eMedicine Specialties > Neurology > Headache and Pain

Pseudotumor Cerebri: Treatment & Medication

Author: James Goodwin, MD, Director of Neuro-Ophthalmology, Associate Professor, Departments of Neurology and Ophthalmology, University of Illinois College of Medicine
Contributor Information and Disclosures

Updated: May 22, 2008

Treatment

Medical Care

  • Patients without visual loss most often are treated with a carbonic anhydrase inhibitor (eg, acetazolamide) to lower the intracranial pressure (ICP). 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.

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.32
    • 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.
    • 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.33
  • 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.34
    • 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 run35 , 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.36
    • 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.37  
  • Comparison of shunt vs optic nerve sheath fenestration
    • Feldon38 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.   

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.
  • Neurosurgeon consultation is required when patients are losing visual field and medical management does not arrest or reverse the process promptly (within hours to days).

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.39,40 Often, a formal weight-loss program is required.

Activity

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

Medication

Specific therapy for idiopathic intracranial hypertension (IIH) is aimed at lowering intracranial pressure (ICP) pharmacologically. Carbonic anhydrase inhibitors and other diuretics are thought to have their effect on ICP by reducing cerebral spinal fluid (CSF) production at the choroid plexus. Cardiac glycosides have a similar effect. Corticosteroids are effective in reducing ICP. However, the mechanism of action is unknown. Corticosteroids are often used as maximum medical management when rapid lowering of ICP is required.

Carbonic anhydrase inhibitors

These agents reduce CSF production and lower ICP.


Acetazolamide (Diamox)

Reduces CSF production by about 50% (Maren, 1972; McCarthy and Reed, 1974) and lowers ICP. Commonly achieves long-lasting control of transient visual obscurations (TVO), headache, and diplopia, all of which are manifestations of intracranial hypertension, even though papilledema does not resolve completely. Effect on ICP has been shown to be unsustained (Plum and Siesio, 1975), and many patients develop adverse effects severe enough to hinder compliance.
Some clinicians prefer Sequels formulation of Diamox, which may be better tolerated than standard version.
Few patients tolerate more than 2 g/d, but 4 g/d may be required to produce measurable pressure-lowering effect (Gucer and Viernstein, 1978); treatment usually initiated at 1 g/d and increased to 2 g/d if symptoms are not controlled and adverse effects are not severe; treatment with Diamox alone not appropriate for patients who are experiencing progressive visual field loss.

Adult

1-4 g PO qd

Pediatric

5 mg/kg/d or 150 mg/m2 PO qd
10-15 mg/kg/d PO divided q6-8h
5-10 mg/kg/dose IV/IM q6h

Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most common adverse effects include perioral and digital paresthesias, anorexia, nausea and vomiting, and metallic taste in mouth; rarely, patients may develop renal stones or aplastic anemia; patients should have baseline CBC and repeat CBC at regular intervals during continuous usage of acetazolamide; patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in diabetes

Cardiac glycosides

These agents reduce CSF production at choroid plexus and reduce ICP.


Digoxin (Lanoxin)

Present in high concentration in choroid plexuses of patients taking standard cardiac doses (Bertler, 1973), has been shown to reduce CSF production by as much as 78% in humans (Neblett, 1972), probably by inhibiting Na-K-ATPase pump (Vates, 1963). Only one report in which a patient with IIH was treated with digoxin, but patient was asymptomatic, so not known whether symptoms would have been controlled (Schott and Holt, 1974).

Adult

0.25 PO qam after breakfast; measure blood levels following 7-10 d of treatment; therapeutic range for IIH is 0.8-2.0 ng/mL (mcg/L), same as for cardiac indications

Pediatric

<2 years: Not established
2-5 years: 7.5-14 mcg/kg PO
5-10 years: 5-12.5 mcg/kg PO
>10 years: 2.5-5.25 mcg/kg PO

Amiodarone, quinidine, cyclosporine, propafenone, indomethacin, itraconazole, alprazolam, and verapamil increase likelihood of digoxin toxicity; erythromycin and tetracyclines can raise level in 10% of cases; hypokalemia induced by drugs (eg, diuretics) and sympathomimetics also increase toxicity (PDR 51st ed, p.1122); potassium-depleting corticosteroids and diuretics are major contributors to digitalis toxicity by causing hypokalemia; sympathomimetics increase chances of cardiac arrhythmia

Documented hypersensitivity; hypertrophic obstructive cardiomyopathy; dysrhythmias caused via accessory nerve tracts; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most dangerous adverse effect is severe ventricular arrhythmia that may be accompanied by complete atrioventricular block, but is rarely seen
More frequent adverse cardiac effects include bradycardia and ventricular extrasystole
Well tolerated compared with acetazolamide and safe in patients who do not have cardiac disease (Beller, 1971; Chung, 1969; Smith and Willerson, 1971; Smith and Haber, 1973); determination of plasma level may be useful for individualization of therapy (blood samples should be taken at earliest 8 h after last dose) or in case of overdose; "therapeutic" range between 1 and 2.6 nmol/L (0.8-2 µg/L)
Gastrointestinal effects include loss of appetite, nausea and upset stomach; occasionally leads to neuropsychiatric complications (eg, confusion, sleep disturbances), gynecomastia, atypical vaginal smear in postmenopausal women, eosinophilia, or thrombocytopenia and exanthema
Visual complications (eg, disturbed sense of color) are rare (For more information, see InfoMed Online – Digoxin.)

Glucocorticoids

These agents reduce ICP through an unknown mechanism.


Prednisone (Deltasone, Orasone, Meticorten)

Mechanism of action by which corticosteroids lower CSF pressure unknown. Some believe that may facilitate outflow at arachnoid granulations.

Adult

60-100 mg/d PO in single dose, followed by tapering schedule as symptoms and visual fields are monitored

Pediatric

4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk, as symptoms resolve

Phenytoin, phenobarbital, ephedrine, and rifampicin may enhance metabolic clearance, resulting in decreased blood levels and lessened physiological activity; may inhibit response to coumarins and may potentiate coumarin response (PDR 51st ed, p. 1679)

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with hypothyroidism or cirrhosis may have enhanced effect; with prolonged treatment, drug dosage should be lowered gradually to avoid signs and symptoms of acute adrenal cortical insufficiency; psychic disturbances may occur, including euphoria, insomnia, mood swings, personality changes, severe depression, and frank psychosis; preexisting emotional disturbance may worsen; weight gain and hyperglycemia may occur with prolonged administration (PDR 51st ed, p. 1679)

More on Pseudotumor Cerebri

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Treatment & Medication: Pseudotumor Cerebri
Follow-up: Pseudotumor Cerebri
Multimedia: Pseudotumor Cerebri
References
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Further Reading

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Keywords

idiopathic intracranial hypertension, IIH, benign intracranial hypertension, pseudotumor cerebri, elevated intracranial pressure, ICP, papilledema, progressive optic atrophy, blindness, cerebral edema, occult cerebral venous outflow abnormalities, vision loss, vision impairment

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Contributor Information and Disclosures

Author

James Goodwin, MD, Director of Neuro-Ophthalmology, Associate Professor, Departments of Neurology and Ophthalmology, University of Illinois College of Medicine
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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing 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.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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: Nothing to disclose.

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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