Skip Navigation LinksHome > June 2004 - Volume 24 - Issue 2 > Idiopathic Intracranial Hypertension
Journal of Neuro-Ophthalmology:
State of the Art

Idiopathic Intracranial Hypertension

Friedman, Deborah I. MD; Jacobson, Daniel M. MD

Free Access
Article Outline
Collapse Box

Author Information

Departments of Ophthalmology and Neurology, University of Rochester School of Medicine and Dentistry Rochester, New York (DIF), and Departments of Neurology and Ophthalmology, Marshfield Clinic, Marshfield, Wisconsin (DMJ).

Address correspondence to Deborah I. Friedman, MD, 601 Elmwood Ave, Box 569, Rochester, NY 14642; E-mail: Deborah_Friedman@urmc.rochester.edu

Collapse Box

Abstract

The syndrome of intracranial hypertension without structural brain or cerebrospinal fluid abnormalities and without identifiable cause, now most appropriately termed idiopathic intracranial hypertension, was described over a century ago. Although the pathogenesis of this condition remains unknown, diagnostic and therapeutic developments during the past two decades have substantially advanced patient management.

Back to Top | Article Outline

DEFINITION

The syndrome of increased intracranial pressure (ICP) without ventriculomegaly or mass lesion, and with normal cerebrospinal fluid (CSF) composition, was first described more than a century ago, yet we still know little about its pathogenesis (1). Often referred to as “pseudotumor cerebri” but more appropriately called “idiopathic intracranial hypertension” (IIH), it is a surprisingly common disorder. In young overweight women, the annual incidence is as high as 20 per 100,000 persons (2).

The definition of IIH has evolved with clinical experience and advances in imaging technology. Currently, IIH can be diagnosed only if the following criteria are met (Table 1): 1) symptoms and signs attributable to increased ICP or papilledema; 2) elevated ICP recorded during lumbar puncture in the lateral decubitus position; 3) normal CSF composition; 4) no imaging evidence of ventriculomegaly or a structural cause for increased ICP, such as a brain parenchymal, ventricular, meningeal, or venous sinus abnormality; and 5) no other cause of intracranial hypertension identified, such as use of certain medications.

Table 1
Table 1
Image Tools

The diagnosis and management of IIH remains based largely on anecdotal evidence. However, substantial developments during the past two decades have provided clinicians with more tools for excluding disorders that mimic IIH and for facilitating its diagnosis and management.

Back to Top | Article Outline

NOMENCLATURE

The nomenclature for IIH remains controversial. “Benign intracranial hypertension” is no longer accepted, as significant visual morbidity may occur with this disorder (3). The term “pseudotumor cerebri,” a historically popular and all-encompassing term, leaves the impression that IIH is not a real disease. IIH is currently the favored term for the primary (idiopathic) disorder. For those patients with an identified cause of intracranial hypertension without structural brain imaging or CSF constituent abnormalities, the appropriate diagnostic term would be “intracranial hypertension secondary to (…).” The typical patient with IIH is an obese woman of childbearing age (4). Atypical patients include men, slim women, prepubescent children, and patients older than age 44 years.

Back to Top | Article Outline

NATURAL HISTORY AND VISUAL PROGNOSIS

There are few prospective data in the era of modern imaging (computed tomography [CT], magnetic resonance imaging [MRI], and magnetic resonance venography [MRV]) to document the natural history of the disorder. Clinical experience, however, suggests that it is common for patients to have a protracted course lasting months to years, during which they may be asymptomatic but have chronic papilledema, or have symptoms that require medical agents to lower their ICP. This suggests that intracranial hypertension, symptomatic or not, persists in many patients with IIH. Indeed, one series found that 10 (83%) of 12 patients in long-term follow-up who underwent repeated lumbar punctures showed persistently elevated ICPs ranging from 220 to 550 mm H2O (5). Recurrent symptoms and papilledema have been reported in 8% to 37% of patients often years after the initial diagnosis (5,6).

The principal morbidity of IIH is papilledema-associated visual loss. A prospective study of 50 patients with IIH found visual field defects at initial presentation in at least one eye in 96% of patients assessed with the Goldmann perimeter, and in 92% of patients assessed with the Humphrey perimeter (4). After treatment, 60% of patients improved, 30% remained stable, and 10% worsened, as assessed with Goldmann perimetry (4). Assessed with the Humphrey perimeter, 50% of patients improved, 28% remained stable, and 22% worsened (4).

Back to Top | Article Outline

DIAGNOSIS

Imaging

With advances in neuroimaging techniques and a growing understanding of the pathophysiology of IIH, the diagnostic criteria for this condition have recently been revised (7) (Table 1). A noncontrast CT was previously considered an adequate imaging study because it can exclude ventriculomegaly or a mass lesion. However, conditions that increase ICP without producing ventriculomegaly or mass lesions, such as gliomatosis cerebri, meningitis, and cerebral venous thrombosis, may mimic IIH yet not have associated CT abnormalities to provide a clue to the true underlying condition. Accordingly, this imaging technique may be suboptimal, particularly for atypical patients. Unless there are external constraints (weight limitations, availability), MRI with MRV is currently the study of choice. Using a special technique, three-dimensional gadolinium-enhanced MRV appears to be more sensitive than conventional MRV for detecting areas of subtle cerebral venous stenosis (8). The clinical relevance of these changes is uncertain, and likely reflects a compensatory response to increased ICP.

Back to Top | Article Outline
CSF Opening Pressure

The medical literature contains various, and sometimes conflicting, recommendations regarding the minimum CSF opening pressure required for diagnosing IIH. In general, however, a CSF pressure greater than 250 mm H2O is consistent with the diagnosis, less than 200 mm H2O is normal, and 201 to 249 mm H2O is nondiagnostic (9). Contrary to popular belief, there is no evidence that body weight influences these cutoff values. The upper limit of normal CSF pressure in children is generally considered to be 180 to 200 mm H2O; the effect of obesity in children has not been studied.

Back to Top | Article Outline
Visual Fields

Although visual acuity and color perception are generally preserved in papilledema unless it enters a chronic and atrophic stage (10–12), visual fields and contrast sensitivity may be abnormal earlier. Visual field testing is far more sensitive for detecting optic nerve damage producing visual loss, particularly in the early stages of the disorder. Quantitative perimetry with static or kinetic methods is the current standard for assessing visual fields in IIH. The sensitivity to the detection of visual field defects is similar using either technique, assuming an experienced perimetrist performs the kinetic test (11,13).

