History of Present Illness: This patient is a 29-year-old white female who noticed that her vision had been getting progressively worse in the right eye (OD) over the past two weeks. Past Ocular History: She had a similar episode four years prior to the current episode involving the left eye (OS). Medical History: Three miscarriages at the end of the first trimester, otherwise unremarkable.
OS—clear media, pale optic nerve, normal cup-to-disc ratio with peripapillary atrophy, normal macula, normal vessels, small chorioretinal scar in the far inferior periphery.
A presumptive diagnosis of neuroretinitis was made based on the patient's clinical appearance.
At here next appointment (one month later) she felt that her vision had improved to some extent in the right eye. Laboratory work revealed negative testing for syphilis (RPR), Bartonella Henselae, and Lyme. In contrast to the above stated clinical course, there exists a subset of patients who suffer repeated attacks of neuroretinitis involving the same or opposite eye. To our knowledge, there has only been one case series reported in the literature of idiopathic recurrent neuroretinitis and potential treatment options.
The disc edema caused by group 4 hypertension and that caused by increasing intracranial pressure appear essentially the same. A small group of patients with papilledema have preretinal hemorrhages that may be located in front of the disc or the macula (Fig. Intraocular hemorrhages secondary to subarachnoid hemorrhage occur in about 20% of patients. Mechanisms for the production of fundus and optic nerve sheath hemorrhages have been put forward by Ballantyne, Walsh and I ledges, and Muller and Deck. Subhyaloid hemorrhage may occur from neovascularization of the retina, as in diabetes, or from the neovascularization following a central retinal vein occlusion. The predominant picture in central retinal vein occlusion (Plate 2.IID) is one of blood, not edema or exudate. The decrease in visual acuity associated with central retinal vein occlusion is usually marked and rapid in onset. The diseases to be considered in determining the cause of central retinal vein occlusion are glaucoma, diabetes, dysproteinemias, multiple myeloma, and polycythemia vera.
These disorders are discussed together because of the sign they have in common Roth's spots (hemorrhages with white centers) (Plate 2.IC). A useful diagnostic test for evaluating papillitis with good visual acuity is the afferent pupillary defect, which indicates unilateral optic nerve disease.
Cells in the vitreous humor in front of the dime are an inconstant sign of papillitis or a relrobulbar optic neuritis.
Infiltration of the optic nerve head may give the appearance of papilledema on casual inspection. The four different manifestations of optic nerve involvement in sarcoid are optic atrophy, optic neuritis, optic nerve granuloma invasion of the nerve, and papilledema. The papilledema may occur secondary to infiltration of the perioptic meninges or as papillitis.
Reticulum sarcoma usually presents as a uveitis associated with subretinal and choroidal infiltrates and, occasionally, with disc hyperemia mimicking early papilledema.
Orbital and optic nerve tumors can cause disc edema through obstruction of ocular venous drainage.
Thyroid disease may cause unilateral loss of vision, exophthalmos, disc edema, and horizontal striae in the macular area.
Intracranial tumors, particularly those along the sphenoid ridge, can cause changes that are more marked in one eye than in the other. Longstanding increased intracranial pressure from any cause and tumor of the chiasm both bring about a bilateral decrease in acuity.
The association of a spinal cord tumor and increased intracranial pressure is well known but occurs uncommonly.
Brain abscess usually causes focal neurologic deficit, but occasionally it produces papilledema. A focal chorioretinitis next to the disc may be hard to see because of overlying inflammatory exudates. Posterior scleritis, usually referred to as brawny scleritis, causes retinal edema with horizontal striae in the macula as well as low-grade disc edema.
Cataract operation, even when it is uncomplicated and when the depth of the anterior chamber is normal, may be associated with a low intraocular pressure—in the range of 2 to 4 mm. The physician should strongly suspect temporal arteritis whenever the blood sedimentation rate is elevated. The cause of this condition is considered to be small ciliary vessel occlusive disease, and the condition is not favorably affected by anticoagulant or steroid therapy.
The many causes of intracranial hypertension all have serious consequences for the visual system. Increased intracranial pressure results from only a limited combination of factors: an increase in cerebral mass, an increase in vascular volume, or an increase in fluid in the subarachnoid space. The disease initially called serous meningitis by Quicke and now referred to as idiopathic intracranial hypertension has many different associations with a varied group of disease processes that do not appear to have anything in common.
