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Traumatic Optic Neuropathy
What Is the Traumatic Optic Neuropathy?
Traumatic optic neuropathy (TON) is a clinical diagnosis that presents with typical clinical features. Table 6–1 summarizes these features. The incidence of TON after craniofacial trauma is probably 2 to 5%. Multiple mechanisms have been proposed in TON. Table 6–2 lists the major theories for pathogenesis of TON.
What Is the Evaluation of Traumatic Optic
Neuropathy?
Once the clinical diagnosis of TON is made, neuroimaging should be performed if possible. The incidence of visible canal fracture in TON is variable and does not correlate well with the severity of visual loss (Goldberg, 1992; Seiff, 1990; Steinsapir,
Table 6–1. Clinical Features of Traumatic Optic Neuropathy
History of direct or indirect impact injury to the head, face, or orbit Unilateral or bilateral visual loss
Variable loss of visual acuity (range 20=20 to no light perception) Variable loss of visual field
Relative afferent pupillary defect (unilateral or bilateral but asymmetric cases) Commonly normal or less commonly swollen optic nerve (Brodsky, 1995) Eventual ipsilateral optic atrophy
Exclusion of other etiologies of visual loss in the setting of trauma: Open globe
Traumatic cataract Vitreous hemorrhage Retinal detachment
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120 Clinical Pathways in Neuro-Ophthalmology, second edition
Table 6–2. Proposed Mechanisms of Traumatic
Optic Neuropathy
Compressive or direct mechanical injury
Laceration
Optic nerve contusion, edema, and swelling
Avulsion or transection
Bone fragment or fracture
Hemorrhage
Retrobulbar with increased intraorbital pressure
Subperiosteal hematoma
Optic nerve sheath hematoma
Vascular injury
Vasospasm
Ischemia
Infarction
Source: Aitken, 1991; Mauriello, 1992; Miller, 1990;
Steinsapir, 1994a; Volpe, 1991; Wolin, 1990.
1994a). Computed tomography (CT) may be the best imaging study for the evaluation of TON, detailed examination for bone fractures, evaluation of bone anatomy (Goldberg, 1992), and detection of acute hemorrhage (Knox, 1990; Seiff, 1990). Crowe et al described a case of an intrasheath and intrachiasmal hemorrhage and delayed visual loss (Crowe, 1989). Chou et al in 1996 summarized the literature on TON from 1922 to 1990 and reported optic canal fracture in 92 of 431 cases (21%) (Chou, 1996).
The role of magnetic resonance imaging (MRI) in TON has yet to be clearly defined (Takehara, 1994). In addition, MRI is generally not available in the acute setting and is less useful than CT imaging for the detection of acute hemorrhage, canal fractures, and bone anatomy (class III, level C).
What Is the Treatment of Traumatic Optic
Neuropathy?
The natural history of TON is not well defined but up to 20 to 38% of untreated patients may improve over time. Hughes described 56 cases of untreated TON, of which 44% were permanently blind and 16% gained useful vision (Hughes, 1962). There is, however, no large, well-controlled randomized prospective data regarding the treatment of TON (class III, level U). The literature on medical and surgical treatment of TON is difficult to summarize accurately because of the variations in clinical presentation, treatment modalities (e.g., steroids alone, steroids with surgery, surgery alone), surgical techniques and approaches, study inclusion criteria, and outcome measures, and because of recruitment bias and small sample sizes (class III–IV, level U). Cook et al in 1996 reviewed all cases of TON published in the English-language literature and performed a meta-analysis of treatment results (Cook, 1996). Patients were classified into one of four grades (Table 6–3) depending on visual acuity and the location and type of fracture. Recovery of vision was significantly better in patients who underwent treatment compared with observation alone. No significant difference in improvement was noted in patients treated with corticosteroids alone, surgical decompression alone,
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Table 6–3. Grades of Traumatic Optic Neuropathy
Grade 1: Acuity better than 20=200 without posterior orbital fracture
Grade 2: Acuity 20=200 to light perception (LP) without a posterior orbital fracture
Grade 3: Acuity of no light perception (NLP) or presence of nondisplaced posterior orbital fracture and some remaining vision
Grade 4: NLP and a displaced posterior orbital fracture
Source: Cook, 1996.
or a combination of those modalities. The prognosis for visual recovery worsened with increasing severity of grade. Recovery of vision was better in patients without orbital fractures and in those with anterior rather than posterior fractures.
