Venous Hypertension and Increased Intracranial Pressure
Although the mechanism of idiopathic intracranial hypertension (IIH) is uncertain, the cerebral venous system has been implicated since the 1930s. Dandy (1) hypothesized that the volume of cerebrospinal fluid (CSF) or cerebral blood might be increased. Others postulated that the cerebral microvasculature was the source of cerebral edema in this condition (2–4). Intracranial venous hypertension was subsequently proposed as a unifying mechanism or final common pathway of IIH. Johnston and Paterson (5) first suggested that increased sagittal sinus pressure causing decreased CSF absorption was the underlying cause of IIH.
A syndrome clinically identical to IIH is produced by cerebral venous sinus thrombosis (6–8). Interest in the dural venous sinuses as the source of increased intracranial pressure (ICP) in IIH was heightened in the 1990s, with studies of direct venous manometry in IIH patients and studies performed in IIH patients undergoing bariatric surgery. Intracranial and central systemic venography and manometry were performed in 10 patients with increased ICP associated with various disorders (1 congenital stenosis, 2 idiopathic, 5 morbid obesity, 1 tumor compressing the dural sinus, 1 craniodiaphyseal dysplasia, and bony overgrowth of the skull) (9). All patients had CSF pressures above 200 mm H2O and had no ventriculomegaly. No venous outflow obstruction was found in the obese patients, but some degree of stenosis or occlusion was seen in the other 5 patients (including those with congenital stenosis and tumor). Superior sagittal sinus pressure was elevated in all 7 patients in whom it was measured, including the 5 obese patients. The mean increase was small (1.8 mm Hg above normal) in patients without obstruction, and it is uncertain whether the elevation was statistically significant. Central venous pressure was measured in 6 of the 7 patients who had venous sinus manometry and was abnormal in 5 patients. Patients with venous sinus occlusion were treated with angioplasty/thrombolysis or shunting. The patient with the tumor underwent a CSF diversion procedure (shunt), and the patients with IIH were treated with a combination of shunt, optic nerve sheath fenestration, or gastric stapling. None of the manometric measurements was repeated following treatment.
Dural Venous Sinus Stenosis in IIH
Numerous studies have demonstrated transverse sinus stenosis (TSS) in patients with IIH. Whether TSS causes IIH or whether IIH causes TSS remains unanswered. MR venography (MRV) and conventional angiography with venous imaging are often normal when a substantial pressure gradient is present. The association between IIH and TSS is quite strong as shown by (high-resolution) autotriggered elliptic-centric–ordered (ATECO), 3-dimensional, gadolinium-enhanced MRV (ATECO MRV), which demonstrated transverse dural sinus stenosis in 90% of 29 IIH patients (10) with a high interrater correlation.
King et al (11) studied 9 patients with IIH and 2 patients with minocycline-induced intracranial hypertension by CT, MRI, digital subtraction internal carotid arteriography, and dural sinus venous manometry. Venous pressure was measured in the superior sagittal, left sigmoid, and transverse sinuses. Pullback pressures were measured in the superior sagittal sinus, torcular herophili, proximal and distal transverse sinuses, sigmoid sinuses, and jugular bulbs. Normal controls, however, were not used because the procedures are invasive. All 9 IIH patients had increased pressure in the superior sagittal sinus (14–23 mm Hg; normal = 2–7 mm Hg) and proximal transverse sinus. There was a large (10–20 mm Hg) pressure gradient between the superior sagittal sinus and the internal jugular vein in IIH patients. The angiography findings did not always correlate with the manometry findings. A gradually tapered narrowing of the transverse sinus was frequently observed. The authors proposed that a mural thrombosis associated with thrombotic factors related to obesity was the cause of the dural sinus stenosis and pressure gradient. The 2 patients with minocycline-induced intracranial hypertension had normal studies.