The association of pseudotumor cerebri with vitamin A toxicity is not usually seen in adults. Hydrocephalus and increased intracranial pressure have also occurred in vitamin A–deficient babies in association with other neurologic signs such as increased reflexes and a bulging fontanel.
The usual criteria for establishing the diagnosis of pseudotumor cerebri are signs of increased intracranial pressure confirmed by lumbar puncture. The diagnosis of pseudotumor cerebri usually is suggested by a finding of papilledema corroborated by increased spinal fluid pressure on a spinal tap. The situation of increased intracranial pressure without papilledema is particularly important in judging when the course of idiopathic intracranial hypertension is over. Pseudotumor that occurs in the young pediatric group differs from cases we see in teenagers and older persons. Many patients with idiopathic intracranial hypertension have mild symptoms and do not require treatment. The use of carbonic anhydrase inhibitors such as acetazolamide decreases the production of cerebral spinal fluid just as they reduce aqueous production in the eye. Since Diamox belongs to the sulfonamide family, agranulocytopenia can occur, although rarely.
If the disease process does not abate and the medical treatment is not effective in stopping visual loss, then surgical intervention must be considered.
The surgical procedure is fairly standard, with some small individual variations that each surgeon has learned from experience.
There is no preoperative pupil dilatation, since intraoperative monitoring of pupil function is vital for surgical safety.
The patient should be relatively quiet for 24 hours to reduce chances of bleeding in the orbit or sheath, which can compromise optic nerve function and or the surgical result.
Among younger patients, carotid cavernous sinus fistula is more often seen in men and after trauma.
Peripheral uveitis or pars planitis may cause a vitreitis that, in turn, causes disc edema and macular edema.
In radical neck dissection, a procedure for extensive carcinoma, the possibility that a particular dissection is incomplete with later metastasis to the brain is of real concern. The theory behind ligation of the internal jugular vein or in removing it totally in a radical neck dissection is that the rich collateral venous system draining the head will compensate.
With such patients, the usual studies—skull roentgenograms, brain scan, CT, MRI, neurologic examination, complete ophthalmologic examination including field examination—must be performed.
Papilledema can also occur with other causes of respiratory compromise such as the Pickwickian syndrome. Unilateral inferior disc edema in a diabetic patient with superior altitudinal field loss suggestive of AION. Image focused on the macula of the right eye showing marked subretinal fluid extending into the fovea from the optic nerve.
Specifically, the appearance of the right optic nerve, the profound visual field loss as well as the accumulation of fluid in the outer plexiform layer are very suggestive of this condition.
These signs include unilateral painless visual loss, optic disc edema, macular edema, and the later development of a macular star.
These patients, by definition, have negative serologic studies and thus the disease is referred to as idiopathic recurrent neuroretinitis. The problem arises in trying to differentiate increased intracranial pressure with secondary hypertension from group 4 hypertension with papilledema and hypertensive encephalopathy.
The presence of these hemorrhages is highly significant in predicting the mortality rate from ruptured aneurysms. Some authors, like Ballantyne, believe these hemorrhages are caused by venous obstruction owing to increased intracranial pressure on Intracranial venous structures draining the rye and orbit. Muller and Deck evaluated 46 eyes and their orbits and optic canals in patients with increased intracranial pressure; 87% had optic nerve sheath hemorrhage, and 37% had intraocular hemorrhages.
These hemorrhages result from sudden increases in venous ocular pressure at a level in the nerve that precludes its dissipation by alternate drainage into the facial and pterygoid vessel systems. The branch retinal vein occlusions are more readily diagnosed by those unfamiliar with the fundus picture, because the hemorrhages are limited to one quadrant of the retina.
This decrease in acuity is not seen with increased intracranial pressure, except over a long period of time and with a gradual onset.
The evaluation of diabetes requires a formal glucose tolerance test rather than a postprandial blood glucose determination.
In leukemia the white centers are tumor cells, whereas in septic chorioretinitis they are inflammatory white cells. The appearance of the papillitis is not diagnostic; some patients with optic neuritis have good visual acuity.