Newer perimetric techniques, such as frequency-doubling technology perimetry, short-wavelength automated perimetry, tendency-oriented perimetry, and high-pass resolution (ring) perimetry have been examined in patients with glaucoma, but, with the exception of high-pass resolution perimetry (14), not well-studied in other optic neuropathies or in IIH. Motion perimetry, in which computer graphics generate small circular regions of coherent motion perception targets throughout the central visual field, identified the visual field defects in patients with IIH detected with conventional automated perimetry, as well as some defects that were not identified using automated perimetry (15). These results, and those elicited with other newer perimetric techniques, must be confirmed and validated before the newer tools replace the current visual field testing methods.

Back to Top | Article Outline
Monitoring the Optic Nerve Head

Whereas the results of visual field testing provide functional information concerning the degree of optic nerve damage, assessment of the degree of papilledema change over time often provides a useful structural measure of the clinical course and effect of treatment. In some patients, however, papilledema never resolves completely despite resolution of symptoms and stabilization of visual function. It is important to document the appearance of the optic disc with photographs, ideally at the first evaluation and whenever there is a change.

Confocal scanning tomography is a new tool that can quantify the degree of papilledema and measure changes over time (16). Tomographic parameters of the optic nerve head seem to correlate with visual field sensitivity loss (17). For routine patient care, however, confocal scanning tomography is not a practical tool and may not provide more useful information than carefully performed and interpreted visual fields. Future studies are needed before deciding if this technique will find a place in routine patient management.

Back to Top | Article Outline
Visual Acuity

Loss of visual acuity generally does not occur in acute papilledema unless there is macular edema. As untreated papilledema becomes more chronic, however, progressive impairment of visual acuity can be expected from a variety of causes (Table 2).

Table 2
Table 2
Image Tools
Back to Top | Article Outline
Contrast Sensitivity

Loss of contrast sensitivity is frequently identified patients with IIH, regardless of the technique used (10–12) For that reason, some investigators recommend contrast sensitivity testing as an adjunctive measure to assess optic nerve function. Whereas this tool may detect a global ab normality of optic nerve function when other standard mea sures are normal (11), its specificity for optic nerve dys function is low.

Back to Top | Article Outline
Visual Evoked Potentials

Assessment of visual evoked potentials (VEP) is of ten performed to screen for injury to the optic nerve. How ever, this technique probes only the central 10 degrees visual field, a region that is insensitive to visual loss in pap illedema (11). Thus, there is no role for VEP in evaluating patients with IIH. The future role of multifocal VEP, which is capable of assessing nonfoveal neurotransmission, re mains to be determined.

Back to Top | Article Outline

RISK FACTORS FOR VISUAL LOSS

Several clinical series have identified factors that may influence visual outcome in patients with IIH (Table 3) (2,18–22). The reliability of these variables in clinical prac tice may be limited on an individual case basis because they were determined from retrospective studies. Some reports provide conflicting results.

Table 3
Table 3
Image Tools
Back to Top | Article Outline

MIMICKERS OF IIH

As long as the diagnostic guidelines outlined in Table 1 are followed, there is little chance of failing to diagnose ominous mimicker of IIH. Still, some cases of cerebral ve nous sinus thrombosis, gliomatosis cerebri, and leptomen ingeal infiltration by a chronic neoplastic or infectious process may escape detection with brain imaging and CSF analysis until late in their course. Red flags that should signal the possible presence of a mimicker are outlined in Table 4 (23–26).

Table 4
Table 4
Image Tools

One should be particularly cautious about falsely diagnosing IIH in patients with abnormal visual fields that are psychogenic in nature, in those with anomalous optic discs, and when the opening pressure during lumbar puncture was improperly measured. Because concentric visual field constriction is a finding common to both psychogenic visual loss and IIH, misinterpretation of this visual field defect is a particularly frequent problem (5).

Back to Top | Article Outline

TREATMENT

Indications for Treatment

Not all patients with IIH require treatment. After establishing the diagnosis, asymptomatic individuals with normal vision and minimal papilledema can be monitored frequently for the development of symptoms or visual decline. A small percentage of patients improve after their diagnostic lumbar puncture (LP). The reason for the apparent cure is uncertain and may relate to re-establishing normal CSF homeostasis or cerebral venous pressure when normal CSF pressure is temporarily restored (27). Patients experiencing transient visual obscurations with normal visual function may be observed unless they have moderately severe papilledema. Some patients with headaches and minimal visual signs (visual field loss limited to a slightly enlarged blind spot) may also be managed conservatively.

Therapy is initiated in the presence of visual acuity or visual field loss (apart from mild enlargement of the blind spot), moderate to severe (Frisén grade 3–5) papilledema or persistent headaches (28). Visual signs and symptoms often co-exist with headache, but the two manifestations are approached independently. Treatment is always indicated when patients are aware of their visual deficit.

Back to Top | Article Outline
Dietary Management

Dietary management and weight loss are time-honored treatments, supported by several observational studies (29–36). The earliest report described rapid resolution of papilledema in nine obese patients treated with a very low-calorie (400–1,000 calories daily) rice diet (29). One retrospective study correlated weight loss to papilledema in 15 women with IIH who were treated with acetazolamide at the time of diagnosis (30). Within the 24-week study period, 11 patients had improvement or resolution of papilledema. The six patients who had complete resolution of marked papilledema underwent a mean weight loss of 6.2% total body weight. Patients who were unable to achieve the same degree of weight loss had lesser degrees of improvement in their papilledema grade. The four patients with unchanged optic disc swelling had no weight loss during the study period.

Another retrospective series evaluated the effect of weight loss on visual function and papilledema grade in 58 patients (31). There was more rapid improvement in papilledema and visual fields in overweight women with IIH who lost weight (mean weight loss 13.3 ± SD 9.9 lb) than in those who did not lose weight (mean weight loss 0.2 ± SD 0.6 lb). Surgically induced weight loss (mean loss 57 ± 5 kg) was associated with decreased CSF pressure and resolution of papilledema in eight patients examined 34 ± 8 months postoperatively (32). Various procedures used over the 11-year study period included horizontal gastroplasty, vertical banded gastroplasty, proximal Roux-en-Y gastric bypass, and distal gastric bypass.

There is little scientifically robust information regarding specific dietary measures for IIH. Limiting vitamin A consumption and a low tyramine diet may be beneficial (33–36). Dietary sources rich in vitamin A include fish, eggs, carrots, sweet potatoes, leafy greens, broccoli, red bell peppers, tomatoes, apricots, and cantaloupe. Supplemental vitamin A preparations are available over-the-counter. Tyramine naturally accumulates in food during the aging process. Foods and beverage that have high tyramine content include aged cheese and meat, pickled foods, overripe or dried fruit, beer, and wine. As many of the high-tyramine foods are also migraine triggers, patients may be instructed to use resources that are available to migraineurs regarding diet.

