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, 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).
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 |
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.
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, 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.
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.
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 follow-up (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 = 9), (2) corticosteroids (n = 85), or (3) optic canal decompression (n = 33). Corticosteroid therapy was categorized according to initial daily dose of methylprednisolone (or equivalent corticosteroid) as (1) megadose for ≥ 5400 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 ≥3 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 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.
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