Preface

x Preface

We would again like to thank our mentor, colleague, and friend Dr. Neil R. Miller for his encouragement and example. Dr. Brazis would also like to thank the following individuals for their guidance: Drs. James Corbett, Jonathan Trobe, James Bolling, and Frank Rubino. He is appreciative of the encouragement and support of his family, especially Elizabeth, Erica, Paul, and Kelly Brazis.

Dr. Lee acknowledges the support and encouragement of the three chairmen with whom he has served over the years: Drs. Mort Goldberg, Dan B. Jones, and Thomas Weingeist. He is grateful to his colleagues at the University of Iowa, Drs. Randy Kardon, Michael Wall, and Stan Thompson, for their insight, support, and friendship. He thanks his parents Drs. Alberto C. Lee and Rosalind G. Lee for instilling in a young man the thirst for knowledge and intellectual curiosity. He is particularly thankful to his loving, patient, and tolerant wife, Dr. Hilary A. Beaver, who made a baby (Rachael E. Lee) while he made a book.

We appreciate the assistance of our editors at Thieme Medical Publishers. We thank the faculty and residents of the Departments of Ophthalmology, Neurology, and Neurosurgery at the University of Iowa Hospitals and Clinics, and the Departments of Neurology and Ophthalmology at the Mayo Clinic in Jacksonville, Florida, for their academic stimulation. We especially appreciate and extend our love to our wives and families.

Andrew G. Lee, M.D.

Paul W. Brazis, M.D.

2 Clinical Pathways in Neuro-Ophthalmology, second edition

atrophy, including glaucoma, central retinal artery occlusion (CRAO), ischemic optic neuropathy (ION), optic neuritis (ON), hereditary optic neuropathy (Leber’s and nonLeber’s types), compressive optic neuropathy (CON), and traumatic optic neuropathy (TON) (Trobe, 1980). These photographs were reviewed by five ophthalmologists as ‘‘unknowns.’’ Glaucoma, CRAO, and ION were correctly identified as the etiology by at least one of the five observers with an accuracy above 80%, but the remaining etiologies were correctly identified in less than 50% of cases! Helpful features in differentiating the entities included:

1.The presence of retinal arteriolar attenuation and sheathing in ischemic lesions (e.g., CRAO or ION).

2.Temporal pallor in entities selectively involving central vision and central visual field with sparing of peripheral visual field (e.g., optic neuritis and toxic optic neuropathies).

3.Superior or inferior (sector) optic disc pallor in ION.

Although optic disc cupping was often identified in glaucoma, it was also seen in 20% of cases not associated with glaucoma. Optic disc cupping in glaucoma cases, however, was more profound than in nonglaucomatous cases and greater neuroretinal rim pallor occurred in the nonglaucomatous cases. In patients with glaucoma, there is often absence of at least part of the neuroretinal rim, and the color of the remaining rim is normal. With nonglaucomatous optic neuropathy, rarely is any area of the rim completely absent and the remaining rim is often pale. Interestingly, only 11% of these cases with a known history of papillitis or ION had sufficient clues to identify previous disc swelling (Trobe, 1980).

Another study suggested that optic disc appearance may help differentiate anterior ischemic optic neuropathy (AION) from ON, although there are overlapping features. Optic disc stereographs were reviewed by masked observers (87 AION and 68 ON) (Warner, 1997). Altitudinal disc swelling was more than three times more common in AION than ON, although most discs were diffusely swollen. Most patients with AION had hemorrhages, whereas most ON cases did not. Almost all discs with ON had normal color or were hyperemic; only 35% of discs with AION had pallid swelling. Pallid swelling was so rare in ON, however, that of discs with pallor, 93% had AION. Arterial attenuation was also much more typical of AION. AION was the clinical diagnosis in 82% of cases with altitudinal edema, 81% of cases with disc hemorrhage, 93% of cases with pallid edema, and 90% of cases with arterial attenuation. A pale optic nerve with hemorrhage, regardless of type of edema, always represented AION (100%). A normal color nerve without hemorrhage reflected ON in 91% of cases, increased from only 76% if hemorrhage was not considered. A hyperemic nerve with hemorrhage represented AION in 82% of cases, but if altitudinal edema was also present, AION incidence increased to 93%.

In addition, numerous authors have stressed the localizing value to the optic chiasm or optic tract of a special type of optic atrophy caused by specific involvement of the nerve fiber layer of the nasal and temporal retina, respectively. Involvement of these fibers results in atrophy of the nasal and temporal optic disc with sparing of the inferior and superior poles (‘‘band’’ or ‘‘bow tie’’ atrophy). Band atrophy occurs in the eye contralateral to the involved optic tract and may be unilateral or bilateral with lesions of the optic chiasm.

Neither the pattern (e.g., central scotoma, arcuate, altitudinal) of ipsilateral visual field impairment nor the severity of visual loss is pathognomonic for a specific optic

neuropathy, and virtually any visual field defect may occur with any optic neuropathy (Trobe, 1978). In their report on 35 eyes in 20 patients with CON and 70 eyes in 54 patients with ON, Trobe and Glaser found central scotomas in 33% of cases of CON (vs. 75% in ON) and felt that a central scotoma could not be used as a differentiating feature between the two entities (Trobe, 1978).

The following sections describe the evaluation of optic neuropathy; this approach is summarized in Figure 1–1. We begin with an age-based differential diagnosis of an acute optic neuropathy. Two of the most common causes of acute optic neuropathy are AION and ON. Although there is considerable overlap in their clinical presentation, age can be used as an initial differentiating feature in many cases (Rizzo, 1991). In younger patients (< 40 years old) with acute unilateral optic disc edema and evidence for an optic neuropathy, ON is more likely than AION. Conversely, in the older patient with acute optic disc edema and visual loss, AION is more common (class III).

Is the Clinical Presentation Typical for

Anterior Ischemic Optic Neuropathy?

