Review article
Visual loss due to optic nerve injury after closed head trauma constitutes a formidable diagnostic and therapeutic
challenge for the clinician. Assessment must be made of the site of optic nerve injury, and this is often difficult in the
patient with an altered level of consciousness. A decision regarding optic nerve decompression must be formulated, yet
the literature is confusing with regard to operative indications. In reviewing current pathogenetic theories, clinicopath-
ological data, and therapeutic options, this report attempts to clarify the role of surgical intervention in indirect optic
nerve injury. (Neurosurgery 14:756—764, 1984)
Key words: Head trauma. Indirect injury, Optic nerve trauma, Visual loss
Approximately 5% of all patients with head trauma mani- Each optic nerve is approximately 50 mm in length, ex-
fest an injury to some portion of the visual system (12). The tending from the posterior aspect of the eye to the optic
diagnostic challenge facing the clinician during the initial chiasm. It is generally divided into four segments: intraocular,
evaluation of such patients is considerable. Assessment of intraorbital, intracanalicular. and intracranial.
visual function is often difficult in an individual with an
altered state of consciousness. If vision is found to be im-
paired, decisions must be made regarding further evaluation
and management based on the site of injury.
1
JuneThe intraocular portion of the optic nerve is about 1 mm in
1984 theINDIRECT
dura mater, arachnoid,
INJURYand OFpiaTHE
materOPTIC
of the brain.
NERVE The 2
length with a diameter of 1.5 mm. The optic nerve exits the intraorbital segment is longer than the distance between the
globe approximately 3 mm nasal to and slightly above the optic disc and the orbital apex, making the optic nerve
fovea. Surrounded by retina and choroid, the intraocular optic somewhat redundant and mobile within the orbit. It is
nerve is visible ophthalmoscopically as the optic disc. This
portion of the nerve lies anterior to the lamina cribrosa, which surrounded by orbital fat and the extraocular muscles. The
is a thin, sievelike canal in the sclera through which the axons long and short posterior ciliary arteries and nerves surround
of the retinal ganglion cells pass. Posterior to the lamina the optic nerve and are closely related to the dural sheath
cribrosa, the optic nerve becomes myelinated and the septal immediately behind the globe. The central retinal artery and
network, which is continuous with the pia mater, begins. The vein course forward in the orbit below the optic nerve, outside
vascular supply of the intraocular optic nerve is derived but adherent to the dural sheath. Ten to fifteen millimetres
principally from an incomplete arterial circle (Zinn-Haller), posterior to the globe, these vessels enter the optic nerve,
which receives contributions from the posterior ciliary arteries, piercing the dura mater and arachnoid. At the apex of the orbit,
the pial arterial plexus, and the peripapillary choroid. The latter the four rectus muscles arise from a tendinous ring, the anulus
also sends small arterioles directly to the prelaminar disc
substance. The central retinal artery perfuses the retina, but of Zinn. which encircles the optic nerve and the ophthalmic
probably contributes very little to the optic disc. artery. In this area, the dura mater of the optic nerve fuses with
The intraorbital portion of the optic nerve extends from the the periosteum of the optic canal and orbit and also with the
posterior aspect of the globe to the optic canal, measuring 25 anulus of Zinn. The anterior intraorbital portion of the optic
to 30 mm in length and 3 to 4 mm in diameter. It is covered by nerve is vascularized by centrifuga
3 KLINE et al. Neurosurgery, Vol. 14, No. 6
l in the retinal vasculature, and a cherry-red spot in the macula
(21). In other instances, retinal vascular spasm without
thrombosis has been observed (21). Traumatic ischemic optic
neuropathy with a diffusely swollen disc and the remainder of
branches of the central retinal artery and centripetal the fundus normal in appearance has also been reported (18,
branches of the pial vessels, whereas the remainder of the 55). Fluorescein angiography in these cases supports
