Current Neurovascular Research - Volume 17, Issue 4, 2020

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na,⁺, K⁺-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na⁺, K⁺-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na⁺, K⁺-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na⁺, K⁺-ATPase activity and increased oxidative stress.

Our knowledge of the vascularization of the precentral gyrus by branches of the anterior cerebral artery (ACA) relies mainly on anatomical cadaveric dissection. A distal branch of the ACA known as the posterior internal frontal artery (PIFA) is thought to vascularize the precentral gyrus responsible for proximal arm movement; however, no clinical correlation has yet been reported to confirm this relation. In this manuscript, we report a case of coil migration in the PIFA, causing proximal arm weakness in a 58-year-old woman treated for aneurysmal subarachnoid hemorrhage. The occurrence of clinical signs immediately following coil migration into the PIFA, combined with evidence of stroke in the cortical territory related to arm movement as seen on imaging, indicates that the PIFA indeed can vascularize this lateral portion of the precentral gyrus. This case confirms our current understanding of the vascularization of the precentral gyrus by distal ACA branches, in particular the PIFA.

Coronavirus is an enveloped, non-segmented, positive-polarity and single-stranded RNA virus. It has four types of genera that infect mammals and birds, with only alpha and beta types found to affect humans with varying severity. A specific clade of beta coronaviruses is reported as lethal zoonotic viruses and has created major epidemic troubles, starting with the severe acute respiratory syndrome (SARS) in 2002, then the Middle East respiratory syndrome (MERS) in 2012, and lastly Coronavirus Disease 2019 (COVID-19) in 2019. However, many neurological complications reported in COVID-19 patients have highlighted a critical pattern of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Awareness of such an association could create new insight to consider neurological manifestations as a COVID-19 differential diagnosis during the pandemic period of COVID-19 to avoid delayed diagnosis and prevent further transmission. This mini-review aims to collect the current knowledge regarding the mechanism behind the neuroinvasive capacity of SARS-CoV-2, to summarize the common documented neurological symptoms and associated complications in COVID-19 patients, and to review the impact of neurological manifestations on COVID-19 mortality.