The features of typical AION are discussed in Chapter 4. If these features are present, the patient should undergo an evaluation for underlying vasculopathic risk factors and giant cell arteritis (class III–IV, level B).

Is the Clinical Presentation Typical for Optic

Neuritis?

The features and evaluation of typical ON are described in Chapter 2.

Is the Clinical Presentation Consistent with Optic Disc Edema with a Macular Star (ODEMS)?

The evaluation of optic disc edema with a macular star (ODEMS) is outlined in Chapter 3.

Is a Compressive Optic Neuropathy Present?

Compressive optic neuropathy (CON) usually causes painless, progressive, gradual loss of visual function (visual acuity, visual field, and color vision), a relative afferent pupillary defect (in unilateral or asymmetric cases), and optic disc edema or atrophy (but the optic disc may initially appear normal) (Burde, 1992; Miller, 1998; Trobe, 1978). Unfortunately, CON may also present acutely or be steroid responsive and may masquerade as an inflammatory or demyelinating optic neuropathy.

CON that is due to orbital or intracanalicular lesions may result in ipsilateral optic disc edema followed by optic atrophy and may be associated with the development of abnormal blood vessels on the disc head called optociliary shunt vessels. These vessels

probably represent collateral circulation between the retinal and choroidal venous circulation that allows venous blood to bypass the compression at the level of the optic nerve. The presence of an unexplained relative afferent pupillary defect or unexplained optic atrophy should prompt appropriate neuroimaging studies (usually magnetic resonance imaging of the involved optic nerve) (Guy, 1990). Orbital signs such as proptosis, chemosis, or conjunctival injection should direct the imaging studies to the orbit (class III–IV, level B). Table 1–2 lists some possible causes of CON. Tables 1–3, 1–4, 1–5, and 1–6, and Figures 1–2 and 1–3, review the main clinical features of meningioma affecting the anterior visual pathways, optic nerve glioma, and craniopharyngioma.

Is There Clinical Evidence for an Infiltrative or

Inflammatory Optic Neuropathy?

Infiltrative or inflammatory optic neuropathy may present with the typical features of an optic neuropathy discussed above. As described in Chapter 2, the clinical profile of typical ON (e.g., pain with eye movement, typical age of onset, etc.) should be

Table 1–2. Lesions Causing Compressive Optic Neuropathy

Intracranial or intraorbital benign and malignant tumors (Burde, 1992; Golnik, 1996; Katz, 1991; Kazim, 1992; Kodsi, 1993; Lee, 1997b)

Meningioma (see Table 1–3) Glioma (see Tables 1–4 and 1–5) Craniopharyngioma (see Table 1–6) Pituitary adenoma

Lymphoma and leukemia (Brazis, 1995; Nygaard, 1991; Park, 1993; Roth, 2000) Germinoma (Nakajima, 2001)

Sinus histocytosis with lymphadenopathy (Goldberg, 1998) Nasopharyngeal cancer

Metastasis (Kattah, 1993; Newsom, 1999; Pengel, 1997) Extramedullary hematopoiesis (Aarabi, 1998)

Orbital fractures Pneumatocele (Wein, 1999)

Inflammatory or infectious diseases (e.g., mucoceles, sclerosing orbital inflammation) (Hao, 1994; Loehrl, 2000; Thorne, 2002; Yamaguchi, 1997)

Idiopathic hypertrophic cranial pachymeningitis (Tamai, 2000)

Primary bone diseases (e.g., osteopetrosis, fibrous dysplasia, craniometaphyseal dysplasia, fibrosclerosis, Paget’s disease, aneurysmal bone cyst, pneumosinus dilatans, etc.) (Arroyo, 1991; Bland, 1992; Bocca, 1998; Caldermeyer, 1995; Chen, 1997; Daly, 1994; Grimm, 1995; Joseph, 1995; Katz, 1998; Michael, 2000; Saito, 1990; Schaffler, 2000; Skolnick, 2000; Steel, 1995; Stretch, 1992; Weisman, 1990)

Vascular etiologies

Orbital hemorrhage (Amrith, 1990; Buus, 1990; Dolman, 1991; Moorthy, 1992; Muthukumar, 1997) Orbital venous anomalies

Carotid artery and anterior communicating artery aneurysms (Bakker, 1999; Miller, 1995; Misra, 1991; Ortiz, 1991; Shutter, 1993; Vargas, 1994)

Dolichoectasia of the carotid artery (Colapinto, 1996; Jacobson, 1999; Savy, 1996)

(continued)

6 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–2. (continued)

Compression by supraclinoid carotid artery (Ishikawa, 2000; Jacobson, 1999) Arteriovenous malformations

Thyroid ophthalmopathy (see Chapter 16) Hydrocephalus

Iatrogenic

Intracranial catheters (Shults, 1993) Intranasal balloon catheter

Intracranial oxidized cellulose hemostat

Postoperative (e.g., post–optic canal decompression, sinus surgery) (Carter, 1998; Edelstein, 1998) Muslinoma (Bhatti, 2000; Lee, 1997a)

differentiated from atypical ON (e.g., lack of pain, atypical age of onset, anterior or posterior segment inflammation, etc.). Atypical cases should undergo an evaluation for infiltrative or inflammatory etiologies as listed in Table 1–7 (class IV, level C).

