Pseudotumor Cerebri 

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

Background

Pseudotumor cerebri, also known as idiopathic intracranial hypertension (IIH) is a disorder of unknown etiology. It affects predominantly obese women of childbearing age.[1] 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.[1]

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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.[2] 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.[3] 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.[4]

More recently, Bateman et al proposed a mathematical model to account for collapsible dural venous sinuses in the pathogenesis of IIH since this has been shown to be an important factor in many cases. The model includes arterial inflow volume, venous outflow resistance, and CSF pressure. They used combined flow rates in the 2 carotid arteries and the basilar artery as measured by MRI in individual patients as the measure of inflow blood volume and measured values from the literature for the pressure gradient from superior sagittal sinus to jugular bulb and venous outflow resistance.

The model predicts 2 CSF pressure equilibrium points for the collapsible dural sinus cases with greater than 40% stenosis (usually of the transverse sinus)—one point in the normal range and the other in the range encountered in IIH patients. This accounts for the prolonged remission of symptoms that follows removal of CSF at lumbar puncture, presumably because this relieves the venous sinus stenosis. Without dural sinus collapse and stenosis, as is encountered in some patients with IIH, the model requires increased arterial inflow volume to account for the elevated intracranial pressure. Interestingly, the model did not require increased resistance to outflow of CSF across the arachnoid villi.[5]

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Epidemiology

Frequency

United States

  • Annual incidence of pseudotumor cerebri in Iowa and Louisiana[6]
    • 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 1990[7]
    • 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 years[8]
    • 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[9, 10]
    • 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 1994[11] , 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 Iowa[6] ).
    • 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.[1]
  • Specific numbers are available from the epidemiological studies.
    • Durcan et al[6] - Female-to-male ratio 8:1
    • Radhakrishnan[7] - Female-to-male ratio 8:1 (N = 9)
    • Radhakrishnan[7] - 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.

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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.

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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.
 
 
 
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