eMedicine Specialties > Neurology > Headache and Pain

Pseudotumor Cerebri

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

Introduction

Background

Pseudotumor cerebri, also known as idiopathic intracranial hypertension (IIH) is a disorder of unknown etiology. It affects predominantly obese women of childbearing age. The primary problem is chronically elevated intracranial pressure (ICP), and the most important neurologic manifestation is papilledema, which may lead to progressive optic atrophy and blindness.

Pathophysiology

A dominant early theory concerning the pathogenesis of elevated ICP in these patients was cerebral edema. Against this is the fact that no altered level of alertness, cognitive impairment, or focal neurological findings are associated with the elevated ICP. In addition, no pathologic signs of cerebral edema have been documented in these patients. Early reports describing edema were later considered to represent fixation artifact (ie, from tissue preparation) rather than in vivo edema.

Current theories include increased resistance to cerebrospinal fluid (CSF) outflow at the arachnoid granulations that line the dural venous sinuses and through which CSF reabsorption is thought to occur by bulk flow. Alternatively, occult cerebral venous outflow abnormalities may produce IIH.

Farb and colleagues have demonstrated that, in a series of 29 patients with IIH, narrowing of the transverse dural venous sinus was demonstrable on MR venography, while none of the 59 control subjects had this finding.1 These authors suggest that the narrowing is a consequence of elevated intracranial pressure, and, when the narrowing develops, it exacerbates the pressure elevation by increasing venous pressure in the superior sagittal sinus.

  • CSF production rate (mL/min) should be equal to the CSF reabsorption rate.
  • If production exceeds absorption, ICP rises until it exceeds mean arterial pressure, which, if sustained, would be fatal.
  • In IIH the production rate equals the reabsorption rate; however, a higher than normal pressure is required to achieve this owing to the increased resistance at the arachnoid granulations.
Bateman has shown that some patients with IIH with normal dural venous drainage have increased arterial inflow suggesting that collateral venous drainage occurs in addition to that provided by the superior sagittal sinus and transverse sinuses.2 The same investigator measured MR venography and MR flow quantification in cerebral arteries and veins in a series of 40 patients with IIH, of which 21 patients had venous stenosis. The arterial inflow was 21% higher than normal and superior sagittal sinus outflow was normal, resulting in reduced percentage of venous outflow compared to inflow. The remainder of arterial inflow volume is presumed to have drained via collateral venous channels. With clinical remission of symptoms, the arterial inflow volumes returned to normal.3

Frequency

United States

  • Annual incidence of pseudotumor cerebri in Iowa and Louisiana4  
    • 0.9 case per 100,000 population
    • 13 cases per 100,000 (Iowa) and 14.85 per 100,000 (Louisiana) in women aged 20-44 years and 10% over ideal weight
    • 19.3 cases per 100,000 in women 20% over ideal weight
    • Female-to-male ratio 8:1 for mean weight 38% over ideal weight for height
  • Annual incidence at Mayo Clinic (Rochester, MN) between 1976 and 19905
    • 0.9 case per 100,000 population
    • 1.6 cases per 100,000 women
    • 3.3 cases per 100,000 females aged 15-44 years
    • 7.9 cases per 100,000 obese women aged 15-44 years

International

  • Annual incidence of idiopathic intracranial hypertension in Benghazi, Libya, in a study conducted between 1982 and 1989 comprising 81 patients (76 females and 5 males) aged 8-55 years6
    • 2.2 cases per 100,000 population
    • 4.3 cases per 100,000 women of all ages
    • 12 cases per 100,000 women aged 15-44 years
    • 21.4 cases per 100,000 obese women aged 15-44 years

Mortality/Morbidity

  • IIH is associated with no known specific mortality risk. The increased mortality rate associated with morbid obesity has a selective expression in this group because of the strong predilection of the disease to affect obese females.
  • Vision loss
    • The only permanent morbidity in IIH is vision loss from decompensation of papilledema with progressive optic atrophy. The frequency and degree to which visual loss occurs in this disease is difficult to establish from the existing literature.
    • As outlined by Radhakrishnan et al in 19947 , the reported incidence of vision impairment is much higher in series published from referral centers (as many as 96% of cases with some degree of visual field loss) compared to population-based series (eg, 22% in Iowa4 ).
    • Two equally valid explanations for this discrepancy have been proposed.
      • The referral centers perform more extensive vision testing, including Goldmann and computerized automated threshold perimetry, and thus discovered visual deficits that were not tested for in the community-based studies.
      • The worst cases are referred for tertiary care consultation and thus the referral center series are biased toward more severe vision loss cases than the community-based studies.