Patients with inflammatory autoimmune optic neuropathy often have a progressive or recurrent steroid responsive or steroid dependent clinical course. A more detailed discussion of the evaluation of atypical ON and these alternative etiologies is found in Chapter 2. In patients with a possible inflammatory or infiltrative optic neuropathy, a

Table 1–3. Clinical Features of Meningiomas Affecting the Anterior Visual Pathway

Most commonly middle aged (peak in the 5th decade)

Female : male ¼ 3 : 1

White > African-American

Increased frequency in neurofibromatosis

May grow in pregnancy

Symptoms

Painless (rarely retro-orbital pain)

Gradually progressive loss of vision or visual field defects

If frontal, may have mental status changes

May have diplopia if cavernous sinus involvement

Olfactory groove may have anosmia

Ophthalmic signs

May have relative afferent pupillary defect (RAPD)

Optic disc edema (including papilledema) and=or optic atrophy

May see optociliary shunt vessel (disc collaterals, visual loss, and optic atrophy—characteristic triad)

Indocyanine green videoangiography may show abnormal hemodynamics of choroidal circulation in patients with sheath meningiomas (Muci-Mendoza, 1999)

Visual acuity loss or visual field defects

Generalized depression or constriction (orbital=canal=sphenoid) Central, paracentral, or cecocentral (orbital=canal) Homonymous hemianopsia (suprasellar=sphenoid)

Bitemporal hemianopsia (suprasellar=sphenoid) May have proptosis (orbital=sphenoid)

Motility deficits

Table 1–3. (continued)

Sixth nerve palsy (most common), but any ocular motor palsy (third, fourth, sixth, combination) Restrictive extraocular muscle mechanical limitation if orbital lesion

Paretic pattern if suprasellar=sphenoid=cavernous sinus Differential diagnosis of optic nerve sheath meningioma

Sarcoidosis and other granulomatous diseases Optic nerve sheath meningocele (Garrity, 1990) Idiopathic hypertrophic cranial pachymeningitis Idiopathic inflammatory perioptic neuritis

Metastasis (e.g., breast cancer) and other tumors (Newman, 1996)

Source: Al-Mefty, 1990; Cunliffe, 1992; DeMonte, 1994; Dutton, 1991, 1992; Fayaz, 1999; Fineman, 1999; Garrity, 1990; Goldsmith, 1994a,b; Grunberg, 1991; Hirsch, 1993; Kinjo, 1995; Klink, 2000; Kotapka, 1994; Larson, 1995; Lee, 1996; Lee Wan, 1990; Lundsford, 1994; Mafee, 1999; Maroon, 1994; Moyer, 2000; Muci-Mendoza, 1999; Newman, 1994, 1996; Rubinstein, 1994; Sadun, 1993; Stafford, 1998; Vaphiades, 2001; Weaver, 1993; Wilson, 1994; Wroe, 1991; Zimmerman, 1990b.

Table 1–4. Clinical Features of Optic Glioma

Age

Can present at any age Usually < 10 years old (75%)

Mean 8.8 years (90%< 20 years old) No gender predilection

Association with neurofibromatosis type 1 (NF1) 29% of optic nerve gliomas occur in setting of NF1

15% of NF1 who have no visual symptoms have glioma

Patients with NF1 may have borderline favorable or no different prognosis than patients without NF1

Location of infiltration (topographic localization) One or both optic nerves (nerve alone in 24%) Optic disc (1.6%)

Optic chiasm (75.7%) or tract

In general, the more anterior the lesion, the better the prognosis Signs and symptoms

Proptosis

Painless progressive visual loss (optic neuropathy) Visual loss at presentation in 87.5%

Hypothalamic symptoms (26%) or endocrinologic: diabetes insipidus, diencephalic wasting, precocious puberty, somnolence, growth failure

Disc swelling (35%) or atrophy (59%) Rare optociliary shunt vessels Strabismus

Nystagmus (23%) (spasmus nutans–like nystagmus) Visual field defects (central or bitemporal) Headache (23%)

Intrinsic enlargement of optic nerve with variable contrast enhancement

(continued)

8 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–4. (continued)

Neuroimaging

Magnetic resonance (MR) scan with gadolinium superior to computed tomography (CT) scan Differential diagnosis

Parenchymal optic nerve enlargement Sarcoid

Tuberculosis Syphilis

Optic neuritis (e.g., multiple sclerosis)

Optic nerve infiltration (e.g., leukemia, lymphoma) Extraparenchymal

Optic nerve sheath meningioma Optic nerve sheath metastasis

Treatment Controversial

Gliomas are often static lesions

May enlarge and cause progressive visual loss in one or both eyes Treatment recommendations outlined in Figure 1–3 (Lee, 1999)

Observation in stable cases is reasonable (class III–IV, level B) Radiation therapy (class III–IV, level C)

Usually 5400 cGy in daily dose fractions 150–180 cGy

Radiation risks include cerebrovascular disease, moyamoya disease, cerebral atrophy, subnormal intelligence or learning disabilities, secondary malignancies (e.g., astrocytomas), cataracts, radiation retinopathy or optic neuropathy, endocrinopathy, hypothalamic dysfunction

Chemotherapy—various agents in various combinations: actinomycin-D, vincristine, 2 chloroethyl- cyclohexyl-1-nitrosourea (CCNU), 6-thioguanine, procarbazine, dibromodulatol, topotecan, carboplatin, etoposide (class III–IV, level C)

Surgical therapy (class III–IV, level C)

Optic nerve glioma with no useful vision or progression may be resected Chiasmal hypothalamic, optic tract glioma cannot be resected

Exophytic component of tumor may be debulked Hydrocephalus may require shunting procedure

Prognosis

80% have stable vision after an initial period of visual loss 10-year survival rate 85–100% in various series Spontaneous regression may occur

Source: Brodovsky, 1997; Chateil, 2001; Cre´ange, 1999; Cummings, 2000; Deliganis, 1996; DiMario, 1993; Drake, 1991; Dunn, 1990; Dutton, 1994; Epstein, 1992; Friedman, 1997; Fuss, 1999; Garvey, 1996; Gayre, 2001; Grill, 1999; Hoffman, 1993; Imes, 1991; Janss, 1995; Jenkin, 1993; Kestle, 1993; Kovalic, 1990; Levin, 1992; Listernick, 1992, 1994, 1997; Liu, 1992a, 2001; Moghrabi, 1993; Nishio, 1993; Oaks, 1990; Packer, 1993, 1994; Parsa, 2001; Petronio, 1991; Pierce, 1990; Rodriguez, 1990; Shuper, 1997; Sutton, 1994, 1995; Wisoff, 1990a,b.

lumbar puncture and additional laboratory studies (e.g., complete blood count, syphilis serology, antinuclear antibody, Lyme titer, chest radiograph, etc.) should be considered. The appropriate specific laboratory studies should be directed by pertinent history and examination findings. Table 1–8 reviews the evaluation of an atypical or unexplained optic neuropathy (class IV, level C).

