Arachnoid granulation affected by subarachnoid hemorrhage

Abstract

The purpose of this study was to investigate using light microscopy the fibrocellular components of arachnoid granulations affected by mild and severe subarachnoid hemorrhage. The erythrocytes were in the channels delimited by collagenous and elastic bundles and arachnoid cells, showing their tortuous and inter-communicating row from the pedicle to the fibrous capsule. The core portion of the pedicle and the center represented a principal route to the bulk outflow of cerebrospinal fluid and erythrocytes. In the severe hemorrhage, the fibrocellular components are disorganized, increasing the extracellular channels. We could see arachnoid granulations without erythrocytes, which cells showed big round nucleus suggesting their transformation into phagocytic cells.

Tridimensional architecture of the collagen element in the arachnoid granulations in humans: a study on scanning electron microscopy

“…Neto et al 11 , and Chopard et al 12 , agree with the association of both of these mechanisms for the absorption of cerebrospinal fluid.…”

A new perspective on cerebrospinal fluid dynamics after subarachnoid hemorrhage: From normal physiology to pathophysiological changes

“…114 In addition to the blood clot, collagen and fibrin deposition were also found to block the arachnoid granulation-mediated CSF drainage in the autopsy. 84,115 Proliferation of leptomeningeal cells with increased collagen synthesis enzyme (prolyl 4-hydroxylase) prompts CSF collagen production in response to the circulating toxic products of blood, which further block the arachnoid granulations. 84,116 After SAH, the physiological structure of arachnoid granulations is destroyed by the increased ICP and by the chemical effects of digestive enzymes released from inflammatory cells, 84 which consequently stimulates the fibro-cells to facilitate granulation fibrosis.…”

“…84,116 After SAH, the physiological structure of arachnoid granulations is destroyed by the increased ICP and by the chemical effects of digestive enzymes released from inflammatory cells, 84 which consequently stimulates the fibro-cells to facilitate granulation fibrosis. 115 Fibrin/fibrinogen derived from the impaired BBB could be an additional source of granulation fibrin deposition. 117 Knowledge regarding post-SAH pathophysiological changes of arachnoid villi has stagnated, as most studies were performed 20 years ago.…”

Inhibition of caspase-1-mediated inflammasome activation reduced blood coagulation in cerebrospinal fluid after subarachnoid haemorrhage

“…7À10 The blood coagulation response to SAH in the subarachnoid space is considered the leading cause of CSF flow abnormalities, 2,3,8,9,11 which directly blocks the ventricular system and arachnoid granules with the resultant CSF retention and acute hydrocephalus. 12,13 The coagulation cascade leads to fibrin clotting and deposition in the subarachnoid space and perivascular space, which further blocks the CSFinterstitial fluid (ISF) exchange and induces cerebral vasospasm and the neuroinflammatory response. 8,9,11,14 Besides, fibrin deposition on the choroid plexus has also been suggested as the cause of CSF hypersecretion.…”