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PubMed1991

Accuracy of papilledema and pseudopapilledema detection: a multispecialty study.

BACKGROUND: Present trends in medical care suggest that primary care physicians will exert increasing control over patient access to medical specialty consultation and diagnostic testing. Therefore, it is important to determine whether primary care physicians can reliably identify papilledema. METHODS: A prospective study involving 429 physicians was undertaken to assess the accuracy of papilledema and pseudopapilledema detection by five groups of physicians, family practice physicians, neurologists, neuro-ophthalmologists, neurosurgeons, and ophthalmologists. RESULTS: Neuro-ophthalmologists and ophthalmologists did better than family physicians, neurologists, and neurosurgeons in identifying both papilledema and pseudopapilledema (P less than .05). Neuro-ophthalmologists more accurately identified pseudopapilledema than all other groups in the study (P less than .05). Family physicians did as well as, or better than, neurologists and neurosurgeons in identifying all classifications of acute and chronic papilledema defined in the study. Family physicians did not perform as well as the other four groups in differentiating pseudopapilledema from papilledema (P less than .05). CONCLUSIONS: Although the sensitivity of detecting papilledema was high (84.5%) for family physicians, the specificity was low (59.3%). Preliminary data indicate that family physicians with prior exposure to clinical ophthalmology in medical school did better than those who had not had training. It is possible that additional exposure to clinical ophthalmology during residency training might yield improved performance.

Clinical Competence↗

PubMed2001

Optical coherence tomography demonstrates subretinal macular edema from papilledema.

OBJECTIVE: To evaluate macular changes in eyes with papilledema from increased intracranial pressure using optical coherence tomography (OCT). METHODS: Fifty-five patients with papilledema seen during 1998 and 1999 were studied with OCT of the optic nerve and retinal nerve fiber layer. Nineteen of these also had OCT of the macula during periods of acute, subacute, or recurrent papilledema and were evaluated in detail for this report. RESULTS: Seven patients had OCT evidence of subretinal fluid involving the macula. All had some reduction in visual acuity. The subretinal fluid appeared to arise from the peripapillary region, and all showed some improvement in central vision as the fluid resolved. CONCLUSIONS: Subretinal fluid accumulations can cause decreased visual acuity in patients with papilledema. Optical coherence tomography can demonstrate subretinal fluid and can be used to follow the course of this important visual complication of papilledema.

Acute Disease↗

PubMed1977

Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema.

Tritiated leucine was injected intravitreously into the eyes of rhesus monkeys that had developed papilledema secondary to implantation of intracranial balloons. Autoradiographic studies of the optic nerve head showed that six hours after intravitreous injection of the isotope the fast component of axoplasmic transport accumulated in the regions of the lamina choroidalis and lamina scleralis. The slow component arrived at the optic nerve head two to four days after injection, and the swollen axons of the entire optic nerve head were filled with radioactive isotopes. Twelve days after injection of isotope, the axons in the optic nerve head were still diffusely labeled. Disturbance of axoplasmic transport was one of the primary events resulting in swelling of axons in papilledema. The pattern of axoplasmic disturbances in papilledema secondary to raised intracranial pressure was similar to that observed in papilledema secondary to ocular hypotony or increased intraocular pressure. Ocular hypotony, raised intracranial pressure, and increased intraocular pressure appear to share a final common pathway. All these conditions apparently converge into this final common pathway of disturbance of axoplasmic transport to give rise to papilledema.

Animals↗

PubMed2001

Unilateral papilledema caused by a fronto-temporo-parietal arachnoid cyst.

PURPOSE: To report a case of unilateral papilledema caused by an arachnoid cyst. METHODS: Interventional case report. RESULTS: A 36-year-old woman presented with unilateral papilledema in the left eye. Magnetic resonance imaging (MRI) of the brain demonstrated a large fronto-temporo-parietal arachnoid cyst in the left hemisphere. The papilledema resolved after placement of a cysto-peritoneal shunt that drained the cerebrospinal fluid directly from the arachnoid cyst into the peritoneum. CONCLUSION: Papilledema caused by increased intracranial pressure is usually bilateral; unilateral papilledema is possible under special anatomical circumstances.

Adult↗

PubMed2002

Resolution of papilledema after neurosurgical decompression for primary Chiari I malformation.

