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.

The prognosis for vision in most patients with pseudotumor cerebri is excellent; however, visual loss, which is the only serious complication, may occur either early or late in the course of the disease. A group of 57 patients was followed up five to 41 years with visual fields, visual acuity, and fundus photographs. Blinding visual loss or severe visual impairment in one or both eyes occurred in 14 patients, and in seven patients, this occurred months to years after the initial symptoms. Systemic hypertension was a significant risk factor for visual loss in patients with pseudotumor cerebri, and blindness occurred in eight of 13 patients who were hypertensive. Despite suggestions that blind spot measurement is useful for following up patients with this condition, we believe that sequential quantitative perimetry gives more complete information and is essential to rational decision making in the treatment of pseudotumor cerebri.

[1]  J. Antel,et al.  Bilateral juxtapapillary subretinal neovascularization associated with pseudotumor cerebri. , 1981, American journal of ophthalmology.

[2]  R. Ruff,et al.  A blind spot tester. , 1981, Journal of neurology, neurosurgery, and psychiatry.

[3]  Rush Ja.  Pseudotumor cerebri: clinical profile and visual outcome in 63 patients. , 1980, Mayo Clinic proceedings.

[4]  R. Burde,et al.  Disappearing opticociliary shunt vessels and pseudotumor cerebri. , 1980, American journal of ophthalmology.

[5]  M. Sanders,et al.  Acquired optociliary shunt vessels in papilloedema. , 1980, The British journal of ophthalmology.

[6]  M. Sanders,et al.  Peripheral retinal haemorrhages with papilloedema. , 1980, The British journal of ophthalmology.

[7]  J. Loewenstein,et al.  Ischemic optic neuropathy in chronic papilledema. , 1980, Archives of ophthalmology.

[8]  C. Ellenberger,et al.  Ischemic optic neuropathy as a possible early complication of vascular hypertension. , 1979, American journal of ophthalmology.

[9]  B. Troost,et al.  Sudden monocular visual loss in pseudotumor cerebri. , 1979, Archives of neurology.

[10]  H. V. Crevel,et al.  Benign intracranial hypertension A retrospective and follow-up study , 1979, Journal of the Neurological Sciences.

[11]  A. H. Bunt,et al.  Axoplasmic transport in ocular hypotony and papilledema in the monkey. , 1977, Archives of ophthalmology.

[12]  M. Tso,et al.  Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema. , 1977, Archives of ophthalmology.

[13]  H. Quigley,et al.  The dynamics and location of axonal transport blockade by acute intraocular pressure elevation in primate optic nerve. , 1976, Investigative ophthalmology.

[14]  A Jefferson,et al.  Treatment of benign intracranial hypertension by dehydrating agents with particular reference to the measurement of the blind spot area as a means of recording improvement. , 1976, Journal of neurology, neurosurgery, and psychiatry.

[15]  R. Penn,et al.  Computed tomography in the diagnosis of pseudotumor cerebri. , 1976, Radiology.

[16]  K. Foley,et al.  Does pseudotumor cerebri cause the empty sella syndrome? , 1975, Neurology.

[17]  J. G. Wood,et al.  Visual improvement after chiasmapexy for primary empty sella turcica. , 1975, Surgical neurology.

[18]  A. Paterson,et al.  Benign intracranial hypertension. I. Diagnosis and prognosis. , 1974, Brain : a journal of neurology.

[19]  O Gilland,et al.  Normal cerebrospinal-fluid pressure. , 1974, The New England journal of medicine.

[20]  M. Sanders,et al.  Choroidal folds in association with papilloedema. , 1973, The British journal of ophthalmology.

[21]  J. Stears,et al.  Chiasmapexy for the correction of traction on the optic nerves and chiasm associated with their descent into an empty sella turcica. Case report. , 1971, Journal of neurosurgery.

[22]  D. N. Grant,et al.  Benign intracranial hypertension , 1971, Archives of disease in childhood.

[23]  H. J. Svien,et al.  Long-term follow-up on patients with diagnosis of pseudotumor cerebri. , 1966, Journal of neurosurgery.

[24]  B. Schwartz,et al.  Effects of long-term systemic steroids on ocular pressure and tonographic values. , 1962, Archives of ophthalmology.

[25]  N. Schlezinger,et al.  Inferior Nasal Quadrantanopsia in Pseudotumor Cerebri , 1959 .

[26]  J. Foley.  Benign forms of intracranial hypertension; toxic and otitic hydrocephalus. , 1955, Brain : a journal of neurology.

[27]  S. Ethelberg,et al.  Obscurations and further time-related paroxysmal disorders in intracranial tumors; syndrome of initial herniation of parts of the brain through the tentorial incisure. , 1952, A.M.A. archives of neurology and psychiatry.

[28]  H A Quigley,et al.  Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. , 1981, Archives of ophthalmology.

[29]  R. Jamison,et al.  Subretinal neovascularization and papilledema associated with pseudotumor cerebri. , 1978, American journal of ophthalmology.

[30]  A. H. Bunt,et al.  Radioautographic and cytochemical ultrastructural studies of axoplasmic transport in the monkey optic nerve head. , 1978, Investigative ophthalmology & visual science.

[31]  P. J. Savino,et al.  Pseudopapilledema versus Papilledema , 1977, International ophthalmology clinics.

[32]  M. Aminoff,et al.  "Benign" intracranial hypertension. A survey of the clinical and radiological features, and long-term prognosis. , 1974, Brain : a journal of neurology.

[33]  G. Bonamour.  La papille optique , 1968 .

[34]  B. Schwartz.  The response of ocular pressure to corticosteroids. , 1966, International ophthalmology clinics.