26 Venous Sinus Stenting for Intracranial Hypertension
Abstract
Intracranial hypertension has long been considered an idiopathic disease. Advances in endovascular evaluation and management, however, increasingly suggest that venous hypertension plays a role in its pathogenesis, with many patients exhibiting signs of venous stenosis located within the cerebral venous sinuses. Venous sinus stenting for the treatment of intracranial hypertension has become an accepted treatment for patients that have failed more conservative management. Although long-term follow-up is lacking, recent studies suggest that, in carefully selected patients, this treatment option compares favorably to traditional invasive treatments such as ventriculoperitoneal shunting.
Keywords: intracranial hypertension, venous sinus stenosis, venous sinus stenting, pseudotumor cerebri, pulsatile tinnitus, transverse sinus, sigmoid sinus
26.1 Goals
1. Review the literature that informs current understanding of the pathogenesis of intracranial hypertension.
2. Critically analyze the literature on the treatment options for intracranial hypertension.
3. Review the literature that evaluates outcomes of treatment of intracranial hypertension with venous sinus stenting.
26.2 Case Example
26.2.1 History of Present Illness
A 27-year-old female presented with 8 months of progressive daily headaches, rated a 7/10 on the visual analog pain scale. She developed blurry vision and subsequent ophthalmological examination revealed bilateral papilledema, Frisen grade II. She denied pulsatile tinnitus.
A lumbar puncture was performed in the lateral decubitus position with a measured opening pressure of 27 cm H20. She developed a postlumbar puncture headache requiring epidural blood patch and subsequently noted transient improvement in her headaches and vision for several days.
The patient had attempted diet and weight loss without success. She had transient improvement in her headaches with acetazolamide but was unable to tolerate the side effects. She underwent a trial of topiramate without improvement.
Past medical history: Polycystic ovarian syndrome, anxiety, irritable bowel syndrome, ocular migraine.
Past surgical history: Cholecystectomy, dilatation, and curettage of uterus.
Family history: Noncontributory.
Social history: Denies alcohol or tobacco use.
Neurological examination: Unremarkable.
Imaging studies:Magneticresonance venography (MRV) demonstrated a dominant right transverse sinus with signal dropout at the transverse sigmoid junction along with a non-dominant left transverse sinus with signal dropout at the left transverse sigmoid junction (▶ Fig. 26.1a, b).
26.2.2 Treatment Plan
Treatment options were discussed in depth with the patient, including optic nerve sheath fenestration (ONSF), cerebrospinal fluid (CSF) diversion, and venography with potential venous sinus stenting. She elected to pursue venography and possible venous sinus stenting. Venography was performed under light conscious sedation. This confirmed a hypoplastic left transverse sinus with focal narrowing at the transverse-sigmoid junction (▶ Fig. 26.2a) as well as a dominant right transverse sinus with focal narrowing at the transverse-sigmoid junction (▶ Fig. 26.2b). Venous pressure manometry was performed showing a pressure of 21 mm Hg in the superior sagittal sinus, 21 mm Hg in the right transverse sinus, 14 mm Hg in the left transverse sinus, 7 mm Hg in the left sigmoid sinus, and 9 mm Hg in the right sigmoid sinus. Given the pressure gradient of 12 mm Hg in the dominant transverse sinus, the patient was offered transverse sinus stenting, and she elected to proceed. She was placed on 325 mg of aspirin and 75 mg of clopidogrel for 7 days and subsequently underwent uneventful placement of a stent within the right transverse sigmoid junction (▶ Fig. 26.3).
Fig. 26.1 Magnetic resonance venography (MRV) of the brain lateral (a) and anteroposterior (AP) (b) views showing a dominant right transverse sinus with a nondominant left transverse sinus. There is signal dropout at the bilateral transverse-sigmoid junctions suggesting venous stenosis.
Fig. 26.3 Lateral unsubtracted (a) and subtracted (b) angiography following placement of a stent within the right transverse-sigmoid junction. There is a significantly improved caliber and flow following stent placement.
26.2.3 Follow-up
The patient developed the expected postoperative headache that resolved after 10 to 14 days. She was maintained on aspirin and clopidogrel for 6 months at which point a CTA demonstrated wide patency of the stent and the clopidogrel was discontinued. At her 1-year follow-up, her papilledema had resolved, and she was no longer suffering from headaches.
26.3 Case Summary
1. What are the criteria for diagnosis of idiopathic intracranial hypertension?
While multiple classification and diagnostic schemes have been proposed for intracranial hypertension,1,2,3 the most widely cited and adopted criteria for the diagnosis of idiopathic intracranial hypertension are the modified Dandy criteria, proposed by Smith in 1985 (▶ Table 26.1).4 These criteria include signs and symptoms of increased intracranial pressure (such as papilledema and headache) in the setting of CSF pressure of greater than 200 mm of water relative to the level of the left atrium in a patient that is alert and oriented with no localizing neurological findings (except possible cranial nerve VI palsy). In addition, there can be no evidence of abnormalities within the ventricular system and no other obvious source of increased intracranial pressure. For CSF pressures of 200 to 250 mm H20, at least one of the following is also required: pulse synchronous tinnitus, cranial nerve VI palsy, Frisen grade II papilledema, MRV with transverse sinus stenosis/collapse, partially empty sella or optic nerve sheath with filled out CSF spaces on magnetic resonance imaging (MRI), echography for drusen negative. This patient meets the modified Dandy criteria for the diagnosis of idiopathic intracranial hypertension.