This phenomenon may be seen when damage to the nerve oc-curs for any reason, causing a conduction defect, even in cases of neuritis with good visual acuity. The light must be moved rapidly from one eye to the other so as not to lose the constrictor effect from the normal eye. They can be seen only with the fundus contact lens, and they are not seen grossly with the ophthalmoscope. Even in optic neuritis with good visual acuity, the ability to recognize the plates may be markedly different in each eye. Fortunately, infiltration of the disc is rare and usually occurs unilaterally, which should alert one to an alternative diagnosis to true papilledema.
It may also occur secondary to true increased intracranial pressure from a mass effect or, more rarely, from direct infiltration of the disc. These cases may present as cranial nerve involvement, of which seventh nerve paresis is the most common, or with hypothalamic involvement and symptoms of diabetes insipidus.
We have seen lymphoma produce this ocular presentation on several occasions; however, these patients were well known to us as patients with lymphoma and did not have optic infiltration as their initial systemic complaint. They may also cause decrease in visual acuity, field defects, decrease in motility, and proptosis. Tumors that are truly retroorbital or are in the muscle cone are the most difficult to diagnose, but they can be diagnosed by the ultrasound technique or CT. Although these conditions also suggest orbital tumor, a positive forced duction test and lid retraction point toward thyroid disease as the primary cause. In disc edema caused by venous compression in the superior orbital fissure, the veins appear to be disproportionately larger than in papilledema caused by increased intracranial pressure.
Bilateral papilledema with a decrease in acuity can be confused with bilateral optic neuritis, a mistake that is likely to occur when the CT and MRI of the sphenoid ridge and sella turcica are reported as normal. The focal nature of the changes suggests the diagnosis, since the rest of the nerve looks normal. The low pressure causes mild swelling of the disc and macula, with chronic loss of vision caused by macular disease.
This condition is usually thought of as occurring in older people who show signs of headache and a temporal artery that is prominent, very tender, and noncompressible. The usual elevation is 45 mm or more, but even minimal elevations (in the range of 30 mm) warrant a temporal artery biopsy.
Anterior ischemic optic neuropathy (AION) is associated with ischemic disc edema more often than is temporal arteritis.
Although no effective specific therapy exists, associated conditions that decrease the vascular profusion ratio of the eye should be evaluated. Acute blood loss, such as occurs in gastrointestinal and uterine hemorrhages, does not commonly cause loss of vision or disc edema. Sahs and Joynt did brain biopsies on 10 patients and found an increase in intracellular edema.
It has been repeatedly reported in patients taking vitamin A, tetracycline, nalidixic acid, and penicillin.
I have seen it in one 19-year-old girl who chronically ingested an excess of vitamin A to treat her acne. The spinal fluid, except for Increased pressure, should be entirely normal or show a slight decrease in spinal fluid proteins, a finding that has been reported in as many as 70% of cases.
The headache is generalized, nonlocalizing, and made worse by increasing the intracranial pressure such as during a Valsalva maneuver. Although these two findings would seem interchangeable—if you have one, you have the other—this does not hold in all cases. A low tap in the face of papilledema creates a diagnostic dilemma; an elevated spinal fluid tap in the absence of papilledema is equally confusing.


Even after the papilledema disappears, severe visual consequences may occur if the intracranial pressure is still elevated or the idiopathic intracranial hypertension recurs without the production of papilledema. Therefore, we cannot assume that a minor amount of edema is less serious than 4 diopters of papilledema. However, they need to be followed just as closely as those who have severe complaints, because of possible visual system deficits. An intervenous bolus of 1 g has been shown to decrease cerebral spinal fluid secretion for 2 hours.
Steroids in themselves have serious side effects and have been implicated in causing benign intracranial hypertension in association with the nephrotic syndrome.
Among older patients, it is more often seen in women and secondary to arteriosclerotic rupture of an in-tracavernous aneurysm.
Examination of the far periphery of the fundus with the indirect ophthalmoscope is indispensable. If the patient later has a mild disc edema and engorged veins, the question of cerebral metastasis with increased intracranial pressure is raised.