The same researchers subsequently performed an elegant study confirming the reciprocal relationship between cerebral venous pressure and CSF pressure (12). Twenty-one patients with confirmed IIH underwent digital subtraction internal and external carotid angiography, dural sinus venography, and manometry. Immediately afterward, 8 of the patients underwent lateral C1-2 puncture and their CSF pressure was recorded before and after 20–25 mL of CSF was removed, after which the cerebral venous pressure measurement was repeated. Control subjects consisted of patients with other diagnoses or those who were suspected of having IIH, but the diagnosis was later proven incorrect. Nineteen of the 21 IIH patients showed a large pressure gradient across the transverse venous sinus. Lowering of the ICP by removal of CSF produced a pressure drop within the transverse sinus between 12 and 41 mm Hg in 6 patients. The pressure drop in the other 2 patients was 4 and 6 mm Hg, respectively; both patients had only a small drop in CSF pressure after the cervical puncture. The drop in pressure in the proximal transverse sinus was most dramatic in patients with the highest pressures before the cervical puncture. Their results correlate nicely with the previous studies showing that at high ICPs, the transverse sinuses could collapse, producing increased superior sagittal sinus pressure. The TSS in such patients resolved after interventions to lower the CSF pressure, such as lumbar puncture or shunting (13,14). Based on these studies, many investigators have concluded that increased venous pressure results from, rather than causes, increased ICP in IIH in most cases (15).
PRO—Stenting for transverse sinus stenosis in idiopathic intracranial hypertension: Rebekah Ahmed and G. Michael Halmagyi
When maximum medical treatment (e.g., weight loss, acetazolamide, furosemide, and topiramate) fails in IIH, invasive treatments, such as optic nerve sheath fenestration or CSF shunting, are often recommended. Although these can be effective initially, they can also have significant complication and failure rates. The mortality rate of intracranial shunts can be as high as 1% (16), and the morbidity from all CSF shunting procedures (17) includes shunt migration or dislocation, infection, acquired tonsil herniation, and intracerebral hemorrhage (18). In addition, up to 64% of ventriculoperitoneal and lumboperitoneal shunts fail within 6 months and require revision due to recurrence of headache and papilledema (19). Likewise, optic nerve sheath fenestration has a reported surgical complication rate of up to 40% (20), including visual loss, motility and pupillary dysfunction, and vascular complications. Such poor results have been tolerated due to a lack of a viable alternative (21). We propose that stenting a transverse sinus in IIH patients unresponsive to maximal medical therapy, who have stenosis of a dominant transverse sinus or stenosis of both transverse sinuses, is now a viable and effective alternative to CSF shunting procedures.
The first report of TSS stenting in IIH by Higgins et al in 2002 (22) was of an overweight female patient unresponsive to medical treatment, with bilateral TSSs and raised lumbar CSF and cerebral venous sinus pressures. Transverse sinus stenting abolished the pressure gradient across the stenosis and improved the patient's symptoms and signs. Since then, individual case reports and small case series have appeared (23–25). Higgins et al (26) reported 12 more cases of venous sinus stenting; of whom 5 became asymptomatic, 2 improved, and 5 remained unchanged. However, 5 of their patients had undergone previous CSF diversion procedures, 2 had functioning ventriculoperitoneal shunts at the time of the stent—they did not improve. Our group (27) reported 4 stented IIH cases: headache improved in all 4 and vision improved in 3. Donnet et al (28) reported 10 IIH patients, stented without complication, 6 being “cured” and 4 improved. Bussiere et al (29) reported 10 IIH patients who were stented, with resolution of the venous hypertension in all patients and symptom improvement in most.
We have now stented a further 46 patients with IIH and papilledema, all either unresponsive to maximal medical treatment or with fulminant IIH (30). We have reviewed their clinical, venographic, and ICP data before and after TSS stenting and followed up them for 2 months to 9 years. In these 46 patients, stenting 1 transverse sinus and providing 1 functioning sinus lowered venous pressures and abolished papilledema and accompanying symptoms.