Back to Top | Article Outline
Repeated Lumbar Punctures

Repeated LPs are sometimes used in patients with occasional symptom relapses, in pregnant women, or in the setting of rapidly declining vision to temporarily lower the CSF pressure while planning a more aggressive treatment. However, the procedure may be painful, technically difficult to perform, and cause a low-pressure headache (37). Other complications of LP, such as infection, tonsillar herniation, radiculopathy, and arachnoiditis, are rare. Considering that 50 mL of CSF are produced in a day in humans at a rate of approximately 0.35 mL/min, 20 mL of CSF removed by LP is replenished in one hour, provided there is no persistent CSF loss through the dural puncture site or alteration in CSF production caused by the LP (38).

Back to Top | Article Outline
Carbonic Anhydrase Inhibitors

Acetazolamide is generally accepted as a first-line medication for lowering the intracranial hypertension in patients with IIH. Its carbonic anhydrase inhibition decreases the secretion of CSF by the choroid plexus. Doses of 1 to 2 g are generally used and some advocate increasing to the maximum tolerated dose if necessary. Side effects are common but are better accepted when patients are aware of their potential occurrence and medication doses are built up gradually. Alternatively, methazolamide may be used but it has no particular therapeutic advantage over acetazolamide. Topiramate, an anti-epileptic medication with carbonic anhydrase inhibitory properties, may prove to be useful for IIH, particularly because it is also useful for headache prophylaxis and often produces weight loss (39). Currently, treatment of IIH with topiramate has not been studied and is considered off-label usage.

Back to Top | Article Outline
Other Diuretics

Furosemide also has beneficial effects on CSF secretion and may be used (39). Other diuretics are used but no consistent therapeutic trend has been reported. Most diuretics contain a sulfa moiety that may be problematic in patients who are allergic to sulfa. Triamterene and spironolactone are useful in this circumstance, although they have no proven effect on CSF production.

Back to Top | Article Outline
Corticosteroids

Corticosteroids are not advocated for routine or long-term management of IIH. They are useful as an adjunctive treatment in patients with rapid deterioration while arranging a surgical procedure (see “malignant” IIH) (40). Withdrawal of corticosteroids may lead to a rebound increase in ICP (41,42). Moreover, their side effects (weight gain, fluid retention, hyperglycemia) are problematic in IIH patients.

Back to Top | Article Outline
Management of Headaches

The chronic headaches of IIH are best treated with conventional headache prophylaxis, although in some cases lowering the ICP with medical methods is effective (37). Because of the potential dangers, we do not advocate CSF shunting procedures for headache alone. At the same time, many of the agents used for headache prophylaxis in IIH (tricyclic antidepressants, selective serotonin reuptake inhibitors, sodium valproate, calcium channel blockers) may produce weight gain or edema that is undesirable in this population. Many patients with IIH also have migraine, tension-type headaches, or analgesic overuse headaches (43). Headache prevention is recommended in IIH as long as the patient is monitored for medication-induced weight gain (43).

Medical treatment of IIH is seldom life-long. When the patient's visual status and optic nerve appearance have stabilized, or when the disease has been in remission for at least six months, ICP-lowering agents may be tapered and discontinued. Patients should still be periodically monitored at this point because recurrences are not rare. Weight gain is associated with recurrence in some patients (44). Recurrence of symptoms may warrant reinstitution of medications but headaches are typically managed without diuretics or carbonic anhydrase inhibitors unless there is evidence of elevated ICP.

Back to Top | Article Outline

SURGICAL TREATMENT

Surgery is considered under the following circumstances: 1) progressive loss of vision despite maximal medical therapy; 2) severe or rapid visual loss at onset (see “malignant IIH”), including the development of an afferent pupillary defect or signs of advancing optic nerve dysfunction; and 3) severe papilledema causing macular edema or exudates (37,45).

Surgical procedures used for the treatment of visual loss include optic nerve sheath decompression (ONSD) and CSF diversion procedures. Whether one procedure is superior to the other is controversial and the decision often depends on available resources and expertise. The success rate is comparable between ONSD and lumboperitoneal shunt (46). Advantages of ONSD are shorter anesthesia and hospitalization times. ONSD avoids the complications of shunting (Table 6). Approximately 50% of patients experience improvement in the nonoperated eye after a single ONSD (47).

Table 6
Table 6
Image Tools
Back to Top | Article Outline
Optic Nerve Sheath Decompression

The mechanism by which ONSD benefits IIH is uncertain. One possibility is a filtering effect with local CSF pressure reduction improving the peripapillary circulation (47). A second possibility is a generalized decrease in ICP, which has been demonstrated after ONSD (48,49). A third possibility is that scarring of the arachnoid after the procedure may protect the nerve head from the elevated CSF pressure. ONSD in monkeys produces connective tissue proliferation and obliteration of the subarachnoid space near the area of operation (50); similar changes were found in one human postmortem study (51).

The complication rate of ONSD ranges broadly from 4.8% to 45%, with a mean of 12.9% (52–62). Meta-analysis is difficult because there are so many variables, including the surgical approach (medial versus lateral), surgical experience, duration of follow-up, criteria for an event to be considered a complication, and primary procedure versus reoperation. Complications of ONSD are listed in Table 5. In a review of 317 published cases by Anthony Arnold, MD (presented at the International Neuro-Ophthalmology Society Meeting, 2002), failure (progressive visual loss postoperatively or need for reoperation) occurred in 42 cases (13%). The most commonly reported complications are extraocular motility dysfunction (often transient) and pupillary abnormalities. Extraocular movement dysfunction, usually caused by lateral rectus palsy, generally resolves. Visually threatening complications are rare. Transient and protracted postoperative blindness have been reported (59,60) and are attributed to ischemic injury to the optic nerve. The complication risks after reoperation are approximately the same as those for the first procedure (61,62).