intraorbital optic nerve receives only the pial contribution. compromise of the posterior ciliary arterial circulation. Varying
degrees of avulsion of the intraocular optic nerve from the
globe may also be seen after head trauma. Anterior marginal
The intracanalicular portion of the optic nerve measures tears are characterized by optic nerve dysfunction with a
about 10 mm in length and is 4 mm in diameter. It traverses the hemorrhage at the disc margin that rarely exceeds more than a
optic canal, which is formed by the union of the two roots of third of its circumference (21). Within 2 weeks the hemorrhage
the lesser wing of the sphenoid bone. The canal is 4 to 9 mm resolves, leaving a heavily pigmented scar at the disc margin,
long and 4 to 6 mm wide and runs posteriorly and medially. In and within 1 month disc pallor, often mild, is evident. In
addition to the optic nerve, the canal contains the ophthalmic general, there is good correlation between the visual field
artery, postganglionic fibers of the carotid sympathetic plexus, defect and the visible abnormality at the disc margin. Visual
and extensions of the meningeal sheaths. In contrast to the acuity is variable, but is usually poor. Infrequently. complete
intraorbital optic nerve, which moves freely as the eye moves, avulsion of the optic nervehead may occur, causing total
the intracanalicular optic nerve is fixed within the optic canal blindness (19). Initial ophthalmological examination reveals a
by the dura mater, which is tightly adherent to the bone within deep round hole with a clear sharp rim surrounded by a bared
the optic canal. Within the orbit, the dura divides into two ring of sclera. Over the following 1 to 2 months, this hole is
layers: one remains as the outer sheath of the optic nerve, and filled with white connective tissue and the retina is thrown into
the other becomes the orbital periosteum. Intracranially. the thick folds. Circulation in the branch retinal arterioles and
dura mater leaves the optic nerve to become the periosteum of veins is interrupted initially, but is reestablished within 2 to 3
the sphenoid bone. The subarachnoid space, however, does weeks of injury.
communicate through the optic canal and around the optic
nerve to the posterior aspect of the globe. In the optic canal, Posterior indirect optic nerve injury
the optic nerve receives pial branches derived from the
ophthalmic and internal carotid arteries.
The intracranial segment of the optic nerve, an average of 10 The diagnosis of posterior optic nerve injury is based on
mm in length (range, 3-16 mm), has a diameter of 4 to 7 mm. evidence of optic nerve dysfunction in the absence of fundu-
It is located above the diaphragma sella. Lateral to the optic scopic abnormalities on initial examination and no evidence of
nerve is the internal carotid artery, which gives off the chiasmal injury. Over 4 to 8 weeks after head trauma, optic
ophthalmic artery just inferior to the nerve. The frontal lobes of disc pallor and loss of the retinal nerve fiber layer becomes
the brain lie above each optic nerve. On the ventral surface of apparent. It is presumed that the lesion lies somewhere be-
each frontal lobe, the olfactory tract is separated from the optic tween the entry of the central retinal artery into the optic nerve
nerve by the anterior cerebral and anterior communicating and the optic chiasm. Because of the anatomic considerations
arteries. The intracranial portion of the optic nerve terminates and those instances in which pathological correlation has been
at the optic chiasm. The intracranial optic nerve receives small made, the intracanalicular portion of the optic nerve is by far
pial vessels originating from the internal carotid. the A-l the most frequent site of injury.
segment of the anterior cerebral, and the anterior It is difficult to analyze the clinical data dealing with
communicating arteries. posterior injury of the optic nerve (Table 1). The nature of head
injury varies from case to case, and there is great variability in
TYPES OF INDIRECT OPTIC NERVE INJURY the type and sophistication of radiological evaluation and in
methods of therapy, both medical and surgical. The ultimate
visual acuity is variable regardless of the type of treatment.
