Idiopathic Intracranial Hypertension Follow-up

  • Author: Mark S Gans, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 5, 2012
 

Further Outpatient Care

  • The frequency of the follow-up visits is determined by a number of factors, to include the following:
    • Initial visual function of the patient
    • Underlying disease causing increased intracranial pressure
    • Perceived compliance of the patient with respect to medical therapy
  • Once the initial diagnosis has been established, investigations have been performed, and the therapy has been initiated, the patient can be observed every 3-4 weeks. However, patients who present with a significant visual function deficit or marked papilledema should be monitored daily for a week until they demonstrate some improvement and subsequent stability in their visual function. The clinician should be prepared to titrate the patient's treatment to the status of the visual function and should not hesitate to refer the patient for surgical treatment (optic nerve sheath fenestration or a neurosurgical shunting procedure) in the absence of stabilization of the visual function.
  • During follow-up visits, the best-corrected visual acuity for distant and near vision, color vision (using pseudoisochromatic plates), static perimetry, and optic nerve appearance (including the status of spontaneous venous pulsations) should be recorded. Patients who do not perform well on static perimetry testing may be better followed with kinetic perimetry testing. The spontaneous pulsation of large retinal veins generally indicates a normal intracranial pressure. If the patient continues to remark on the persistence of a significant headache despite the presence of spontaneous venous pulsations, evaluating a source other than idiopathic intracranial hypertension for the headache is important.
  • When a patient appears to have stabilized with respect to visual function and treatment, follow-up visits can extend to once every 2-4 months.
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Complications

  • The main complication of this disorder is progressive optic neuropathy. Despite timely treatment, some patients develop an optic neuropathy related to the optic nerve edema.
  • Generally, this dysfunction presents in a progressive fashion with constriction of the peripheral visual field; worsening nerve fiber bundle visual field defects; a decrease of color vision; and, in end-stage disease, a drop in the central visual function.
  • Occasionally, a patient may develop an acute loss of vision due to ischemic optic neuropathy or a retinal vascular occlusion associated with the papilledema.
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Prognosis

  • The visual prognosis in timely and appropriately treated patients can be encouraging in cases of idiopathic intracranial hypertension.
  • Unfortunately, the incidence of visual loss has been reported to be significant in some studies of this disease. Corbett et al documented visual dysfunction in close to one half of patients with idiopathic intracranial hypertension.[9]
  • Since the increase in intracranial pressure tends to be chronic in nature, all patients with this disorder must be monitored for years after presentation. If necessary, medical treatment should be continued on a long-term basis.
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Patient Education

  • Informing patients who are overweight that weight control is a long-term factor in idiopathic intracranial hypertension is important. Asking patients about their weight loss at the beginning of each visit reinforces this concept. In addition, it may be worthwhile to mention that the loss of as little as 6% of body weight may lead to the termination of this disorder and also may significantly diminish the risk of its recurrence.
  • Although the disease may appear to be self-limiting, it is considered to be a chronic disorder; therefore, once the medication is tapered off, patients should be alerted to return to an ophthalmologist if symptoms of increased intracranial pressure recur.
  • If a particular agent, such as tetracycline, is associated with the rise in intracranial pressure, the patient should be educated to avoid this agent.
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Contributor Information and Disclosures
Author

Mark S Gans, MD  Associate Professor, Director of Neuro-Ophthalmology, Department of Ophthalmology, McGill University; Clinical Director, Department of Ophthalmology, Adult Sites, McGill University Hospital Center, Interim Chairman of the Department of Ophthalmology, McGill University

Mark S Gans, MD is a member of the following medical societies: American Academy of Ophthalmology, Canadian Medical Association, Canadian Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Edsel Ing, MD, FRCSC  Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada

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

Brian R Younge, MD  Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

References

  1. Friedman DI, Jacobson DM. Idiopathic intracranial hypertension. J Neuroophthalmol. Jun 2004;24(2):138-45. [Medline].

  2. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology. Nov 26 2002;59(10):1492-5. [Medline].

  3. Miller NR, Newman NJ. Pseudotumor cerebri (benign intracranial hypertension). In: Walsh and Hoyt's Clinical Neuro-Ophthalmology. Vol 1. 5th ed. 1999:523-38.

  4. 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].

  5. Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri). Curr Neurol Neurosci Rep. Mar 2008;8(2):87-93. [Medline].

  6. Corbett JJ. The first Jacobson Lecture. Familial idiopathic intracranial hypertension. J Neuroophthalmol. Dec 2008;28(4):337-47. [Medline].

  7. Daniels AB, Liu GT, Volpe NJ, et al. Profiles of obesity, weight gain, and quality of life in idiopathic intracranial hypertension (pseudotumor cerebri). Am J Ophthalmol. Apr 2007;143(4):635-41. [Medline].

  8. Digre KB, Nakamoto BK, Warner JE, Langeberg WJ, Baggaley SK, Katz BJ. A comparison of idiopathic intracranial hypertension with and without papilledema. Headache. Feb 2009;49(2):185-93. [Medline].

  9. 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. Aug 1982;39(8):461-74. [Medline].

  10. Ney JJ, Volpe NJ, Liu GT, Balcer LJ, Moster ML, Galetta SL. Functional Visual Loss in Idiopathic Intracranial Hypertension. Ophthalmology. Jul 28 2009;[Medline].

  11. Bruce BB, Kedar S, Van Stavern GP, et al. Idiopathic intracranial hypertension in men. Neurology. Jan 27 2009;72(4):304-9. [Medline].

  12. Jiraskova N, Rozsival P. Idiopathic intracranial hypertension in pediatric patients. Clin Ophthalmol. Dec 2008;2(4):723-6. [Medline].

  13. Gonzalez-Hernandez A, Fabre-Pi O, Diaz-Nicolas S, Lopez-Fernandez JC, Lopez-Veloso C, Jimenez-Mateos A. [Headache in idiopathic intracranial hypertension]. Rev Neurol. Jul 1-15 2009;49(1):17-20. [Medline].

  14. Mollan SP, Ball AK, Sinclair AJ, et al. Idiopathic intracranial hypertension associated with iron deficiency anaemia: a lesson for management. Eur Neurol. 2009;62(2):105-8. [Medline].

  15. Lin A, Foroozan R, Danesh-Meyer HV, De Salvo G, Savino PJ, Sergott RC. Occurrence of cerebral venous sinus thrombosis in patients with presumed idiopathic intracranial hypertension. Ophthalmology. Dec 2006;113(12):2281-4. [Medline].

  16. Johnson LN, Krohel GB, Madsen RW, March GA Jr. The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumor cerebri). Ophthalmology. Dec 1998;105(12):2313-7. [Medline].

  17. Brazis PW. Clinical review: the surgical treatment of idiopathic pseudotumour cerebri (idiopathic intracranial hypertension). Cephalalgia. Dec 2008;28(12):1361-73. [Medline].

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

  19. Sinclair AJ, Kuruvath S, Sen D, et al. Is cerebrospinal fluid shunting in idiopathic intracranial hypertension worthwhile? A 10-year review. Cephalalgia. Dec 2011;31(16):1627-33. [Medline].

 
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