebral circulation leading to transient or acute cerebrovascular accidents. In this paper, we aimed to evaluate the effects of COVID-related hypoxemia and direct viral invasion on the cerebral circulation, with special respect to the postulated pathomechanism, vulnerable groups of patients, clinical course and outcomes, as well as diagnostic imaging findings.
Subject(s)
Blood Coagulation Disorders , COVID-19 , Angiotensin-Converting Enzyme 2 , COVID-19/complications , Humans , Hypoxia , Pandemics , SARS-CoV-2ABSTRACT
We present a case of a woman who reported to the emergency unit due to recurrent episodes of severe headache and collapse. MRI examination revealed no relevant findings apart from small meningioma of the right parietal region. The patient was diagnosed with epilepsy and received outpatient treatment, which was changed due to poor toleration. A follow-up MRI was performed which revealed an isolated, focal lesion of the splenium of the corpus callosum. The patient underwent extensive laboratory testing and antiseizure medications were started again. Another MRI indicated substantial regression of the splenium of the corpus callosum (SCC) lesion. Both the complete clinical image and results of the diagnostic evaluation spoke in favor of cytotoxicity of the corpus callosum associated with anti-epileptic drug treatment. Pathologies involving the corpus callosum include congenital, demyelination, infection, neoplasm, trauma and vascular changes. Isolated, non-specific lesions of the splenium of corpus callosum usually indicate multiple sclerosis; however, other pathologies should be considered. Anti-epileptic drugs may evoke cytotoxic lesions of the corpus callosum (CLOCCs).
ABSTRACT
In this review we attempt to collate the existing scientific evidence regarding the possible role of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the pathophysiology of Parkinson's disease (PD), as well as to investigate the impact of PD/parkinsonism on the clinical course of the viral infection itself. Since etiology of PD is not completely understood, various studies suggest different potential links between coronavirus disease 2019 (COVID-19) and PD. Suggested connections include, among others, similar prodromal symptoms, renin-angiotensin-aldosterone system involvement, or gut microbiome dysbiosis participation. Despite the initial assumptions that, as a mainly elderly population suffering from rigidity of respiratory muscles, impairment of cough reflex, and dyspnea, PD patients would be more susceptible to viral infection, and would experience a more aggressive course of COVID-19, the published scientific reports contain mutually exclusive data that require further investigation and meta-analysis.