Visual field defects fall into two main categories, central
The intracanalicular portion of the optic nerve is that most scotomas and nerve fiber bundle defects. Skull fractures seen
frequently damaged as a consequence of closed head trauma on plain films or bony tomograms usually bear no relationship
(21. 35. 49). Occasionally, the intraocular segment is damaged. to the degree of visual loss. In addition, no consistently
and ophthalmoscopic findings are then evident. In general, the effective therapy can be demonstrated.
intraorbital portion is spared because of its relative laxity
within the orbit and the protection offered by the surrounding
orbital fat and extraocular muscles. Similarly, the intracranial PATHOLOGICAL STUDIES
portion of the nerve is rarely involved because of its relative
mobility within the head.
From a practical standpoint, indirect optic nerve injuries can There are few reports in the literature correlating surgical
be divided into two categories: anterior, in which fundu- scopic and pathological findings in indirect optic nerve injury (15, 20-
abnormalities are evident, and posterior, in which the fundus 22, 24, 33, 35, 41). Review of these cases is essential in
initially appears normal. attempting to understand the pathophysiological mechanisms
involved and the potential role of neurosurgical intervention.
Anterior indirect optic nerve injury
Anterior injury denotes involvement of the intraocular optic
nerve (optic disc) and that portion of the intraocular segment
containing the central retinal artery. In all instances, Observations of the optic nerves made during surgical
ophthalmoscopic abnormalities are visible. There may be a exploration vary widely. Descriptions include grossly normal
central retinal artery occlusion with an edematous retina, a pale appearance, arachnoid adhesions, hemorrhage into the optic
optic disc, threadlike arterioles, visible sludging of blood flow nerve sheaths or within the nerve itself, direct compression by
bony fragments of the optic canal or anterior clinoid process,
4 KLINE et al. Neurosurgery. Vol. 14, No. 6
and partial or complete laceration of the intracanal- instantaneous mechanism of injury possibly caused
TABLE 1
Posterior Indirect Optic Nerve Injury
Author. Year (Ref.) No. Final Visual Acuity Visual Fields Neuroradiological Studies Treatment
Cases
Davidson, 1938 (5) 37 20/20-20/400 = 11 less CC; NFB de- None
Skull fracture = 29 (optic
than 20/400 = 20 NLP = fects: "con- canal = 1)
6 tracted”
Turner, 1943 (47) 46 20/20-20/400 = 23 less CC; NFB defects Skull fracture = 27 (optic None
than 20/400= 10 NLP = canal = 4)
13
Roger. 1943 (36) 20 20/20-20/400 = 6 less NFB defects; Skull fracture = 9 None
than 20/400 = 7 NLP =7 "constriction”
“Abbreviations: NLP, no light perception; CC central scotoma; NFB, nerve fiber bundle.
icular optic nerve (15. 20-22, 24. 33, 35, 41). by shearing forces disrupting the nerve fibers.
Histological abnormalities have been consistently Ramsay reported the case of a 72-year-old woman
demonstrated. regardless of the gross appearance of who sustained blindness of the left eye after closed
the nerve either at surgical exploration or at head trauma and died 4 days later (35). Histological
postmortem examination. Hughes reported two cases study revealed an epidural hemorrhage of the left
studied pathologically (21). In one. examination of optic nerve associated with a fracture of the optic
the optic nerve at operation was canal. There was minimal hemorrhage in the dura
unremarkable.However, at autopsy, microscopic stuuy mater and no disruption of the nerve or sheath. From
of the intracanalicu- lar segment revealed an area of the level of approximately 1 mm anterior to the
chronic inflammation with phagocytes containing fracture of the optic canal and extending posteriorly 3
iron pigment and lipid. Throughout the area of mm posterior to the cranial opening of the canal, the
degeneration, no intact axons could be demonstrated. nerve was totally infarcted, showing scattered
In the other cases, complete disruption of the hemorrhages and neutrophil infiltration. At no level
intracan- alicular optic nerve was identified at was there evidence of rupture of small arterioles
operation. Histological study confirmed necrosis of within the nerve or sheath. The author postulated two
this portion of the nerve, with degeneration of myelin possible mechanisms of injury. The shearing force at
and loss of axons. Based on these cases, Hughes the fracture site might have caused rupture of a small
concluded that, although there are instances of arteriole supplying the nerve, resulting in infarction,
contusion and laceration of the optic nerve within the and subsequent hemorrhage and edema of the nerve
canal, most posterior indirect optic nerve injuries within the canal then led to extension of the infarction
resulted from vascular insufficiency and infarction of to involve the whole nerve. Alternatively, the shearing
the intracanalicular segment and thus would probably forces might have produced edema of the canalicular
not benefit from surgical decompression. optic nerve, causing infarction through compression.
