Also appropriate to mention here are CSF leaks that occur after cranial, nasal, or spinal surgery. These are suspected in the postoperative period, although the precise origin of the leak may be difficult to determine, but they give rise to some of the most intractable low-pressure syndromes and must be investigated by radiologic and nuclide studies. In our experience, several such leaks have been intermittent, adding to the difficulty in diagnosis.
The treatment of spontaneous intracranial hypotension is similar to that mentioned earlier under the treatment of postlumbar puncture headache. Kantor and Silberstein pointed out that some patients who fail to respond to conservative management with bed rest, abdominal binders, hydration, caffeine, theophylline, and corticosteroids, and who have also failed with lumbar epidural blood patch, will respond to a cervical epidural blood patch. This should be administered by those who are skilled in their use and are aware of the risk of compression of the spinal cord.
The effects of bacterial invasion of the pia-arachnoid, cerebrospinal subarachnoid space, ventricles, and ependyma are described in Chap. 31 and summarized in Table 31-1. The point being made here is that these structures may also be involved in a number of noninfective processes, some of obscure origin.
Because the ventricular and subarachnoid spaces are in continuity, one would expect that a noxious agent entering any one part would extend throughout the CSF pathway. Such is not always the case. The lower spinal roots or spinal cord alone may be implicated in “spinal arachnoiditis.” A similar process may affect the optic nerves and chiasm exclusively (“opticochiasmatic arachnoiditis,” see further). A predominant localization to these basal or cervical structures may be apparent even in cases of diffuse cerebrospinal meningeal reactions, perhaps because of an uneven concentration of the noxious agent. The mechanisms by which these meningeal reactions affect parenchymal structures (brain, cord, and nerve roots) are not fully understood. The most obvious sequela is an obstruction to the flow of CSF in hydrocephalus; here, simple fibrotic narrowing of the CSF circulatory pathway is causative. Progressive constriction of nerve roots and spinal cord, literally a strangulation of these structures, is another plausible mechanism, but it is difficult to separate vascular factors from mechanical ones. Because any toxic agent or inflammatory response in the subarachnoid space has free access via Virchow-Robin spaces and thereby to the superficial parts of the brain and spinal cord, direct parenchymal injury may follow. Perivascular reactions of subpial vessels, as in infectious processes, would be a plausible mechanism of injury to optic nerves and spinal cord, where long stretches of myelinated fibers abut the pia.
Arachnoiditis limited to the lumbosacral roots has followed ruptured discs, myelograms, and spinal surgery. Usually, there is sciatica and chronic pain in the back and lower extremities, but sensorimotor and reflex changes in the legs are variable. The MRI shows irregularly enhancing roots and arachnoidal thickening; myelography discloses loculated pockets of imaging media. This condition is discussed further in Chap. 10.