Table 1–5. Clinical Features of Adult Malignant Gliomas of the Anterior Visual Pathway

Age at presentation: middle-age; range 6–79, mean 47.8; 73% were 40 or older Sex: 65% males and 35% females

Clinical signs and symptoms Decreased vision

Bilateral or unilateral

Visual acuity usually falls to blindness over average of 11.1 weeks (range 1–60 weeks) Optic nerve visual field defects

Normal discs, optic disc swelling or atrophy Proptosis

Ophthalmoplegia Retro-orbital pain common

Macular edema, cherry-red spot, and flame hemorrhage or hemorrhagic papillopathy may simulate central retinal vein occlusion (CRVO)

Not associated with NF1 (neurofibromatosis) Location

Involves chiasm and at least one contiguous optic nerve; often involves hypothalamus, third ventricle, basal ganglia, temporal lobe

Primarily affects chiasm and intracranial optic nerves Treatment

Radiation Chemotherapy

Treatment may temporarily improve or rarely stabilize vision Pathology: malignant astrocytoma

Prognosis

Poor

Overall mortality 97%

Mean survival 8.7 months (3 to 24 months)

Is There Evidence for Traumatic Optic

Neuropathy?

The features and evaluation of TON are discussed in Chapter 6.

Is There Evidence for a Toxic or Nutritional

Optic Neuropathy?

Patients with toxic optic neuropathies usually present with painless, bilaterally symmetric, and slowly progressive visual loss. The visual field defect is typically bilateral central or cecocentral scotomas. The optic nerves may appear normal until late in the course of the disease when optic atrophy (often temporal pallor) usually develops. Occasionally the discs may be swollen and slightly hyperemic. A number of medications and toxins may result in optic neuropathy (Brazis, 1998; Danesh-Meyer, 2000; Sedwick, 1991, 1992). These are summarized in Table 1–9. Most of these etiologies can be excluded by a careful and detailed exposure and occupational history.

10 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–6. Clinical Feature of Craniopharyngiomas

Any age

Bimodal incidence

Peak age < 20 and 50 to 70 years old Equal sex distribution

Clinical

Decreased visual acuity (optic nerve, chiasm, optic tract) In children—often decreased acuity and papilledema (50%) In adults—less commonly papilledema

Signs of increased intracranial pressure (headache, nausea, vomiting) Endocrine

Absent or precocious sexual development Growth disturbances

Variable hypopituitarism Diabetes insipidus Obesity

Impotence Amenorrhea=galactorrhea

Somnolence, confusion, or dementia (especially in older patients) Ocular findings

Seesaw nystagmus Visual field defects

Inferior bitemporal field defect (most have field defects) May have incongruous, asymmetric defect

May involve optic tract

May cause ocular motor nerve palsies Neuroimaging

Magnetic resonance imaging (MRI) delineates tumor and intracranial anatomy Computed tomography (CT) shows calcification better

Occasionally may infiltrate optic nerve, chiasm tract, mimicking primary intrinsic tumor such as optic glioma (‘‘potbelly’’ appearance of optic nerve)

Treatment

Surgical: complete vs. partial resection Radiotherapy

Cyst aspiration and P32 instillation

Consider intracystic chemotherapy (bleomycin)

Secondary malignant glioma can develop after radiation therapy

Source: Brummitt, 1992; Crotty, 1995; El-Mahdy, 1998; Fahlbusch, 1999; Honegger, 1999; Petito, 1996; Rao, 1995; Weiner, 1994; Youl, 1990.

Ethambutol is a commonly used medication that may cause toxic optic neuropathy. The mechanism of ethambutol toxicity is poorly understood but may be related to zinc depletion (Schild, 1991). The incidence of toxicity is dose and duration dependent (Choi, 1997; Harcombe, 1991; Kumar, 1993; Russo, 1994; Schild, 1991; Seth, 1991; Thomas, 1994; Tsai, 1997), with the incidence of optic neuropathy being as high as 6% at doses of 25 mg=kg=day. Doses less than 15 mg=kg=day are thought to be relatively safe, but optic neuropathy may occur even at ‘‘safe’’ doses.

Figure 1–2. Treatment algorithm for meningiomas affecting optic pathway.

Barron et al reported ethambutol optic neuropathy in 3 of 304 (0.99%) patients treated with ethambutol at 25 mg=kg=day for 60 days followed by 15 mg=kg=day (Barron, 1974). Leibold described two types of visual loss due to ethambutol toxicity: a central toxicity (e.g., decreased visual acuity, central scotomas, and impaired color perception) and a periaxial toxicity (e.g., normal or almost normal visual acuity, normal color perception, and peripheral quadrantic scotomas or constriction) (Leibold, 1966). There was a 20% incidence of central toxicity and an 11% incidence of periaxial toxicity in 35 patients receiving doses higher than 35 mg=kg=day for a minimum of 185 days. A 5.3% incidence of periaxial toxicity occurred in the 38 patients receiving less than 35 mg=kg=day (Leibold, 1966). Although many authors feel that doses of 25 mg=kg=day =day for less than 2 months followed by maintenance doses of 15 mg=kg=day are safe, there are cases of visual loss even at ‘‘safe’’ doses (Alvarez, 1993; Thomas, 1994; Tsai, 1997). Bronte-Stewart et al reported five patients with severe visual loss after 25 mg=kg=day for 2 months followed by 15 mg=kg=day (Bronte-Stewart, 1976). Three

12 Clinical Pathways in Neuro-Ophthalmology, second edition

Figure 1–3. Treatment algorithm for optic pathway gliomas based on location. (Reprinted from Lee, 1999, with permission from # Swets & Zeitlinger.)