These collaterals include the orbital, occipital, pharyngeal, pterygoid, and emissary venous systems, to name only a few. If the other signs of increased intracranial pressure are present, contrast studies must be considered. Despite the large numbers of people whom we see with various grades of chronic obstructive pulmonary disease (COPD), the occurrence of papilledema is rare. The patient went to her local optometrist and was then referred to the University of Iowa for further evaluation. In addition, she had a history of a similar episode in the left eye associated with a swollen optic nerve years before. An MRI scan of the brain and orbits was performed on this date due to the atypical nature of the case. Goldmann visual field of the right eye one month after initial presentation demonstrating some improvement, however there is still marked constriction of all isopters and loss of the smaller isopters (I1e, I2e). The papilledema secondary to increased intracranial pressure is limited to the posterior pole, whereas that caused by hypertension is accompanied by marked hypertensive changes that extend to the peripheral retina (Plate 2.IIC). The mortality rate is about 60% when fundus hemorrhages are present but only 27% when they are absent according to Manschot, Richardson and Hyland, and Fahmy.
They may occur initially as large hemorrhages breaking out into the vitreous or secondarily from a subhyaloid hemorrhage that subsequently breaks the posterior vitreous face and invades the vitreous body. In an old central retinal vein occlusion, the vein looks white, with vessels sprouting from the site of the obstruction. The dysproteinemias, such as Waldenstrom's macroglobulinemia, are best diagnosed by an electrophoresis of the patient's blood serum. In these, the field defect may he so subtle that the patient is not aware of it; it must be looked for carefully. The test should be done several limes to differentiate the condition from a dilatation of the pupil owing to hippus.
Cells in the vitreous humor can be seen in a variety of conditions—pars planitis, chorioretinitis, and cyclitis. This finding can be carried over into the field examination, in which a field defect may be more easily detected with colored test objects than with small white ones. Infiltration or masses on the nerve head can be seen with several disorders, such as tuberous sclerosis, sarcoid, and lymphoma (Plate 13.ID).
A patient reported by Jampol, Woodfin, and McLean and seen by us responded dramatically to systemic steroids (Plate 13.IB). The optic nerve masses resolved under therapy but left an infarcted nerve from the infiltration (Plate 13.ID). The exophthalmos may be subtle, and exophthalmometer measurements should be part of the evaluation of unilateral papilledema or loss of acuity.
Slow progressive loss of acuity is not caused by optic neuritis, however, so a compressive lesion must he considered. When no intracranial reason for the papilledema can be found and before pseudotumor cerebri is accepted as the diagnosis, investigation for a spinal cord tumor should be considered.
Since juxta-papillary choroiditis most frequently occurs on the temporal side of the disc, it is unlikely to be papilledema, which occurs first on the nasal side.
The loss of vision in patients with AION is gradual rather than cataclysmic; it tends to be a piecemeal loss of vision. These conditions are increased ocular pressure, decreased blood pressure, such as occurs in too sudden and too severe treatment for hypertension, and decreased carotid pressure owing to silent carotid occlusive disease, as evidenced by a decrease in ophthalmodynamometry.
In the United States, it usually occurs in women who have begun a pregnancy with a low hemoglobin level and then compounded the problem with no prenatal care, thus making the hemoglobin level drop even lower. One such disease process that requires cautious and prolonged observations is idiopathic intracranial hypertension, also called pseudotumor cerebri. Other investigators have identified the microvasculature as the source of the problem with secondary tissue swelling. There is also an association in patients with plumbism, carbon dioxide retention, hypoparathyroidism, and lupus erythematosus. Headache is usually present in benign intracranial hypertension and frequently is the reason patients seek medical consultation. One theory is that a swollen brain with displacement causes trigeminal nerve stretching over the petrous bone or compression of the nerve root at the petrous apex as it is about to enter the trigeminal cistern and become the gasserian ganglion. Many reports indicate that in idiopathic intracranial hypertension, there is wide fluctuation in intracranial pressure; thus, at any given moment, a tap may show normal, borderline, or elevated pressure. The problem has been to establish what factors predict those patients at risk for visual loss. However there are only two cases of this in the literature, and it appears to be a safe drug after the 20th week of pregnancy. Most physicians treating benign intracranial hypertension recommend only a short course of steroid treatment, usually lasting no more than several weeks. The first is the lumboperitoneal shunt, which has the advantage of rapidly normalizing the intracranial pressure and reducing the papilledema.
This technique has been effective in reversing visual loss from increased intracranial pressure, although the exact mechanism of its effect is not well understood. Local anesthesia may interfere with pupil functions, and there is always the problem of a retrobulbar hemorrhage, which could make a marginally functioning nerve worse as well as postpone surgery beyond an optimal time.
Diplopia and pupillary abnormalities have also been noted but appear to be more common in the lateral surgical approach.
