Endothelial Cell Dysfunction and Injury in Subarachnoid Hemorrhage

Kumar, T. Peeyush; McBride, Devin W.; Dash, Pramod K.; Matsumura, Kanako; Rubi, Alba; Blackburn, Spiros

doi:10.1007/s12035-018-1213-7

Cited by 68 publications

(72 citation statements)

References 207 publications

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“…In spite of the relatively small number of patients who underwent autopsy in our case series, the histopathological pattern was similar presenting with multiorgan failure ( Figure 3 and Figure 4 ). In the brain, vascular endothelial cells primarily form the blood–brain–barrier (BBB) and maintain the interface between central nervous system and circulating blood [ 19 ]. Thereby, systemic vascular endotheliitis in COVID-19 may promote severe vessel weakening, blood vessel ruptures, and thus form a procoagulative state with subsequent intracerebral hemorrhage [ 6 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

Clinical and Imaging Characteristics in Patients with SARS-CoV-2 Infection and Acute Intracranial Hemorrhage

Nawabi

Morotti²,

Wildgruber

et al. 2020

JCM

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Background and Purpose: Intracranial hemorrhage has been observed in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19), but the clinical, imaging, and pathophysiological features of intracranial bleeding during COVID-19 infection remain poorly characterized. This study describes clinical and imaging characteristics of patients with COVID-19 infection who presented with intracranial bleeding in a European multicenter cohort. Methods: This is a multicenter retrospective, observational case series including 18 consecutive patients with COVID-19 infection and intracranial hemorrhage. Data were collected from February to May 2020 at five designated European special care centers for COVID-19. The diagnosis of COVID-19 was based on laboratory-confirmed diagnosis of SARS-CoV-2. Intracranial bleeding was diagnosed on computed tomography (CT) of the brain within one month of the date of COVID-19 diagnosis. The clinical, laboratory, radiologic, and pathologic findings, therapy and outcomes in COVID-19 patients presenting with intracranial bleeding were analyzed. Results: Eighteen patients had evidence of acute intracranial bleeding within 11 days (IQR 9–29) of admission. Six patients had parenchymal hemorrhage (33.3%), 11 had subarachnoid hemorrhage (SAH) (61.1%), and one patient had subdural hemorrhage (5.6%). Three patients presented with intraventricular hemorrhage (IVH) (16.7%). Conclusion: This study represents the largest case series of patients with intracranial hemorrhage diagnosed with COVID-19 based on key European countries with geospatial hotspots of SARS-CoV-2. Isolated SAH along the convexity may be a predominant bleeding manifestation and may occur in a late temporal course of severe COVID-19.

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Section: Discussionmentioning

confidence: 99%

Clinical and Imaging Characteristics in Patients with SARS-CoV-2 Infection and Acute Intracranial Hemorrhage

Nawabi

Morotti²,

Wildgruber

et al. 2020

JCM

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“…Experimental studies have shown that blood components and blood breakdown products in CSF can induce endothelial dysfunction and increase permeability of microvascular barriers, on the basis of which extravasation of serum from the vascular lumen into brain parenchyma would cause vasogenic edema. [ 21 – 23 ] Indeed, global vasogenic edema in white matter and deep gray matter, although mild only measured by elevated apparent diffusion coefficient, was reported in the subacute stage of subarachnoid hemorrhage. [ 24 ] Furthermore, the cell-free hemoglobin in the CSF disrupted dilatory NO signaling and increased endothelin-1, a powerful vasoconstrictor peptide, in cerebral arteries network, which shifted vascular tone balance from dilation to constriction.…”

Section: Discussionmentioning

confidence: 99%

Posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome associated spinal subdural hematoma