Ramsay preferred the latter explanation because
there was no evidence to suggest rupture of an in the nerve; and (cj there were orbital roof and optic
arteriole supplying the optic nerve in the region of the canal fractures both with and without direct optic
fracture. The extension of the infarction posteriorly nerve decompression (22). In a postmortem study of
may have resulted from compression of the pial 70 patients who died from head injury. Walsh and
Lindenberg classified the resultant optic nerve lesions
branches supplying the intracanalicular optic nerve as primary and secondary (54). Primary refers to all
that arise from the ophthalmic artery within the orbit alterations caused by mechanical force and
and pass posteriorly through the region of the originating at the moment of impact. This includes:
fracture. (a) hemorrhages into the nerve, dura mater, and
sheath spaces; (b) tears in the nerve: and (c) contusion
necrosis of the nerve. Secondary lesions include all
These reports illustrate that histopathological alterations that originate at any time after impact,
findings vary in cases of indirect optic nerve trauma including: (a) edema of the nerve; (b) necrosis from
and suggest that multiple pathophysiological local vascular compression or systemic circulating
mechanisms may be operative. failure; and (c) infarction of the optic nerve related to
In support of this concept, Imachi and coworkers vascular obstruction (spasm, thrombosis).
(22) and Walsh and Lindenberg (54) have reviewed
optic nerve injury in patients who died from head PATHOPHYSIOLOGY OF INDIRECT OPTIC
trauma. In 55 cases, Imachi and coworkers NERVE INJURY
demonstrated a variety of histopathological findings: The mechanisms by which closed head trauma leads
(a) “in a high percentage” there was hemorrhage in to optic nerve injury are not yet determined, primarily
the optic nerve sheath, dura mater, subdural and
subarachnoid spaces, pia, fibrous septa, and optic because of the lack of clinicopathological material
nerve bundles; (b) there were partial or complete tears available for study. The literature suggests multiple
causes (Table 2)
.Included in virtually all reports of indirect optic documented cases of visual recovery after the removal
nerve trauma is the concept of mechanical damage to of bone compressing the optic nerve. Thus, surgical
the nerve itself. Descriptive terms frequently used intervention may be of benefit.
include “stretching.” “tearing," and “torsion” (21. 33.
49). This may lead to partial or complete disruption of
the nerve. This type of injury occurs most often in the Recently, Anderson and coworkers used the
area of the cranial opening of the optic canal and less technique of holographic interferometry to evaluate
commonly at the orbital opening. This injury is orbital and optic canal stress without fracture (1). This
primarily due to immobilization of the nerve within method is extremely sensitive in demonstrating
the optic canal and its freedom of movement both surface perturbations on an object in response to
intracranially and intraorbitally. Sudden movements surface loading. Examination of the response of a
of the brain produce significant shearing forces number of skulls to loading over the supraorbital
adjacent to the optic canal, where the nerve is fixed in ridge revealed stress concentration in the orbital roof
position. about 5 to 8 mm from the optic foramen. This
suggests that forces from frontal trauma may be
transmitted to the optic nerve and its supporting
Deformation or fracture of the bony structures structures and suggests that deformation of sur-
surrounding the optic nerve clearly produces injury in rounding bone without fracture is a potential
a small number of cases (20, 22, 24, 33. 35). Fractures mechanism for optic nerve injury.