The increased venous flow to the eye, as well as the increased venous pressure, may cause only edema of the disc and fullness of the retinal veins without dilated veins on the conjunctiva, sclera, and lids.
The more subtle pulsations are diagnosed when the physician uses direct ophthalmoscopy, noting that the fundus is going in and out of focus synchronously with the pulse at the wrist. The physician may not consider the possibility of decreased venous drainage from the head and presume that the other jugular system is able to drain the head adequately. The appearance of optic atrophy and the inferior nasal scotoma in the left eye suggest that the previous episode also affected both the inner and outer retinal layers.
The majority of cases are thought to be due to current or previous infection with Bartonella henselae, a Gram-negative proteobacteria, however, infection with a number of different agents has been postulated to lead to the disease.
Patients may develop permanent central or cecocentral scotomas, optic disc atrophy, and macular and retinal nerve fiber layer thinning.
These hemorrhages probably do not result from increased intracranial pressure being transmitted to the orbital venous structures. Hemorrhages of this magnitude represent even more serious consequences from the intracranial disease than just preretinal hemorrhages. The disc in papilledema with vision loss shows a gliotic grayish appearance with white sheathing of the vessels. The physician shines a light in the affected eye, and the pupil in that eye responds, as expected, by constricting.
In all these disorders, the cells cause a visible haze or debris in the vitreous humor and are not localized to the disc area.
An increase in the serum angiotensin-converting enzyme has also shown promise as a laboratory aid in the diagnosis, but it is not universally elevated in all cases of sarcoid. As the tumor enlarges and the intracranial pressure increases, the relationship of papilledema and venous engorgement is more typical of true papilledema. Suprasellar masses, such as meningioma, craniopharyngioma, or aneurysm, may cause compression of the nerves without evidence of bony changes, even with adequate tomograms of the sella turcica. The usual lower extremity symptoms should dismiss serious consideration of pseudotumor cerebri. A detailed view of the ciliary body may reveal ciliary body detachment, with secondary decrease in aqueous production. If asked about any previous signs and symptoms, the patient may admit to them but dismiss them as "just old age" or "wearing out." Frequently, temporal arteritis causes disc edema, but it is of the pale and ischemic variety, with small vessels, rather than the plethoric type seen with increased intracranial pressure.
If the condition is strongly suspected because of an elevated sedimentation rate, systemic steroid therapy should be started immediately, even if the biopsy cannot be done for as long as 48 hours. In persons with AION, the other eye tends to be affected more consistently, although usually not simultaneously. About 25% of those who develop disc edema do so immediately, and the remainder develop it in the next few days or weeks. The edema is low grade and closer to the ischemic variety than the edema in increased intracranial pressure. The disease is seen most commonly in obese young females with menstrual irregularities and in the first trimester of pregnancy. The acute variety occurs when the patient ingests food with a high vitamin A content such as polar bear meat or shark liver.
In the past, invasive studies such as a pneumoencephalogram were required to demonstrate ventricular size. However, headache is not always present despite the increased intracranial pressure and may come and go despite constant increased intracranial pressure. Macular pigmentary changes have been reported in papilledema secondary to pseudotumor cerebri. In the pediatric group, changes in personality like apathy, somnolence, irritability, dizziness, and ataxia were the usual presenting signs. Several decades ago, Walter Dandy, the famous neurosurgeon, had four criteria—all visual—for surgical intervention in this disease: decreasing visual acuity, progressive contraction of the field, gliosis of the disc, and increasing transient obscurations. Visual loss can occur late or early in the course of the disease, although the amount of visual loss does increase with the duration of the disease. Since the spinal fluid pressure usually restores itself to the previous level in about 2 hours, I am not convinced of the rationale for its use in a chronic disease. Side effects at this dosage level or even less include gastrointestinal symptoms, disturbances in acid-base balance, and perioral and digital pares-thesias. Although any competent neurosurgeon can do this surgery, the operation, like all operations, is not perfect.
Some workers contend that opening up the optic nerve sheath reduces pressure in the nerve and allows for better vascular profusion of the nerve. The degree of globe manipulation and compression of orbital contents are easier under general anesthesia. The larger blade-type speculum can force the lids wider apart but may create more orbital pressure. The cellular reaction is more generalized than that seen in papillitis located just in front of the disc. It may be caused by decreased venous drainage from the head into the chest, or it may be secondary to an increase in blood Pco2.