of these five patients had renal disease that may have increased drug levels because 70% of the ethambutol dose is excreted by the kidneys (Citron, 1986). Tsai and Lee reported 10 patients with ethambutol optic neuropathy from ‘‘safe’’ doses, stressing that there is in fact no safe dose of ethambutol. Toxicity in this study was most prominent in individuals over the age of 60 years, and thus this drug must be used with caution, especially in elderly patients (Tsai, 1997). Isoniazid (isonicotinic acid hydrazide, INH), especially in combination with ethambutol, has also been reported to cause a toxic optic neuropathy, and isoniazid toxicity should be suspected as the etiology in cases of persistent visual loss despite discontinuation of ethambutol (Jimenez-Lucho, 1987). Visual evoked potential studies may be useful in evaluating patients with early ethambutol toxicity (Kumar, 1993).

Nutritional deficiencies may result in optic neuropathy (Bourne, 1998; Lessell, 1998). Some vitamin and nutrient deficiencies causing an optic neuropathy are listed in Table 1–10.

Pernicious anemia or dietary deficiency (e.g., vegetarian) may result in a vitamin B12 deficiency optic neuropathy. The pathophysiology of ‘‘alcohol amblyopia’’ is probably related to a deficiency (nutritional amblyopia) of B12, thiamine, and=or folate (rather than a direct toxic effect of alcohol). The ability of tobacco alone to cause a toxic optic neuropathy has been asserted by several authors (Samples and Younge, 1981). Samples and Younge (1981), for example, state that central and cecocentral scotomas may occur in association with smoking alone, especially cigar smoking. A toxic effect of cyanide may be the basis for tobacco optic neuropathy (Bronte-Stewart, 1976). Smoking may also impair intestinal vitamin B12 absorption.

Patients suspected of harboring a toxic or nutritional optic neuropathy should be screened for nutritional deficiencies and treated with appropriate supplementation (class IV, level C). These patients should be urged to discontinue alcohol and tobacco

Table 1–7. Infiltrative or Inflammatory Optic Neuropathies

Neoplastic

Plasmacytoma and multiple myeloma (Maini, 1997)

Carcinomatous meningitis (Freilich, 1995; Ing, 1996; Katz, 1991; McFadzean, 1994; Sung, 1998; Teare, 1991)

Leukemia (Brown, 1992a; Camera, 1993; Costagliola, 1992; Cramer, 1996; Horton, 1992; Pierro, 1992; Shibasaki, 1992; Wallace, 1991)

Lymphoma (Dunker, 1996; Fierz, 2001; Forman, 1998; Guyer, 1990; Noda, 1993; Siatkowski, 1992; Strominger, 1993; Yamamoto, 1994; Zaman, 1993)

Infiltrative orbitopathy in POEMS syndrome

Reactive lymphocytosis with pseudolymphoma from phenytoin (Galetta, 1991)

Paraneoplastic disease (Ing, 1996; Lieberman, 1999; Luiz, 1998; Malik, 1992; Oohira, 1991; Thambisetty, 2001)

Idiopathic hypertrophic cranial pachymeningitis (Aylward, 1995; Botella, 1994; Girkin, 1998; Hamilton, 1993; Jacobson, 1996; Kawano, 1995; Lam, 1994; Levine, 1993; Mamelak, 1993; Nishizaki, 1997; Olmos, 1993; Parney, 1997; Rootman, 1994)

Infectious etiologies

Cryptococcal meningitis (Cohen, 1993)

Aspergillus (Brown, 1994; Dinowitz, 2001; Hutnik, 1997; Johnson, 1999) Mucormycosis (Balch, 1997)

Cysticercosis (Chandra, 2000; Gulliani, 2001; Gurha, 1999) Lyme disease (Lesser, 1990)

Tuberculosis Toxoplasmosis (Song, 2002)

Syphilis (Danesh-Meyer, 1999) Cat-scratch disease (Golnik, 1994b) HIV (AIDS) (Cacciatori, 1996)

Inflammatory diseases (Burde, 1992) Churg-Strauss (Acheson, 1993) Contiguous sinus disease Behc¸et’s disease

Sarcoidosis (Achiron, 1995; Beck, 1994; Carmody, 1994; DeBroff, 1993; Ing, 1997; Kosmorsky, 1996; Pelton, 1999; Sharma, 1991; Silver, 1994; Thorne, 1998)

Wegener’s granulomatosis (Belden, 1993)

Systemic lupus erythematosus (Ahmadieh, 1994; Rosenbaum, 1997; Siatkowski, 2001) Sjo¨gren’s syndrome

Relapsing polychondritis Polyarteritis nodosa Inflammatory bowel disease

Granulomatous hypophysitis (Arsava, 2001) Isolated optic nerve pseudotumor (Patankar, 2000) Sclerosing orbital inflammation (Thorne, 2002)

use. Both serum and erythrocyte folate levels should be checked because there may be variability in the serum folate level alone (especially related to recent meals) (Golnik, 1994).