Table 5
Table 5
Image Tools
Back to Top | Article Outline
CSF Diversion Procedures

A CSF diversion procedure treats IIH by lowering ICP but requires insertion of a foreign body. Lumboperitoneal shunting is more commonly performed than ventriculoperitoneal (VP) shunting because insertion and maintenance of patency may be more difficult in the latter procedure. However, VP and cisterna magna shunting may be successfully used (63,64,67). Complications of shunts are summarized in Table 6. The revision rate for lumboperitoneal shunts ranges from 38% to 64%, with an overall revision rate of 52% (78 of 150 cases) (46,61–66). The number of revisions per patient is 2.3% to 6.6% (mean 3.9%), but this value may be skewed because of the small number of reported patients. The reported interval between shunt placement to first revision is 9 to 27 months (46,66,67). Major causes of shunt failure include catheter obstruction, low ICP, catheter migration, and lumbar radiculopathy (66,68). A programmable shunt valve usually prevents low-pressure headaches, obviating the need for reoperation; this complication is less frequent in VP than in lumboperitoneal shunting. Visual loss may herald shunt malfunction, but may also occur with a functioning shunt (66–75). Uncommonly, patients may become “shunt dependent” after being in remission for years, with worsening of signs and symptoms when the shunt is obstructed or removed. Severe, acute ICP elevation upon insertion or removal of a shunt has been reported (70).

Over-shunting may lead to an acquired Chiari malformation or chronic intracranial hypotension. The symptoms and signs of low ICP are often similar to those of elevated ICP. Most patients will experience a postural headache that worsens with sitting or standing. Neck pain, vomiting, photosensitivity, blurred vision, transient visual obscurations, peripheral visual field loss, and sixth nerve paresis may occur (71). MRI changes of intracranial hypotension include leptomeningeal enhancement, tonsillar herniation, and sub-dural effusions (72,73).

Back to Top | Article Outline
Bariatric Surgery

Bariatric surgery may be considered in morbidly obese patients in whom medical and surgical treatments are ineffective (31). Although the procedure has risk, it offers the additional health benefits of reduced cardiovascular risk, type II diabetes, and lumbar disc degeneration that occur with significant weight loss. Bariatric surgery may be considered for long-term management but is not an appropriate treatment of patients with actively worsening vision.

Back to Top | Article Outline

SPECIAL CONSIDERATIONS

“Malignant” IIH

Aggressive treatment is required for patients in whom rapid visual decline (“malignant” IIH) develops. Significant visual field loss and marked papilledema are evident at presentation, often with decreased visual acuity. Visual loss may occur rapidly over days to weeks. Temporizing management includes serial lumbar punctures or insertion of a lumbar drain, and the administration of intravenous acetazolamide and corticosteroids (76). Prompt surgical treatment is indicated with ONSD, shunting, or both procedures. Cerebral venous sinus thrombosis is an important diagnostic exclusion as it is managed with heparinization and, in some cases, thrombolytic treatment. Occasionally, the thrombosis may not be apparent on the initial MRI study, and re-imaging or catheter angiography may be fruitful.

Back to Top | Article Outline
IIH in Pregnancy

Although pregnancy is not considered an independent risk factor for IIH, the disease may start or worsen during pregnancy (21,77). IIH during pregnancy is managed in cooperation with the obstetrician. Often the condition is successfully controlled with headache management and serial LPs. Patients are advised to avoid excessive weight gain with guidance from their obstetrician. Low-calorie diets and weight reduction are not recommended. Acetazolamide is a category C medication in pregnancy (risk cannot be ruled out because data are lacking). However, large clinical experience among neuro-ophthalmologists indicates overall safety without known teratogenic effects on the fetus, especially if the medication is used after the first trimester. Another option is chlorthalidone, a diuretic with a category B rating (no evidence of risk in humans). Corticosteroids may be administered without undue risk if needed for visual loss. Surgery is rarely required. If it is, ONSD is preferred over shunting because of potential shunt obstruction by the enlarging uterus (77). No special measures are required for delivery, and vaginal delivery is not contraindicated.

Back to Top | Article Outline
IIH in Children

Treatment of children with IIH is similar to that of adults, with the caveat that a secondary cause is often found in children (78–81). IIH in children may follow a febrile illness, and common secondary causes are tetracycline (including minocycline), hypervitaminosis A (including retinoid use), and cerebral venous sinus thrombosis (81).

Back to Top | Article Outline

REFERENCES

1. Bandyopadhyay S. Pseudotumor cerebri. Arch Neurol 2001;58:1699–701.

2. Durcan FJ, Corbett JJ, Wall M. The incidence of pseudotumor cerebri. Population studies in Iowa and Louisiana. Arch Neurol 1988;45:757–7.

3. Corbett JJ, Savino PJ, Thompson HS, et al. Visual loss in pseudotumor cerebri. Follow up of 57 patients from five to 41 years and a profile of 14 patients with permanent severe visual loss. Arch Neurol 1982;39:461–74.

4. Wall M, George D. Idiopathic intracranial hypertension. A prospective study of 50 patients. Brain 1991;114:155–80.

5. Corbett JJ, Savino PJ, Thompson HS, et al. Visual loss in pseudotumor cerebri. Follow-up of 57 patients from five to 41 years and a profile of 14 patients with permanent severe visual loss. Arch Neurol 1982;39:461–74.

6. Rush JA. Pseudotumor cerebri. Clinical profile and visual outcome in 63 patients. Mayo Clin Proc 1980;55:541–6.

7. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology 2002;59:1492–5.

8. Farb RI, Vanek I, Scott JN, et al. Idiopathic intracranial hypertension. The prevalence and morphology of sinovenous stenosis. Neurology 2003;60:1418–24.

9. Corbett JJ, Mehta MP. Cerebrospinal fluid pressure in normal obese subjects and patients with pseudotumor cerebri. Neurology 1983;33:1386–8.

10. Wall M. Sensory visual testing in idiopathic intracranial hypertension: measures sensitive to change. Neurology 1990;40:1859–64.

11. Rowe FJ, Sarkies NJ. Assessment of visual function in idiopathic intracranial hypertension: a prospective study. Eye 1988;12:111–8.

12. Verplanck M, Kaufman DI, Parsons T, et al. Electrophysiology versus psychophysics in the detection of visual loss in pseudotumor cerebri. Neurology 1988;38:1789–92.

13. Wall M, George D. Visual loss in pseudotumor cerebri: incidence and defects related to visual field strategy. Arch Neurol 1987;44:170–5

14. Frisén L. High-pass resolution perimetry. A clinical review. Doc Ophthalmol 1993;83:1–25.

15. Wall M, Montgomery EB. Using motion perimetry to detect visual field defects in patients with idiopathic intracranial hypertension: a comparison with conventional automated perimetry. Neurology 1995;45:1169–75.

16. Trick GL, Vesti E, Tawansy K, et al. Quantitative evaluation of papilledema in pseudotumor cerebri. Invest Ophthalmol Vis Sci 1998;39:1964–71.

17. Salgarello T, Falsini B, Tedesco S, et al. Correlation of optic nerve head tomography with visual field sensitivity in papilledema. Invest Ophthalmol Vis Sci 2001;42:1487–94.