Kety showed that by raising the level of CO2 in the blood, secondary vascular dilatation occurs, resulting in increased intracranial pressure.
One month after this follow up visit, the patient developed symptoms of decreased vision in the left eye. Fundus photo of the right eye showing near complete resolution of the optic disc edema, optic nerve pallor, and the presence of a prominent macular star in the right eye. Most patients with typical neuroretinitis generally suffer a single attack, with slow resolution of symptoms, with or without treatment. A number of case reports exists in the literature regarding this disease, its clinical course, and therapeutic options. In each patient, treatment was initiated after several attacks of neuroretinitis which were generally treated acutely with a short course of oral steroids or antibiotics. If the hemorrhage is located in front of the macula, it causes a severe decrease in vision. Also, any increased orbital venous pressure can be dissipated by alternate venous drainage into the facial and pterygoicl vessels.
Papillophlebitis as initially described by Lyle and Wybar and subsequently by Lonn and Hoyt should not be confused with papilledema secondary to increased intracranial pressure. When Roth's spots are present, they are located at the posterior pole and need not be looked for at the equator or beyond. A variation of this condition is the Foster Kennedy syndrome, in which the tumor, usually a frontal lobe glioma or an olfactory groove meningioma, compresses the optic nerve, causing optic atrophy. MRI with contrast of the lumbosacral region may show atrophy and widening of the interpedicular distance.
Seidel's test with fluorescein should be done, and the physician should look for a leak of the wound if an ob-vious filtering bleb is not present. The diagnosis of temporal arteritis should be considered in a patient over 55 years of age, particularly one over 65 years of age, when sudden loss of vision occurs in one or both eyes. Such a brief course of steroid therapy does not affect the biopsy, and it may protect the other eye.


AION is not associated with an increased sedimentation rate, and the temporal artery biopsy is negative. The loss of vision is usually unilateral, and it may be complete or partial or even present as a field defect, such as an attitudinal hemianopsia. They injected 131T RISA in two patients and found a decrease in absorption from the spinal fluid compartment into the intravascular compartment. At one time it was also commonly seen in female patients on the pill, but this is a rare association now. The toxicity is manifested by headache, nausea and vomiting, a decreased sensorium, and irritability. The lack of or cessation of a headache, therefore, does not always mean a decrease in intracranial pressure and is not a reason for complacency. In this group the fontanels are frequently open, and the sutures are not set; as a result papilledema is infrequent. Methazolamide theoretically may be preferable to acetazolamide because it crosses the blood-brain barrier better than acetazolamide. The shunt may fail with return of increased intracranial pressure; at the other extreme, it may filter excessively and lead to increased headache due to shifting of the intracranial contents and stretching of the nerves. Others contend that the dural window in the optic nerve sheath acts as a draining point for cerebrospinal fluid and, therefore, helps reduce the intracranial pressure. However, the disadvantage of general anesthesia is that too much compression can be used in an attempt to increase visualization.
Rarely, disc edema may even begin in the contralateral eye if a superior ophthalmic vein thrombosis occurs ipsilateral with the fistula. The variation of the tonometer reading may be interpreted as unsteadiness of the patient in the headrest of the slit lamp.
For instance, left jugular compression usually causes a more pronounced rise in cerebral spinal fluid pressure than does right jugular compression. The secondary anoxia these patients suffer over a long period rarely causes optic nerve ischemia and decreased vision. In the current case, we decided to treat the patient with a short course of oral azithromycin to target Bartonella henselae as well as a short course of steroids to help decrease inflammation. Unless it breaks into the vitreous humor, however, it will be absorbed, and previous vision will return. These two facts militate against optic nerve sheath hemorrhages resulting from intracranial subarachnoid blood being pushed into the optic nerve sheath.
The white centers in Roth's spots frequently are transient, and when they are looked for the next day, they may be filled in with blood and look like an ordinary retinal hemorrhage.
The light is then moved quickly from the affected eye to the other eye—and the degree of pupillary constriction in both eyes comes down more. The mass responded to steroids, and all of the symptoms and signs were relieved or markedly improved. Careful inspection of the plain roentgenograms may reveal subtle calcification in some cases of meningioma and aneurysm. Temporal arteritis has been reported and confirmed by biopsy in much younger people, but only rarely. Since temporal arteritis is a segmental disease, it is imperative to get serial sections done on the specimen because the pathologic area may be missed. The visual loss may be made worse by antecedent carotid occlusive disease or small vessel disease in the optic nerve or in the retina, which has already decreased the perfusion of the eye.