All these patients either had 1 hypoplastic transverse sinus and a stenosis of the other sinus or bilateral TSS. In our experience, the presence of 1 functioning transverse sinus precludes the development of venous hypertension due to stenosis of the other. The mean superior sagittal sinus pressure before stenting was 34 mm Hg, with a mean TSS gradient of 20 mm Hg. Figure 1 shows the gradient across the stenosis vs the sagittal sinus pressure in our patients. The mean lumbar CSF pressure before stenting was 320 mm H2O. In all the 46 patients, stenting immediately abolished the TSS pressure gradient, rapidly improved IIH symptoms, abolished papilledema, and lowered the superior sagittal sinus pressure to a mean of 16 mm Hg (210 mm H2O). In 6 patients, symptom relapse (headache) was associated with increased venous pressures and recurrent stenosis adjacent to the previous stent. In these cases, placement of another stent again abolished the TSS pressure gradient and improved symptoms. Of the 46 patients in our series, 43 have been cured of all IIH symptoms. Three have ongoing headaches but normal venous pressures on venography, suggesting another cause for the headaches.
Our complication rate was 11% and included transient unilateral headache, transient unilateral hearing loss in 2 patients, allergic reaction to antiplatelets in 2 patients, an anaphylactic reaction to the anesthetic agent in 1 patient, and the development of subdural and subarachnoid blood during the procedure in 2 patients requiring immediate craniotomy (both patients made a full recovery). One female patient was not included in our study, as she had a functioning ventriculoperitoneal shunt and underwent TSS stenting after 30 previous shunt revisions. Unfortunately, at the end of the procedure, despite a patent stent and venous sinuses, she developed uncontrollable intracranial hypertension and died. An autopsy found that she had died of intracranial hypertension secondary to hypoventilation and the resultant hypercapnia at the end of the anesthesia. We believe that it is likely that this complication would have occurred regardless of the invasive intervention performed if she had been hypoventilated.
Is TSS a cause or an effect of the high ICP in IIH (15)? Since the association of IIH and TSS was shown (11), much has been written about whether the TSS causes (31) or is caused by the IIH (12,14,32,33). With the development of ATECO MRV (34), it is now possible to show the TSS noninvasively and decide whether the stenosis is likely due to intrinsic or extrinsic factors (10). Previously with time-of-flight MRV, a TSS was often interpreted as a flow-related artifact (35). Direct retrograde cerebral venography and manometry allows direct measurement of the venous sinus pressures and the pressure gradient across the stenosis (11). Regardless of whether TSS is the cause or the effect of IIH, we believe that by stenting just 1 transverse sinus and providing a normally functioning sinus, venous pressures are lowered and papilledema resolves in IIH.
We propose that venous hypertension develops in IIH by 1 of 2 mechanisms. In the minority of cases, arachnoid granulations or septal bands (36) swell, causing intrinsic stenosis of the sinus. In the majority of cases, the key feature is the collapsible transverse sinus (a Starling-like resistor), which is vulnerable to extrinsic compression from intracranial hypertension itself. Preventing collapse of the sinus with a rigid wall stent is the key to the effectiveness of transverse sinus stenting. A mathematical model (37) predicts that intracranial hypertension compresses a collapsible transverse sinus causing venous outflow obstruction, which results in further venous hypertension, which then decreases CSF absorption and causes further increases in ICP, which then feeds back causing further external compression of the transverse sinus and further stenosis (Fig. 2).
In the presence of a collapsible sinus, various perturbations in the model produce a transition from a normal-pressure state to a high-pressure state or vice versa. Such perturbations include an increase in cerebral blood flow, an infusion of CSF (leading to transition from the normal to elevated state), withdrawal of CSF, or reduction in the rate of CSF production (leading to transition from the elevated to normal state). Treatment with acetazolamide (which reduces CSF production) or a CSF shunt (which provides an alternate drainage pathway for CSF) induces transition from a high-pressure to normal-pressure state. Repeated lumbar punctures with the removal of CSF might have a similar effect. In a simulation of the high-pressure state, insertion of a stent, modeled by removing the Starling-like resistor, giving a rigid-walled venous sinus, results in transition to the normal-pressure state (now the only stable state), with further perturbations no longer leading to a high-pressure state (Fig. 3).