may involve the optic canal, the anterior clinoid The most widely accepted explanation of the
process, and the orbital roof. The generally held pathogenesis of indirect optic nerve injury is vascular
concept is that there is disruption in the continuity of insufficiency. If the visual loss is transient vasospasm
the canal with compression or laceration of the nerve. may be responsible, but if it is permanent optic nerve
Falconer reported compression of the optic nerve by a infarction has presumably oc-
bone spicule, which was successfully removed with
subsequent improvement of vision (52). In one of the
cases reported by Hooper, the intracranial portion of TABU: 2
the right optic nerve was contused by a fractured and Mechanisms of Indirect Optic Nerve Injury
displaced anterior clinoid process (20). Surgical
intervention produced no improvement. A similar I. L
experience was reported by Anderson et al. in a
repairing a displaced fracture of the left optic canal: c
total blindness remained in the eye (1). Kennerdell et e
al. (24) and Schmaltz and Schcrmann (40) r
a
6 KLINE et al. Neurosurgery. Vol. 14, No. 6
function in both (32). Hammer and Am bos reported Pupillary reactivity. An assessment of pupillary
four cases of visual loss after closed head trauma (15). reactivity is of critical importance in the ocular
Using a transfrontal approach to decompress the examination of a patient who has sustained head
intraorbital optic nerve, the authors found “a trauma, whether he is alert and oriented or unable to
hematoma of the optic nerve sheath" in each case. All respond to visual testing. After reviewing 22 cases of
patients reportedly achieved complete recovery of optic nerve injury after head trauma, Edmund and
vision after evacuation of the hematoma. Godtfredsen concluded that the direct pupillary
response to light is the most reliable sign of the extent
of optic nerve injury (6). Roentgenographic studies,
Intraneural hemorrhage may also occur as a severity of head trauma, and ophthalmoscopic
consequence of indirect optic nerve injury (22, 54), findings were all considerably less valuable than the
arising from traumatic rupture of capillaries or small status of the pupillary light reflex. After unilateral
veins and resulting in the accumulation of optic nerve injury, the pupil on the side of the injured
perivascular blood that compresses surrounding nerve nerve is equal in size to the opposite pupil, but is less
fibers. Resorption of this blood may explain the reactive to direct light stimulation. The pupil on the
improvement in vision and visual field defects in affected side will, however, react consensually. This
some cases. Imachi and coworkers emphasized the indicates the presence of an afferent lesion in the
frequency of intraneural hemorrhage, stating " . . . pupillary light reflex pathway, specifically a
vascular or neurovascular friction is the cause of these conduction defect involving the optic nerve on the
hemorrhages” (22). side of the less reactive pupil. The opposite pupil will
It can be seen that a variety of mechanisms react to direct light stimulation, but will have a
contribute to optic nerve injury after closed head reduced consensual response. The difference in
trauma. Undoubtedly, many of the mechanisms pupillary reactions with the light first in one and then
discussed occur simultaneously and are in the other eye may be enhanced by swinging a
interdependent. For example, bony fracture of the flashlight back and forth from one eye to the other
optic canal may lead to vascular insufficiency and (26). Each time the light is brought from the abnormal
edema of the nerve, and this edema may further to the intact eye, there is pupillary constriction. When
compromise the vascular supply of the nerve, the light is moved from the intact to the abnormal
extending the area of infarction. (afferent defect) eye, so-called paradoxical dilation is
seen. This response to the swinging flashlight test has
CLINICAL EVALUATION OF INDIRECT OPTIC been termed the Marcus Gunn pupil (Gunn's pupillary
NERVE INJURY test) (25).