Race

No evidence exists to suggest predilection for any particular racial or ethnic group apart from variation in the prevalence of obesity in the different groups.

Sex

  • Obese females of childbearing age are affected selectively by IIH.
  • Specific numbers are available from the epidemiological studies.
    • Durcan et al4 - Female-to-male ratio 8:1
    • Radhakrishnan5 - Female-to-male ratio 8:1 (N = 9)
    • Radhakrishnan5 - Female-to-male ratio 8:1 (N = 76)

Age

Please refer to the incidence statistics in Frequency. The highest incidence is among obese women of childbearing age. For most of the epidemiological series, this was women aged 15-44 years.

Clinical

History

  • Symptoms of elevated intracranial pressure (ICP)
    • Headache that is nonspecific and varies in type, location, and frequency
    • Pulsatile tinnitus - A rhythmic sound, heard in one or both ears, with pulsing synchronous rhythm that may be exacerbated by the supine or bending position
    • Horizontal diplopia - A symptom of a false-localizing sixth cranial nerve palsy
    • Radicular pain (usually in the arms) - An uncommon symptom
  • Symptoms of papilledema
    • Transient visual obscurations (eg, dimming or blackout of vision in one or both eyes lasting for a few seconds) may be present. They may be predominantly or uniformly orthostatic (ie, after bending over).
    • Progressive loss of peripheral vision in one or both of the eyes may be noted, most often starting in the nasal inferior quadrant, followed by loss of central visual field (possibly affecting visual acuity) and, lastly, loss of color vision.
    • Blurring and distortion (ie, metamorphopsia) of central vision is caused by macular wrinkling and subretinal fluid spreading from the swollen optic disc.
    • Sudden visual loss is due to intraocular hemorrhage secondary to peripapillary subretinal neovascularization related to chronic papilledema.

Physical

Visual function testing, in particular, visual field, funduscopy, and ocular motility examination, are the most important parts of the neurologic examination for diagnosing and monitoring patients with idiopathic intracranial hypertension (IIH).

  • Papilledema
    • Peripapillary flame hemorrhages, venous engorgement, and hard exudates are features consistent with acute papilledema.
    • Telangiectatic vessels on the disc surface, optociliary shunt veins (which exit the disc at its margin), and optic disc pallor are associated with chronic papilledema (see Image 1).
  • Visual fields
    • The first sign of incipient postpapilledema optic atrophy is constriction of the inferior nasal quadrant of the visual field with a border respecting the nasal horizontal midline (nasal step). This starts in the most peripheral points in the visual field (ie, 50 degrees from fixation) and progresses inward (see Image 2).
    • Goldmann-type dynamic perimetry is the best test, since it provides reliable information concerning the most peripheral parts of the visual field.
    • Computerized automated Humphrey-type static perimetry is generally unreliable beyond 30 degrees eccentricity and may not be as sensitive as dynamic perimetry for this problem.
  • Visual acuity: This is usually normal until significant peripheral visual field loss with progressive postpapilledema optic atrophy has occurred.
  • Color vision: This usually is tested in the office with color-confusion type plates, most commonly the Ishihara or Hardy-Rand-Rittler (HRR). Unlike visual acuity testing, it is not sensitive in picking up early postpapilledema optic atrophy, since color perception is concentrated in the central visual field.
  • Ocular motility
    • Occasionally limited abduction of one or both of the eyes results from increased ICP. This is termed false-localizing sixth cranial nerve palsy.
    • This usually can be observed as the patient follows the examiner's hand to the right and the left with both eyes. The involved eye does not move fully outward (ie, abduction), leaving some white sclera showing lateral to the cornea on the involved side compared to the other side. Speed of the abducting movement in the paretic eye also usually is slower than in the normal eye.
    • Some patients with full abduction still show some sclera; therefore, when using this sign demonstrating asymmetry between the eyes in abduction is important.
    • Diplopia testing is another way to detect even a low-grade sixth nerve paresis.
      • The patient is told to look at a focal light source (eg, penlight, Finnoff head), preferably placed more than 10 ft away. Either a red glass or a Maddox rod is placed in front of the patient's right eye. The Maddox rod creates an image of a vertical red line when the patient views a focal light source through it.
      • In a positive test for limited abduction, the red image (focal light or line) is displaced to the right of the light (homonymous or uncrossed diplopia) in the patient's view. This indicates that the visual axes are convergent with respect to one another (ie, esotropia, relative weakness of the lateral rectus muscle or muscles, sixth cranial nerve palsy).
    • Alternate cover testing also may reveal a slight corrective saccade when the other eye is covered in patients with sixth nerve palsies.