PURPOSE: To report a causal relationship between Chiari I malformation and its rare, but recognized manifestation of bilateral papilledema. DESIGN: Interventional case series. METHODS: Four adult female patients (mean age, 48, age range 25-59 years) with bilateral papilledema, signs and symptoms of increased intracranial pressure, and cranial magnetic resonance imaging (MRI) evidence of a Chiari I malformation ranging from 7 to 22 mm of tonsillar herniation underwent suboccipital decompression. RESULTS: In all four patients, suboccipital decompression was followed by resolution of bilateral papilledema and signs and symptoms of increased intracranial pressure. CONCLUSION: Patients with bilateral papilledema and presumed pseudotumor cerebri require a cranial MRI to determine if they have a Chiari I malformation, because patients with increased intracranial pressure and papilledema from a Chiari I malformation may benefit from suboccipital decompression.

Adult↗

PubMed1996

Insidious craniosynostosis and chronic papilledema in childhood.

PURPOSE: We studied a case of chronic papilledema in a 5-year-old child with visual loss who presented no obvious cosmetic abnormalities. METHODS: Neuroradiologic investigations were suggestive of craniosynostosis. The child underwent decompressive cranial surgery. Postoperatively, the papilledema totally regressed, and visual acuity recovered to 20/20 in both eyes. RESULTS: The chronic papilledema was confirmed to be related to harmonious oxycephaly. CONCLUSION: Insidious craniosynostosis is an unusual cause of chronic papilledema in childhood. The papilledema may be resolved and visual loss prevented by surgery.

Child, Preschool↗

PubMed1992

Unilateral and highly asymmetric papilledema in pseudotumor cerebri.

I compared six subjects with pseudotumor cerebri and unilateral or highly asymmetric papilledema with 20 such patients with bilateral papilledema. Patients with unilateral papilledema were significantly older than those with bilateral papilledema, but there were no significant differences between the two groups in disease duration, elevation of intracranial pressure, visual fields and acuity, and presence of headaches or transient visual obscurations. I hypothesize that, in patients with unilateral papilledema, one optic nerve is protected from pressure effects by optic nerve sheath anomalies or lamina cribrosa changes due to increased collagen and decreased elasticity with aging.

Adult↗

PubMed1992

Papilledema: clinical clues and differential diagnosis.

The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache, nausea, vomiting, diplopia, ataxia or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.

Diagnosis, Differential↗

PubMed1991

[Papilledema and dural fistula].

A retrospective analysis of three cases of papilledema was made, initially attributed to idiopathic raised intracranial pressure on the basis of the following data: symptoms and signs of raised intracranial pressure, no other neurological signs, normal electroencephalogram, normal computerised tomography, and normal cerebrospinal fluid. The discovery of a dural arteriovenous malformation was made only after a period over six months, by cerebral angiography. After a survey of medical data concerning the incidence of papilledema in dural fistulae, a description of the supposed pathogenic mechanisms of papilledema formation in this disease is proposed. Venous hypertension was found to be the main factor leading to papilledema. It could be in relation with obstruction of the involved venous sinus, and with the high level of blood flow of the dural arteriovenous malformation. It appeared that drainage with involvement of subarachnoid veins was the main characteristic for arteriovenous malformations to be directly responsible for papilledema. The possible lack or delay of suggestive signs such as intracranial bruit and the potential seriousness of the vital and visual prognosis led us to routinely carry out angiologic investigations comprising first doppler ultra-sound of the cervical vessels and secondly cerebral angiography, before diagnosing benign raised intracranial pressure.

Adult↗

PubMed1998

Quantitative evaluation of papilledema in pseudotumor cerebri.

PURPOSE: To determine the feasibility of adapting confocal scanning laser (CSL) tomography of the optic disc for quantitative evaluation of papilledema in pseudotumor cerebri (PTC). METHODS: Confocal scanning laser tomography of the optic disc was performed in 11 patients with diagnosed PTC and 12 visually normal control subjects of similar age. In five patients with active papilledema, CSL tomography was performed serially over several months. To quantify optic disc characteristics, surface topography was measured in 0.1-mm steps along the horizontal and vertical meridians and four oblique meridians. Best fit polynomial functions, describing surface topography along each meridian, were derived using linear regression analysis. RESULTS: Third-order polynomials provided excellent fits (significantly better than the second-order functions) to the surface topography for all meridians in the control subjects and patients with PTC. In control subjects and PTC patients an asymmetry in the slope of the optic disc contours was evident along the horizontal but not the vertical meridian. In patients with active papilledema a significant elevation of the center of the disc was accompanied by a change in overall surface topography. Each of the PTC patients followed up serially had a pronounced posterior deformation of the disc (i.e., a reduction in papilledema) that was initially apparent in the temporal meridian and did not proceed uniformly across all meridians. CONCLUSIONS: Confocal scanning laser tomography can quantify the magnitude and monitor the resolution of papilledema in PTC. Studies of optic nerve head topography may provide further insight into optic nerve compliance with elevated intracranial pressure.

