COVID‐19 outbreak as a probable cause of increased risk of intracranial rebleeding in partially treated cerebral arteriovenous malformations

Abstract

Patients who are infected with COVID‐19 and have cerebral arteriovenous malformations which are partially treated or untreated may be more liable to rupture or bleed than not infected patients.

Neurotropism of SARS-CoV-2: A Pathological Examination of Neurosurgical Specimens

“…39 An apparent increased rupture risk of vascular lesions (intracranial aneurysms, AVMs, and cavernomas) and increased stroke risk with COVID-19 infection also suggests a pathophysiological involvement of the cerebrovasculature. [21][22][23]28,40,41 Cerebrospinal fluid sampling for SARS-CoV-2 has largely been negative 19,39 , raising the possibility of an indirect systemic inflammatory response involving cytokine storms, activation of the coagulation cascade, and autoimmune attacks as the primary mechanism for the neuropathology of COVID-19 infection rather than direct viral invasion. 9,10,19 Although none of the patients in this study had definitive neuropathological manifestations of COVID-19 infection, 4 of 5 patients (80%) had acute neurovascular pathologies coinciding with COVID-19 infection (3 patients had hemorrhagic vascular lesions [AVM, aneurysm, and cavernoma], and 1 patient had a large vessel occlusion).…”

“…39 An apparent increased rupture risk of vascular lesions (intracranial aneurysms, AVMs, and cavernomas) and increased stroke risk with COVID-19 infection also suggests a pathophysiological involvement of the cerebrovasculature. 21-23,28,40,41 Cerebrospinal fluid sampling for SARS-CoV-2 has largely been negative 19,39 , raising the possibility of an indirect systemic inflammatory response involving cytokine storms, activation of the coagulation cascade, and autoimmune attacks as the primary mechanism for the neuropathology of COVID-19 infection rather than direct viral invasion. 9,10,19…”

“…The acute and short-term CNS manifestations of COVID-19 infection are well-documented, including encephalitis and hemorrhagic, ischemic, and thrombotic events in typically lowerrisk patient populations. [21][22][23][24][25][26][27][28] Longer-term neurological sequalae are poorly understood because of the novelty of the virus and its rapidly emerging variants, but likely based on an examination of prior viral respiratory outbreaks. For example, an increased incidence of Parkinsonism was seen after the 1918 H1N1 influenza pandemic, 29 as was an increased incidence of cerebrovascular pathologies, demyelinating disorders, and neuromuscular diseases found after the coronavirus outbreaks SARS-CoV-1 and MERS-CoV in 2002 and 2012, respectively.…”

Another Face of COVID-19: A Pediatric Case of Cerebral Arteriovenous Malformation Rupture

“…2 Although the exact pathophysiological mechanism is not fully understood, it was hypothesized that COVID-19, like other well-known viruses, may result in inflammation of the vessel wall secondary to hypercytokinemia. 2,3 An alternative theory posits that the virus enters cells via angiotensin-converting enzyme II, inducing vasoconstriction and disrupting receptor function, ultimately resulting in impaired vascular autoregulation and elevation in blood pressure. 2,4 Although the patient’s cerebrospinal fluid was not tested for COVID-19 at the initial presentation, we considered it could account for the clinical picture.…”

Intracranial Hemorrhage Due to Potential Rupture of an Arteriovenous Malformation after BNT162b2 COVID-19 mRNA Vaccination in a Young Korean Woman: Case Report

“…Cerebral arteriovenous malformation (AVM) is an abnormal tangling of blood vessels in the brain with arteries connecting directly to veins without intervening cerebral tissue [ 1 ]. The majority of cases of AVM are asymptomatic, with most patients with AVM remaining unaware of this condition prior to manifesting neurological symptoms, such as convulsions or headache.…”