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The Venous Distension Sign: A Diagnostic Sign of Intracranial Hypotension at MR Imaging of the Brain - AJNR News Digest
October 2013
Brain

The Venous Distension Sign: A Diagnostic Sign of Intracranial Hypotension at MR Imaging of the Brain

Richard I. Farb

Richard I. Farb

Gadolinium-enhanced MR venography has provided neuroradiologists with the ability to visualize the effect that altered intracranial pressure (ICP) has on the appearance of the dural venous sinuses. Specifically, the dural sinuses appear mildly compressed when ICP is elevated and will distend when ICP is abnormally low. This changing contour of the dural sinuses has been shown to be a dynamic phenomenon, and is displayed nicely by the transverse sinuses. Narrowing of the distal transverse sinus associated with elevated ICP is best visualized with gadolinium-enhanced MR venography and typically seen in idiopathic intracranial hypertension as well as other pathologic states associated with elevated ICP. Enlargement of the dural venous sinuses is one of the well-recognized stigmata of intracranial hypotension. Clearly, in imaging patients with headache, it would be beneficial to be able to comment on the presence or absence of intracranial hypotension without the use of gadolinium.

After reviewing several patients with this clinical syndrome it became evident that by applying the criteria of the “venous distension sign” (VDS)—a convex undersurface of the middle third of the dominant transverse sinus—we could determine, in a binary fashion, whether there was presence or absence of intracranial hypotension. We have found the VDS particularly useful when evaluating patients with subdural hemorrhage or hygroma. A positive VDS in a patient with subdural collections indicates that intracranial hypotension is present and is likely the primary abnormality. Conversely, it is worth checking for the VDS in patients suspected of having Chiari type I malformations. The greatest challenge in imaging intracranial hypotension is not in the diagnosis but in identifying the cause.

Popular opinion suggests that spontaneous intracranial hypotension is always related to mechanical leakage of CSF from the thecal sac. In many cases an obvious site of leakage can indeed be found. However, commonly, symptoms and signs of hypotension persist despite 2 or even 3 "blind" epidural blood patches, and the site of CSF leakage cannot be identified despite the use of high-resolution CT myelography and even MR myelography with intrathecal gadolinium. Management of these patients can be quite challenging. Do these patients have abnormal CSF physiology, as suggested by some authors?

I look forward to a better understanding of CSF physiology as well as standardization of diagnostic imaging and management algorithms to benefit patients with this disease.

 

Read this article at AJNR.org . . .