Whatever visual loss ensues can be made worse by an associated eclampsia or hypertension that causes further ischemia. In view of the varied disease processes that have been associated with idiopathic intracranial hypertension, there may well not be one underlying pathologic picture for this disease.
Idiopathic intracranial hypertension is also seen as a consequence of cerebral sinus thrombosis either spontaneously, secondary to mastoid disease, or postpartum.
Acute toxicity in children may be caused by an accidental overdose of vitamins that the infant had access to.
In the absence of neurologic signs and before the advent of CT examinations, the possibility of a posterior fossa tumor made lumbar spinal taps dangerous in the face of increased intracranlal pressure. It is during the neurologic examination that papilledema is discovered and the rest of the diagnosis is considered.
My own experience and the reports by Corbett et al., by Orcutt, Page, and Sanders, and by Wall, Hart, and Burde provide additional information about prognostic factors in benign intracranial hypertension. In more chronic cases, peripapillary subretinal hemorrhage sec-ondary to neovascularization occurs and is a bad prognostic sign for visual loss. Repeated taps may cause tears in the dura, with chronic leaking of spinal fluid and perhaps worsening of the headache.
The report of Kaye, Galbraith, and King on a 51-year-old female with a 14-month history of papilledema and pseudotumor cerebri addresses this controversy. With the Schiotz tonometer, however, the arm has wide rhythmic swings in the range of six scale readings rather than the usual two to three scale readings. This type of response probably explains the increase in intracranial pressure that follows radial neck dissections and the increased cerebral venous pressure from chronic chest pathology.
If another complicating factor occurs, such as a reduction in optic nerve perfusion pressure, then decrease in vision can occur. Blood was drawn for testing of syphilis (RPR), antinuclear antigen (ANA), Bartonella Henselae, complete blood count (CBC), Lyme titers, and angiotensin converting enzyme (ACE). This therapy was initiated upon our first clinical encounter with the patient, when the diagnosis of typical neuroretinitis was considered. Hemorrhages can be found on the optic nerve sheath in cases of increased intracranial pressure without subarachnoicl hemorrhage.
The fundus picture is usually much worse than the patient's complaints of minimal blurriness. Roth's spots lire seen in other diseases, including subacute bacterial endocarditis, pernicious anemia, scurvy, lupus erythematosus, and sickle cell anemia. Then as the tumor grows, increased intracranial pressure develops, and the other nerve shows papilledema while the atrophic side does not. Suprasellar calcification can be seen in more than 85% of childhood craniopharyngiomas, but it is uncommon in the adult variety. The cause of the papilledema is not necessarily mechanical obstruction of cerebrospinal fluid flow as has been shown by myelography. The condition usually attacks one eye at a time, but since the other eye may be affected within days, a diagnosis should be made promptly, and therapy begun immediately.
It is important to get a positive biopsy early so that patients who do not require steroid therapy will not continue to receive it.
Chronic intoxication is a more common presentation with the signs and symptoms of idiopathic intracranial hypertension.
However, a CT examination can rule out a posterior fossa tumor or aqueduct stenosis with secondary enlargement of the ventricles. Macular stars do not portend visual loss but only substantiate the chronicity of the process.
Hayreh's fenestration experiments revealed fibrous adhesions to the nerve as a late finding. A conjunctival peritomy is then performed beginning 4 mm from the limbus over the medial rectus muscle'. She was treated with a five day course of oral azithromycin and two weeks of oral prednisone and asked to return in one month. However, as all of her serologic testing was negative, and she developed recurrent symptoms in the opposite eye, a diagnosis of idiopathic recurrent neuroretinitis was made.
These hemorrhages in the nerve sheath occur predominantly in the subdural rather than the subarachnoid space. The edema and hemorrhages on the disc and in the retina are more consistent with a vein occlusion than with papilledema. When the Foster Kennedy syndrome occurs in persons 65 years of age or older, however, it is commonly caused by vascular disease. If the Foster Kennedy syndrome is caused by an olfactory groove meningioma, anosmia ipsilateral with the optic atrophy also occurs. Since increased cerebrospinal fluid protein is a constant finding in these cases, the protein may obstruct the turnover of cerebrospinal fluid as occurs in the Guillain-Barre syndrome.
