Intracranial Hypotension Syndrome

Abstract

Intracranial hypotension syndrome is characterized by orthostatic headache and low CSF pressure and volume. Intracranial hypotension is either primary, also known as spontaneous intracranial hypotension, or secondary to cervical manipulation, lumbar puncture, or cranial/spinal surgery at the origin of a dural breach. Spontaneous intracranial hypotension can be observed in patients with dural weakness, e.g., in Marfan disease after mild trauma or in the presence of large Tarlov cysts. Sometimes the location of the dural breach can be demonstrated or suspected on spinal MR study. Invasive methods such as radionuclide cisternography are no longer carried out. An epidural blood patch provides the most efficient treatment for intracranial hypotension syndrome. MR findings in intracranial hypotension syndrome include dural thickening, dural enhancement, decreased ventricle size, subdural collections, tonsillar herniation, collapsed cisterns, venous distension signs and in the sellar region, and bulging of the pituitary gland (Fig. 46.1). It is hypothesized that enlargement of the pituitary gland is related to hyperemia of the gland in the same way as venous hyperemia and enhancement occur in pachymeninges. We have observed that a prominent inferior intercavernous sinus is frequent in patients with intracranial hypotension syndrome, and probably reflects an engorgement of parasellar veins. Enlargement of inferior intercavernous sinus can also participate in the bulging of the pituitary gland. A prominent inferior intercavernous sinus is seen as a more or less thick T1-hypointense band doubling the sellar floor; the signal is variable on T2WI, either hyper- or hypointense depending on the flow velocity (Fig. 46.2). Thus, in the presence of an enlarged pituitary gland of unknown origin, demonstration of a prominent inferior intercavernous sinus leads one to consider the diagnosis of intracranial hypotension syndrome. After medical treatment and/or lumbar blood patch, shrinkage of the inferior intercavernous sinus is usually observed, simultaneously with clinical improvement (Fig. 46.3).