Chou et al in 1996 summarized the treatment results from the literature (28 reports) and found improvement in 94 (53%) of 176 medical treatment patients; 219 (46%) of 477 surgical treatment patients; and 25 of 81 (31%) patients without treatment (Chou, 1996). These authors divided the patients undergoing medical and surgical treatment into two groups: patients with no light perception (NLP) vision and those with better than light perception (LP) vision. They reported that the NLP group had an improvement rate of 36% (14 of 39 patients) following medical treatment and 34% (19 of 56 patients) following surgical treatment, versus the better than LP group that had an improvement rate of 70% (55 of 79) after medical treatment and 70% (69 of 98) after surgical treatment (class II, level C) (Chou, 1996).
Levin et al studied a total of 133 patients with TON (127 unilateral and 6 bilateral) who had initial visual assessment within 3 days of injury and at least 1 month of followup (Levin, 1999). On the basis of treatment received within 7 days of injury, patients with unilateral injuries were categorized as being in one of three treatment groups: (1) untreated (n ¼9), (2) corticosteroids (n ¼85), or (3) optic canal decompression (n ¼33). Corticosteroid therapy was categorized according to initial daily dose of methylprednisolone (or equivalent corticosteroid) as (1) megadose for 55400 mg (40%), (2) very high dose for 2000–5399 mg (18%), (3) high dose for 500–1999 mg (16%), (4) moderate dose for 100–499 mg (9%), and (5) low dose for <1000 mg (8%). Visual loss was severe in most eyes, being hand motion or worse level of vision in about two thirds. The surgical approach consisted of an external ethmoidectomy in 36%, medial orbitopathy in 12%, endonasal in 39%, craniotomy in 9%, and was not specified in 3%. At follow-up, visual acuity increased by 53 lines in 32% of surgery group, 57% of untreated group, and 52% of the steroid group. The surgery group had more patients whose initial vision was NLP. After adjustment for the baseline visual acuity, there were no significant differences between any of the treatment groups. There was no indication that the dosage or timing of corticosteroid treatment or the timing of surgery was associated with an increased probability of visual improvement. The authors concluded that no clear benefit was found for either corticosteroid therapy or optic canal decompression surgery (class II, level C). The number of patients studied was considered sufficient to rule out major effects in the treatment groups, although clinically relevant effects in specific
122 Clinical Pathways in Neuro-Ophthalmology, second edition
subgroups could have been missed. These results were thought to provide sufficient evidence to conclude that neither corticosteroid treatment nor optic canal surgery should be considered the standard of care for patients with TON. The authors felt that it is therefore clinically reasonable to treat or not treat on an individual patient basis (class II, level C).
The study of Levin et al had several potential problems:
1.The study was not randomized, controlled, or masked, and treatment decisions followed the investigators ‘‘customary practice.’’
2.Selection bias may have been present.
3.Some patients were initially treated with corticosteroids, and it is possible that the decision to perform surgery was related to a lack of positive response to the steroid treatment. This could have biased the results by removing nonresponders from the steroid group and adding patients less likely to improve to the surgery group.
4.Although the data suggested that neither the presence nor the absence of any particular CT finding (e.g., optic nerve compression from a bone fragment or comminuted canal fracture) affected visual outcome, a standardized methodology was not used for either CT technique or grading, and the number of patients with specific CT findings was small.
How Much and What Dose of Corticosteroids
Should Be Used?
Although the mainstay of medical treatment for TON has been corticosteroids, there is no prospective well-controlled study (i.e., no class I evidence) to support the efficacy of treatment or the validity of the various steroid preparations, dosages, or duration of therapy (Anderson, 1982; Lam, 1990; Mauriello, 1992; Volpe, 1991). Anderson et al proposed dexamethasone 3 to 5 mg=kg=day for all patients with TON and advocated surgery for patients with delayed visual loss who failed medical treatment or those with initial visual improvement followed by worsening despite medical treatment (Anderson, 1982). Three (50%) of six patients had visual recovery after steroids, and four patients underwent transethmoidal-sphenoidal decompression with return of vision in one case (25%). Seiff reported a nonconsecutive, nonrandomized retrospective series of 36 patients with TON (Seiff, 1990). Eighteen patients experienced visual improvement, including 5 of 15 (33%) patients who did not receive corticosteroids, and 13 of 21 (62%) patients treated with dexamethasone 1 mg=kg=day. This difference was not found to be statistically significant. Spoor et al reported an uncontrolled, nonconsecutive, retrospective series of 22 eyes in 21 patients with TON (Spoor, 1990). Of these 21 patients, 8 received intravenous (IV) dexamethasone 20 mg every 6 hours and 13 received IV methylprednisolone (MP) 30 mg=kg load followed by 15 mg=kg every 6 hours. Visual improvement occurred in 7 of 9 patients in the dexamethasone group, and 12 of the 13 patients in the MP group. Lessell described 33 cases of TON. Vision improved in 5 of 25 untreated cases, 1 of 4 treated with corticosteroids, and 3 of 4 treated with transethmoidal decompression (Lessell, 1989). Kitthaweesin and Yospaiboon (2001) performed a randomized, double-blind study comparing dexamethasone and methylprednisolone in 20 patients with TON. There were no significant differences in visual improvement
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between the two groups. Chen et al (1998) reviewed 30 cases of TON (Chen, 1998). Thirteen of 21 cases treated with IV methylprednisolone improved and patients with vision better than light perception had a better prognosis.