Causes

  • In 1994, Radhakrishnan et al reviewed the literature on IIH associated with other diseases and with drugs. These authors insisted that, to be included in the list of causally related associations, the following criteria should be met:7
    • At least 2 cases should have been described.
    • The reported cases should have met all the criteria for the diagnosis of IIH.
    • Intracranial dural sinus thrombosis should have been ruled out with reasonable certainty.
  • The following data were obtained from this 1994 study and subsequent case reports. The authors' organization of categories is preserved here.
    • Endocrine risk factors confirmed in epidemiological studies
      • Female sex
      • Reproductive age group
      • Menstrual irregularity
      • Obesity
      • Recent weight gain
    • Endocrine risk factors that meet minimal criteria, unconfirmed in case-controlled studies
      • Adrenal insufficiency
      • Cushing disease
      • Hypoparathyroidism
      • Hypothyroidism
      • Excessive thyroxine replacement in children (ie, low thyrotrophin levels)
    • Medication risk factors that meet minimal criteria, unconfirmed in case-controlled studies
      • Cimetidine, corticosteroids, danazol, isotretinoin (Accutane), levothyroxine, lithium, minocycline, nalidixic acid, nitrofurantoin, tamoxifen, tetracycline, trimethoprim-sulfamethoxazole7
      • All-trans -retinoic acid (ATRA) used in the treatment of promyelocytic leukemia, cyclosporine, levonorgestrel implant (Norplant; 39 women reported to US Food and Drug Administration [FDA] from February 1991-December 1993), pancreatin (pancreatic enzyme replacement for cystic fibrosis patients)
      • Recombinant human growth hormone (7 children in 3 papers)/natural growth hormone (somatotropin)
      • Vitamin A in infants
    • Miscellaneous risk factors that meet minimal criteria, unconfirmed in case-controlled studies
    • References cited for additions since 1994 include Rogers, 19998 ; Howell, 19989 ; Crock, 199810 ; Williams, 199711 ; Raghavan, 199712 ; Sacchi, 199713 ; Tanaka, 1997; Visani, 1996; Cruz, 1996; Querfeld, 1996; Blethen, 1996; Visani and Bontempo, 199614 ; Selleri, 199615 ; Ahmad, 199616 ; Varadi, 199517 ; Sivin, 199518 ; Baqui, 199519 ; Alder, 199520 ; Malozowski, 199521 ; Campos and Olitsky, 199522 ; Nasr and Schaffert, 199523 ; Wysowski and Green, 1995; and Price, 199524 .
  • Increased venous red blood cell aggregation and relatively elevated fibrinogen concentration were demonstrated in patients with IIH compared with matched controls.25
  • The retinol/retinol-binding protein ratio is elevated in the CSF of patients with IIH compared with non-IIH neurologic controls and with normal controls.26

More on Pseudotumor Cerebri

Overview: Pseudotumor Cerebri
Differential Diagnoses & Workup: Pseudotumor Cerebri
Treatment & Medication: Pseudotumor Cerebri
Follow-up: Pseudotumor Cerebri
Multimedia: Pseudotumor Cerebri
References
[ CLOSE WINDOW ]

References

  1. Farb RI, Vanek I, Scott JN, et al. Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis. Neurology. May 13 2003;60(9):1418-24. [Medline].

  2. Bateman GA. Association between arterial inflow and venous outflow in idiopathic and secondary intracranial hypertension. J Clin Neurosci. Jun 2006;13(5):550-6; discussion 557. [Medline].