It has been proposed that prior to stenting, the MRV should be repeated after lumbar puncture and CSF removal, to see if the stenosis resolves. This would suggest a reversible high ICP-related stenosis (32). We have done this in several patients and have found that after several weeks, once the ICP rises again and the effects of the CSF removal from the lumbar puncture “wear off” the stenosis returns. In our opinion, to perform repeated lumbar punctures and venous imaging (especially CT) is neither practical nor cost-effective. It does not matter if the stenosis is the “chicken or the egg” (15). By stenting the collapsible transverse sinus, patients no longer flip between a normal-pressure state and high-pressure state but instead remain in the normal-pressure state. We have found that further lumbar punctures and medications are not required after stenting the transverse sinus.
Regardless of whether TSS is the cause or effect of IIH, some patients require additional treatment, other than optic nerve sheath fenestration, subtemporal decompression, or CSF shunting, in order to save vision and/or control intractable headache. We believe that transverse sinus stenting is such a treatment. In our study, although 13% required a repeat stent, this is a significantly lower rate than the current failure rate of CSF shunting. We propose that patients with IIH being considered for CSF shunting or optic nerve sheath fenestration should undergo an MR venogram (using the ATECO technique) or a CT venogram. If this study suggests TSS, then we recommend cerebral venography with manometry and consideration for transverse sinus stenting.
CON—Stenting of the transverse sinuses is not a reasonable treatment for most patients with idiopathic intracranial hypertension: Deborah I. Friedman
Stenting in IIH
To date, the data regarding stenting for IIH have only come from a small and uncontrolled case series of selected patients. There have been no randomized trials with a control group or sham stenting. Various authors attribute the lack of a control group to the invasive nature of the procedure, but there are clinical trial designs that could overcome this argument. The various series (n = 8 with 31 patients) were reviewed in detail by Arac et al (38), who added 1 additional patient. This series now will be summarized.
Venous sinus stenting was performed on 12 cases of IIH (26). All patients had intractable headaches and a visual disturbance lasting 5 months to 12 years. Two patients had severe visual loss and 8 had chronic papilledema. All had previously received medical treatment, optic nerve sheath fenestration, or a shunt procedure. No surgery had been performed within 10 months of stenting. Carotid angiography, cerebral venography, and manometry were performed on all patients. Stenting was done under general anesthesia. Ten patients underwent unilateral sinus stenting only and 2 underwent contralateral stent placement later. At follow-up, 5 patients were asymptomatic, 2 had improved except for residual headache, and 5 were unchanged. Papilledema resolved in 4 patients and improved in 1. Two patients received thrombolytic treatment successfully in the immediate postprocedural period for an intraluminal thrombus. Venography after stenting showed a reduction in intrasinus pressure that did not necessarily correlate with clinical improvement.
The same authors reported the results of stenting in an additional 8 patients with IIH (39). The duration of disease and previous treatment were not indicated in the report. All had papilledema prior to stenting that resolved after the procedure. Seven patients had headaches over the stenting site that resolved in days to weeks. Six of 7 had long-term improvement in vision that was dramatic in 1 case (light perception to almost normal vision within weeks). Another had resolution of bilateral abducens palsies.
Nine consecutive patients at another center were evaluated with direct retrograde cerebral venography and manometry with simultaneous CSF pressure measurement in 2 patients (27). All patients had been previously treated with various modalities, including acetazolamide (3 patients), optic nerve sheath fenestration (3 patients), shunt (6 patients, 5 of whom had numerous revisions), and subtemporal decompression (1 patient). Five patients had partial transverse sinus obstruction and 4 were treated with stents. One patient with complex venous anatomy was not stented but had a shunt placed with a successful outcome. Four patients were feeling well and required no additional treatment. The authors postulated that IIH may be caused by dural venous sinus thrombosis in some patients and cause venous stenosis in others. Donnet et al (28) reported their experience with stenting in 10 patients with “refractory” IIH. “Refractory” in this series was defined as lack of response to acetazolamide (dose not specified), which would hardly be considered refractory by most neuro-ophthalmologists treating IIH.
While these reports are encouraging, complications of stenting reported in the literature include headache, transient hearing loss, transient unsteadiness, and a life-threatening acute subdural hematoma (39). The subdural hematoma developed during venography and stenting in a patient who also had an optic nerve sheath fenestration and external ventricular drainage. I am personally aware of another patient who suffered a life-threatening subdural hematoma requiring a ventriculostomy and craniectomy following an unsuccessful stenting procedure. Venous re-stenosis has also occurred.
