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0148-396X/84/1406-0756S02.

00/0 N EUROS URGERY


Copyright © 1984 by the Congress of Neurological Surgeons Vol. 14, No. 6. 1984
Printed in U.S.A.

Review article

Indirect Injury of the Optic Nerve


Lanning B. Kline, M.D., Richard B. Morawetz, M.D., and Swaid N. Swaid, M.D.
Combined Program in Ophthalmology (L.B.K.) and Department of Neurosurgery (L.B.K.. R.B.M., S.N.S.), University of
Alabama School of
Medicine, Birmingham, Alabama

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.

This review deals with those patients who sustain indirect


injury to the optic nerves. Walsh and Hoyt define this as
“traumatic loss of vision which occurs without external or
initial ophthalmoscopic evidence of injury to the eye or its
nerve” (53). Thus, the optic nerves are not damaged directly by
an overt open or penetrating injury such as that caused by a
missile or another foreign body, but rather are damaged in
conjunction with closed head trauma (0.5 to 1.5% of cases) (3,
47). Typically, such an injury results from an ipsilateral blow
to the head, usually frontal, occasionally temporal, and rarely
occipital. Infrequently, the eye on the side opposite the head
trauma is involved. In most instances, there is loss of
consciousness, yet visual loss may also follow an apparently
trivial blow that produces no other neurological abnormalities
(45, 48).
Conflicting recommendations appear in the literature re-
garding the treatment of optic nerve injuries (6, 10. 11, 20, 31,
32, 44). We attempt to provide guidelines in dealing with
patients who sustain indirect optic nerve trauma. Optic nerve
anatomy, classification of optic nerve injuries, clinicopatho-
logical data, pathophysiological mechanisms, clinical exami-
nation techniques, neuroradiological studies, and therapeutic
modalities are discussed.
OPTIC NERVE ANATOMY (30,38.51)

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”

Hughes. 1962 (21) 67 20/20-20/400 = 7 less CC: NFB defects Operation in 5


than 20/400 = 9 NLP = Skull fracture = 43 (optic canal =
32 3; anterior clinoid = 2)
Edmund & Godtfredsen. 22 20/20-20/400 = 0 less CC; NFB defects Skull fracture = 11 (optic Operation in 6
1963 (6) than 20/400 = 12 NLP = canal = 5)
10
Anderson et al„ 1982 (1) 7 20/20-20/400 = 3 less NFB defects Skull fracture = 3 (optic Operation in 5: high
than 20/400 = 1 NLP = 3 canal = 2) dose steroids in 7

“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

Seitz removed the entire optic nerve from the blind


eye in one case of indirect optic nerve injury (41).
Although it appeared grossly normal, he found axon
interruption deep in the nerve, without vascular or
connective tissue changes. These findings favor an
June 1984 INDIRECT INJURY OF THE OPTIC NERVE 5