Chen¹,

Xu²,

Yuan³

2020

Medicine

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Rationale: Posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) are separate clinical entities with distinct pathophysiological features. But in some special conditions PRES and RCVS can occur simultaneously. Patient concerns: We report the unique case of a 40-year-old female presented with crescendo headache, blurred vision, and recurrent generalized tonic–clonic seizure. She had a minor neck injury 1 week before but attracted no more attention. Neurological tests on admission yielded a Glasgow Coma Scale score of 13. No obvious focal neurological deficit apart from positive signs of meningeal irritation was presented. Diagnoses: Xanthochromia and hemorrhagic cerebrospinal fluid with pleocytosis was found on lumbar puncture. Cranial computed tomography was negative but magnetic resonance imaging demonstrated bilateral areas of vasogenic edema in the parieto-occipital lobes and cerebellum consistent with PRES. An incidental subacute spinal subdural hematoma extending from the level of C6 to T1 was depicted by spinal magnetic resonance imaging, presumably as a complication of negligible neck trauma. Spinal digital subtraction angiography showed no evidence of spinal aneurysm, arteriovenous malformation, or dural arteriovenous fistula. Cerebral digital subtraction angiography showed segmental narrowing and dilatation of vessels, a potential feature of RCVS, involving the circle of Willis and their branches. Interventions: The patient was treated with nimodipine for vasodilation and other symptomatic therapies. The spinal subdural hematoma was not warranted for surgical intervention and managed with simple analgesics. Outcomes: The patient experienced a dramatic improvement in neurological symptoms and was discharged without sequelae. Follow-up imaging showed complete resolution of all radiological changes. Lessons: Clinician should be aware of spinal subdural hematoma as the potential trigger in development of PRES and RCVS. We speculate that endothelial dysfunction and vascular tone dysregulation may be implicated to play the major pathophysiologic role.

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“…These proinflammatory cytokines and mediators upregulate specific cell adhesion molecules on endothelial cells and induce neuroinflammation as well as the degradation of the inter-endothelial tight junctions and basal membrane in brain capillaries, which leads to BBB disruption and apoptosis of various cells, aggravating tissue damage after stroke (16,20,91). MMP-9 is a proinflammatory mediator induced by inflammatory cytokines and reactive oxygen species, and degrades components of the ECM of the cerebral microvessel basal lamina such as collagen IV, laminin, and fibronectin, as well as inter-endothelial tight junction proteins such as ZO-1, causing BBB disruption (92,93). TNC amplifies the expression levels through positive feedback mechanisms utilizing the TLR4 signaling pathway, leading to further activation of the signaling transduction and the development or aggravation of secondary brain injury, as TNC itself is a ligand of TLR4 (16,22).…”

Section: Tlr4 Cascades and Tnc In Strokementioning

confidence: 99%

The Role of Tenascin-C in Tissue Injury and Repair After Stroke

Okada

Suzuki

2021

Front. Immunol.

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Stroke is still one of the most common causes for mortality and morbidity worldwide. Following acute stroke onset, biochemical and cellular changes induce further brain injury such as neuroinflammation, cell death, and blood-brain barrier disruption. Matricellular proteins are non-structural proteins induced by many stimuli and tissue damage including stroke induction, while its levels are generally low in a normal physiological condition in adult tissues. Currently, a matricellular protein tenascin-C (TNC) is considered to be an important inducer to promote neuroinflammatory cascades and the resultant pathology in stroke. TNC is upregulated in cerebral arteries and brain tissues including astrocytes, neurons, and brain capillary endothelial cells following subarachnoid hemorrhage (SAH). TNC may be involved in blood-brain barrier disruption, neuronal apoptosis, and cerebral vasospasm via the activation of mitogen-activated protein kinases and nuclear factor-kappa B following SAH. In addition, post-SAH TNC levels in cerebrospinal fluid predicted the development of delayed cerebral ischemia and angiographic vasospasm in clinical settings. On the other hand, TNC is reported to promote fibrosis and exert repair effects for an experimental aneurysm via macrophages-induced migration and proliferation of smooth muscle cells. The authors review TNC-induced inflammatory signal cascades and the relationships with other matricellular proteins in stroke-related pathology.

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Endothelial Cell Dysfunction and Injury in Subarachnoid Hemorrhage

Cited by 68 publications

References 207 publications

Clinical and Imaging Characteristics in Patients with SARS-CoV-2 Infection and Acute Intracranial Hemorrhage

Clinical and Imaging Characteristics in Patients with SARS-CoV-2 Infection and Acute Intracranial Hemorrhage

Posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome associated spinal subdural hematoma

The Role of Tenascin-C in Tissue Injury and Repair After Stroke

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