An update from the Sydney Group reported above, having the most experience worldwide performing TSS stenting for IIH, was presented at the 2011 annual meetings of the North American Neuro-Ophthalmology Society (February 2011) and the American Academy of Neurology (April 2011) (personal communications) (40). These 46 patients had symptomatic improvement within hours in most patients, resolution of papilledema in all patients over weeks, and persisting improvement in visual symptoms and visual fields in 43 patients. Six patients had a relapse with recurrent stenosis adjacent to the previous stent. These patients underwent placement of another stent with improvement. The most troubling aspect of their stenting experience was the complications. “Minor” complications included anaphylaxis and hearing loss. “Major” complications included subarachnoid hemorrhage and subdural hematoma. One patient with a mural thrombus developed a subdural hematoma after urokinase treatment. There was death in a patient with uncontrollable cerebral edema following the procedure that was attributed to anesthetic technique. The overall safety profile of the procedure is difficult to ascertain, largely because of publication bias as there is an unknown number of poor stent outcomes that likely have not been published. Although there is a small but real mortality risk with CSF shunting procedures, to my knowledge, there have not been any deaths associated with an optic nerve sheath fenestration. It would be difficult to recommend stenting and its associated morbidity and mortality if the indication is visual loss and optic nerve sheath fenestration is easily available.
It is difficult to interpret the findings of various reports, as the criteria for stenting are variable between centers and “treatment failure” is poorly defined. Surgical intervention for IIH is generally reserved for patients with visual loss. Optic nerve sheath fenestration may improve headaches in some cases but is not used for the treatment of headache alone. Although shunting is often considered the “definitive” treatment for IIH-associated headaches, large case series suggest otherwise. The long-term efficacy of shunting for headache control is poor (41,42). Chronic headache as a measure of treatment failure is an imprecise criterion for stenting. The details of headache treatments used in the Sydney group's patients are not provided, and all invasive treatments for headache tend to have a good success rate. There is a high placebo response rate in all studies of treatments used for headache disorders, particularly for migraine. Resolution of papilledema is an important and objective outcome measure, although the headache severity in IIH does not correlate with the degree of papilledema. Stenting patients with mild disease may offer no benefit—and much greater risk—than maximal medical therapy.
Although there is biologically plausible rationale for stenting in selected patients with IIH and TSS, there is no randomized controlled clinical trial evidence to document efficacy. However, patients sometimes fail to improve with conventional therapy, and no currently used treatment is particularly helpful in those with fulminant IIH. One may consider stenting in IIH only when the following conditions are met: 1) The procedure is performed by an interventionalist with experience in venous sinus angiography and stenting, in a facility with neurosurgical backup available in case of a neurologic emergency or complication, 2) potential candidates are screened for reversibility of the venous sinus stenosis upon lowering of the CSF pressure prior to considering stenting, 3) conventional treatments, including medical therapy and surgical therapy (e.g., shunt, optic nerve sheath fenestration) are tried without success, 4) the patient's vision continues to deteriorate despite ongoing conventional therapy. The rate of serious complications is worrisome, particularly when compared to existing treatments.
Even if dural venous blockage is a cause or the only cause of IIH, larger clinical studies of stenting must demonstrate the long-term safety and efficacy of this procedure before it can be adopted for IIH cases refractory to standard treatment methods. Because standard medical treatment is generally successful and much less invasive, stenting should not be adopted until such measures have failed.
Rebuttal: Rebekah Ahmed and G. Michael Halmagyi
The main argument presented against TSS stenting in IIH is the lack of a randomized controlled trial to document its efficacy and complication rate, yet there is also no randomized controlled data to document the efficacy of CSF shunting or optic nerve sheath fenestration. In our reported series, the complication rate was 11%. Headache and hearing loss were transient complications. Although 2 early patients suffered subdural and subarachnoid bleeding, both recovered fully. The death reported was found to be due to the anesthetic. The other alternatives are not without complications. There is a risk of mortality with shunting (1%) and a greater than 50% failure rate. It is proposed in the con argument that if the reason to stent is to save vision, then optic nerve sheath fenestration is a safer and more effective alternative. There are a number of problems with this argument. First, optic nerve sheath fenestration is not available in all centers; second, it has an overall complication rate of up to 40%, including visual loss; and third, while it may cause some improvement in headache, the degree to which it lowers ICP is not known. Transverse sinus stenting not only resolves papilledema and saves vision but also significantly reduces ICP and treats the other symptoms of IIH, including headache and pulsatile tinnitus.
