Abstract
Coronaviruses (CoVs) are enveloped RNA viruses and have been shown to cause mild to severe respiratory infections in humans, with some severe cases inducing neurological manifestations. The lethality and Neurological effects of the Severe Acute Respiratory Syndrome (SARS-CoV), Middle-East Respiratory Syndrome (MERS-CoV), and recently the Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) have been well documented though currently there is little literature regarding long term effects and the implications for neurorehabilitation. SARS-CoV-2 and MERS-CoV have been linked to the infection associated inflammatory cytokine storms and induced hypercoagulopathic states that affect the entire vascular system including that of the brain. This mini-review provides an overview of the commonalities among studies published on all three types of the coronavirus related to acute ischemic stroke (AIS). The aim was to elucidate the physiological mechanisms underpinning COVID-2 and to reflect the similarities with the chronic inflammation induced symptoms of AIS that are likely to prove a further challenge for neurorehabilitation clinicians post COVID. In terms of increased incidence of COVID and AIS, it is likely that in depth knowledge of increased thrombotic risk in this population will require appropriate anticoagulation treatment, and other therapeutic interventions as well as neurorehabilitation interventions. Lastly the risk of spreading the virus requires further balancing of the provision of neurorehabiliatation services useful to the patient.
Highlights
Four genera of Coronavirina have been identified, three of which can infect mammals [1]
Impairment of normal functioning of the angiotensin-converting enzyme 2 (ACE2) receptors following the invasion of the virus leads to down regulation of the Renin Angiotensin Aldosterone system (RAAS) and cascade of inflammatory events culminating in pneumonia, severe acute respiratory distress syndrome, multi-organ failure and has led to numerous fatalities during earlier regional outbreaks in China (SARS-CoV), Saudi Arabia (MERS-CoV), and globally severe Retrospective cohort acute respiratory syndrome (SARS)-CoV-2 [6]
It is important that medical staff are cognizant of potential neurological complications when treating COVID-19
Summary
Four genera of Coronavirina have been identified, three of which can infect mammals [1]. Impairment of normal functioning of the ACE2 receptors following the invasion of the virus leads to down regulation of the Renin Angiotensin Aldosterone system (RAAS) and cascade of inflammatory events culminating in pneumonia, severe acute respiratory distress syndrome, multi-organ failure and has led to numerous fatalities during earlier regional outbreaks in China (SARS-CoV), Saudi Arabia (MERS-CoV), and globally SARS-CoV-2 [6]. Neurological manifestations of coronaviruses were first described during the SARS CoV epidemic in 2002 [10]. Tsai et al reported cases of neuropathies, myopathies, and strokes during the SARS I epidemic while encephalitis and acute inflammatory demyelinating polyneuropathy (AIDP), and Gullian-Barre syndrome (GBS) have been described in patients with MERS-CoV by Kim et al [10, 11]. During the SARS-CoV-2 pandemic, an increasing number of patients have presented with stroke and other neurovascular complications as well as the aforementioned manifestations [9, 12]
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