Arachnoiditis

Anatomy

The arachnoid mater is an avascular region that lies between two vascularized membranes: the pia mater and the dura mater. The arachnoid is attached to the underlying pia by numerous trabeculae, which create a space between the arachnoid and the pia. This space, or potential space in some instances, transmits arterioles and is referred to as the subarachnoid space. The arachnoid is composed of layers of squamous cells held together by a network of connective tissue. The arachnoid contains intercellular pores that allow for the passage of molecules.

Pathogenesis

A chronic infection or irritation can cause the arachnoid membrane to become thickened and adherent to both the overlying dura mater and the underlying pia mater. The pia-arachnoid carries the blood vessels to the spinal cord, and this layer contains mesenchymal cells. In 1951, Smolik and Nash recognized that when the outer arachnoid layer is injured both the blood vessels and mesenchymal cells lend themselves to extensive proliferation. The ensuing reaction between the pia-arachnoid and the dura mater leads to obliterative arachnoiditis.

When the arachnoid membrane is exposed to an insult, an inflammatory response ensues, which is characterized by fibrinous exudates, neovascularization, and a relative paucity of inflammatory cellular exudates. ^, Vascular occlusive changes can occur that may lead to spinal cord ischemia. ^, The small perforating blood vessels that supply portions of the white matter may be obliterated, with resultant necrosis and cavitation of the spinal cord parenchyma. ^{, ,} In addition to ischemia, blockage of venous return from the spinal cord or occlusion of cerebrospinal fluid (CSF) pathways may occur. When CSF pathways occlude, syringomyelia formation may result.

Burton described the stages of progressive inflammation of the arachnoid that occur in lumbosacral arachnoiditis. The initial stage, radiculitis, consists of an inflamed pia-arachnoid with associated hyperemia and swelling of the nerve roots. The second stage, arachnoiditis, is characterized by fibroblast proliferation and collagen deposition. During this stage, nerve root swelling decreases, and the nerve roots adhere to each other and to the pia-arachnoid. The final stage, adhesive arachnoiditis, is the resolution of the inflammatory process and is characterized by dense collagen deposition. There is marked proliferation of the pia-arachnoid layers, as well as complete nerve root encapsulation, hypoxemia, and progressive atrophy. For reasons that are not fully understood, the adhesions occur preferentially on the dorsal segments. The exact time course of these three phases has not been elucidated. Furthermore, it is not known how the specific causative insult for the development of arachnoiditis might affect the time course of each of the three phases.

Yamagami and colleagues postulated that the pathological changes in arachnoiditis may be secondary to diminished nutritional supply. They found that, in an experimental rat model, the development of arachnoiditis and neural degeneration directly corresponded to the magnitude of extradural inflammation and wound-healing processes that occurred after a laminectomy with or without foreign bodies. Furthermore, adhesions of the arachnoid cause the nerve roots to lump together, and in the process these nerve roots are isolated from contact with the CSF, with resultant nutritional compromise.