We agree that stenting should only be performed by an experienced neurointerventionalist, just as optic nerve sheath fenestration should only be done by a surgeon experienced with the procedure. We do not agree that stenting should only be tried once shunting and optic nerve sheath fenestration have failed. In our opinion, this only results in patients undergoing additional unnecessary procedures.
Patients who have failed maximal medical management for treatment of IIH and are being considered for shunt placement or optic nerve sheath fenestration should also undergo MRV (ATECO technique) and cerebral venography and manometry to see if they are candidates for stenting. Even if the stenosis disappears with the lowering of ICP and recurs with high ICP, these patients should be considered for stenting. We consider stenting to be like democracy; it might not be perfect, but it is better than the alternatives.
Rebuttal: Deborah I. Friedman
We are in agreement that the currently used surgical treatments for IIH are suboptimal. In my own experience, I only proceed with shunting for patients with fulminant IIH and rapidly declining vision or those with very poor vision in both eyes at presentation. I do not recommend shunting for headache alone because of the high failure rate of shunts and the very real possibility of shunt dependence. Better treatments are certainly needed. A randomized trial for stenting or optic nerve sheath fenestration has been considered but deemed unfeasible at this time because of the number of subjects needed to detect a statistically significant treatment effect. The limited availability of optic nerve sheath fenestration is not justification for a procedure that has a small, but potentially life-threatening, complication rate. IIH has devastating consequences in a small percentage of patients who are rendered blind, but it is not a fatal disease. Comparing the percentages of complications between various procedures is misleading. There is no comparison between transient diplopia or a worsening visual field defect after optic nerve sheath fenestration and a subdural hematoma with brain herniation, even if the patient recovers. Despite the small number of patients who experience this devastating complication, the morbidity and expense of intensive care and additional neurosurgical treatments needed to save these patients are not trivial. Moreover, while optic nerve sheath fenestration is not offered at all centers, the availability of neurointerventionalists who have experience with stenting is also limited.
My only direct experience with the democratic process in the United States does not support the contention that choosing a candidate who is “better than the alternative” leads to a good outcome. Although there is much political influence in medicine, medicine is not politics and we try to use scientifically based evidence to make thoughtful treatment decisions. Primum non nocere.
Summary: Andrew G. Lee and Valérie Biousse
Although venous stenoses play some role in IIH, much remains to be understood before supporting routine endovascular stenting of stenosed intracranial venous sinuses in patients with IIH. Pilot data have opened the door to a completely new type of treatment, whose indications, efficacy, and safety remain insufficient at this point. A recently launched prospective pilot study evaluating venous stenting in IIH will hopefully provide more insight into this new treatment (43).
