Pseudotumor Cerebri Clinical Presentation

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

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.
Next

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, shown below. Left optic disc with moderate chronic papilledema Left optic disc with moderate chronic papilledema in a patient with pseudotumor cerebri. Paton lines (arc-shaped retinal wrinkles concentric with disc margin) are seen along the temporal side of the inferior pole of the disc.
  • 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, depicted below. Right optic disc with postpapilledema optic atrophRight optic disc with postpapilledema optic atrophy in a patient with pseudotumor cerebri. Diffuse pallor of the disc and absence of small arterial vessels on the surface are noted, with very little disc elevation. The disc margin at the upper and lower poles and nasally is obscured by some residual edema in the nerve fiber layer and gliosis that often persists even after all the edema has resolved.
    • 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.
Previous
Next

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:[11]
    • 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,[12] minocycline, nalidixic acid, nitrofurantoin, tamoxifen, tetracycline, trimethoprim-sulfamethoxazole[11]
      • 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, 1999[13] ; Howell, 1998[14] ; Crock, 1998[15] ; Williams, 1997[16] ; Raghavan, 1997[17] ; Sacchi, 1997[18] ; Tanaka, 1997; Visani, 1996; Cruz, 1996; Querfeld, 1996; Blethen, 1996; Visani and Bontempo, 1996[19] ; Selleri, 1996[20] ; Ahmad, 1996[21] ; Varadi, 1995[22] ; Sivin, 1995[23] ; Baqui, 1995[24] ; Alder, 1995[25] ; Malozowski, 1995[26] ; Campos and Olitsky, 1995[27] ; Nasr and Schaffert, 1995[28] ; Wysowski and Green, 1995; and Price, 1995[29] .
  • Increased venous red blood cell aggregation and relatively elevated fibrinogen concentration were demonstrated in patients with IIH compared with matched controls.[30]
  • 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.[31]
  • Because IIH is concentrated in women between puberty and menopause, Fraser and colleagues emphasized the potential role of sex hormones in the pathogenesis of IIH. They also point out that obstructive sleep apnea has been proposed as a risk factor. Since women taking exogenous estrogen and pregnant women are not at particular risk for IIH, they suggest that low levels of testosterone may be the important hormonal link in women with IIH. The authors administered 2 standardized questionnaires embedded in a telephone interview of 24 men with IIH and 48 controls matched for gender, age, race and WHO BMI category. The questionnaires were 1) Androgen Deficiency in Aging Males (ADAM) and 2) Obstructive Sleep Apnea (OSA). They found that the men with IIH were significantly more likely than controls to have symptoms of testosterone deficiency and obstructive sleep apnea.[32]
Previous
Proceed to Differential Diagnoses
 
 
Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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

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

Disclosure: Nothing to disclose.

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

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

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

Chief Editor

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

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

Disclosure: Nothing to disclose.

References

  1. Jindal M, Hiam L, Raman A, Rejali D. Idiopathic intracranial hypertension in otolaryngology. Eur Arch Otorhinolaryngol. Jun 2009;266(6):803-6. [Medline].

  2. 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].

  3. 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].

  4. 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].

  5. Bateman GA, Stevens SA, Stimpson J. A mathematical model of idiopathic intracranial hypertension incorporating increased arterial inflow and variable venous outflow collapsibility. J Neurosurg. Mar 2009;110(3):446-56. [Medline].

  6. 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].

  7. 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].

  8. 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].

  9. Agostoni E, Aliprandi A. Alterations in the cerebral venous circulation as a cause of headache. Neurol Sci. May 2009;30 Suppl 1:S7-10. [Medline].

  10. Ney JJ, Volpe NJ, Liu GT, Balcer LJ, Moster ML, Galetta SL. Functional visual loss in idiopathic intracranial hypertension. Ophthalmology. Sep 2009;116(9):1808-1813.e1. [Medline].

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

  12. Kelly SJ, O'Donnell T, Fleming JC, Einhaus S. Pseudotumor cerebri associated with lithium use in an 11-year-old boy. J AAPOS. Apr 2009;13(2):204-6. [Medline].

  13. 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].

  14. 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].

  15. 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].

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

  17. 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].

  18. 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].

  19. 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].

  20. 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].

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

  22. 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].

  23. 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].

  24. 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].

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

  26. 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].

  27. 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].

  28. 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].

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

  30. 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].

  31. 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].

  32. Fraser JA, Bruce BB, Rucker J, Fraser LA, Atkins EJ, Newman NJ, et al. Risk factors for idiopathic intracranial hypertension in men: a case-control study. J Neurol Sci. Mar 15 2010;290(1-2):86-9. [Medline].

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

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

  35. 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].

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

  37. 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].

  38. Stone MB. Ultrasound diagnosis of papilledema and increased intracranial pressure in pseudotumor cerebri. Am J Emerg Med. Mar 2009;27(3):376.e1-376.e2. [Medline].

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

  40. 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].

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

  42. 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].

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

  44. 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].

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

  46. Bussière M, Falero R, Nicolle D, Proulx A, Patel V, Pelz D. Unilateral Transverse Sinus Stenting of Patients with Idiopathic Intracranial Hypertension. AJNR Am J Neuroradiol. Nov 26 2009;[Medline].

  47. Arac A, Lee M, Steinberg GK, Marcellus M, Marks MP. Efficacy of endovascular stenting in dural venous sinus stenosis for the treatment of idiopathic intracranial hypertension. Neurosurg Focus. Nov 2009;27(5):E14. [Medline].

  48. Fridley J, Foroozan R, Sherman V, Brandt ML, Yoshor D. Bariatric surgery for the treatment of idiopathic intracranial hypertension. J Neurosurg. Jan 22 2010;[Medline].

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

  50. 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].

  51. 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].

  52. 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].

  53. 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].

  54. 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].

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

  56. 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].

  57. 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].

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

  59. 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].

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

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

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

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

  64. 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].

  65. 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].

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

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

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

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

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

  71. 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].

  72. 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].

  73. 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].

  74. Wilkes BN, Siatkowski RM. Progressive optic neuropathy in idiopathic intracranial hypertension after optic nerve sheath fenestration. J Neuroophthalmol. Dec 2009;29(4):281-3. [Medline].

 
Previous
Next
 
Left optic disc with moderate chronic papilledema in a patient with pseudotumor cerebri. Paton lines (arc-shaped retinal wrinkles concentric with disc margin) are seen along the temporal side of the inferior pole of the disc.
Right optic disc with postpapilledema optic atrophy in a patient with pseudotumor cerebri. Diffuse pallor of the disc and absence of small arterial vessels on the surface are noted, with very little disc elevation. The disc margin at the upper and lower poles and nasally is obscured by some residual edema in the nerve fiber layer and gliosis that often persists even after all the edema has resolved.
The most common early visual field defect in papilledema as the optic nerve develops optic atrophy is an inferior nasal defect as shown in the left eye field chart (left side of figure). The shaded area indicates the defective portion of the field. Note the sharp line of demarcation between defective lower nasal quadrant and normal upper nasal quadrant along the horizontal midline. This is characteristic of early papilledema optic atrophy and is called a nasal step or inferonasal step.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
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.