Pseudotumor Cerebri Treatment & Management

  • Author: James Goodwin, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: May 7, 2010
 

Medical Care

  • Patients without visual loss most often are treated with a carbonic anhydrase inhibitor (eg, acetazolamide) to lower the intracranial pressure (ICP). The starting dose is typically brand name Diamox at 500 mg bid. Some authors believe digoxin has the same effect and is associated with fewer adverse effects.
  • In patients with severe symptoms, early visual field loss, or poor response to standard medical therapy, some clinicians utilize a short course of high-dose corticosteroids (eg, prednisone).
  • When new visual field loss is documented, medical management should be coupled with plans for emergency surgical intervention if the visual function continues to deteriorate or does not improve immediately with corticosteroid treatment.
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Surgical Care

For patients with idiopathic intracranial hypertension (IIH) who have progressive visual field loss, currently 2 general surgical approaches can be considered: CSF shunting procedures or optic nerve sheath fenestration.

  • Neurosurgical operations
    • Lumboperitoneal shunt is the traditional method for providing prompt reduction of ICP in patients with IIH.[39] However, this procedure has a high 1-year failure rate.
    • Some neurosurgeons prefer ventriculoperitoneal or ventriculoatrial shunts over lumboperitoneal shunting.
    • The reason for this preference is that ventricular shunts can be monitored for function using an extracranial subcutaneous compressible bulb and one-way valve (intracranial to abdominal flow) in series with the intracranial and abdominal ends of the shunt.
      • The bulb will resist digital compression if the distal (abdominal or atrial) end is obstructed.
      • The bulb will collapse under digital pressure but will fail to re-inflate if the intracranial end is obstructed.
      • Many neurosurgeons have been reluctant to place ventricular shunts in patients with IIH because the ventricles are small and difficult to cannulate without radiographic guidance. There are also a significant number of complications including infection, stroke, seizures, and shunt failure.
    • However, Woodworth and colleagues have recently shown that, using a stereotactic frame, they were uniformly able to place ventricular shunts even in slit ventricles in patients with IIH using a single pass in all patients, with good long-term viability.[40]
  • Ophthalmic approach - Optic nerve sheath fenestration
    • The ophthalmic surgical approach to managing patients with progressive vision loss and papilledema involves cutting slits or rectangular patches in the dura surrounding the optic nerve immediately behind the globe.[41]
    • This allows egress of CSF directly into the orbital fat where it is absorbed into the venous circulation.
    • Lumbar puncture following this procedure does not consistently show significant reduction of CSF pressure, and headache is not reliably relieved by this approach.
    • Despite general lack of an ICP-lowering effect, papilledema in both eyes may regress following fenestration of one optic nerve.
    • Visual function stabilizes or improves following optic nerve sheath decompression in most cases in the short run[42] , but in at least a third of cases, secondary visual decline may occur within 3-5 years and may require repeat surgery or an alternative treatment.[43]
    • A study of optic nerve sheath fenestration on 41 eyes from 21 patients with vision loss from either IIH or intracranial hypertension from cerebral venous thrombosis found best-corrected visual acuity and visual field stabilization or improvement in 32 of 34 eyes (94%) over a 3-month follow-up interval. Transient benign complications were apparent in 4 eyes. Only marginal improvement was shown in 4 eyes with no light perception vision; these were not analyzed with the remainder of the group.[44]
  • Comparison of shunt vs optic nerve sheath fenestration
    • Feldon[45] performed a meta-analysis of existing literature comparing visual outcomes after the following:
      • 17 intracranial venous sinus stent placements; improved/resolved visual defects 47%
      • 31 ventriculoperitoneal (VP) shunt placements; improved/resolved visual defects 38.7%
      • 44 lumboperitoneal (LP) shunt placements; improved/resolved visual defects 44.6%
      • 252 optic nerve sheath decompressions; improved/resolved visual defects 80%
      • Visual worsening was rare for all procedures. The author concluded that visual outcome was best documented for optic nerve sheath fenestration and appeared to be the best surgical procedure for vision loss in IIH
  • Dural venous sinus stent
    • Following up on the work of Farb et al, Bussiere and coworkers studied 13 patients with IIH that was refractory to medical management who were found to have stenosis of 1 or both transverse dural sinuses on time-of-flight MR venography. Ten of these also had increased pressure gradient across the stenotic dural venous sinus (>10 mm Hg) and these underwent stent placement without significant complications. All 10 of these patients had complete headache resolution or significant improvement, and papilledema resolved completely or almost completely in 8 of them. The authors suggest only that a randomized controlled study of transverse dural venous sinus stenting in the management of IIH is needed to establish the safety and efficacy of the procedure in this setting.[46]
    • Arac and colleagues reported 1 case of endovascular stenting for IIH and reviewed the same published series as did Bussière et al, arriving at essentially the same conclusions. They also discuss Bateman’s recently proposed mathematical model of the relationship among intracranial arterial inflow, CSF pressure, and venous outflow.[47] (See Bateman above.)
  • Bariatric surgery for obesity in IIHP: Fridley et al reviewed the literature on bariatric surgery for obese patients with IIH. They found a total of 62 patients, of which 52 (92%) had resolution of the presenting symptoms. Of 35 patients who had postoperative fundoscopy, 34 had resolution of papilledema. Of 12 patients who had pre- and postoperative visual field examinations, 11 had resolution of visual field defects. Among 13 patients with pre- and postoperative cerebrospinal fluid pressure measurements, there was an average postoperative decrease of 254 mm H2 O. The authors call for prospective controlled studies to confirm the effectiveness of this surgery for IIH patients in long-term follow-up.[48]
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Consultations

