Ординатура / Офтальмология / Английские материалы / Neuro-Ophthalmology_Kidd, Newman, Biousse_2008

132Neuro-Ophthalmology: Blue Books of Neurology

17.Fry CL, Carter JE, Kanter MD, et al: Anterior ischemic optic neuropathy is not associated with carotid artery atherosclerosis. Stroke 1993;24:539–542.

18.Biousse V, Schaison M, Touboul PJ, D’Anglejan-Chatillon J, Bousser MG: Ischemic optic neuropathy associated with internal carotid artery dissection. Arch Neurol 1998;55:715–719.

19.Feldon SE: Anterior ischemic optic neuropathy: trouble waiting to happen. Ophthalmology 1999;4:651–652.

20.Salomon O, Huna-Baron R, Kurtz S, et al: Analysis of prothrombotic and vascular risk factors in patients with nonarteritic anterior ischemic optic neuropathy. Ophthalmology 1999;106: 739–742.

21.Weger M, Stanger O, Deutschmann H, et al: Hyperhomocysteinemia, but not MTHFR C677T mutation, as a risk factor for non-arteritic ischaemic optic neuropathy. Br J Ophthalmol 2001;85:803–806.

22.Lee AG: Prothrombotic and vascular risk factors in non-arteritic anterior ischemic optic neuropathy. Ophthalmology 2000;107:2231.

23.Biousse V: The coagulation system. J Neuro-ophthalmol 2003;23:50–62.

24.Murphy MA, Murphy JF: Amiodarone and optic neuropathy: The heart of the matter. J Neuroophthalmol 2005;25:232–326.

25.Chiari M, Manzoni GC, Van de Geijn EJ: Ischemic optic neuropathy after sumatriptan in a migraine with aura patient. Headache 1994;34:237–238.

26.Fivgas G, Newman NJ: Anterior ischemic optic neuropathy following the use of a nasal decongestant. Am J Ophthalmol 1999;127:104–106.

27.Lee AG, Newman NJ: Erectile dysfunction drugs and non-arteritic anterior ischemic optic neuropathy. Am J Ophthalmol 2005;140:707–708.

28.Lee AG, Kohnen T, Ebner R, et al: Optic neuropathy associated with laser in situ keratomileusis. J Cataract Refract Surg 2000;26:1581–1584.

29.McCulley TJ, Lam BL, Feuer WJ: Non-arteritic anterior ischemic optic neuropathy and surgery of the anterior segment: Temporal relationship analysis. Am J Ophthalmol 2003;136:1171–1172.

30.Slavin ML, Margulis M: Anterior ischemic optic neuropathy following acute angle-closure glaucoma. Arch Ophthalmol 2001;119:1215.

31.Arnold AC, Hepler RS, Lieber M, Alexander JM: Hyperbaric oxygen therapy for non-arteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1996;122:535–541.

32.Botelho PJ, Johnson LN, Arnold AC: The effect of aspirin on the visual outcome of non-arteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1996;121:450–451.

33.Johnson LN, Guy ME, Krohel GB, Madsen RW: Levodopa may improve vision loss in recentonset, nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2000;107:521–526.

34.Soheilian M, Koocheck A, Yazdani S, Peyman GA: Transvitreal optic neurotomy for nonarteritic anterior ischemic optic neuropathy. Retina 2003;23:692–697.

35.Fazzone HE, Kupersmith MJ, Leibmann J: Does topical brimonidine tartrate help NAION? Br J Ophthalmol 2003;87:1193–1194.

36.Kupersmith M, Frohman L, Sanderson M, et al: Aspirin reduces the incidence of non-arteritic anterior ischemic neuropathy: A retrospective study. J Neuro-ophthalmol 1997;17:250–253.

37.Beck RW, Hayreh SS, Podhajsky PA, et al: Aspirin therapy in non-arteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997;123:212–217.

38.Salomon O, Huna-Baron R, Steinberg DM, et al: Role of aspirin in reducing the frequency of second eye involvement in patients with non-arteritic ischaemic optic neuropathy. Eye 1999;13:357–359.

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42.Hayreh SS, Podhajsky PA, Zimmerman B: Occult giant cell arteritis: Ocular manifestations. Am J Ophthalmol 1998;125:521–526.