Toxic or nutritional optic neuropathies are painless, subacute in onset, and bilateral, and usually involve central visual acuity and visual fields (e.g., central and cecocentral

14 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–8. Evaluation of an Atypical or Unexplained Optic Neuropathy

First-line testing

Magnetic resonance imaging of optic nerve(s) Erythrocyte sedimentation rate

Complete blood count with differential Syphilis serology

Antinuclear antibody (ANA) Chest radiograph

Angiotensin-converting enzyme (antineutrophil cytoplasmic antibody, ANCA) Lumbar puncture

Second-line testing

Gallium scan if sarcoidosis suspected

Purified protein derivative (PPD) skin testing if tuberculosis suspected

Anti–double-stranded DNA, complement levels, etc., if systemic lupus erythematosus or other collagen vascular disease suspected

Leber’s hereditary optic neuropathy mutation blood test Heavy metal screen

Serum vitamin B12 and folate levels

Lyme titer if endemic area or exposure history

Paraneoplastic antibody profile (e.g., autoantibodies for collapsin response mediated protein (CRMP)-5 may be associated with optic neuropathy in patients with lung cancer, especially small-cell type, or thymoma) (Cross, 2002; Thambisetty, 2001; Yu, 2001)

Consider more specific serologic studies if infectious process suspect (e.g., Bartonella titers for cat-scratch disease, toxoplasmosis titers, toxocara titers, etc.)

scotomas), but their clinical presentations may be variable. Unfortunately, CON may mimic the clinical presentation of toxic optic neuropathy, and neuroimaging is recommended. The determination of presumed toxic or nutritional optic neuropathy should include a complete evaluation to exclude other etiologies of bilateral, painless, and progressive optic neuropathies (e.g., hereditary optic neuropathy, bilateral compressive optic neuropathy, etc.). The evaluation of presumed toxic optic neuropathy is outlined in Table 1–11 (class IV, level C).

Is There a History of Radiation Exposure to the Optic Nerves?

Radiation optic neuropathy (RON) is thought to be an ischemic disorder of the optic nerve that usually results in irreversible severe visual loss months to years after radiation therapy to the brain or orbit (Arnold, 1995; Borruat, 1993, 1996; Ebner, 1995; Girkin, 1997; Glantz, 1994; Goldsmith, 1992; Guy, 1991, 1995; Hudgins, 1992; Jiang, 1994; Landau, 1996; Leber, 1998; Liu, 1992; McClellan, 1995; Parsons, 1994; Polak, 1995; Roden, 1990; Tachibana, 1990; Young, 1992; Zimmerman, 1990). It is most often a retrobulbar optic neuropathy, and thus the optic nerve may appear normal on initial examination. Approximately three fourths of patients have bilateral involvement. The visual loss is characteristically rapid and progressive, with the disc becoming pale over a period of 4 to 6 weeks. Final vision is NLP in 45% and worse than 20=200 in an

Table 1–9. Etiologies for Toxic Optic Neuropathy

Common etiologies

Ethambutol—tuberculosis therapy (Harcombe, 1991; Kumar, 1993; Russo, 1994; Schild, 1991; Seth, 1991; Thomas, 1994; Tsai, 1997)

Ethanol and tobacco (tobacco alcohol amblyopia) (Danesh-Meyer, 2000; Sedwick, 1991, 1992) Less common etiologies

Amantadine—antiviral, Parkinson’s disease

Amiodarone (Cardarone)—cardiac disease (Macaluso, 1999; Sedwick, 1992; Speicher, 2000; Sreih, 1999)

Amoproxan—vasodilator and antiarrhythmic Aniline dyes

Aspidium (male fern) Barbiturates—sedative, anticonvulsant Cafergot—headache

Carbon disulfide—manufacture of viscose rayon fibers and cellophane films Carbon monoxide (Simmons, 1998)

Carbon tetrachloride—manufacturing of refrigerants and aerosols, dry-cleaning fluid, fat solvent, fire extinguishers, insecticides, shampoo

Cephaloridine—antibiotic Chloramphenicol—antibiotic (Thomas, 1994) Chloronitrobenzene and dinitrobenzene—explosives Chlorpromazine (Thorazine)—antipsychotic Chlorpropamide (Diabenese)—diabetes

Cimetidine (Sa’adah, 1999)

Ciprofloxacin (Cipro)—antibiotic (Vrabec, 1990)

Cisplatin plus carboplatin—chemotherapy (Caraaceni, 1997) Cisplatin plus carmustine—chemotherapy (Wang, 2000) Clioquinol—antibiotic

Cobalt chloride Corticosteroids (Teus, 1991) Cyanide intoxication (dietary)

Cyclosporine—chemotherapy (Avery, 1991) D-penicillamine—rheumatologic

Deferoxamine—for removal of excess iron in patients requiring long-term transfusions (Pinna, 2001)

Dichlorodiphenyltrichloroethane (DDT)—insecticide Digitalis (Digoxin)—cardiac disease Diiodohydroxyquin—amoebocide Dinitrotoluene—explosive

Disulfiram (Antabuse)—alcohol addiction Elcatonin—synthetic analogue of calcitonin (Kimura, 1996) Emetine—amoebocide

Ethylchlorvynol (Placidyl)—hypnotic

Ethylene glycol—antifreeze, moistener for tobacco, lacquer softener, solvent Etoposide phosphate and carboplatin (intracarotid)—chemotherapy (Lauer, 1999) 5-Fluorouracil—antineoplastic

Gallium nitrate—antineoplastic (Csaky, 1997)

(continued)

16 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–9. (continued)

Halogenated hydroxyquinolone (e.g., Clioquinol, boxyquinolone [Colipar],

chlorquinadol [Steroxin], diiodohydroxyquin [Diodoquin], iodochlorhydroxyquin [EnteroVioform], Vioform)—gastrointestinal disorders

Heavy metals (e.g., arsenic, lead, mercury) Hexachlorophene (Phiso-Hex)—detergent cleanser Iodoform—disinfectant

Iodopyracet (Diodrast)—radiologic contrast media Isoniazid (INH)—tuberculosis therapy (Thomas, 1994) Lead intoxication

Lysol—disinfectant

Manganese—skin exposure or inhalation of fumes in pottery or electroplating industry (Lewis, 2001)

Melatonin, Zoloft (sertraline), and a high-protein diet (Lehman, 1999) Methamphetamine (intranasal abuse) (Wijaya, 1999)

Methanol—wood alcohol, solvent, combustible, antifreeze, adulterant of alcohol (Sullivan-Mee, 1998)

Methotrexate—antineoplastic and rheumatologic (Johansson, 1992)

Methyl acetate—solvent for nitrocellulose, resins, and oils and manufacture of artificial leather Methyl bromide—fumigant, fire extinguishers, refrigerant, insecticide Octamoxin—monoamine oxidase inhibitor