18. Orcutt JC, Page NG, Sanders MD. Factors affecting visual loss in benign intracranial hypertension. Ophthalmology 1984;91:1303–12.

19. Tolander LM, Corbett JJ, Cremer S. Pseudotumor cerebri: first predictors of visual loss. Ann Neurol 1988;24:169–70 (Abstract).

20. Arseni C, Simoca I, Jipescu I, et al. Pseudotumor cerebri: risk factors, clinical course, prognostic criteria. Rom J Neurol Psychiat 1992;30:115–32.

21. Wall M, White WN. Asymmetric papilledema in idiopathic intracranial hypertension: prospective interocular comparison of sensory visual function. Invest Ophthalmol Vis Sci 1998;39:134–42.

22. Digre KB, Varner MW, Corbett JJ. Pseudotumor cerebri and pregnancy. Neurology 1984;34:721–9.

23. Corbett JJ. Problems in the diagnosis and treatment of pseudotumor cerebri. Can J Neurol Sci 1983;10:221–9.

24. Friedman DI, Forman S, Levi L, et al. Unusual ocular motility disturbances with increased intracranial pressure. Neurology 1998;50:1893–6.

25. Purvin VA, Trobe JD, Kosmorsky G. Neuro-ophthalmic features of cerebral venous obstruction. Arch Neurol 1995;52:880–5.

26. Biousse V, Ameri A, Bousser MG. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology 1999;53:1537–42.

27. King JO, Mitchell PJ, Thomson KR, et al. Manometry combined with cervical puncture in idiopathic intracranial hypertension. Neurology 2002:58:26–30.

28. Frisén L. Swelling of the optic nerve head: a staging scheme. J Neurol Neurosurg Psychiatr 1982;45:13–8.

29. Newborg B. Pseudotumor cerebri treated by rice/reduction diet. Arch Intern Med 1974;133:802–7

30. Johnson LN, Krohel GB, Madsen RW, et al. The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumor cerebri). Ophthalmology 1998:105:2313–7.

31. Kupersmith MJ, Gamell L, Turbin R, et al. Effects of weight loss on the course of idiopathic intracranial hypertension in women. Neurology 1998;50:1094–8.

32. Sugarman HJ, Felton WL III, Salvant JB, Jr, et al. Effects of surgically induced weight loss in idiopathic intracranial hypertension in morbid obesity. Neurology 1995;45:1655–9

33. Jacobson DM, Berg R, Wall M, et al. Serum vitamin A concentration is elevated in idiopathic intracranial hypertension. Neurology 1999;53:1114–8.

34. Selhorst JB, Kulkantrakorn K, Corbett JJ, et al. Retinol-binding protein in idiopathic intracranial hypertension (IIH). J Neuro-ophthalmol 2000;20(4):250–2.

35. Sirdofsky M, Kattah J, Macedo P. Intracranial hypertension in a dieting patient. J Neuro-ophthalmol 1994;14:9–11.

36. Friedman DI, Ingram P, Rogers MAM. Low tyramine diet in the treatment of idiopathic intracranial hypertension: a pilot study. Neurology 1998;50:A5.

37. Corbett JJ, Thompson HS. The rational management of idiopathic intracranial hypertension. Arch Neurol 1989;46:1049–51.

38. Fishman RA. Cerebrospinal fluid in Diseases of the Nervous System, 2nd edition. Philadelphia: W.B. Saunders; 1992:25–30.

39. Physicians' Desk Reference, 56th edition. Montvale, NJ: Medical Economics Company, Inc; 2002:2590–2595.

40. Liu GT, Glaser JS, Schatz NJ. High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri. Am J Ophthalmol 1994;118:88–96.

41. Liu GT, Kay MD, Bienfang DC, et al. Pseudotumor cerebri associated with corticosteroids withdrawal in inflammatory bowel disease. Am J Ophthalmol 1994;117:352–7.

42. Neville BG, Wilson J. Benign intracranial hypertension following corticosteroids withdrawal in childhood. Br Med J 1970;3:554–6.

43. Friedman DI, Rausch EA. Headache diagnoses in patients with treated idiopathic intracranial hypertension. Neurology 2002;58:1551–3.

44. Giuseffi V, Wall M, Siegel PZ, et al. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): A case-control study. Neurology 1991;41:239–44.

45. Carter S, Seiff SR. Macular changes in pseudotumor cerebri before and after optic nerve sheath fenestration. Ophthalmology 1995;102:937–41.

46. Rosenberg ML, Corbett JJ, Smith C, et al. Cerebrospinal fluid diversion procedures in pseudotumor cerebri. Neurology 1993;43:1071–2.

47. Keltner JL. Optic nerve sheath decompression. How does it work? Has its time come?Arch Ophthalmol 1988;106:1365–9.

48. Ngyun R, Carta A, Geleris A, et al. Long-term effect of optic nerve sheath decompression on intracranial pressure in pseudotumor cerebri. Invest Ophth Vis Sci 1997:38:S388.

49. Mittra RA, Sergott RC, Flaharty PM, et al. Optic nerve decompression improves hemodynamic parameters in papilledema. Ophthalmology 1993;100:987–97.

50. Hayreh SS. Pathogenesis of oedema of the optic disc. Doc Ophthalmol 1968;24:289–411.

51. Tsai JC, Petrovich MS, Sadun AA. Histopathological and ultra-structural examination of optic nerve sheath decompression. Br J Ophthalmol 1995;79:1825.

52. Brourman ND, Spoor TC, Ramocki JM. Optic nerve sheath decompression for pseudotumor cerebri. Arch Ophthalmol 1988;106:1378–83.

53. Corbett JJ, Nerad JA, Tse DA, et al. Results of optic nerve sheath fenestration for pseudotumor cerebri: the lateral orbitotomy approach. Arch Ophthalmol 1988;106:1391–7.

54. Sergott RC, Savino PJ, Bosley TM. Modified optic nerve sheath decompression provides long-term visual improvement for pseudotumor cerebri. Arch Ophthalmol 1988;106:1384–9.

55. Kelman SE, Heaps R, Wolf A, et al. Optic nerve decompression surgery improves visual function in patients with pseudotumor cerebri. Neurosurgery 1992;30:391–5.

56. Spoor TC, McHenry JG. Long-term effectiveness of optic nerve sheath decompression for pseudotumor cerebri. Arch Ophthalmol 1993;111:632–5.

57. Plotnik JL, Kosmorsky GS. Operative complications of optic nerve sheath decompression. Ophthalmology 1993;100:683–90.

