The “Subdural” Space

Abstract

This review considers the structure of the meninges, as seen at the electron microscopic level, with particular emphasis on the dura-arachnoid junction and whether a naturally occurring space is found at this interface. The classic view has been that a so-called subdural space is located between the arachnoid and dura and that subdural hematomas or hygromas are the result of blood or cerebrospinal fluid accumulating in this (preexisting) space. The dura is composed of elongated, flattened fibroblasts and copious amounts of extracellular collagen. A specialized layer of fibroblasts, the dural border cell layer, is found at the dura-arachnoid junction and is characterized by flattened fibroblasts, no extracellular collagen, extracellular spaces, and few cell junctions. These features combine to create a layer of the inner dura that is structurally weak when compared with external portions of the dura and the internally located arachnoid. The arachnoid layer is composed of larger cells with numerous cell junctions, no extracellular space, and no extracellular collagen. The occurrence of many tight junctions in this layer also serves as a barrier to the movement of fluids and ions. Fibroblasts specialized to form the arachnoid trabeculae attach to the inner surface of the arachnoid layer, bridge the subarachnoid space, and surround vessels in the subarachnoid space as well as attach to pia on the surface of the brain. Under normal conditions, there is no evidence of a naturally occurring space being extant at the dura-arachnoid junction. A space may appear at this point subsequent to pathological/traumatic processes that result in tissue damage with a cleaving opening of the structurally weakest plane in the meninges--through the dural border cell layer. Furthermore, when a space does appear, it is not "subdural" in location but rather within a morphologically distinct cell layer.

Dynamics of subdural hygroma following decompressive craniectomy: a comparative study

“…Based on electron microscopy studies, 25,63 necropsy findings, 15,49 and the entrance of contrast material into the hygroma cavity after contrast cisternography, 46 it is hypothesized that injury to the arachnoid-dura interface layer is the central pathology in SDGs. Spillage of the CSF into the subdural space peaked at 3-4 weeks after DC, and this pathological process gradually ceased from 14-17 weeks postoperatively.…”

“…Whereas a significant number of collagen fibers bond the cellular structure of periosteal and meningeal dura, the dural border cell layer contains very little collagen, and instead, cellular elements are loosely held together by an amorphous material prone to disruption by physical stress. 25,63 Protecting the subarachnoid space and its trabeculae is the arachnoid barrier cell layer in which the cellular elements are tightly packed together by desmosomes, tight junctions, and gap junctions. 25,63 Shearing stress generated by kinetic energy can tear arachnoid barrier cells and damage the integrity of the arachnoid-dura interface layer.…”

“…25,63 Protecting the subarachnoid space and its trabeculae is the arachnoid barrier cell layer in which the cellular elements are tightly packed together by desmosomes, tight junctions, and gap junctions. 25,63 Shearing stress generated by kinetic energy can tear arachnoid barrier cells and damage the integrity of the arachnoid-dura interface layer. 25 In our study patients who had been in MVAs were significantly more prone to SDGs (p < 0.0007) than were those who had fallen.…”

“…25,63 Shearing stress generated by kinetic energy can tear arachnoid barrier cells and damage the integrity of the arachnoid-dura interface layer. 25 In our study patients who had been in MVAs were significantly more prone to SDGs (p < 0.0007) than were those who had fallen. It is quite likely that the former patients had a significantly more damaged arachnoiddura interface layer during sudden exposure to a highly dynamic kinetic energy.…”

Acute-on-Chronic Subdural Hematoma: Not Uncommon Events

“…The reason was that the bleeder was usually venous or capillary, either from bridging veins or fragile new vessels in the neomembrane. The outer membrane contains many fragile sinusoidal vessels that are often the source of repeated multifocal bleeding 4,14) . Like the repeated hemorrhages from the outer membrane, repeated trauma may cause acute bleeding over the chronic SDH as a mechanism of hematoma enlargement.…”