Examination techniques
Visual field testing. There are no pathognomonic
visual field defects associated with indirect optic
Examination of the visual system after head trauma nerve injuries. All visual field abnormalities fall into
may be difficult or impossible. Nevertheless, every the general categories of central scotoma and nerve
effort should be made to assess visual function using fiber bundle defects. Although visual field
the following techniques. examination using the tangent screen or perimeter is
preferred, a confrontation technique usually must be
employed initially in examining patients after head
Visual acuity. When possible, visual acuity in each trauma. Discovery of a hemianopic defect, either
eye should be assessed. Ideally, a Snellen acuity chart bitemporal or homonymous, excludes consideration
or a Rosenbaum near vision card should be used. of optic nerve decompression. Again, the value of
Failing this a newspaper or some other form of readily serial determinations of visual field function is
available printed material should be shown to the important; documentation of a deteriorating unilateral
patient. If this cannot be seen, the patient should be visual field defect may be an indication for optic
asked to count fingers while the testing distance is nerve decompression.
varied to quantitate the response. If fingers cannot be
seen, an assessment of light perception should be
carried out. Even if the patient does not consistently Funduscopic examination. In all cases of posterior
respond to a light stimulus, photophobia and lid indirect optic nerve injury, the optic disc will initially
closure indicates probable light perception. As is appear normal, as will the entire fundus. Within 3 to 6
outlined under “Treatment of Indirect Optic Nerve weeks, optic disc pallor will be seen; the more
Trauma,” serial quantitation of vision is important in anterior the lesion involving the optic nerve, the
the injured patient. A case of progressive visual loss sooner the optic atrophy will become apparent.
after head injury may indicate the need for surgical
intervention.
8 KLINE et al. Neurosurgery. Vol. 14, No. 6
FIG. 1. A 26-year-old man sustained left frontal head trauma in an automobile accident. The patient lost consciousness for approximately 10
minutes and was evaluated 30 minutes later. His vision was 20/20 in the right eye and 1/200 in the left.
Reconstructions of the optic canals. Top illustrations are of the right optic canal and bottom images are of the left canal.
Top left, lines on axial CT indicate the level of the reformatted image. Top right, normal right optic canal (arrowj seen on an image
reformation perpendicular to the axis of the canal. Bottom left, level of the reformatted image indicated on an axial scan. Arrows demonstrate
multiple fractures of the left lateral orbital wall. Bottom right, reformatted image reveals a disrupted left optic canal (arrows). Note that the
underlying sphenoid air cells are opacified.
11 KLINE et al. Neurosurgery, Vol. 14. No. 6
ghead trauma with evidence of sphenoethmoid sinus hemor- the management of patients with indirect optic nerve trauma. It
rhage on conventional radiography or loss of visual acuity is evident from the nonsurgical group that a significant number
should undergo cranial CT as well as full ophthalmological of patients improve spontaneously. In general, there is no clear
examination. In addition, recently developed CT reconstruction trend toward improved vision in the patients who underwent
algorithms allow scan data to be assigned a smaller pixel
matrix with an expanded CT number range (27). The resolution operation. The notable exception is the report by Fukado (11).
of images so produced (e.g.. ReView. General Electric Corp.) Although it is difficult to interpret the exact indications and
surpasses the previously available resolution of osseous results in this study, virtually all of 400 cases treated by
structures by CT. These algorithms probably will play a major transethmoidal surgical decompression of the optic nerve were
role in the evaluation of cranial trauma, including optic canal stated to improve. Only a few of these patients had no light
fractures (Fig. 1). perception before operation, and most had only “impaired
CT also provides valuable information regarding soft tissue vision." It is well known that partial visual decrease may occur
structures in patients with visual loss. In the case reported by from a number of factors after blunt injury around the orbit,
Shaked et al.. CT demonstrated right proptosis and stretching and there is a tendency for vision to improve with time without
of the optic nerve due to orbital edema (42). In one patient
reported by Anderson and coworkers. CT revealed a mass in surgical intervention. However, there is still no explanation for
the superonasal aspect of the left orbit that proved to be a the uniform improvement of the cases in Fukado’s series.