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

ti There is pathological evidence supporting this


o vascular theory. In two cases reported by Hughes,
n examination of the intracanalicular optic nerve
s revealed changes compatible with ischemic infarction
I of both neural and glial elements (21). The
n pathological findings in the case studied by Ramsay
c also demonstrated infarction of portions of the
o intracanalicular and intracranial segments of the optic
m nerve (35). Support for a vascular cause is
p summarized by Hughes: “That the vessels supplying
l the optic nerve within the canal are damaged in some
e way so that all or part of the nerve is deprived of its
t blood supply would seem to be an explanation fitting
e most of the facts” (21).
C
o
m
Concussion has been proposed as a mechanism of
p
indirect optic nerve injury when there is transient
l
visual loss (38. 49, 50). Concussion is defined as “a
e
clinical syndrome characterized by immediate and
t
transient impairment of neural function .. . due to
e
mechanical forces” (17). As Walsh points out,
II. Bone deformation concussion cannot be identified histologically: rather,
and/or fracture Optic it is a clinical description (50).
canal
Anterior
clinoid Contusion is defined histologically as structural
process alteration of neural tissue characterized by
Orbital roof extravasation of blood and cell death (17). Walsh
classified contusion necrosis as a primary lesion of
III. Vascular indirect optic nerve injury resulting from shearing
insufficienc forces transmitted to the nerve at the time of head
y Ischemia injury. The lesion has a characteristic triangular shape
Infarction with the apex internal to the base (49). Although
contusion necrosis of the optic nerve is identified
IV. Concussion
infrequently, it is significant because the ensuing
V. Contusion visual loss is permanent. Walsh believed it to be an
operative mechanism in instantaneous blindness due
VI. Hemorrhag to indirect optic nerve injury.
e Nerve
sheath
Intraneural
Hemorrhage within the optic nerve sheaths or into
the nerve itself may produce or accompany visual
loss. Hemorrhage within the sheaths may be
curred (2. 21, 46). Anatomical factors make the blood intradural, subdural, or subarachnoid. Pringle
supply of the intracanalicular portion of the optic performed 174 postmortem examinations in patients
nerve very susceptible to trauma. As described under unconscious from the time of head injury until death
“optic nerve anatomy,” the nerve is firmly attached to (34). He identified blood in the optic nerve sheaths
the periosteum of the optic canal, particularly along and postulated that optic nerve injuries were caused
its superior aspect. The blood supply of this portion of by compression by blood. Subsequently, he operated
the nerve arises from small branches of the on three patients with monocular blindness following
ophthalmic artery, which produce a pial network closed head injury, and in all three he found blood
surrounding the nerve. Penetrating vessels exit at right under tension within the nerve sheath, but none of the
angles from this network to supply the nerve bundles. patients had return of vision. Turner was skeptical of
In addition, the central retinal artery may give off a nerve sheath hemorrhage as a cause of optic nerve
recurrent branch that extends posteriorly to the optic injury (47). Walsh shared this opinion until witnessing
foramen. Rupture of small penetrating vessels due to a case in which incision of the optic nerve dura mater
movement of the nerve relative to the bony canal or released a blood clot and visual acuity returned to
fracture of the canal would lead to vascular impair- normal (49). Niho and coworkers reported
ment of the optic nerve. decompression of intradural hemorrhage in two
patients resulting in minimal improvement of visual
June 1984 INDIRECT INJURY OF THE OPTIC NERVE 7

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

An abnormal fundus signifies optic nerve injury


either at its junction with the globe or along the
intraorbital portion containing the central retinal
artery and the central retinal vein. The spectrum of
funduscopic abnormalities has been discussed.

Visual evoked response. For assessment of visual


loss and localization of the site of injury in the visual
pathways, ophthalmological testing requires the
patient’s attention and cooperation. Examination of
the visual system during the acute phase after head
injury is often difficult because of the patient’s altered
level of consciousness, and the visual evoked
response (VER) to flash stimulation may provide
valuable objective data. This type of evaluation was
described by Feinsod and Auerbach (9) using a
combination of two elec- trophysiological tests: the
electroretinogram (ERG) to assess the retinal activity
and the VER to test optic nerve function. Of 75
patients examined by Feinsod, 35 had suffered optic
nerve injury, which was unilateral in 21 (8). There
was usually good correlation between the initial VER
and the ultimate visual acuity. Other reports have
confirmed this (1, 42). To date, there has been no
patient with a nonrecordable VER in whom there was
return of vision after optic nerve decompression.

Greenberg and coworkers found that the VER was


more accurate than clinical examination in the
diagnosis of retrobulbar visual dysfunction in the
patient with acute head trauma (13). Retrobulbar
visual dysfunction was defined by
neuroophthalmological examination at 3 months or
longer after injury and was present in 10 of 13
patients examined. In the acute setting (mean of Day
3 after injury), the clinical evaluation of visual
dysfunction was correct in 30% of the cases (3 of 10),
whereas electrophysiological evaluation was correct
in 90%.
Thus, in the comatose patient the VER provides
some assessment of visual function. However, the
limited availability and impracticality of performing
VER testing in a patient after acute head trauma limit
the usefulness of this diagnostic modality.
Neuroradiological evaluation

With the advent of high resolution computed


tomography (CT), the role of traditional radiological
studies has diminished. The reported frequency of
radiological abnormalities after indirect optic nerve
trauma is highly variable (Table 1). Rollet et al. (37)
and Davidson (5) reported radiological abnormalities
in approximately 80% of cases. In contrast.
June 1984 INDIRECT INJURY OF THE OPTIC NERVE 9

autopsy was subjected to complete radiological


examination after discovery of the fracture, including
plain films of the left optic foramen and horizontal
Turner found that only 4 of 46 cases of optic nerve hypocycloidal axial tomography. Despite knowledge
injury were associated with radiographic evidence of of the fracture site, it could not be demonstrated
optic canal fracture (47). In Turner’s 46 cases, special radiographically.
views of the optic foramina were obtained in all but 9
cases, and 33 of the 37 were interpreted as being
normal. Thus, the limitations of plain film
roentgenography must be recognized.