  3. Bateman GA. Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses. J Clin Neurosci. Apr 2008;15(4):402-8. [Medline].

  4. Durcan FJ, Corbett JJ, Wall M. The incidence of pseudotumor cerebri. Population studies in Iowa and Louisiana. Arch Neurol. Aug 1988;45(8):875-7. [Medline].

  5. Radhakrishnan K, Ahlskog JE, Cross SA, et al. Idiopathic intracranial hypertension (pseudotumor cerebri). Descriptive epidemiology in Rochester, Minn, 1976 to 1990. Arch Neurol. Jan 1993;50(1):78-80. [Medline].

  6. Radhakrishnan K, Thacker AK, Bohlaga NH, et al. Epidemiology of idiopathic intracranial hypertension: a prospective and case-control study. J Neurol Sci. May 1993;116(1):18-28. [Medline].

  7. Radhakrishnan K, Ahlskog JE, Garrity JA, Kurland LT. Idiopathic intracranial hypertension. Mayo Clin Proc. Feb 1994;69(2):169-80. [Medline].

  8. Rogers AH, Rogers GL, Bremer DL, McGregor ML. Pseudotumor cerebri in children receiving recombinant human growth hormone. Ophthalmology. Jun 1999;106(6):1186-9; discussion 1189-90. [Medline].

  9. Howell SJ, Wilton P, Shalet SM. Growth hormone replacement in patients with Langerhan''s cell histiocytosis. Arch Dis Child. May 1998;78(5):469-73. [Medline].

  10. Crock PA, McKenzie JD, Nicoll AM, et al. Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand. Acta Paediatr. Apr 1998;87(4):381-6. [Medline].

  11. Williams JB. Adverse effects of thyroid hormones. Drugs Aging. Dec 1997;11(6):460-9. [Medline].

  12. Raghavan S, DiMartino-Nardi J, Saenger P, Linder B. Pseudotumor cerebri in an infant after L-thyroxine therapy for transient neonatal hypothyroidism. J Pediatr. Mar 1997;130(3):478-80. [Medline].

  13. Sacchi S, Russo D, Avvisati G, et al. All-trans retinoic acid in hematological malignancies, an update. GER (Gruppo Ematologico Retinoidi). Haematologica. Jan-Feb 1997;82(1):106-21. [Medline].

  14. Visani G, Bontempo G, Manfroi S, et al. All-trans-retinoic acid and pseudotumor cerebri in a young adult with acute promyelocytic leukemia: a possible disease association. Haematologica. Mar-Apr 1996;81(2):152-4. [Medline].

  15. Selleri C, Pane F, Notaro R, et al. All-trans-retinoic acid (ATRA) responsive skin relapses of acute promyelocytic leukaemia followed by ATRA-induced pseudotumour cerebri. Br J Haematol. Mar 1996;92(4):937-40. [Medline].

  16. Ahmad S. Amiodarone and reversible benign intracranial hypertension. Cardiology. Jan-Feb 1996;87(1):90. [Medline].

  17. Varadi G, Lossos A, Or R, et al. Successful allogeneic bone marrow transplantation in a patient with ATRA-inducedpseudotumor cerebri. Am J Hematol. Oct 1995;50(2):147-8. [Medline].

  18. Sivin I. Serious adverse events in Norplant users reported to the Food and Drug Administration's MedWatch Spontaneous Reporting System. Obstet Gynecol. Aug 1995;86(2):318-20. [Medline].

  19. Baqui AH, de Francisco A, Arifeen SE, et al. Bulging fontanelle after supplementation with 25,000 IU of vitamin A in infancy using immunization contacts. Acta Paediatr. Aug 1995;84(8):863-6. [Medline].

  20. Alder JB, Fraunfelder FT, Edwards R. Levonorgestrel implants and intracranial hypertension. N Engl J Med. Jun 22 1995;332(25):1720-1. [Medline].

  21. Malozowski S, Tanner LA, Wysowski DK, et al. Benign intracranial hypertension in children with growth hormone deficiency treated with growth hormone. J Pediatr. Jun 1995;126(6):996-9. [Medline].

  22. Campos SP, Olitsky S. Idiopathic intracranial hypertension after L-thyroxine therapy for acquired primary hypothyroidism. Clin Pediatr (Phila). Jun 1995;34(6):334-7. [Medline].

