Walsh & Hoyt: Traumatic Optic Neuropathies: Pharmacology - Experimental

Over the past thirty years, research in acute spinal cord trauma has demonstrated a pharmacology for very high doses of corticosteroids that is distinct from the pharmacology of steroids in the doses more typically encountered in clinical practice. In the doses usually encountered in clinical practice, corticosteroids are thought to act by decreasing the rate of protein synthesis. Receptor proteins in the cytosol mediate this action. In lymphocytes, this steroid-receptor complex stimulates the synthesis of an inhibitory protein. In addition, glucocorticoids inhibit the release of arachidonic acid from phospholipids, decreasing the production of prostaglandin endoperoxides and thromboxane

Walsh & Hoyt: Traumatic Optic Neuropathies

Optic nerve injuries are classically divided into direct and indirect injuries. Direct injuries are open injuries where an external object penetrates the tissues to impact the optic nerve. Indirect optic nerve injuries occur when the force of collision is imparted into the skull and this energy is absorbed by the optic nerve. The prognostic value in knowing that an injury was direct or indirect is unclear. Historically, direct optic nerve injury is associated with a poor visual outcome. It may be safe to classify an optic nerve injury as direct if orbital imaging reveals a bullet at the orbital apex, but this provides no insight into the cellular injury mechanism. The classification does not illuminate whether the nerve is severed with no hope of recovery or only mildly injured with significant recovery potential. This becomes important as strategies for treating nerve injuries evolve

Walsh & Hoyt: Classification

Optic nerve injuries are classically divided into direct and indirect injuries. Direct injuries are open injuries where an external object penetrates the tissues to impact the optic nerve. Indirect optic nerve injuries occur when the force of collision is imparted into the skull and this energy is absorbed by the optic nerve. The prognostic value in knowing that an injury was direct or indirect is unclear. Historically, direct optic nerve injury is associated with a poor visual outcome. It may be safe to classify an optic nerve injury as direct if orbital imaging reveals a bullet at the orbital apex, but this provides no insight into the cellular injury mechanism. The classification does not illuminate whether the nerve is severed with no hope of recovery or only mildly injured with significant recovery potential. This becomes important as strategies for treating nerve injuries evolve

Walsh & Hoyt: Traumatic Optic Neuropathies: Epidemiology

Traumatic optic neuropathy occurs in association with high momentum deceleration injuries. Optic nerve injury is often associated with midface trauma. Table 9.1 lists the most common causes of traumatic optic neuropathy. Motor vehicle and bicycle accidents are the most frequent cause, accounting for 1763% of cases, depending on the series. Motorcycle accident victims may be particularly vulnerable to traumatic optic neuropathy. A consecutive series of 101 patients with head trauma after a motorcycle accident found 18 cases of traumatic optic neuropathy (18%) (10). Falls are the next most common cause, producing 1450% of cases. Traumatic optic neuropathy has also resulted from frontal impact by falling debris (11,12), assault (11), stab wounds (13), gun shot wounds (13,14), skateboarding (11), bottlecork injuries (15), following seemingly trivial injuries (3,16), and following endoscopic sinus surgery (1720). Iatrogenic optic nerve trauma with visual loss is rare following elective LeFort I osteotomy. When it does occur, it may be related to uncontrolled and unpredictable pterygomaxillary disjunction with propagation of the fractures into the optic canal (22)

Walsh & Hoyt: Traumatic Optic Neuropathies: Imaging

The superior imaging afforded by computed tomography and magnetic resonance imaging has made plain films and hypoclinoidal tomograms obsolete. Manfredi and coworkers reviewed the medical records of 379 patients with facial fractures. Twenty-one patients lost all vision in one eye (6%) and 3 of these 21 lost vision in both eyes; 12 of the 21 patients with visual loss had CT scans of the head as part of the initial assessment and of these 12, visual loss was attributed to traumatic globe injuries in 7 cases. CT scans in the remaining 5 patients demonstrated a fracture through the optic canal. The fracture may injure the optic nerve directly or it may serve as a marker of the severity of force transferred into the optic nerve. Seiff et al. reported CT results of nine patients with traumatic optic neuropathy. Six of the nine patients demonstrated fractures of the optic canal. Fractures were present in adjacent structures but not extending into the optic canal in two additional patients. In a follow-up study, canal fractures were found in 16 of 36 patients and fractures of the bones adjacent to the optic canal, but not involving the optic canal, in an additional 10 of 36 patients. However, 63% of the patients with canal fractures presented with no light perception compared with a 40% incidence of no light perception when there was no fracture or the fracture did not extend to the optic canal

Walsh & Hoyt: Traumatic Optic Neuropathies: Management - Early Studies

Early reports concerning surgical decompression suggested it to be of little value in treating traumatic optic neuropathy. In these cases decompression was performed transcranially. Hooper operated on five patients with traumatic optic neuropathy. Two patients recovered vision, but only one patient had optic canal decompression. Hughes explored 8 cases in his series of 90 patients, with no visual improvement. Edmund and Godtfredsen operated on 6 patients in their series of 22 patients. The vision of only one patient improved following surgery, changing from no light perception to light perception. Based on this experience and the available pathologic material, Walsh felt that visual recovery was unlikely if amaurosis occurred at the moment of impact and advised against surgical intervention. He also cautioned against operating on unconscious patients. However, in cases of delayed visual loss, Walsh suggested that surgical decompression might be more promising

Walsh & Hoyt: Traumatic Optic Neuropathies: Examination

Visual acuity following indirect optic nerve trauma is often significantly reduced. Each patient in Hughes series of 56 cases presented with no light perception. All 46 patients described by Turner also presented with no light perception on the side with optic nerve injury. In Hoopers series, 14 of 21 patients presented with no light perception. In the series reported by Edmund, 17 of 22 patients presented with no light perception. While vision better than 20/400 is not inconsistent with traumatic optic neuropathy, it is unusual in older reported cases. Pupillary reflexes. Biomicroscopy and fundoscopy

Walsh & Hoyt: Traumatic Optic Neuropathies: Pathology

Pringle conducted 174 autopsies on patients who were left unconscious from the time of head injury until death. In 16 cases, blood was found in the optic nerve sheath, leading him to hypothesize that indirect injury to the optic nerve was caused by hemorrhage compressing the optic nerve. These observations are also supported by the work of Hughes who explored six nerves in five patients

Walsh & Hoyt: Traumatic Optic Neuropathies: Management

The management of traumatic optic neuropathy should be guided by the Hippocratic adage to do no harm. Almost all case reports and most case series of traumatic optic neuropathy present treated cases. The older series are biased toward cases with severe visual loss. Contemporary studies contain much larger numbers of patients with mild optic nerve injuries. Consequently it is very difficult to use the retrospective data in the literature to characterize the natural history of traumatic optic neuropathy, making meaningful meta-analysis difficult. Without an accurate knowledge of the natural history of this injury, measuring the beneficial effect of a medical, surgical or combined approach is very difficult. This section will critically review the studies that are in the literature and summarize what is currently known concerning the clinical management of traumatic optic neuropathy

Walsh & Hoyt: Optic Disc Avulsion

Figure 9.