Organophosphate pesticides

Pamidronate—treatment of hypercalcemia (des Grottes, 1997)

Penicillamine (Cupramine)—treatment of Wilson’s disease, rheumatologic diseases Phenazone (antipyrine)—analgesic and antipyretic

Pheniprazine (Catron)—monoamine oxidase inhibitor for hypertension and depression Plasmocid—antimalarial

Quinine—antimalarial, cramps Sodium fluoride Streptomycin—tuberculosis therapy

Styrene (vinyl benzyl)—synthetic rubber and fiberglass production Sulfonamides—antibiotics

Tacrolimus (FK 506)—immunosuppressant (Brazis, 2000) Thallium—rodenticides and insecticides

Tobutamide (Orinase)—diabetes Toluene—glue sniffing (Kiyokawa, 1999)

Trichloroethylene—industrial solvent and degreasing compound used in dry cleaning and in manufacture of rubber

Tricresyl phosphate—plasticizer and lubricant Vincristine—antineoplastic agent

additional 40% of affected eyes (i.e., 85% of eyes with RON have a final visual acuity of 20=200 or worse). More rarely, RON may present as an anterior optic neuropathy with optic disc swelling (Parsons, 1994). Such cases usually occur in the setting of radiation retinopathy following treatment of orbital or intraocular lesions. Associated findings of radiation retinopathy resemble those of diabetic retinopathy and variably include peripapillary hard exudates, hemorrhages, subretinal fluid, cotton-wool spots, focal

Table 1–10. Etiologies of Nutritional Optic Neuropathy

B6 deficiency

B12 deficiency (e.g., pernicious anemia) Folate deficiency (Golnik, 1994a) Niacin deficiency

Riboflavin deficiency Thiamine (B1) deficiency

Iatrogenic malabsorption (e.g., post-biliopancreatic bypass procedure) (Smets, 1999)

arteriolar narrowing, macular edema, capillary nonperfusion, capillary telangiectasia, microaneurysms, neovascularization of disc and retina, perivascular sheathing, vitreous hemorrhage, neovascular glaucoma, central retinal artery occlusion, and central retinal vein occlusion. Loss of vision with anterior cases may be due to macular edema, macular hemorrhages, macular exudates, or perifoveal capillary nonperfusion, as well as from optic nerve involvement. The clinical features of RON are outlined in Table 1–12.

The diagnosis of RON is suspected from the clinical setting and may usually be confirmed by magnetic resonance imaging. In RON, the unenhanced T1and T2weighted images show no abnormalities, but there is enhancement of the optic nerves, chiasm, and possibly the optic tracts in some cases (Borruat, 1993; Guy, 1991; Hudgins, 1992; McClellan, 1995; Tachibana, 1990; Young, 1992; Zimmerman, 1990). This enhancement usually resolves over several months. The differential diagnosis of RON is presented in Table 1–13. Recurrence of the primary tumor and radiation-induced tumors must be especially considered.

Patients with RON may rarely improve with corticosteroids. Hyperbaric oxygen therapy may be of benefit if given early in the course (e.g., within 72 hours of onset of symptoms), although some patients show no improvement (Borruat, 1993, 1996; Liu, 1992; Roden, 1990). Anticoagulation therapy was of no help in one case (Barbosa, 1999). There is no proven effective therapy for RON (class IV, level U).

Table 1–11. Evaluation of Painless Progressive Bilateral Optic Neuropathy (Presumed Toxic or Nutritional Optic Neuropathy)

Magnetic resonance imaging of the optic nerves (exclude compressive optic neuropathy [CON]) Vitamin B12 level (serum)

Folate level (serum and erythrocyte) Complete blood count with differential

Urine heavy metal screen (mercury, lead, arsenic) if history suggestive

Syphilis serology (e.g., rapid plasma reagent [RPR], fluorescent treponemal antibody absorption [FTA-ABS])

Leber’s hereditary optic neuropathy mutational analysis

Consider lumbar puncture and other laboratory studies (e.g., chest x-ray, antinuclear antibody [ANA], sedimentation rate, angiotensin-1-converting enzyme [ACE], antineutrophil cytoplasmic antibody [ANCA], paraneoplastic antibody screen, etc.) if an inflammatory or infiltrative process is suspected

Table 1–13. The Differential Diagnosis of Radiation Optic Neuropathy

Recurrent tumor (main consideration!) Empty sella syndrome (arachnoiditis)

Secondary new tumor in field of radiation (long latency 3 to 41 years; mean 15 years) Meningiomas or gliomas

Dural tumors (e.g., fibrosarcoma) Cranial bone tumors (e.g., osteosarcoma)

Peripheral nerve tumors (e.g., malignant schwannoma) Neurofibromatosis type I and ataxia telangiectasia are risk factors

Adhesive arachnoiditis Ischemic optic neuropathy Carcinomatous meningitis

Paraneoplastic optic neuropathy or retinopathy Chemotherapy-related complications or toxicity

Tamoxifen

Cisplatinum

Intraarterial bis 2-(chloroethyl)-1 nitrosourea (BCNU), etoposide phosphate and carboplatin

Primary optic nerve tumors Metastatic tumor

Increased intracranial pressure Venous sinus thrombosis

Is There Clinical Evidence for a Hereditary

Optic Neuropathy?

Miller and Newman have divided the hereditary optic neuropathies into three groups (Miller, 1998):

1.Patients without associated neurologic signs and symptoms.

2.Patients with neurologic signs and symptoms.

3.Patients in whom the optic neuropathy is secondary to the underlying systemic disease.

The hereditary optic neuropathies may have an isolated, dominant (e.g., Kjer optic neuropathy), recessive, or mitochondrial (e.g., Leber’s hereditary optic neuropathy) inheritance pattern. The clinical features of Kjer autosomal-dominant optic neuropathy are outlined in Table 1–14, and the clinical features of Leber’s hereditary optic neuropathy are outlined in Table 1–15. We will not discuss other forms of hereditary optic neuropathy, as outlined in Table 1–16.