1. Dandy W. Intracranial pressure without brain tumor: diagnosis and treatment. Ann Surg. 1937;106:492–513
2. Foley J. Benign forms of intracranial hypertension—“toxic” and “otitic hydrocephalus.” Brain. 1955;78:1–41
3. Sahs AL, Joynt RJ. Brain swelling of unknown cause. Neurology. 1956;6:791–803
4. Raichle ME, Grubb RL Jr., Phelps ME, Gado MH, Caronna JJ. Cerebral hemodynamics and metabolism in pseudotumor cerebri. Ann Neurol. 1978;4:104–111
5. Johnston IH, Paterson S. Benign intracranial hypertension: II. Cerebrospinal fluid pressure and circulation. Brain. 1974;97:301–312
6. Biousse V, Ameri A, Bousser M-G. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology. 1999;53:1537–1542
7. Lam BL, Schatz NJ, Glaser JS, Bowen BC. Pseudotumor cerebri from cranial venous obstruction. Ophthalmology. 1992;99:706–712
8. Kim AW, Trobe JD. Syndrome simulating pseudotumor cerebri caused by partial transverse venous sinus obstruction in metastatic prostate cancer. Am J Ophthalmol. 2000;129:254–256
9. Karahalios DG, Rekate HL, Khayata MH, Apostolides PJ. Elevated intracranial venous pressure as a universal mechanism in pseudotumor cerebri of varying etiologies. Neurology. 1996;46:198–202
10. Farb RI, Vanek I, Scott JN, Mikulis DJ, Willinsky RA, Tomlinson G, terBrugge KG. Idiopathic intracranial hypertension. The prevalence and morphology of sinovenous stenosis. Neurology. 2003;60:1418–1424
11. King JO, Mitchell PJ, Thomson KR, Tress BM. Cerebral venography and manometry in idiopathic intracranial hypertension. Neurology. 1995;45:2224–2228
12. King JO, Mitchell PJ, Thomson KR, Tress BM. Manometry combined with cervical puncture in idiopathic intracranial hypertension. Neurology. 2002;58:26–30
13. McGonigal A, Bone I, Teasdale E. Resolution of transverse sinus stenosis in idiopathic intracranial hypertension after L-P shunt. Neurology. 2004;62:514–515
14. Higgins JN, Pickard JD. Lateral sinus stenosis in idiopathic intracranial hypertension resolving after CSF diversion. Neurology. 2004;62:1907–1908
15. Corbett JJ, Digre KB. Idiopathic intracranial hypertension: an answer to, “the chicken or the egg?”. Neurology. 2002;58:5–6
16. Curry WT, Butler WE, Barker FG. Rapidly rising incidence of cerebrospinal fluid shunting procedures for idiopathic intracranial hypertension in the United States, 1988–2002. Neurosurgery. 2005;57:97–108
17. Wang VY, Barbaro NM, Lawton MT, Pitts L, Kunwar S, Parsa AT, Gupta N, McDermott MW. Complications of lumboperitoneal shunts. Neurosurgery. 2007;60:1045–1048
18. Suri A, Pandey P, Mehta VS. Subarachnoid hemorrhage and intracerebral hematoma following lumboperitoneal shunt for pseudotumour cerebri: a rare complication. Neurol India. 2002;50:508–510
19. Rosenberg ML, Corbett JJ, Smith C, Goodwin J, Sergott R, Savino P, Schatz N. Cerebrospinal fluid diversion procedures in pseudotumor cerebri. Neurology. 1993;43:1071–1072
20. Brazis PW. Clinical review: the surgical treatment of idiopathic pseudotumour cerebri (idiopathic intracranial hypertension). Cephalgia. 2008;28:1361–1373
21. Owler BK. CSF shunt failure: an ongoing epidemic? J Neurol Neurosurg Psychiatry. 2009;80:1185
22. Higgins JN, Owler BK, Cousins C, Pickard JD. Venous sinus stenting for refractory benign intracranial hypertension. Lancet. 2002;359:228–230
23. Ogungbo B, Roy D, Gholkar A, Mendelow AD. Endovascular stenting of the transverse sinus in a patient presenting with benign intracranial hypertension. Br J Neurosurg. 2003;17:565–568
24. Rajpal S, Niemann DB, Turk AS. Transverse venous sinus stent placement as treatment for benign intracranial hypertension in a young male: case report and review of the literature. J Neurosurg. 2005;102:342–346
25. Métellus P, Levrier O, Fuentes S, Adetchessi T, Dufour H, Donnet A, Grisoli F. Endovascular treatment of benign intracranial hypertension by stent placement in the transverse sinus. Therapeutic and pathophysiological considerations illustrated by a case report. Neurochirurgie. 2005;51:113–120
