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with severely reduced vision should not be attributed to papilledema; instead, intraorbital optic neuritis (papillitis) or infarction of the nerve head (ischemic optic neuropathy), both of which are described further on, are then the cause of disc edema The examiner is also aided by the fact that papilledema due to raised intracranial pressure is generally bilateral, although, as mentioned earlier, the degree of disc swelling tends not to be symmetrical In contrast, papillitis and infarction of the nerve head usually affect one eye, but there are exceptions to both of these statements Also, the pupillary reaction to light is muted only with infarction and optic neuritis, not with papilledema The occurrence of papilledema on one side and optic atrophy on the other is referred to as the Foster Kennedy syndrome and is attributable to a frontal lobe tumor or an olfactory meningioma on the side of the atrophic disc In its complete form, which is seen only rarely, there is also anosmia on the side of the optic atrophy Papilledema due to increased intracranial pressure must also be distinguished from combined edema of the optic nerve and retina, which typi es both malignant hypertension and from posterior uveitis Papilledema due to infarction of the nerve head is characterized by extension of the swelling beyond the nerve head, as described below, whereas the papilledema of increased pressure is associated with peripapillary hemorrhages Often these distinctions cannot be made on the basis of the funduscopic appearance alone, in which case the most reliable distinguishing feature is again the presence or absence of visual loss (Table 13-1) Chronic papilledema, as occurs in pseudotumor cerebri (see Chap 31), presents a special problem in diagnosis and represents a risk for permanent reduction in visual acuity and, eventually, optic atrophy In addition to testing visual acuity at regular intervals, our colleagues advise serial evaluation of the visual elds; a constriction of the nasal eld, detectable by automated perimetry and tangent screen testing, is an early and ominous sign The essential element in the pathogenesis of papilledema is an increase in pressure in the sheaths of the optic nerve, which communicate directly with the subarachnoid space of the brain This was demonstrated convincingly by Hayreh (1964), who produced bilateral chronic papilledema in monkeys by in ating balloons in the temporal subarachnoid space and then opening the sheath of one optic nerve; the papilledema promptly subsided on the operated side but not on the opposite side The pathogenesis of papilledema has also been ascribed to a blockage of axoplasmic ow in the optic nerve bers (Minckler et al; Tso and Hayreh) It was found that compression of the optic nerve bers by elevated cerebrospinal uid (CSF) pressure resulted in swelling of axons behind the optic nerve head and leakage of their contents into the extracellular spaces of the disc In our opinion, the block in axonic ow alone could not account for the marked congestion of vessels and hemorrhages that accompany papilledema The mechanism of papilledema that on rare occasions accompanies spinal tumors, particularly oligodendrogliomas, and the Guillain-Barre syndrome is not entirely clear Usually the CSF pro tein is more than 1000 mg/100 mL, but this cannot be the entire explanation, since instances occur in which the protein concentration is only slightly elevated (also the concentration of protein in the ventricular and cerebral subarachnoid spaces is considerably lower than in the lumbar sac, where it is usually sampled; see Chap 30) In other diseases that at times give rise to papilledema eg, chronic lung disease with hypercarbia, cancer with meningeal in ltration, or dural arteriovenous malformation the mechanism is most often one of a generalized increase of intracranial pressure
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Puzzling are cases of papilledema without raised intracranial pressure, as may occur in children with cyanotic congenital heart disease and other forms of polycythemia and possibly with hypocalcemia
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