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At least 19 recordsLinked to original sources
PubMed1976

"Twin peaks" papilledema: the appearance of papilledema with optic tract atrophy.

A woman with a right middle fossa meningioma causing right optic tract atrophy and papilledema had distinctive funduscopic changes. The ipsilateral eye showed temporal disc pallor and nasal edema. The contralateral disc showed edema of the upper and lower poles which was separated by a horizontal band of optic atrophy. The fluorescein angiographic changes clearly illustrate this pattern. Apart from its theoretical interest this appearance of papilledema and atrophy provides definite localizing information.

Adult↗
PubMed1998

Asymmetric papilledema in idiopathic intracranial hypertension: prospective interocular comparison of sensory visual function.

PURPOSE: Visual loss is the main morbidity of idiopathic intracranial hypertension (IIH). The relationship between papilledema grade and visual loss is unclear. The goal of this study was to determine whether there is a relationship between papilledema grade and visual loss. METHODS: Fundus photographs of 478 patients with IIH were reviewed, and their degree of papilledema was graded using Frisén's scheme. We identified 46 patients (10%) with IIH and highly asymmetric papilledema, as defined by an interocular difference of two or more grades. Nine of these patients with active asymmetry agreed to return for a series of visual tests. They underwent three visual field tests-Humphrey visual field analyzer 24-2, motion perimetry, and ring perimetry. The perimetry outcome measures were mean deviation, foveal threshold, and means for eccentric zones (3 degrees, 9 degrees, 15 degrees, and 21 degrees). The patients participated also in visual acuity, Farnsworth-Munsell 100-hue, Pelli-Robson contrast sensitivity, and foveal flicker fusion testing. Their relative afferent pupillary defect was graded using neutral density filters. RESULTS: The intereye comparisons showed vision to be worse in the eye with the high-grade papilledema for all outcome measures. The magnitude of the loss with the perimetry tests increased with eccentricity. The measures of central visual function, although in the normal range, were relatively depressed in the eye with high-grade papilledema. CONCLUSIONS: Visual loss in patients with asymmetric papilledema caused by IIH was most pronounced in the eye with the higher grade of papilledema. Foveal visual functions, although they remained in the normal range, were also decreased in patients with high-grade papilledema. In patients with high-grade papilledema, visual loss appeared to affect the entire visual field, and the peripheral field showed the most deficit. Our findings showed that high-grade papilledema was associated with visual dysfunction in patients with IIH.

Adult↗
PubMed1996

The effectiveness of papilledema as an indicator of raised intracranial pressure in children with craniosynostosis.

Craniosynostosis management partially depends on the detection and treatment of elevated intracranial pressure (ICP). Examination for papilledema is considered to be the most reliable screening method for identifying raised ICP, but its effectiveness has not been defined. One hundred and twenty-two children with craniosynostosis who underwent funduscopic examinations and then Camino ICP monitoring were studied. All eye examinations were performed by an ophthalmologist after pharmacological pupillary dilation. Fifteen patients (12%) had papilledema. Subsequent ICP monitoring showed that the median ICP was 12.7 mm Hg, with 41 patients (34%) having elevated ICPs (> 15 mm Hg). Those with papilledema had higher ICPs (17.5 +/- 3.2 versus 12.7 +/- 5.5 mm Hg), were older (5.9 +/- 4.7 versus 1.9 +/- 2.6 years), and were more likely to have craniofacial syndromes (73 versus 41%) than those without papilledema (P < 0.05). Patients with both elevated ICPs and papilledema were older (5.9 +/- 4.7 versus 1.6 +/- 1.4 years) and more likely to have multiple-suture synostosis (92 versus 61%) than those with elevated ICPs and no papilledema (P < 0.05). The presence of papilledema was a specific (98%) indicator of raised ICP, but its sensitivity was age-dependent. It was 100% sensitive in children older than 8 years, but it indicated elevated ICP in only 22% of younger patients. These results suggest that ICP monitoring to document elevated ICP is unnecessary in children older than 8 years who have detailed ophthalmological examinations. In the younger child, the presence of papilledema reliably indicates elevated ICP but its absence does not rule out elevated ICP; formal ICP measurement has a greater role in detecting elevated ICP in these patients.

Adolescent↗
PubMed1985

Papilledema after acute head injury.

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.

Acute Disease↗
PubMedDate not supplied

Papilledema: its recognition and relation to increased intracranial pressure.