subperiosteal hematoma, the removal of which produced
improvement of vision (1). Grove emphasized the value of CT
in visualizing soft tissues, foreign bodies, and bone details in In 1966, Walsh proposed the following guidelines in con-
cases of orbital trauma (14). sidering surgical decompression of the optic nerve (49):
The following general principles which might add to our knowledge
TREATMENT OF INDIRECT OPTIC NERVE of unroofing the optic nerve are now stated: 1) It should never be
INJURY undertaken as an elective procedure on an unconscious patient. 2) If
the loss of vision is associated with a nonreactive pupil, and the loss
occurred at the moment of impact, the procedure probably is
contraindicated. 3) If the loss of vision or loss of pupillary response
From the material reviewed, it is evident that multiple to light developed after the moment of impact the possibility of an
factors may be operative in the development of indirect optic operation improving the situation should be considered. 4) If it
nerve injury. Coupled with the unpredictability of visual cannot be determined that the loss of vision or pupillary response to
recovery, it is difficult to evaluate the literature dealing with light was delayed, it should be sound judgement to wait and watch
surgical intervention. Previous authors have expressed a wide for four to six days because spontaneous i mprovement occurs in
divergence of opinion. Lyle suggested that operation for de- some such cases. If improvement does not occur, it might be
reasonable to undertake the procedure
compression of the optic nerve should be carried out as soon as
the patient’s condition permits (28). whereas Stallard asserted
that such procedures are rarely of value (44). Tables 3 and 4
summarize reported nonsurgical and surgical results in Since these guidelines were published, there have been no
reports either substantiating or refuting them. Walsh later
reemphasized the third guideline listed above (50): " . . . we
have decided that unroofing of the optic canal should be
TABLE 4
Surgical Results in Indirect Optic Nerve Injury
No. Time between Trauma No. No. Not
Author. Year (Ref.)
Patients and Operation Improved improved
Pringle. 1922 (34) 3 2-4 wk 0 3
Daum et al. 1951 (4) 12 10-72 d 0 12
Hooper. 1951 (20) 4 18 hr-18 mo 1 3
TABLE 3
Nonsurgical Therapy in Indirect Optic Nerve Injury7
Nihoetal.. 1961 (32) 5-263 d 5 2
Hughes. 1962 (21) 5 20 hr-2 mo 0 5
Edmund
Author, No.
& Godtfredsen. 1963 (6)
Year (Ref.) No. 6 No. Not
—
Comment 1 5
Imachi et al.. 1968 (22) Patients Improved
61 Improved — 43 15
—
Schmaltz
Davidson. 1938& (5)Schurmann. 1971 (40)
37 11 13 26 1 12
Turner.
Hammer
1943 (47)
& Ambos. 1971 (15) 46 23 4 “within
23 1 wk” 4 0
Fukado.
Hooper. 19511975
(20) (11) 17 5 400 "less
12 than 7 to greater than 90 d” 400 0
Karniketetal..
Anderson al..1982
1981(1)
(23) 10 “less than 1Use
wk to
ofmore than 1 steroids
megadose mo" (>1 mg2 of dexamethasone
8 sodium
Anderson et al.. 1982 (1) 2 2 4 0
12-48 hr i 3
phosphate per kg per dav)
12 KLINE et al. Neurosurgery. Vol. 14, No. 6
27. Littleton JT, Shaffer KA, Callahan WP, Durizch ML: 49. Walsh FB: Pathological-clinical correlations: 1. Indirect
Temporal bone: Comparison of pluridirectional trauma to the optic nerves and chiasm. II. Certain
tomography and high resolution computed tomography. cerebral involvements associated with defective blood
AJR 137:835-845, 1981. supply. Invest Ophthalmol 5:433— 449, 1966.
50. Walsh FB: Trauma involving the anterior visual
28. Lvle DJ: Neuro-ophlhalmologv. Springfield, Charles pathways, in Freeman HM (ed): Ocular Trauma.
C Thomas. 1945. New York, Appelton-Cen- tury-Crofts, 1979, ch 35, pp
29. Manfredi SJ, Raji MR, Sprinkle PM, Weinstein GW, 335-351.
Minardi LM, Swanson TJ: Computerized tomographic 51. Walsh FB, Hoyt WF: Clinical Neuro-
scan findings in ophthalmology. Baltimore, Williams & Wilkins,
facial fractures associated with blindness. Plast 1969, pp 12-18.