26. Higgins JN, Cousins C, Owler BK, Sarkies N, Pickard JD. Idiopathic intracranial hypertension: 12 cases treated by venous sinus stenting. J Neurol Neurosurg Psychiatry. 2003;74:1662–1666
27. Owler BK, Parker G, Halmagyi GM, Dunne VG, Grinnell V, McDowell D, Besser M. Pseudotumour cerebri syndrome: venous sinus obstruction and its treatment with stent placement. J Neurosurg. 2003;98:1045–1055
28. Donnet A, Metellus P, Levrier O, Mekkaoui C, Fuentes S, Dufour H, Conrath J, Grisoli F. Endovascular treatment of idiopathic intracranial hypertension: clinical and radiologic outcome of 10 consecutive patients. Neurology. 2008;70:641–647
29. Bussiere M, Falero R, Nicolle D, Proulx A, Patel V, Pelz D. Unilateral transverse sinus stenting of patients with idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2010;31:645–650
30. Ahmed R, Wilkinson M, Parker G, Thurtell M, Macdonald J, McCluskey P, Allan R, Dunne V, Hanlon M, Owler B, Halmagyi GM. Transverse sinus stenting for idiopathic intracranial hypertension: a review of 52 patients and of model predictions. AJNR Am J Neuroradiol. 2011;32:1408–1414
31. Bono F, Gilberto C, Mastrandrea C, Cristiano D, Lavano A, Fera F, Quattrone A. Transverse sinus stenoses persists after normalization of the CSF pressure in IIH. Neurology. 2005;65:1990–1093
32. Rohr A, Dorner L, Stingele R, Buhl R, Alfke K, Jansen O. Reversibility of venous sinus obstruction in idiopathic intracranial hypertension. AJNR Am J Neuroradiol. 2007;28:656–659
33. De Simone R, Marano E, Fiorillo C, Briganti F, Disalle F, Volpe A, Bonavita V. Sudden re-opening of collapsed transverse sinuses and longstanding clinical remission after a single lumbar puncture in a case of idiopathic intracranial hypertension. Pathogenetic implications. Neurol Sci. 2005;25:342–344
34. Farb R, Scott J, Willinsky R, Montanera WA, Wright GA, terBrugge KG. Intracranial venous system: gadolinium-enhanced three-dimensional MR venography with auto-triggered elliptic centric-ordered sequence—intial experience. Radiology. 2003;206:203–209
35. Ayanzen RH, Bird CR, Keller PJ, McCully FJ, Theobald MR, Heiserman JE. Cerebral MR venography: normal anatomy and potential diagnostic pitfalls. AJNR Am J Neuroradiol. 2000;21:74–78
36. Strydom MA, Briers N, Bosman MC, Steyn S. The anatomical basis of venographic filling defects of the transverse sinus. Clin Anat. 2010;23:153–159
37. Stevens SA, Previte M. Idiopathic intracranial hypertension and transverse sinus stenosis: a modelling study. Math Med Biol. 2007;24:85–109
38. Arac A, Lee M, Steinberg GK, Marcellus M, Marks MP. Efficacy of endovascular stenting in dural venous sinus stenosis for the treatment of idiopathic intracranial hypertension. Neurosurg Focus. 2009;27:E14
39. Owler BK, Parker G, Halmagyi GM, Johnston IH, Besser M, Pickard JD, Higgins JN. Cranial venous outflow obstruction and pseudotumor cerebri syndrome. Adv Tech Stand Neurosurg. 2005;30:108–174
40. Ahmed RA, Wilkinson M, Parker G, Thurtell M, MacDonald J, McCluskey PJ, Dunne V, Hanlon M, Owler B, Halmagyi M. Transverse sinus stenting for pseudotumor cerebri: a review of 43 patients and of model predictions. Presented at the Annual Meeting of the American Academy of Neurology, Honolulu, HI, 2011. S47.004
41. Eggenberger ER, Miller NR, Vitale S. Lumboperitoneal shunt for the treatment of pseudotumor cerebri. Neurology. 1996;46:1524–1530
© 2011 Lippincott Williams & Wilkins, Inc.
42. McGirt MJ, Woodworth G, Thomas G, Miller NR, Williams M, Rigamonti D. Cerebrospinal fluid shunt placement for pseudotumor cerebri-associated intractable headache: predictors of treatment response and analysis of long term outcomes. J Neurosurg. 2004;101:627–632