Dorsal Thoracic Arachnoid Abnormalities


Introduction

Deformities along the dorsal aspect of the thoracic spinal cord are occasionally identified on magnetic resonance imaging (MRI), often in patients presenting with myelopathy ( Fig. 36.1 ). A variety of nontumoral etiologies result in deformities of the dorsal thoracic cord, of which many are related to abnormalities of the dorsal arachnoid. These abnormalities include intradural arachnoid cyst as well as dorsal thoracic arachnoid webs, bands, or pouches. Clinically the presenting symptoms include upper or lower extremity paresthesia or weakness, gait disturbances, neck or upper back pain, or some combination. The clinical course is typically chronic and progressive. Although these entities display significant overlap in their clinical presentation and appearance on MRI, they have distinct anatomic origins, which can be identified preoperatively.

Figure 36.1, Dorsal thoracic cord deformity.

Anatomic Principles of the Spinal Meninges

The spinal cord is intimately associated with a surrounding lattice of meningeal connective tissue ( Fig. 36.2 ). Generally speaking the outermost component is termed the dura , which is a thick sac-like structure that maintains the outer margin of the cerebrospinal fluid (CSF) space. The innermost layer is the pia , which is closely apposed to the spinal cord, cauda equina, and nerve roots. The space between the pia and dura is the subarachnoid space , which is occupied by a fine, filamentous, diaphanous lattice of arachnoid trabeculae bathed in CSF. The outer layer of the arachnoid is attached to the dura by thin strands of collagen. Centrally, the arachnoid and pia merge. Nerve roots and blood vessels coursing through the subarachnoid space are enveloped by arachnoid tissue. Stronger supportive structures—such as the denticulate ligaments on either side of the cord and dorsal septum—are also present, sometimes evident on imaging particularly within the cervical spine. The spinal subarachnoid space can be subdivided into ventral and dorsal compartments or chambers, as delineated by the laterally projecting denticulate ligaments. Importantly, arachnoid trabeculae are much more plentiful in the dorsal chamber.

Figure 36.2, Anatomy of the spinal meninges.

Arachnoid-Related Abnormalities in Greater Depth

Derangements of the arachnoid may take various forms, including cyst-like abnormalities that may manifest as a complete cyst with intact walls, a porous cyst with communications to the remainder of the subarachnoid space, or an open-ended “windsock”-type cystic structure, to name a few. In addition, arachnoid thickening, banding, or a web-like networks may be encountered. It is precisely this variety of potential morphologies within the context of continuous pulsatile CSF flow that explains some of the differences in the natural history of such lesions.

Arachnoid Cysts and Pouches

Arachnoid cysts may be intra- or extradural as defined by the Nabors classification, with extradural arachnoid cysts referring to a CSF-filled cyst-like structure occurring as a result of arachnoid herniation through the confines of the dura ( Fig. 36.3 ). The current discussion refers to intradural arachnoid cysts, which are CSF-filled cyst-like structures that occur within the subarachnoid space. A variety of mechanisms for their formation have been postulated, including splitting or duplication of the arachnoid, although the exact cause is yet unknown. They can be congenital or acquired and most frequently occur in the thoracic spine (80% of cases). Typically the intradural arachnoid cysts responsible for cord deformities occur posterior to the cord and cause ventral cord displacement and flattening ( Fig. 36.4 ). In cases where the degree of mass effect is subtle, the presence of such a cyst might only be inferred by indirect imaging findings. Specifically, arachnoid cysts may have such diminished communication with the remainder of the subarachnoid space that the CSF within the cyst is devoid of CSF pulsation artifact. This indirect finding can be one of the best clues for diagnosis on sagittal imaging. On axial imaging, flattening of the dorsal cord's surface is another clue that aids in the diagnosis.

Figure 36.3, Intradural arachnoid cyst (A) and pouch (B) indenting the dorsal cord.

Figure 36.4, Arachnoid cyst.

If the resolution of imaging is high enough or if the cyst wall is thick enough, an oval, thin, smooth wall may be evident. Unfortunately visualization of the cyst walls is often beyond the resolution of routine imaging technology. Thin-section heavily T2-weighted MRI sequences as well as more recently employed steady-state imaging techniques (such as CISS, FIESTA, and DRIVE) may more accurately define the wall of the cyst. Alternatively, computed tomography (CT) myelography may be helpful if a complete or nearly complete arachnoid cyst is present, as myelographic contrast will be excluded from the cyst or will fill in a delayed fashion.

Somewhat complicating matters are the fenestrated cysts or pouch-like arachnoid cystic lesions that may be encountered. Fenestrated cysts or pouches may confuse the uninformed imaging interpreter in evaluating the results of a CT myelogram performed for a suspected arachnoid cyst. This is because one would expect an “arachnoid cyst” to not communicate freely with the subarachnoid space. However, as arachnoid pouches and fenestrated cysts communicate with the subarachnoid space, their CSF contents will be isodense to that of the subarachnoid space on myelography. Therefore rapid filling of an ill-defined, questionable cyst-like arachnoid lesion on myelography may be erroneously interpreted as confirmation that an arachnoid cyst is not present.

Arachnoid cysts and pouches can be treated conservatively or surgically and generally have a good prognosis. Most surgically treated cases result in symptomatic improvement dependent on the chronicity of the lesion prior to surgical intervention. On imaging, there is typically resolution of the cord deformity (see Fig. 36.4C ), but in cases of severe chronic compression there may be subtle residual loss of spinal cord volume resulting from long-standing compressive myelomalacia.

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