Reconstr Surg 52. Walsh FB, Hoyt WF: Clinical Neuro-
68:479-490, 1981. ophlhalmologv. Baltimore, Williams & Wilkins,
30. Miller NR: Walsh and Hoyt's Clinical Neuro- 1969, p 2380.
ophthalmology. Baltimore. Williams & Wilkins. 53. Walsh FB, Hoyt WF: Clinical Neuro-
1982. pp 41-58. ophlhalmologv. Baltimore. Williams & Wilkins,
31. Niho S. Niho M. Niho K: Decompression of the optic 1969. pp 2375-2380.
canal by the transethmoidal route and decompression of 54. Walsh FB, Lindenberg R: In Die Veränderungen des
the superior orbital fissure. Can J Ophthalmol 5:22-40, Sehnerven bei indirectem Trauma, in Entwicklung
1970. und Fortschritt in der Augenheilkunde-
32. Niho S. Yasuda K, Sato T, Sugita S, Murayama K, Fortbildungskurs für Augenärzte, Hamburg,
Ogino N: Decompression of the optic canal by the 1962. Stuttgart, Ferdinand Enke Verlag, 1963.
transethmoidal route. Am J Ophthalmol 51:659-665, 55. Wyllie AM, McLeod D, Cullen JF: Traumatic
1961. ischaemic optic neuropathy. Br J Ophthalmol 56:851-
33. Obenchain TG, Killeffer FA, Stern WE: Indirect injury 853. 1972.
of the optic nerves and chiasm with closed head injury.
Bull Los Angeles Neurol Soc 38:13-20, 1973.
34. Pringle JH: Atrophy of the optic nerve following
diffused violence to the skull. Br Med J 2:1156-1157,
1922.
35. Ramsey JH: Optic nerve injury in fracture of the canal.
Br J Ophthalmol 63:607-610, 1979.'
36. Roger FC: Unilateral involvement of the optic nerve in
head injuries. Br J Ophthalmol 27:23-33, 1943.
37. Rollet J, Paufiquc J, Levy A: Fractures of the optic
canal. Arch Ophthalmol (Paris) 47:737-763, 1930.
38. Runyan TE: Concussive and Penetrating Injuries of the
Globe and Optic Nerve. St Louis, CV Mosby, 1975, ch
11, PP 143-164.
39. Saul TG, Ducker TB, Salcman M, Carro E: Steroids in
severe head injury: A prospective randomized clinical
trial. J Neurosurg 54:596-600. 1981.
40. Schmaltz B, Schumann K: Traumatische
Optikusschäden: Probleme der Ätiologie und der
operativen Behandlung. Klin Mon- atsbl Augenheilkd
159:33-40. 1971.
4L Seitz R: Ätiologie und Genese der akuten Erblindung als
Folge stumpfer Schädelverletzungen: Ein Beitrag zur
Frage der expiratorischen Freilegung des Canalis
opticus. KJin Monatsbl Augenheilkd 143:414-429,
1963.
42. Shaked A, Hadani M, Feinsod M: CT and VER follow-
up of reversible visual loss with fracture of the optic
canal. Acta Neu- rochir (Wien) 62:91-94, 1982.
43. Sofferman RA: Sphenoethmoid approach to the optic
nerve. Laryngoscope 91:184-196, 1981.
44. Stallard HB: Eye Surgery. Bristol, John Wright and
Sons, 1946.
45. Sullivan G, Helveston EM: Optic atrophy after
seemingly trivial trauma. Arch Ophthalmol 81:159-161,
1969.
46. Traquair HM, Dott NM, Russell WR: Traumatic lesion
of the optic chiasma. Brain 58:398-411, 1935.
47. Turner JWA: Indirect injury of the optic nerves. Brain
66:140- 151, 1943.
48. Venable HP, Wilson S, Allan WC, Prensky AL: Total
blindness after trivial frontal head trauma: Bilateral
indirect optic nerve injury. Neurology (NY) 28:1066-
1068, 1978.