  • Diagnosis and long-term management of patients with IIH requires the performance of lumbar puncture, typically performed by neurologists or internists, and careful monitoring of visual status (most importantly peripheral visual field and fundus photography). Vision examination and fundus photography are in the domain of ophthalmologists, and neuro-ophthalmologists are especially expert in examining visual fields. A team approach is, therefore, needed for most, if not all, patients.
  • Neurosurgical consultation is required for ventriculoperitoneal shunting when patients are losing visual field and medical management does not arrest or reverse the process promptly (within hours to days). Consultation with an Orbit/Plastic surgeon is required for optic nerve sheath fenestration for the same clinical indications.
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Diet

On initial diagnosis, a weight-reduction diet coupled with an exercise program should be strongly advised to all patients with IIH. Some recent evidence suggests that weight loss is associated with improvement of papilledema in these patients.[49, 50] Often, a formal weight-loss program is required.

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Activity

No activity restriction is required in this disease. In fact, exercise programs are strongly recommended along with a weight-reduction diet.

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Contributor Information and Disclosures
Author

James Goodwin, MD  Associate Professor, Departments of Neurology and Ophthalmology, University of Illinois College of Medicine; Director, Neuro-Ophthalmology Service, University of Illinois Eye and Ear Infirmary

James Goodwin, MD is a member of the following medical societies: American Academy of Neurology, Illinois State Medical Society, North American Neuro-Ophthalmology Society, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Eric R Eggenberger, DO, MS, FAAN  Professor, Vice-Chairman, Department of Neurology and Ophthalmology, Colleges of Osteopathic Medicine and Human Medicine, Michigan State University; Director of Michigan State University Ocular Motility Laboratory; Director of National Multiple Sclerosis Society Clinic, Michigan State University

Eric R Eggenberger, DO, MS, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Ophthalmology, American Osteopathic Association, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

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Left optic disc with moderate chronic papilledema in a patient with pseudotumor cerebri. Paton lines (arc-shaped retinal wrinkles concentric with disc margin) are seen along the temporal side of the inferior pole of the disc.
Right optic disc with postpapilledema optic atrophy in a patient with pseudotumor cerebri. Diffuse pallor of the disc and absence of small arterial vessels on the surface are noted, with very little disc elevation. The disc margin at the upper and lower poles and nasally is obscured by some residual edema in the nerve fiber layer and gliosis that often persists even after all the edema has resolved.
The most common early visual field defect in papilledema as the optic nerve develops optic atrophy is an inferior nasal defect as shown in the left eye field chart (left side of figure). The shaded area indicates the defective portion of the field. Note the sharp line of demarcation between defective lower nasal quadrant and normal upper nasal quadrant along the horizontal midline. This is characteristic of early papilledema optic atrophy and is called a nasal step or inferonasal step.
 
 
 
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