Since they are in the age group that tolerates steroids poorly and is prone to such diseases as diabetes and hypertension, a positive biopsy also puts the treatment on a firmer basis.
This allows a safe spinal tap from below to establish the diagnosis of pseudotumor cerebri. This scarring appears to shift the pressure away from the low pressure vascular system at the laminar cribrosa. The anesthesiologist must be told to not let the patients blood pressure drop at all during the procedure. It is impor-tant to start the peritomy 4 mm back rather than at the limbus so the conjunctival repair at the end of the procedure can be tight and nonleaking.
This hyperviscosity of the blood may cause sludging and vascular congestion at the nerve head, with the appearance of papilledema. At that time we discussed the option with the patient of treatment with systemic immunosuppressive agents, but it was decided not to pursue this treatment, as she was trying to conceive. Muller and Deck believe that the hemorrhages in the sheath may be caused by the rupture of pial vessels when the sheath is rapidly expanded during a sudden severe rise of intracranial pressure. It has been suggested that doing a temporal artery arteriogram will show the occluded areas more precisely and thus increase chances of a positive biopsy. In the presence of the venous flow disturbance in cerebral sinus thrombosis, these patients hear a noise; it is not a bruit, but rather is called a venous souffle. This would explain the ipsilateral eye but not cases with contralateral improvement from unilateral fenestration.
A drop in blood pressure may add to any lack of nerve perfusion from the previous problem and the operative manipulations.
The peritomy extends from over the medial rectus to beyond the superior and inferior rectus 'muscles. The increased volume of the blood also causes an increase in the intravascular space in the cranial vault, further increasing the intracranial pressure. Like vein occlusion in adults, however, there is no effective treatment unless some systemic cause is revealed.
However, a combination of anemia and hypertension may increase the chances of visual loss because of the increased ischemic effect of the two together. The medial rectus is now isolated as in any standard disinsertion of the muscle with 6-0 Vicryl sutures placed in the lateral aspects of the muscle in a locking configuration.
When a sudden loss of vision with ischemic disc edema occurs, an important differential diagnosis is infarction of the nerve immediately behind the disc from emboli, particularly from an atheromatous condition of the carotid or aortic arch. Because of worsening symptoms, increasing papilledema, and increasing transient obscurations, bilateral optic nerve sheath decompression was performed.
The superior and inferior rectus muscles are isolated, and 4-0 silk sutures are used as traction sutures.
Intracranial pressure was measured continuously postoperatively, and no significant lowering of the intracranial pressure was recorded.
A 6-0 Vicryl suture is inserted in the scleral stump of the medial rectus muscle insertion in a baseball-type stitch.
They report it as a blowing sound or whisper rather than the loud roaring sound of a bruit. However, the papilledema and symptoms decreased, and the patient was normal 2 months postoperatively. Be sure it encompasses the entire stump; any asymmetric attachment may cause torsion of the globe and make the nerve harder to visualize.
Therefore, optic nerve sheath decompression appears to preserve optic nerve function but does not apparently treat the underlying cause of the increased intracranial pressure by draining the subarachnoid fluid.
At this point, bring in the microscope and focus it in the most advantageous position for observation.
As a result of this variability and apparent inconstancy, patients may not mention this symptom, and the astute clinical historian must seek it.
As you go deeper into the orbit, look for the ridge on the sclera that identifies the long ciliary artery.
The conjunctiva and tenons capsule are now dissected up by blunt dissection to reduce bleeding. Farther on, you encounter orbital fat, and this is retracted by either a small blunt malleable retractor or a cotton-tip applicator.
When the optic nerve is isolated, gently displace the posterior ciliary artery to prevent injuring it. Also locate a dilated area which is most likely to have a fluid level between the sheath and optic nerve.
As you cut dura, some of the arachnoid can be seen and needs to be incised to release the perineural fluid. At this point some surgeons prefer multiple longitudinal slits and others a window as generous as surgically possible.
A Fisher tenotomy hook is moved carefully without pressure longitudinally along the nerve to free up any adhesions. At this point, if there is no bleeding, then reinsert the medial rectus muscle and remove the sutures on the vertical recti.



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