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44.Hayreh SS, Zimmerman B, Kardon RH: Visual improvement with corticosteroid therapy in giant cell arteritis: Report of a large study and review of literature. Acta Ophthalmol Scand 2002;80:353–367.

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Introduction

Optic neuritis is a subacute disorder caused by inflammation within the optic nerve that leads to visual impairment comprising loss of visual acuity, color vision, and contrast sensitivity. It may affect one or both eyes and may arise at any age, and many different disease processes may be associated with it. This chapter deals with the most common cause of the disorder, a primary demyelinating disease in which optic neuritis may develop as the first manifestation or during the course of multiple sclerosis (MS). The next chapter deals with similar disorders of different pathophysiology.

Epidemiology

The natural history of optic neuritis has been investigated in detail in several studies1–8 (Nettleship: 28 cases, Traquair: 160 cases, Carroll: 100 cases, Bagley: 133 cases, Bradley and Whitty: 73 cases, Nikoskelainen: 185 cases, Hutchinson: 144 cases, and Perkin and Rose: 170 cases) over the past 125 years. The most important recent study of optic neuritis has been the carefully planned and followed prospective study, the Optic Neuritis Treatment Trial (ONTT), in which 457 patients were enrolled over a 3-year period in 15 U.S. centers.9 These have

shown that optic neuritis is a disorder of the young, with the majority of patients presenting at 20 to 50 years2,5–9 (mean 32 years). It is more common in females

than in males (Table 6–1). Like MS, it is more common in Caucasians, in particular, in peoples of Northern European genetics.10 The incidence is highest in the spring months.7,11

There have been two formal epidemiologic studies; the first, from Mayo Clinic, identified 156 cases, and the annual ageand sex-adjusted incidence rate of optic neuritis between 1985 and 1991 was 5.1 per 100,000 person-years, with a prevalence of 115 105.12 This is a high prevalence, indeed similar to the prevalence of MS in the United Kingdom,13 but so too is the prevalence of MS in Minnesota.14

The second took place in Stockholm County, Sweden (population 1.6 M), between 1990 and 1995 and revealed 150 consecutive patients with mean age at

onset of 31.7 8.4 years and a female-male ratio of 4.07. The crude mean annual incidence was 1.46 per 105 person-years,10,11 lower than that in Minnesota.

Clinical Features: Symptoms

ORBITAL PAIN AND HEADACHE

Pain within and around the affected eye arises before or at the time of the onset of

visual loss in about 90% of cases and has equal prevalence in those with and without optic disc swelling.5,7–9 Pain most often arises at the onset of visual symptoms,

but in one series it preceded the symptoms by more than 1 week in 19% of cases.5 Characteristically the pain is experienced as a dull ache around the eye initially that worsens over hours or days and becomes sharp and stabbing within the eye. Most experience a worsening of this pain when the eye is moved in a certain

or several directions; 51% of patients in the ONTT noted this feature and a further 35% experienced pain only on eye movement. Pain is presumably related to the trigeminal afferents arising from the inflamed and swollen optic nerve sheath.1,8 Lepore15 found that pain was less common in patients with disc swelling than

without, although this was not seen in the ONTT.9 Pain is less common in anterior ischemic optic neuropathy (AION),16,17 but common, and often more severe, in

other forms of optic neuritis such as that in CRION (chronic relapsing inflammatory optic neuropathy), sarcoid, infections, and that related to sinus mucoceles.

VISUAL LOSS

Visual symptoms begin after the onset of pain, and pain itself tends to diminish as the visual loss develops. It begins in a subacute way and evolves over hours to, more typically, days. Patients often note a gray cloud or veil in front of the eye, particularly involving the central field; those with more severe visual loss note evolution from a veil to a scotoma in which severe blurring or nothing is seen in one part of the field. Although uncommon, visual loss may proceed to no perception of light.

POSITIVE VISUAL PHENOMENA

Phosphenes or photopsias were noted by 30% of ONTT patients9; these are flashes of white or black shapes and showers of sparkles. Often spontaneous, they may also be stimulated by rubbing the eye; moving it; or, rarely, by auditory stimuli.18 Phosphenes or photopsias are more visible in the dark or with the eyes closed, and some patients notice them only under these conditions.