  23. Nasr SZ, Schaffert D. Symptomatic increase in intracranial pressure following pancreatic enzyme replacement therapy for cystic fibrosis. Pediatr Pulmonol. Jun 1995;19(6):396-7. [Medline].

  24. Price DA, Clayton PE, Lloyd IC. Benign intracranial hypertension induced by growth hormone treatment. Lancet. Feb 18 1995;345(8947):458-9. [Medline].

  25. Kesler A, Yatziv Y, Shapira I, et al. Increased red blood cell aggregation in patients with idiopathic intracranial hypertension. A hitherto unexplored pathophysiological pathway. Thromb Haemost. Oct 2006;96(4):483-7. [Medline].

  26. Warner JE, Larson AJ, Bhosale P, Digre KB, Henley C, Alder SC. Retinol-binding protein and retinol analysis in cerebrospinal fluid and serum of patients with and without idiopathic intracranial hypertension. J Neuroophthalmol. Dec 2007;27(4):258-62. [Medline].

  27. Nampoory MR, Johny KV, Gupta RK, et al. Treatable intracranial hypertension in patients with lupus nephritis. Lupus. 1997;6(7):597-602. [Medline].

  28. Leker RR, Steiner I. Anticardiolipin antibodies are frequently present in patients with idiopathic intracranial hypertension. Arch Neurol. Jun 1998;55(6):817-20. [Medline].

  29. Sussman J, Leach M, Greaves M, et al. Potentially prothrombotic abnormalities of coagulation in benign intracranial hypertension. J Neurol Neurosurg Psychiatry. Mar 1997;62(3):229-33. [Medline].

  30. Bachman DT, Srivastava G. Emergency department presentations of Lyme disease in children. Pediatr Emerg Care. Oct 1998;14(5):356-61. [Medline].

  31. Agid R, Farb RI, Willinsky RA, et al. Idiopathic intracranial hypertension: the validity of cross-sectional neuroimaging signs. Neuroradiology. Aug 2006;48(8):521-7. [Medline].

  32. Burgett RA, Purvin VA, Kawasaki A. Lumboperitoneal shunting for pseudotumor cerebri. Neurology. Sep 1997;49(3):734-9. [Medline].

  33. Woodworth GF, McGirt MJ, Elfert P, et al. Frameless stereotactic ventricular shunt placement for idiopathic intracranial hypertension. Stereotact Funct Neurosurg. 2005;83(1):12-6. [Medline].

  34. Goh KY, Schatz NJ, Glaser JS. Optic nerve sheath fenestration for pseudotumor cerebri. J Neuroophthalmol. Jun 1997;17(2):86-91. [Medline].

  35. Chandrasekaran S, McCluskey P, Minassian D, Assaad N. Visual outcomes for optic nerve sheath fenestration in pseudotumour cerebri and related conditions. Clin Experiment Ophthalmol. Sep 2006;34(7):661-5. [Medline].

  36. Spoor TC, McHenry JG. Long-term effectiveness of optic nerve sheath decompression for pseudotumor cerebri. Arch Ophthalmol. May 1993;111(5):632-5. [Medline].

  37. Nithyanandam S, Manayath GJ, Battu RR. Optic nerve sheath decompression for visual loss in intracranial hypertension: Report from a tertiary care center in South India. Indian J Ophthalmol. Mar-Apr 2008;56(2):115-20. [Medline].

  38. Feldon SE. Visual outcomes comparing surgical techniques for management of severe idiopathic intracranial hypertension. Neurosurg Focus. 2007;23(5):E6. [Medline].

  39. Rowe FJ, Sarkies NJ. Assessment of visual function in idiopathic intracranial hypertension: a prospective study. Eye. 1998;12 (Pt 1):111-8. [Medline].

  40. Kupersmith MJ, Gamell L, Turbin R, et al. Effects of weight loss on the course of idiopathic intracranial hypertension in women. Neurology. Apr 1998;50(4):1094-8. [Medline].

  41. Wall M, George D. Visual loss in pseudotumor cerebri. Incidence and defects related to visual field strategy. Arch Neurol. Feb 1987;44(2):170-5. [Medline].