Because there are no double-masked, placebo-controlled, prospective, randomized data for the treatment of TON, many authors have advocated high doses of IV corticosteroids for TON, extrapolating the data on the use of higher dose MP for central nervous system (CNS) injury (Bracken, 1990, 1993). The first National Acute Spinal Cord Injury Study (NASCIS 1) (Bracken, 1993) was a non–placebo-controlled study that concluded there was no beneficial effect of MP 1000 mg bolus followed by 1000 mg per day for 10 days (‘‘high dose’’) compared with MP 100 mg bolus, then 100 mg per day for 10 days (‘‘standard dose’’). NASCIS 2 was a multicenter, placebo-controlled, randomized, double-masked study of acute spinal cord injury that showed that treatment within 8 hours with MP 30 mg=kg bolus followed by 5.4 mg=kg=hour for 24 hours resulted in significant improvement in motor and sensory function compared to placebo. MP delivered after 8 hours did not improve neurologic outcome. It was thought that MP in the 15 to 30 mg=kg dose range had a different pharmacologic effect on CNS injury parameters including blood flow, calcium homeostasis, energy metabolism, and clinical outcome (Bracken, 1990, 1993). The traditional dose calculation for an equivalent dose of dexamethasone compared with MP has been based on the glucocorticoid potency of 5:1. Steinsapir and Goldberg emphasized in 1994 that the potency ratio for dexamethasone to MP in CNS injury may be closer to 2:1 and therefore that dexamethasone 15 mg=kg may be required (compared to the dose of 3 to 6 mg=kg recommended by Anderson and other authors) for the adequate treatment of TON (Steinsapir, 1994a). In a more recent review, Steinsapir (1999) questioned the evidence that high-dose methylprednisolone is beneficial in TON. In one study using a crush injury model in rats, there was a dose-dependent decrease in the number of axons in the methylprednisolone-treated animals compared with saline-treated controls (Steinsapir, 1994a). Despite these limitations, we summarize in Table 6–4 one protocol for the treatment of TON (class II–IV, level C).
Table 6–4. Traumatic Optic Neuropathy Protocol (class II–IV, level C)
Diagnose TON appropriately (exclude alternative etiologies including open globe) (class III, level B).
Perform canthotomy or cantholysis if the orbit is tense. Drain subperiosteal hematoma if present (class III–IV, level C).
Consider starting IV corticosteroids (one regimen: methylprednisolone 30 mg=kg IV bolus, then 5.4 mg=kg=hour IV for 48 hours or 15 mg=kg every 6 hours) even in patients with NLP vision (Joseph, 1990; Lessell, 1989; Spoor, 1990) (class III, level C).
Perform high-resolution computed tomography (CT) scan of the optic canal and orbit. Consider optic nerve decompression if bony fragments impinging on the optic nerve present (class III, level U).
If vision improves on IV methylprednisolone after 48 hours, then start rapid oral taper of prednisone (class III, level C).
If there is no clinical response after 48 hours or if vision deteriorates during the steroid taper, then surgical decompression of the optic canal is offered especially for patients with severe visual loss (worse than 20=800) (class III, level C).
Source: Reprinted from Steinsapir, 1994a, with permission from Elsevier Science.
124 Clinical Pathways in Neuro-Ophthalmology, second edition
What Is the Surgical Treatment of Traumatic
Optic Neuropathy?