Clinical Features: Signs

These are the signs of an optic neuropathy with reduction in central acuity, color vision, and contrast sensitivity; an afferent pupillary abnormality; and a visual field defect. Ophthalmoscopic or slit lamp evidence for an inflammatory disorder is seen in only a small number of cases (see the section entitled “Ophthalmoscopic Abnormalities”).

VISUAL ACUITY

Visual acuity deteriorates over 1 to 7 days to a nadir, which remains for only a short time before recovery begins; in the ONTT the mean visual acuity was 20/80 (6/24), with 162 patients having acuity of 20/40 (6/12) or better, 166 patients with 20/200 (6/60) or worse, and 129 in between; 3.1% had no perception of light. The mean pattern deviation of the visual field was –23.02 dB (–31.9 to –12.25 dB).9

Tests of color vision are important in cases in which central acuity is not or only slightly reduced; Ishihara or Hardy-Rand-Rittler pseudoisochromatic plates reveal often striking abnormalities of color vision even under these circumstances. Others less severely affected will note that the colors of the plates appear washed out or less distinct when compared with the asymptomatic eye. Clearly those with more profound visual loss, particularly those with central field defects, will be unable to perform the test.

Achromatic contrast sensitivity measures the minimum detectable spatial luminance change of vision. It is least likely of all measures to recover completely (see Residual Visual Loss Following Optic Neuritis). In the ONTT, contrast sensitivity thresholds were abnormal in 98% of cases.

THE PUPILLARY REACTIONS

Providing the integrity of the fellow optic nerve is not impaired, the patient will show a relative afferent pupillary defect or Marcus Gunn phenomenon when tested carefully. This was noted in 76% of cases in Perkin and Rose’s study. Patients with previous symptomatic or asymptomatic optic neuritis in the other eye may not show this phenomenon.

VISUAL FIELD

Previously it was considered that central defects alone accounted for the field defects seen in optic neuritis8; however, the ONTT data show that any possible kind of field defect may arise,19 including arcuate, altitudinal, quadrantic, and hemianopic defects as well as peripheral constrictions and multiple paracentral scotomas. In the ONTT, central or centrocecal scotomas were seen only in 8% of cases out of 415 patients tested (Fig. 6–1).

OPHTHALMOSCOPIC ABNORMALITIES

Two percent to 35% of patients show evidence for disc swelling (Fig. 6–2, Table 6–1). The remainder, therefore, have “retrobulbar neuritis.” The degree to which the disc is swollen does not correlate with the degree of visual loss.8 Only a minority of patients show disc or peripapillary hemorrhages, in contrast to that which is seen in AION. The disc may therefore appear completely normal in the acute phase. Disc pallor at the onset of symptoms may indicate a previous asymptomatic episode but should also serve as a warning that an acute worsening of a more chronic compressive lesion (e.g., an aneurysm or a sinus mucocele) may be responsible.

Vitreous cells may be seen but when they are numerous an alternative etiology, for example sarcoidosis, should be considered. Sheathing of retinal vessels (Fig. 6–3), or periphlebitis retinans, may occur, but this is also seen in sarcoidosis, Behc¸et’s syndrome, and other conditions (see next chapter). In one series of 50 consecutive patients with acute optic neuritis seen at Moorfields Eye Hospital, 14 were seen to have ocular abnormalities at the time of presentation; perivenous sheathing arose in 6, of whom 4 had evidence for fluorescein leakage and a further 6 had fluorescein leakage without clinically evident perivenous sheathing. Media cells were seen in a further 2 cases.20 In the ONTT, such abnormalities were less common; 3.3% had vitreous cells, 1.8% had retinal exudates, and 5.6% had peripapillary hemorrhages.

Pars planitis and intermediate uveitis may also be seen and can precede the onset of the demyelinating disorder by many years.21 The prevalence in that study, however, was only 1% of 2628 patients attending MS and uveitis clinics in France. Pars planitis has a particular association with MS; of 36 patients followed up, 12 developed optic neuritis, MS or both, giving a 20.4% risk over