58. Sergott RC, Savino PJ, Bosley TM. Optic nerve sheath decompression: A clinical review and proposed pathophysiologic mechanism. Aust N Z J Ophthalmol 1990;18:365–73.

59. Flynn WJ, Westfall CT, Weisman JS. Transient blindness after optic nerve sheath fenestration. Am J Ophthalmol 1994;117:678–9.

60. Brodsky MC, Rettele GA. Protracted postsurgical blindness with visual recovery following optic nerve sheath fenestration. Arch Ophthalmol 1998;116:107–9.

61. Spoor TC, Ramocki JM, Madion MP, et al. Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression. Am J Ophthalmol 1991;112:177–85.

62. Mauriello JA, Jr, Shaderowfsky BA, Gizzi M, et al. Management of visual loss after optic sheath decompression in patients with pseudotumor cerebri. Ophthalmology 1995;102:441–5.

63. Howard J, Appen RE. Ventriculoperitoneal shunting for pseudotumor cerebri. Presented at the Association for Research in Vision and Ophthalmology, Fort Lauderdale, FL, 2002.

64. Johnston I, Besser M, Morgan M. Cerebrospinal fluid diversion in the treatment of benign intracranial hypertension. J Neurosurg 1988;69:195–202.

65. Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology 1997;49:734–9.

66. Eggenberger ER, Miller NR, Vitale S. Lumboperitoneal shunt for the treatment of pseudotumor cerebri. Neurology 1996;46:1524–30.

67. Johnston IH, Sheridan MM. CSF shunting from the cisterna magna: a report of 16 cases. Br J Neurosurgery 1993;7:39–43.

68. Alleyne CH Jr, Shutter LA, Colohan AR. Cranial migration of a lumboperitoneal shunt catheter. So Med J 1996;89:634–6.

69. Lee AG. Visual loss as the manifesting symptom of ventriculoperitoneal shunt malfunction. Am J Ophthalmol 1996;122:127–9.

70. Liu GT, Volpe NJ, Schatz NJ, et al. Severe sudden visual loss caused by pseudotumor cerebri and lumboperitoneal shunt failure. Am J Ophthalmol 1996;122:129–31.

71. Horton JC, Fishman RA. Neurovisual findings in the syndrome of spontaneous intracranial hypotension from dural cerebrospinal fluid leak. Ophthalmology 1994;101:244–51.

72. Pannullo SC, Reich JB, Krol G, et al. MRI changes in intracranial hypotension. Neurology 1993;43:919–26.

73. Mokri B. Spontaneous cerebrospinal fluid leaks: from intracranial hypotension to cerebrospinal fluid hypovolemia – evolution of a concept. Mayo Clin Proc 1999;74:1113–23.

74. Kelman SE, Sergott RC, Cioffi GA, et al. Modified optic nerve decompression in patients with functioning lumboperitoneal shunts and progressive visual loss. Ophthalmology 1991;98:1449–53.

75. Wall M. Nerve sheath decompression in patients with functioning shunts. Ophthalmology 1992;99:480.

76. Liu GT, Glaser JS, Schatz NJ. High-dose methylprednisolone and acetazolamide for visual loss in pseudotumor cerebri. Am J Ophthalmol 1994;118:88–96

77. Shapiro S, Yee R, Brown H. Surgical management of pseudotumor in pregnancy: case report. Neurosurgery 1995;37:829–31.

78. Lee AG, Patrinely JR, Edmond JC. Optic nerve sheath decompression in pediatric pseudotumor cerebri. Ophthalmic Surgery & Lasers 1998;29:514–7.

79. Cinciripini GS, Donahue S, Borchert MS. Idiopathic intracranial hypertension in prepubertal pediatric patients: characteristics, treatment and outcome. Am J Ophthalmol 1999;127:178–82.

80. Schoeman JF. Childhood pseudotumor cerebri: clinical and intracranial pressure response to acetazolamide and furosemide treatment in a case series. J Child Neurol 1994;9:130–4.

81. Lessell S. Pediatric pseudotumor cerebri (idiopathic intracranial hypertension). Surv Ophthalmol 1992;37:155–66.

Cited By:

This article has been cited 46 time(s).

Cephalalgia
The International Classification of Headache Disorders, 3rd edition (beta version)
Bes, A; Kunkel, R; Lance, JW; Nappi, G; Pfaffenrath, V; Rose, FC; Schoenberg, BS; Soyka, D; Tfelt-Hansen, P; Welch, KMA; Wilkinson, M; Olesen, J; Bousser, MG; Diener, HC; Dodick, D; First, M; Goadsby, PJ; Gobel, H; Lainez, MJA; Lance, JW; Lipton, RB; Nappi, G; Sakai, F; Schoenen, J; Silberstein, SD; Steiner, TJ; Olesen, J; Bendtsen, L; Dodick, D; Ducros, A; Evers, S; First, M; Goadsby, PJ; Hershey, A; Katsarava, Z; Levin, M; Pascual, J; Russell, MB; Schwedt, T; Steiner, TJ; Tassorelli, C; Terwindt, GM; Vincent, M; Wang, SJ; Olesen, J; Evers, S; Charles, A; Hershey, A; Lipton, R; First, M; Bolay, H; Lanteri-Minet, M; MacGregor, EA; Takeshima, T; Schytz, HW; Ashina, S; Goicochea, MT; Hirata, K; Holroyd, K; Lampl, C; Lipton, RB; Mitsikostas, DD; Schoenen, J; Goadsby, P; Boes, C; Bordini, C; Cittadini, E; Cohen, A; Leone, M; May, A; Newman, L; Pareja, J; Park, JW; Rozen, T; Waldenlind, E; Wang, SJ; Ducros, A; Evers, S; Fuh, JL; Ozge, A; Pareja, JA; Pascual, J; Peres, M; Young, W; Yu, SY; Schwedt, T; Abu-Arafeh, I; Gladstone, J; Huang, SJ; Jensen, R; Lainez, JMA; Obelieniene, D; Sandor, P; Scher, AI; Ducros, A
Cephalalgia, 33(9): 629-808.
10.1177/0333102413485658
CrossRef
Neuro-Ophthalmology
Long-Term Results of Optic Nerve Sheath Fenestration for Idiopathic Intracranial Hypertension: Earlier Intervention Favours Improved Outcomes
Pineles, SL; Volpe, NJ
Neuro-Ophthalmology, 37(1): 12-19.
10.3109/01658107.2012.757787
CrossRef
Journal of Cerebral Blood Flow and Metabolism
What went wrong? The flawed concept of cerebrospinal venous insufficiency
Valdueza, JM; Doepp, F; Schreiber, SJ; van Oosten, BW; Schmierer, K; Paul, F; Wattjes, MP
Journal of Cerebral Blood Flow and Metabolism, 33(5): 657-668.
10.1038/jcbfm.2013.31
CrossRef
Journal of Neurosurgery-Pediatrics
Pseudotumor cerebri following tapered corticosteroid treatment in an 8-month-old infant
Ray, WZ; Lee, A; Blackburn, SL; Lueder, GT; Leonard, JR
Journal of Neurosurgery-Pediatrics, 1(1): 88-90.
10.3171/PED-08/01/088
CrossRef
Acta Ophthalmologica
Persistent visual loss in malignant idiopathic intracranial hypertension
Mensah, A; Milea, D; Jensen, R; Fledelius, H
Acta Ophthalmologica, 87(8): 934-936.
10.1111/j.1755-3768.2009.01706.x
CrossRef
Neurology
Long-term follow-up of idiopathic intracranial hypertension - The Iowa experience
Shah, VA; Kardon, RH; Lee, AG; Corbett, JJ; Wall, M
Neurology, 70(8): 634-640.