Adult↗

PubMed1991

Idiopathic intracranial hypertension without papilledema.

We describe 10 patients with idiopathic intracranial hypertension who did not have papilledema. Idiopathic intracranial hypertension without papilledema, although rarely reported, may well be a clinically important headache syndrome. Historical and demographic features of patients with idiopathic intracranial hypertension without papilledema are similar to those of patients with papilledema. Obese women with chronic daily headache and symptoms of increased intracranial pressure, pulsatile tinnitus, history of head trauma or meningitis, an empty sella on imaging studies, or a headache that is unrelieved by standard therapy should have a diagnostic lumbar puncture. Findings from laboratory and neurologic investigations are normal in most patients with idiopathic intracranial hypertension without papilledema. Initial management should include removal of possible inciting agents, weight loss if applicable, and standard headache therapy. Lumbar puncture and diuretic therapy should precede a trial of corticosteroids. Surgery (lumboperitoneal or ventriculoperitoneal shunt or perhaps optic nerve sheath fenestration) may be indicated for prolonged incapacitating headache that is not responsive to medical management or lumbar puncture.

Adult↗

PubMed1996

High-resolution magnetic resonance imaging of the intraorbital optic nerve and subarachnoid space in patients with papilledema and optic atrophy.

OBJECTIVE: To evaluate the orbital portion of the optic nerve and the subarachnoid space using fast spin-echo magnetic resonance imaging in normal subjects and in patients with papilledema or optic atrophy. DESIGN: Measurements of the optic nerve complex on coronal images were made using high-resolution magnetic resonance imaging with fast spin-echo sequences. PATIENTS: Twenty-one patients, including 5 patients with papilledema due to congenital hydrocephalus, intracranial tumors, or meningitis, as well as 16 patients with optic atrophy, were studied. Sixteen healthy volunteers served as controls. MAIN OUTCOME MEASURES: The longitudinal diameter of the optic nerve, the longitudinal outer diameter of the subarachnoid space, the diameter ratio, and the area of the subarachnoid space were determined. RESULTS: In normal subjects, the ring-shaped area of high signal intensity that represented the subarachnoid space was widest behind the globe, then narrowed toward the orbital apex. In patients with papilledema, the area of the subarachnoid space was markedly dilated, the optic nerve was compressed, and the nerve sheath was widened, resulting in a small diameter ratio compared with that of controls. Patients with pallor of the temporal aspect of the optic disc appeared to exhibit dilation of the subarachnoid space; the size of the optic nerve was decreased more than that of the nerve sheath, resulting in a small diameter ratio compared with controls. Patients with complete pallor of the disc, however, exhibited hyperintense optic nerve complexes without a ring-shaped appearance toward the orbital apex. CONCLUSION: Fast spin-echo magnetic resonance imaging appears useful for objectively evaluating the optic nerve and surrounding subarachnoid space in patients with papilledema and optic atrophy.

Adolescent↗

PubMed1976

Experimental papilledema produced by cyclocryotherapy.

Cyclocryotherapy was a reliable method of producing prolonged decreased intraocular pressure and papilledema in the rhesus monkey. Histologic changes in papilledema caused by decreased pressure were indistinguishable from those in papilledema from increased intracranial pressure. Electron microscopic observations in papilledema after cyclocryotherapy suggested that the principal morphologic alteration in the optic disk is axonal swelling. Additionally, many mitochondria accumulated in some swollen axons. These changes, observed at the ultrastructural level, suggest that alternations of axoplasmic transport may play a significant role in the pathogenesis of swelling of the disk.

Animals↗

PubMed1988

Enlargement of the blind spot caused by papilledema.

Blind spot enlargement in papilledema has been attributed to either mechanical disruption of the integrity of the peripapillary percipient elements by the swollen optic disk or to the Stiles-Crawford effect. We investigated the possibility that blind spot enlargement in papilledema is caused, at least in part, by a refractive scotoma due to peripapillary hyperopia. We reduced the enlarged blind spot in a patient with focal peripapillary hyperopia, without papilledema, to near normal size by using progressively stronger plus lenses. Similarly, with the addition of plus sphere, we reduced the size of the blind spot in five of six patients with papilledema, but in none of our normal subjects.