  42. Shah VA, Kardon RH, Lee AG, Corbett JJ, Wall M. Long-term follow-up of idiopathic intracranial hypertension: the Iowa experience. Neurology. Feb 19 2008;70(8):634-40. [Medline].

  43. Sugerman HJ, Felton WL 3rd, Salvant JB Jr. Effects of surgically induced weight loss on idiopathic intracranial hypertension in morbid obesity. Neurology. Sep 1995;45(9):1655-9. [Medline].

  44. Sugerman HJ, Felton WL 3rd, Sismanis A, et al. Gastric surgery for pseudotumor cerebri associated with severe obesity. Ann Surg. May 1999;229(5):634-40; discussion 640-2. [Medline].

  45. Digre KB, Varner MW, Corbett JJ. Pseudotumor cerebri and pregnancy. Neurology. Jun 1984;34(6):721-9. [Medline].

  46. Giuseffi V, Wall M, Siegel PZ, Rojas PB. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): a case-control study. Neurology. Feb 1991;41(2 (Pt 1)):239-44. [Medline].

  47. Beller GA, Smith TW, Abelmann WH, et al. Digitalis intoxication. A prospective clinical study with serum level correlations. N Engl J Med. May 6 1971;284(18):989-97. [Medline].

  48. Bertler A, Andersson KE, Wettrell G. Letter: Concentration of digoxin in choroid plexus. Lancet. Dec 22 1973;2(7843):1453-4. [Medline].

  49. Blethen SL, Allen DB, Graves D, et al. Safety of recombinant deoxyribonucleic acid-derived growth hormone: The National Cooperative Growth Study experience. J Clin Endocrinol Metab. May 1996;81(5):1704-10. [Medline].

  50. Chung EK. Digitalis intoxication. Amsterdam: Excerpta Medical Foundation; 1969.

  51. Cruz OA, Fogg SG, Roper-Hall G. Pseudotumor cerebri associated with cyclosporine use. Am J Ophthalmol. Sep 1996;122(3):436-7. [Medline].

  52. Gucer G, Viernstein L. Long-term intracranial pressure recording in the management of pseudotumor cerebri. J Neurosurg. Aug 1978;49(2):256-63. [Medline].

  53. Maren TH. Bicarbonate formation in cerebrospinal fluid: role in sodium transport and pH regulation. Am J Physiol. Apr 1972;222(4):885-99. [Medline].

  54. McCarthy KD, Reed DJ. The effect of acetazolamide and furosemide on cerebrospinal fluid production and choroid plexus carbonic anhydrase activity. J Pharmacol Exp Ther. Apr 1974;189(1):194-201. [Medline].

  55. Neblett CR, Waltz TA, McNeel DP, et al. Effect of cardiac glycosides on human cerebrospinal-fluid production. Lancet. Nov 11 1972;2(7785):1008-9. [Medline].

  56. Physicans Desk Reference. Physicans Desk Reference. ed. Medical Economics Data, US; 1997:1679.

  57. Plum F, Siesjo BK. Recent advances in CSF physiology. Anesthesiology. Jun 1975;42(6):708-730. [Medline].

  58. Querfeld U. Benign intracranial hypertension (pseudotumour cerebri) during rhGH therapy. Br J Clin Pract Suppl. Aug 1996;85:68. [Medline].

  59. Schott GD, Holt D. Letter: Digoxin in benign intracranial hypertension. Lancet. Mar 2 1974;1(7853):358-9. [Medline].

  60. Smith TW, Haber E. Digitalis. I. N Engl J Med. Nov 1 1973;289(18):945-52. [Medline].

  61. Smith TW, Willerson JT. Suicidal and accidental digoxin ingestion. Report of five cases with serum digoxin level correlations. Circulation. Jul 1971;44(1):29-36. [Medline].

  62. Vates TS, Bonting SL, Oppelt WW. Na-K activated adenosine triphosphatase and formation of cerebrospinal fluid in the cat. Am J Physiol. May 1964;206:1165-72. [Medline].

  63. Visani G, Manfroi S, Tosi P, Martinelli G. All-trans-retinoic acid and pseudotumor cerebri. Leuk Lymphoma. Nov 1996;23(5-6):437-42. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

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

[ CLOSE WINDOW ]

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.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.