New England Journal of Medicine
Reference Range for Cerebrospinal Fluid Opening Pressure in Children
Avery, RA; Shah, SS; Licht, DJ; Seiden, JA; Huh, JW; Boswinkel, J; Ruppe, MD; Chew, A; Mistry, RD; Liu, GT
New England Journal of Medicine, 363(9): 891-893.

Journal of Child Neurology
Increased intracranial pressure in a case of pediatric multiple sclerosis
Williams, BJ; Skinner, HJ; Maria, BL
Journal of Child Neurology, 23(6): 699-702.
10.1177/0883073807313040
CrossRef
Surgery for Obesity and Related Diseases
Clinical resolution of severely symptomatic pseudotumor cerebri after gastric bypass in an adolescent
Chandra, V; Dutta, S; Albanese, CT; Shepard, E; Farrales-Nguyen, S; Morton, J
Surgery for Obesity and Related Diseases, 3(2): 198-200.
10.1016/j.soard.2006.11.015
CrossRef
Journal of Neurology Neurosurgery and Psychiatry
The neurology of enteric disease
Wills, AJ; Tengah, DSNAP; Holmes, GKT
Journal of Neurology Neurosurgery and Psychiatry, 77(7): -.
ARTN 805
CrossRef
Journal of Child Neurology
Idiopathic Intracranial Hypertension in a Pediatric Population: A Retrospective Analysis of the Initial Imaging Evaluation
Standridge, SM; O'Brien, SH
Journal of Child Neurology, 23(): 1308-1311.
10.1177/0883073808318056
CrossRef
Journal of Neurosurgery
Bilateral jugular foraminal stenosis in a patient with benign osteopetrosis associated with pseudotumor cerebri syndrome
Mirsadeghi, SMH; Meybodi, AT; Nejat, F; Saberi, H
Journal of Neurosurgery, 110(4): 804-807.
10.3171/2008.5.17581
CrossRef
Neurology
Fulminant idiopathic intracranial hypertension
Thambisetty, M; Lavin, PJ; Newman, NJ; Biousse, V
Neurology, 68(3): 229-232.

Graefes Archive for Clinical and Experimental Ophthalmology
Acquired choroidal folds: a sign of idiopathic intracranial hypertension
Lavinsky, J; Lavinsky, D; Lavinsky, F; Frutuoso, A
Graefes Archive for Clinical and Experimental Ophthalmology, 245(6): 883-888.
10.1007/s00417-006-0455-7
CrossRef
Survey of Ophthalmology
Pediatric idiopathic intracranial hypertension
Rangwala, LM; Liu, GT
Survey of Ophthalmology, 52(6): 597-617.
10.1016/j.survophthal.2007.08.018
CrossRef
Survey of Ophthalmology
Now you see it ...
Pendse, S; Bilyk, JR; Olivia, C; Biousse, V
Survey of Ophthalmology, 53(2): 177-182.
10.1016/j.survophthal.2007.12.008
CrossRef
Journal of Laboratory and Clinical Medicine
Linking thrombophilia and idiopathic intracranial hypertension
Weksler, BB
Journal of Laboratory and Clinical Medicine, 145(2): 63-64.
10.1016/j.lab.2004.11.003
CrossRef
Acta Neurologica Scandinavica
Perfusion and diffusion magnetic resonance imaging in idiopathic intracranial hypertension
Bicakci, K; Bicakci, S; Aksungur, E
Acta Neurologica Scandinavica, 114(3): 193-197.
10.1111/j.1600-0404.2006.00702.x
CrossRef
Neuro-Ophthalmology
Regression of a Peripapillary Neovascular Membrane Following Lumbar Peritoneal Shunting in a Case of Idiopathic Intracranial Hypertension
Aslan, O; Acaroglu, G; Ozdamar, Y
Neuro-Ophthalmology, 33(4): 195-198.
10.1080/01658100902842641
CrossRef
Journal of Neurology Neurosurgery and Psychiatry
Disorders of the anterior visual pathways
Madill, SA; Riordan-Eva, P
Journal of Neurology Neurosurgery and Psychiatry, 75(): 12-19.
10.1136/jnnp.2004.053421
CrossRef
Headache
Obesity and Migraine: The Effect of Age, Gender and Adipose Tissue Distribution
Peterlin, BL; Rosso, AL; Rapoport, AM; Scher, AI
Headache, 50(1): 52-62.
10.1111/j.1526-4610.2009.01459.x
CrossRef
Paediatrics & Child Health
Case 1: An unusual cause of headaches and priapism in a teenager
Friedman, J; Abbott, LS; Moineau, G; Johnston, DL
Paediatrics & Child Health, 13(4): 299-301.

Archives of Medical Science
Adolescent polycystic ovary syndrome: pathophysiology and implications of the disease
Gupta, S; Chen, D; O'Brien, KO; Chandra, A; Metterle, L; Kesavan, S; Agarwal, A
Archives of Medical Science, 5(): S115-S131.

Annals of Neurology
Chronic Cerebrospinal Venous Insufficiency and Multiple Sclerosis
Khan, O; Filippi, M; Freedman, MS; Barkhof, F; Dore-Duffy, P; Lassmann, H; Trapp, B; Bar-Or, A; Zak, I; Siegel, MJ; Lisak, R
Annals of Neurology, 67(3): 286-290.
10.1002/ana.22001
CrossRef
Neurology India
Retinal nerve fiber layer analysis in idiopathic intracranial hypertension
Uysal, TF; Cengiz, A; Reyhan, G; Hatice, D
Neurology India, 54(2): 168-172.

