The pathophysiologic mechanism of headache symptoms and various neurological deficits in patients with intracranial hypotension is not well understood but likely multifactorial and may be attributed to 1) compensatory venodilitation, blood volume expansion, and dural sinus stretching as the body attempts to maintain a stable intracranial volume in response to decreased CSF volume; and 2) downward traction on the meninges, nerves, and brain parenchyma as the brain loses buoyancy and begins to sag in response to decreased CSF volume. The findings of venodilitation and brain sagging have well-defined imaging findings and have been shown to resolve along with clinical improvement of headache symptoms [16,17]. The 3 main causes of intracranial hypotension are CSF leakage through a dural defect, leaking meningeal diverticulum, and CSF-venous fistula [18-20]. It is important to note that in the upright position, intracranial hydrostatic pressure is slightly negative relative to atmosphere, whereas hydrostatic pressure in the spine is positive relative to atmosphere [21]. Consequently, the spine has been shown to represent the anatomical source of most symptomatic CSF leaks and venous fistulas, such that the imaging investigation of leak source should be directed primarily toward the spine and not intracranially [22]. Imaging plays a critical role in the diagnostic evaluation of intracranial hypotension. The goals of imaging are 2- fold: 1) to confirm the diagnosis of intracranial hypotension and 2) to localize the source of leak for targeted therapy such as epidural blood patch, percutaneous fibrin glue treatment, endovascular venous fistula embolization, and surgical dural repair or venous fistula ligation [23,24]. Intracranial imaging features suggestive of intracranial aMayo Clinic Arizona, Phoenix, Arizona. bPanel Chair, Mallinckrodt Institute of Radiology, Saint Louis, Missouri. cThe Ohio State University Wexner Medical Center, Columbus, Ohio.
Imaging of Suspected Intracranial Hypotension PCAs. The pathophysiologic mechanism of headache symptoms and various neurological deficits in patients with intracranial hypotension is not well understood but likely multifactorial and may be attributed to 1) compensatory venodilitation, blood volume expansion, and dural sinus stretching as the body attempts to maintain a stable intracranial volume in response to decreased CSF volume; and 2) downward traction on the meninges, nerves, and brain parenchyma as the brain loses buoyancy and begins to sag in response to decreased CSF volume. The findings of venodilitation and brain sagging have well-defined imaging findings and have been shown to resolve along with clinical improvement of headache symptoms [16,17]. The 3 main causes of intracranial hypotension are CSF leakage through a dural defect, leaking meningeal diverticulum, and CSF-venous fistula [18-20]. It is important to note that in the upright position, intracranial hydrostatic pressure is slightly negative relative to atmosphere, whereas hydrostatic pressure in the spine is positive relative to atmosphere [21]. Consequently, the spine has been shown to represent the anatomical source of most symptomatic CSF leaks and venous fistulas, such that the imaging investigation of leak source should be directed primarily toward the spine and not intracranially [22]. Imaging plays a critical role in the diagnostic evaluation of intracranial hypotension. The goals of imaging are 2- fold: 1) to confirm the diagnosis of intracranial hypotension and 2) to localize the source of leak for targeted therapy such as epidural blood patch, percutaneous fibrin glue treatment, endovascular venous fistula embolization, and surgical dural repair or venous fistula ligation [23,24]. Intracranial imaging features suggestive of intracranial aMayo Clinic Arizona, Phoenix, Arizona. bPanel Chair, Mallinckrodt Institute of Radiology, Saint Louis, Missouri. cThe Ohio State University Wexner Medical Center, Columbus, Ohio.