This has been a review on the subject of papilledema from a clinical, pathologic and experimental point of view. Terminology has been clarified. The term papilledema should be reserved for those patients with optic disc edema caused by increased intracranial pressure. The forms of papilledema which are identifiable are: 1. Early (incipient) form which develops into an acute type and then into a fully developed form; 2. Fully developed form, characterized by obscured disc margins, hemorrhages and ischemic infarcts; 3. Chronic papilledema which may persist (the name "vintage" papilledema may be applied to those patients affected in varying degrees up to several years); and 4. Chronic atrophic papilledema which, as the name implies, illustrates a form we do not see as frequently as in years past. It is the type we are now trying to prevent and in this effort we are fortunately achieveing some success. The importance of the intracranial expanding lesions and the influence of the rapidity of elevation and duration of intracranial hypertension on the optic nerve has been considered, based on the clinical and experimental work to date. The pathogenesis of papilledema has been considered in some detail. A unified whole is difficult to arrive at in such a complex situation. Recent advances in our understanding of anatomic, mechanical (sheath space pressure), tissue and vascular pressure as related to increased intracranial pressure have been described. A hydrostatic mechanism brings these factors together in a reasonable, although admittedly not completely proven concept of a mechanism for the development of papilledema. Clarification of terminology and clinical appearance of the various forms of disc edema related to intracranial pressure are of practical value in the diagnosis and management of each patient we see with this clinical entity.

Acute Disease↗
PubMed2002

Long-term evolution of papilledema in idiopathic intracranial hypertension: observations concerning two cases.

Chronic headaches, associated with papilledema and pulsatile tinnitus without any neuroradiologic, cytobiochemical or cerebrospinal fluid abnormalities are suggestive of idiopathic intracranial hypertension (IIH). However the absence of the papilledema does not rule out this diagnosis. The reason why some patients do not develop papilledema in IIH is ignored, however there are some hypotheses concerning the structure of the optical nerve. In this study we described two female patients that presented diagnosis of IIH with papilledema, with subsequent resolution of papilledema without the due resolution of intracranial hypertension. The long-term behavior of the optic nerve (ON) facing an increased intracranial pressure was evaluated through repeated measurements of the intracranial pressure. We concluded that the ON submitted to high intracranial pressure for a certain length of time can adapt itself with subsequent disappearance of the papilledema. The presence or not of papilledema in IIH can be related to the period in which the diagnosis is accomplished.

Adult↗
PubMed1989

Pseudodrusen of the optic disc. Papilledema simulating buried drusen of the optic nerve head.

The distinction between true papilledema and pseudopapilledema rests on characteristics of the optic disc when examined ophthalmoscopically. Buried disc drusen frequently simulate papilledema and often result in misdirected diagnostic maneuvers in search of a cause for presumed intracranial hypertension. When an elevated optic disc exhibits an irregular, "lumpy, bumpy" border, a diagnosis of buried drusen of the optic nerve is usually made. We report a case with papilledema secondary to increased intracranial pressure in which the margins of the swollen optic disc presented this lumpy, bumpy border characteristic of buried drusen. The lumpy character of the disc border disappeared with resolution of the papilledema, and ultrasonography demonstrated the absence of any buried drusen. Other characteristics of papilledema, including extension of the disc swelling into the peripapillary nerve fiber layer, telangiectasia of the superficial vessels of the optic disc, and obscuration of the retinal vessels as they crossed the margins of the optic disc, provided strong evidence of true papilledema and remain the most reliable findings allowing a distinction between true papilledema and pseudopapilledema.

Adult↗
PubMed2002

Severe papilledema identified 3 weeks after head injury.

A 62-year-old woman presented with rapidly developed visual disturbance without associated headache or nausea 3 weeks after head injury. Ophthalmologic examination revealed bilateral severe papilledema with retinal hemorrhage, and intracranial pressure (ICP) was 17.5 cmH2O estimated by lumbar puncture. Computed tomography and magnetic resonance (MR) imaging showed no evidence of increased ICP, except dilation of the subarachnoid space around the optic nerves with distortion of the nerves. Her visual acuity remarkably improved after steroid and glycerol treatment, and optic fundus examination revealed bilateral clear optic papillae without atrophic changes. Follow-up MR imaging demonstrated that the bilateral optic nerves had regained the normal appearance. These results indicate that the bilateral papilledema was caused by increased subarachnoid pressure around the bilateral optic nerves. We conclude that papilledema can occur with a mildly increased ICP and trapped subarachnoid cerebrospinal fluid around the optic nerves, and papilledema may progress after the ICP is normalized. Papilledema is a warning sign for increased ICP, associated with future visual loss from retinal hemorrhage. Therefore, repeated funduscopic investigation is necessary for the early diagnosis and treatment of papilledema.

Aged↗
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↗