Canadian Journal of Neurological Sciences
Treatment of secondary tonsillar herniation by lumboperitoneal shunt revision
Lam, FC; Wheatley, MB; Mehta, V
Canadian Journal of Neurological Sciences, 34(2): 237-242.

Translational Research
Changes in weight, papilledema, headache, visual field, and life status in response to diet and metformin in women with idiopathic intracranial hypertension with and without concurrent polycystic ovary syndrome or hyperinsulinemia
Glueck, CJ; Golnik, KC; Aregawi, D; Goldenberg, N; Sieve, L; Wang, P
Translational Research, 148(5): 215-222.
10.1016/j.trsl.2006.05.003
CrossRef
European Journal of Ophthalmology
Idiopathic intracranial hypertension after 40 years of age: Clinical features in 23 patients
Zayit-Soudry, S; Leibovitch, I; Kesler, A
European Journal of Ophthalmology, 18(6): 989-993.

Headache
A Comparison of Idiopathic Intracranial Hypertension With and Without Papilledema
Digre, KB; Nakamoto, BK; Warner, JEA; Langeberg, WJ; Baggaley, SK; Katz, BJ
Headache, 49(2): 185-193.
10.1111/j.1526-4610.2008.01324.x
CrossRef
Neuro-Ophthalmology
Optic nerve sheath fenestration: A five year audit
Knapp, C; Sampath, R
Neuro-Ophthalmology, 29(): 173-177.
10.1080/01658100500481438
CrossRef
Journal of Clinical Neuroscience
Shunt failure in idiopathic intracranial hypertension presenting with spontaneous cerebrospinal fluid leak
Ransom, ER; Komotar, RJ; Mocco, J; Connolly, ES; Mullins, KJ
Journal of Clinical Neuroscience, 13(5): 598-602.
10.1016/j.jocn.2005.08.008
CrossRef
Journal of Neurosurgery
Laser scanning tomography measurement of the extent of papilledema in the follow-up examination of patients with idiopathic intracranial hypertension
Heckmann, JG; Faschingbauer, F; Lang, C; Reulbach, U; Dutsch, M; Mardin, CY; Schwab, S
Journal of Neurosurgery, 107(3): 543-547.

Acta Neurologica Scandinavica
Transcranial Doppler for evaluation of idiopathic intracranial hypertension
Gur, AY; Kesler, A; Shopin, L; Bornstein, NM
Acta Neurologica Scandinavica, 116(4): 239-242.
10.1111/j.1600-0404.2007.00861.x
CrossRef
Revue Neurologique
Bilateral papilledema: Prospective study of fifty patients
Deschamps, R; Dehais, C; Heran, F; Obadia, M; Laloum, L; Fechner, C; Vignal-Clermont, C; Gout, O
Revue Neurologique, 164(1): 42-46.
10.1016/j.neurol.2007.10.004
CrossRef
Neuro-Ophthalmology
What's New in Childhood Idiopathic Intracranial Hypertension?
Goyal, S; Pless, M; Krishnamoorthy, K; Butler, WE; Noviski, N; Gupta, P
Neuro-Ophthalmology, 33(): 23-35.
10.1080/01658100902717074
CrossRef
Brain & Development
Clinical spectrum of the pseudotumor cerebri in children: Etiological, clinical features, treatment and prognosis
Per, H; Canpolat, M; Gumus, H; Poyrazoglu, HG; Yikilmaz, A; Karakucuk, S; Dogan, H; Kumandas, S
Brain & Development, 35(6): 561-568.
10.1016/j.braindev.2012.08.008
CrossRef
Revue Neurologique
Idiopathic intracranial hypertension: Diagnosis, monitoring and treatment
Biousse, V
Revue Neurologique, 168(): 673-683.
10.1016/j.neurol.2012.07.018
CrossRef
Clinical Neurology and Neurosurgery
An update on the management of pseudotumor cerebri
Galgano, MA; Deshaies, EM
Clinical Neurology and Neurosurgery, 115(3): 252-259.
10.1016/j.clineuro.2012.11.018
CrossRef
European Journal of Pediatric Surgery
Juvenile Psammomatoid Ossifying Fibroma of the Forehead, Radical Resection, and Defect Coverage with a Hydroxyl-Apatite Composite-A Case Report
Wehrli, LA; Zweifel, N; Weil, R; Altermatt, S
European Journal of Pediatric Surgery, 22(6): 479-484.
10.1055/s-0032-1313349
CrossRef
Current Opinion in Ophthalmology
Surgical interventions for idiopathic intracranial hypertension
Uretsky, S
Current Opinion in Ophthalmology, 20(6): 451-455.
10.1097/ICU.0b013e3283313c1c
PDF (293) | CrossRef
Current Opinion in Ophthalmology
Headache and the eye
Dafer, RM; Jay, WM
Current Opinion in Ophthalmology, 20(6): 520-524.
10.1097/ICU.0b013e328331270d
PDF (280) | CrossRef
Journal of Neuro-Ophthalmology
Increased Intracranial Pressure: Idiopathic and Otherwise
Corbett, JJ
Journal of Neuro-Ophthalmology, 24(2): 103-105.

PDF (39)
Journal of Neuro-Ophthalmology
Idiopathic Intracranial Hypertension
Rosa, N; Capasso, L; Lanza, M
Journal of Neuro-Ophthalmology, 25(2): 152.

PDF (164)
Neurosurgery
Rapidly Rising Incidence of Cerebrospinal Fluid Shunting Procedures for Idiopathic Intracranial Hypertension in the United States, 1988–2002
Curry, WT; Butler, WE; Barker, FG
Neurosurgery, 57(1): 97-108.
10.1227/01.NEU.0000163094.23923.E5
PDF (731) | CrossRef
Neurosurgery Quarterly
Idiopathic Intracranial Hypertension: A Neurosurgical Perspective
Ament, JD; Hoffman, C; Black, PM
Neurosurgery Quarterly, 17(2): 77-80.
10.1097/WNQ.0b013e318032953b
PDF (88) | CrossRef
Journal of Pediatric Hematology/Oncology
Pseudotumor Cerebri After Allogeneic Bone Marrow Transplant Associated With Cyclosporine A Use for Graft-Versus-Host Disease Prophylaxis
Somech, R; Doyle, J
Journal of Pediatric Hematology/Oncology, 29(1): 66-68.
10.1097/MPH.0b013e318030ac3b
PDF (74) | CrossRef
Back to Top | Article Outline

© 2004 Lippincott Williams & Wilkins, Inc.

Login