Leber’s hereditary optic neuropathy (LHON) usually occurs in young males (up to 80 to 90% of cases in the United States), although it may rarely occur in females and develop at any age (Ajax, 1998; Al-Salem, 1997; Bhatti, 1999; Cock, 1998; Hackett, 1997; Howell, 1997; Jacobson, 1998; Kerrison, 1997; MacMillan, 1998; Mashima, 1998; Purohit, 1997; Saadati, 1998; Tsao, 1999).

20 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–14. The Clinical Features of Dominant Optic Atrophy (Kjer)

Onset in first decade of life (usually 4 to 6 years) in 58% of patients Symptoms

12.5% to 22.6% unaware of visual difficulties

May be discovered to have optic atrophy as consequence of exam of another affected family member

May have nystagmus Visual acuity

20=20 to 20=60 in 40%

20=200 to 20=600 in 15%

Uncommonly hand motions or worse vision 37% of patients 20=60 or better

46% 20=60 to 20=200

17% below 20=200

Often inability to perceive blue color (tritanopia) or generalized dyschromatopsia

Central, paracentral, or cecocentral scotomas; may be characteristic inversion of peripheral field, with the field being more constricted to blue isopters than red

Optic atrophy: occasionally subtle; usually temporal; rarely diffuse

Occasionally peripapillary atrophy, absent foveal reflex, mild macular pigmentary changes, arterial attenuation, and nonglaucomatous cupping

Occasionally mental abnormality (10%) or hearing loss

Occasionally axonal, predominantly sensory hereditary neuropathy (Chalmers, 1996) Visual evoked potential (VEP) may be reduced in amplitude and delayed

Prognosis

Visual prognosis is relatively good in Kjer’s dominant optic atrophy Stable or slow progression of visual loss

Some families showing evidence of linkage to chromosome 3q and 18q

Source: Berninger, 1991; Del Porto, 1994; Eigberg, 1994; Eliott, 1993; Johnston, 1997, 1999; Kerrison, 1999; Kjer, 1996; Votruba, 1998.

Table 1–15. Clinical Features of Leber’s Hereditary Optic Neuropathy (LHON)

Hereditary aspects

‘‘Primary’’ mitochondrial DNA mutations (e.g., 11778, 3460, 14484)

Mother’s egg sole provider of zygote’s cytoplasmic contents—mitochondria only extracellular source of DNA

Every son and daughter of female carrier inherit LHON trait; only women pass trait

Affected woman more likely to have affected children, especially daughters, than unaffected woman carrier

20 to 83% of men at risk develop visual loss 4 to 32% of women at risk develop visual loss

Men affected more than women (80–90% males) Onset 13 to 35 years (range 5–80 years)

Visual acuity loss

Usually acute, rapid, unremitting, and painless Ultimately 20=200 to hand motions (20=20 to NLP range)

Sequential bilateral involvement (second eye in weeks to months later) Interval between onset in two eyes 0 to 15 months

Simultaneous onset in both eyes 42–55%

(continued)

22 Clinical Pathways in Neuro-Ophthalmology, second edition

Table 1–16. Other Hereditary Optic Neuropathies

No associated neurologic deficits

Congenital recessive optic atrophy (extremely rare; existence questioned) Apparent sex-linked optic atrophy

Associated with other neurologic or systemic diseases Autosomal-dominant progressive optic atrophy with congenital deafness

Autosomal-dominant progressive optic atrophy with progressive hearing loss and ataxia Autosomal-dominant progressive optic atrophy with peripheral neuropathy Autosomal-dominant optic atrophy with ataxia and pes cavus

Hereditary optic atrophy with progressive hearing loss and polyneuropathy Familial bulbospinal neuronopathy with optic atrophy

Dominant optic atrophy, deafness, ophthalmoplegia, and myopathy

Autosomal-recessive optic atrophy with progressive hearing loss, spastic quadriplegia, mental deterioration, and death (opticocochleodentate degeneration)

Opticoacoustic atrophy with dementia

Sex-linked recessive optic atrophy, ataxia, deafness, tetraplegia, and areflexia

Progressive encephalopathy with edema, hypsarrhythmia, and optic atrophy (PEHO syndrome)

Juvenile diabetes insipidus, diabetes mellitus, progressive optic atrophy, and deafness (Wolfram’s syndrome or DIDMOAD)

Complicated hereditary infantile optic atrophy (Behr’s syndrome)

Optic atrophy with hereditary ataxias (Friedreich’s ataxia, Marie’s ataxia)

Optic atrophy with Charcot-Marie-Tooth disease (hereditary sensorimotor neuropathy) Optic atrophy with myotonic muscular dystrophy (Gamez, 2001)

Source: Barrett, 1997; Chalmers, 1996; Miller, 1998; Paradiso, 1996; Scolding, 1996.

Some patients with presumed ‘‘tobacco-alcohol amblyopia’’ or nutritional deficiency amblyopia may actual harbor a LHON mutation (Cullom, 1993; Purohit, 1997), and therefore testing for Leber’s mutations may be indicated in patients with presumed toxic or nutritional optic neuropathy. Although the diagnosis of LHON can be confirmed by serologic testing for the known LHON mutations, little consensus exists regarding the treatment of LHON. Some authors have recommended reducing metabolic stress on the optic nerve (e.g., discontinue smoking, alcohol use, known optic nerve toxins, trauma, etc.). Medical therapy remains unproven, but some authors suggest supplementation with multivitamins, folate, vitamin B12, ibedinone and other coenzyme Q10 analogs, and thiamine (class IV, level U).

Is This an Atypical or Unexplained Optic

Neuropathy?

A number of patients with optic neuropathy do not fit into the categories listed in our approach. For patients with unexplained optic neuropathy or atypical optic neuropathy, a suggested evaluation is listed in Table 1–8.

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