2. What are the treatment options for idiopathic intracranial hypertension?
a) Diet and exercise/weight loss:
In the absence of fulminant papilledema or progressive visual changes, treatment options begin with diet and lifestyle modification. In 1974, Newborg demonstrated a complete reversal of papilledema in all of nine patients with a very low-calorie (400-1000 calories per day) and low-sodium (less than 100 mg/d) diet with accompanying fluid restriction.5 More recent studies have shown improvements with less draconian diets, with some studies showing reversal of symptoms in patients who are able to lose 5 to 10% of total body weight.6
b) Carbonic anhydrase inhibitors:
The Idiopathic Intracranial Hypertension Treatment Trial (IIHTT) was the first randomized, controlled trial examining the use of acetazolamide and weight loss for treatment of vision loss related to idiopathic intracranial hypertension. Patients were randomized to weight loss and placebo or weight loss and acetazolamide with a primary outcome measure of perimetric mean deviation (PMD). Secondary outcomes included safety, quality of life, change in Frisen scale papilledema grade, weight loss, and headache disability.
Table 26.1 Modified Dandy criteria for intracranial hypertension
Modified Dandy criteria for intracranial hypertension |
1. Signs and symptoms of increased intracranial pressure |
2. Absence of localizing findings on neurological examination |
3. Absence of deformity, displacement, or obstruction of the ventricular system and otherwise normal neurodiagnostic studies, except for evidence of increased CSF pressure; abnormal neuroimaging except for empty sella, optic nerve sheath with filled out CSF spaces, and smooth-walled non-flow-related venous sinus stenosis or collapse should lead to another diagnosis |
4. Awake and alert |
5. No other cause of increased intracranial pressure present |
For CSF opening pressure of 200-250 mm water at least one of the following is required: |
– Pulse synchronous tinnitus |
– Cranial nerve VI palsy |
– Frisen grade II papilledema |
– Echography for drusen-negative and no other disc anomalies mimicking disc edema present |
– MRV with lateral sinus collapse/stenosis |
– Partially empty sella on coronal or sagittal views and optic nerve sheaths with filled-out CSF spaces next to globe on T2-weighted axial scans |
Abbreviations: CSF, cerebrospinal fluid; MRV, magnetic resonance venography. |
The study was able to demonstrate significant improvements in visual field, CSF opening pressure, papilledema, and quality of life in the acetazolamide and weight-loss groups when compared to the placebo and weight-loss groups. The study did not find a significant improvement in headache severity.
c)Bariatric surgery:
Given the success of weight loss in ameliorating symptoms of intracranial hypertension it is unsurprising that bariatric surgery has been suggested as an invasive treatment option for refractory intracranial hypertension. In a study of 24 morbidly obese females (mean BMI47) with headaches and elevated opening pressure on lumbar puncture who underwent gastric surgery, 18 of the 19 patients not lost to follow-up at 1 year demonstrated resolution of headache. Only 12 of the patients had papilledema preop-eratively and this improved following surgery. Two patients later regained weight with return of symptoms.7 A meta-analysis comparing bariatric surgery and nonsurgical weight loss for treatment of symptoms of intracranial hypertension including a total of 65 patients undergoing surgery and 277 without surgery showed that 100% of the patients with papilledema in the surgical group improved and 90.2% had a reduction in headaches, whereas nonsurgical weight loss led to a reduction in papilledema in 66.7% and an improvement in headache symptoms in 23.2%.8
d) Optic nerve sheath fenestration (ONSF):
Multiple retrospective case series speak to the utility of ONSF in arresting visual deterioration in intracranial hypertension.9,10,11,12 In one representative study, 54% of eyes had stabilization of visual acuity following ONSF, with 22% showing improvement and visual deterioration in 24% of operated eyes.11 These results are in alignment with other studies.10 Although there is a broad agreement on the utility of ONSF for stabilization of visual loss, it seems to be less effective for ameliorating headaches than other surgical interventions. One systematic review found that only 36% of patients had improvement in headaches with ONSF compared to 62.5% with ventriculoperitoneal shunting, 75.2% with lumboperitoneal shunting, and 82.9% with venous stenting.13 Complications can be seen in up to 40% and, although mostly minor disorders of ocular motility, approximately 5% were central retinal artery occlusion with subsequent loss of vision.14
e) CSF diversion:
CSF diversion has been the most widely adopted invasive intervention for intracranial hypertension. Shunting for intracranial hypertension increased 350% between 1988 and 2002.15
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