Multiple surgical approaches (e.g., lateral facial, transantral, transconjunctival= intranasal endoscopic, sublabial transnasal, transfrontal, transethmoidal, or a combination of these approaches, extracranial versus intracranial, etc.) and surgical indications have been offered for the treatment of TON. Unfortunately, there is no well-controlled prospective class I data to support the use of any one surgical approach to the optic nerve over another (Anand, 1991; Fernandez, 1994; Friedman, 1991; Girard, 1992; Joseph, 1990; Knox, 1990; Kuppersmith, 1997; Levin, 1994; Luxenberger, 1998; Steinsapir, 1994a). Of particular interest is the literature from Japan concerning TON. Several papers have suggested that TON is much more common in Japan and more responsive to surgical treatment. Fukado reported 460 canal fractures on stereoscopic radiography of the optic canal in 500 patients with loss of vision following head trauma (Fukado, 1972, 1975). Of 400 patients who underwent transethmoidal canal decompression, almost 100% had improvement. Several authors have raised serious questions about these studies, including the validity of the diagnostic criteria for canal fracture, the lack of complete ocular examination data including visual field information, the paucity of bilateral cases, the high percentage of improvement after surgery, and the suspiciously high frequency of canal fracture (Kennerdell, 1976). Niho et al reported an 80% success rate in 25 patients with TON and transsphenoidal decompression of the canal (Niho, 1970). Matsuzaki et al reported optic canal fractures in 52% of 33 patients with TON (Matsuzaki, 1982). Vision improved in 36% of the 11 cases undergoing surgical decompression of the canal (8 transcranial and 3 transethmoidal). Vision improved in 50% of the 22 patients treated medically with prednisone (40– 100 mg=day for 5 to 7 days), mannitol, and urokinase (if perineural hematoma was suspected). Fujitani et al reported 110 cases of TON, of which 43 cases underwent medical therapy with prednisone 60 mg=day and 70 eyes underwent transethmoidal decompression. The medically treated group had a 44% improvement rate versus a 47% improvement rate after surgery (Fujitani, 1986). Mine et al studied 34 patients with indirect TON (Mine, 1999). Twelve cases (13 eyes) underwent surgery and 24 patients (24 eyes) were managed without surgery. When initial visual acuity was hand motions or better, vision improved significantly more in patients with surgery than in those without surgery. Age and optic canal fracture did not affect visual improvement or influence the decision for or against surgery.
Joseph et al reported 14 patients in a retrospective, nonconsecutive study with TON treated with transethmoidal-sphenoidal canal decompression and dexamethasone preand postoperatively. Eleven of the 14 patients improved, including 3 of 5 patients who presented with NLP vision ( Joseph, 1990). Luxenberger et al retrospectively studied 14 patients who underwent optic nerve decompression surgery (within 48 hours in 67%) and megadose corticosteroid therapy and noted improvement in 7 patients (50%) (Luxenberger, 1998). However, in this study there was no formal measurement of initial vision, the definition of visual improvement was not stated, and the length of follow-up was not stated. Li et al reported the results of 45 consecutive patients treated with extracranial optic nerve decompression after at least 12 to 24 hours of corticosteroid therapy without improvement and noted visual improvement in 32 patients after surgery (71%) (Li, 1999b). Wang et al (2001) reviewed 61 consecutive, nonrandomized
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Figure 6–1. Evaluation and treatment of traumatic optic neuropathy.
126 Clinical Pathways in Neuro-Ophthalmology, second edition
patients with TON. There was no significant difference in visual improvement in patients treated with surgical versus nonsurgical means. No light perception vision, however, or the presence of an orbital fracture (presumably a marker of more severe trauma), were poor prognostic indicators. In this series, 29 of 34 patients (85%) with orbital fractures presented with no light perception. Lubben et al (2001) reported a retrospective analysis of 65 cases of TON who underwent optic nerve decompression. Thirteen of their 65 patients were comatose and the surgical indication for TON was based on the finding of a canal or orbital apex lesion. We generally do not recommend surgery for comatose patients who cannot provide visual information. Kountakis et al (2000) performed a retrospective review of TON treated with endoscopic optic nerve decompression. Eleven of 34 patients treated with high-dose steroids improved and 23 did not improve. Of these 23 patients, 17 underwent endoscopic optic nerve decompression and 14 of 17 (82%) had improved visual acuity. These authors suggested that patients with visual acuity better than 20=200 had a better prognosis with steroids alone than patients with worse than 20=400 visual acuity.
Unfortunately, until a randomized, prospective, double-masked, placebo-controlled clinical trial is performed, the treatment of TON will remain controversial (class II–III, level U). The approach to TON is outlined in Figure 6–1.
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