Adult↗

PubMedDate not supplied

Optic nerve axoplasm and papilledema.

A detailed review of optic nerve axoplasm is presented. A number of hypotheses have been postulated for the pathogenesis of papilledema associated with increased intracranial pressure. These hypotheses, mechanical and nonmechanical, are critically evaluated in relation to five essential features of papilledema. Theories, as well as clinical and experimental studies, of axonal transport are reviewed, and a new hypothesis is proposed: Papilledema is primarily a mechanical, nonvascular phenomenon in which an excess amount of extracellular fluid is present in the prelaminar region of the optic disc and the accumulation of that fluid results from the leakage of axoplasm from optic nerve fibers which are compressed posterior to the lamina cribrosa of the optic disc. The authors believe that this is the only existing hypothesis consistent with all the known facts about papilledema. Discussions by Drs. J. Terry Ernest, Thomas R. Hedges, and S. S. Hayreh follow the review.

Animals↗

PubMed2006

Dengue fever with papilledema: a case of dengue-3 virus infection in central nervous system.

BACKGROUND AND OBJECTIVES: Neurological manifestations of dengue fever are rarely reported during acute illness and clinical presentation commonly observed is of acute encephalitis or one of the post-infectious immune mediated manifestations. We describe a case of dengue fever having mild encephalopathy and papilledema at presentation. CASE REPORT: Twenty-year-old female presented with fever, headache and vomiting. On examination she did not have classical signs of dengue fever and was found to have bilateral papilledema on fundus examination. Detailed work-up did not reveal any other cause of papilledema. Diagnosis of dengue fever was established by blood IgM antibody test on day 7 of illness. Retrospective analysis of CSF (drawn on day 5 of illness) by RT-PCR assay showed a characteristic band of dengue-3 virus. Papilledema was transient and subsided following symptomatic treatment. The patient recovered from acute illness and follow-up was unremarkable. CONCLUSION: Especially in dengue endemic areas, in the patients having acute febrile illness with subtle signs and symptoms suggestive of CNS involvement, dengue virus infection should also be ruled out early in the clinical course.

Adult↗

PubMed2000

Bilateral papilledema from a massive intracranial epidermoid cyst.

PURPOSE: To report an unusual case of bilateral papilledema from a large intracranial epidermoid cyst. METHODS: Case report. RESULTS: A 26-year-old man presented with visual loss, bilateral papilledema, and only a few neurological symptoms. Magnetic resonance imaging disclosed such a large lesion that his right cerebral hemisphere was compressed to one half its normal size. Histopathologic examination of the completely removed tumor revealed an epidermoid cyst. CONCLUSION: This unique case involved a patient with bilateral papilledema caused by a huge intracranial epidermoid cyst. Epidermoid tumors should be considered in the differential diagnosis of papilledema.

Adult↗

PubMed2003

Anemia and papilledema.

PURPOSE: To elucidate the relationship between anemia and raised intracranial pressure (ICP). DESIGN: Interventional case series. METHODS: Retrospective case series and review of the literature. Only patients with documented papilledema, neuroimaging ruling out a space-occupying lesion, and anemia were included. RESULTS: Five women with confirmed idiopathic intracranial hypertension (IIH) (normal brain magnetic resonance imaging, normal cerebrospinal fluid, elevated intracranial pressure), and one man with presumed IIH (normal head computed tomography [CT], no lumbar puncture) were evaluated. All had bilateral papilledema associated with peripapillary hemorrhages. Two had retinal cotton-wool spots (CWS), and two had preretinal hemorrhages. All had severe iron deficiency anemia, which was discovered at the time of their ocular complaints in five of them. Their symptoms and signs improved dramatically after treatment of the anemia. We found 30 well-documented cases in the English and French literature. Among those, 13 were excluded from our analyses (11 had confounding disorders, and two had cerebral venous thrombosis). In the remaining 17 cases, isolated raised ICP associated with anemia was the most likely diagnosis, although in none of these cases was cerebral venous thrombosis excluded. CONCLUSIONS: Anemia may play a role in the occurrence of raised ICP and papilledema. Although only a few cases in the literature support this association, it may be more common than previously thought. Because most patients are not known to be anemic when papilledema is discovered, we suggest that a complete blood count be obtained in patients with IIH, especially in the absence of known associated factors such as obesity or medications or when treatment aimed at lowering ICP fails to improve the patient's symptoms. The underlying mechanisms remain unknown, but cerebral venous thrombosis should be carefully excluded.

Adult↗