A fracture of the optic canal not apparent


radiographically may be discovered during operation
or at postmortem examination. Ramsay described the
autopsy of a 72-year-old woman with indirect optic
nerve injury (35). A block of bone, including the
posterior segments of both orbits, both optic canals,
and both optic nerves and chiasm, was removed in
one piece. A fracture extending medially through the
body of the sphenoid and involving the posterior part
of the left posterior ethmoid sinus was found. Before
the patient’s death, only plain films of the skull and
orbits were obtained and these were interpreted as
normal. The specimen removed at
10 KLINE et al. Neurosurgery. Vol. 14, No. 6

CT is currently the neuroradiological procedure of


choice in evaluating patients with head trauma (7). By
varying window settings and contrast levels, detailed
examination of the cranial cavity for fractures can be
done. CT visualization of the optic canal requires
careful attention in selecting the proper scanning
plane (16). In a study of 379 consecutive patients with
facial fractures, Manfredi et al. found that 16 patients
exhibited evidence of sphenoid and ethmoid sinus
hemorrhage on routine skull and facial films (29).
Five of these patients (31%) had computed
tomographic evidence of an optic canal fracture with
clinical findings of optic nerve injury. The authors
concluded that any patient sustainin

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

undertaken only if vision was present immediately


after the
June 1984 INDIRECT INJURY OF THE OPTIC NERVE 13

nerve swelling is a feature” (49). A prospective


randomized clinical trial of steroids in severe head
injuries showed no statistically significant difference
trauma or was demonstrated to be present by pupil in the outcome of the steroid and nonsteroid groups at
narrowing on exposure to light and then disappeared." 6 months (39). The authors of this study emphasized
This concept is supported in the literature. Case that the effect of steroids may be different for
reports by Hooper (20) and by Hughes (21) describe different patient groups. Definition of these subgroups
situations in which there was visual deterioration would require further clinical trials. Anderson et al.
during observation and after surgical decompression published the only report dealing with the use of
visual function clearly improved. Kennerdell and corticosteroids in the treatment of indirect optic nerve
coworkers reported the case of a 19-year-old woman injury (1). They used “megadose" steroids, defined as
who was struck in the left eyebrow region with no greater than 1 mg of dexamethasone sodium
loss of consciousness or immediate visual impairment phosphate per kg per day. in six patients with
(24). Over the next 3 days, vision progressively traumatic visual loss. None of the three patients who
deteriorated. Bony tomograms revealed an oblique failed to respond to megadose steroids regained vision
linear fracture of the left greater and lesser sphenoid with optic nerve decompression. Three of the six
wings extending into the optic canal. Using a patients had return of good vision with megadose
transantral-ethmoidal approach, the optic nerve was steroids without optic nerve decompression. Two of
decompressed with removal of bone fragments these three patients had a delayed loss of vision before
directly compressing it, and within 24 hours visual the initiation of steroids. The authors concluded that
acuity and visual fields had returned to normal. megadose steroids may be useful in cases of indirect
Documented delayed visual loss due to indirect optic optic nerve injury. Anderson et al. proposed the
nerve injury seems to be a definite indication for optic following indications for optic nerve decompression:
nerve decompression. (a) delayed visual loss after frontal head trauma
unresponsive to 12 hours of megadose steroid therapy
and (b) initial return of vision with megadose steroids
followed by visual decrease while receiving steroids.
The transethmoidal route for optic nerve
decompression was initially reported by Niho et al. in CONCLUSIONS
1961 (32). This procedure may be performed under
local anesthesia. Others have emphasized this
technique as an alternative to unroofing the optic Throughout this report, we have emphasized the
canal by a transfrontal approach (10, 11, 24, 52, 54). difficulty of analyzing the literature dealing with
Niho’s report included 7 patients, and “visual indirect optic nerve injury. This form of optic nerve
recovery was obtained in every case” (32). In a later damage may be caused by a multiplicity of
report including 25 patients with fracture of the optic pathophysiological factors. From the material
canal, Niho et al. noted “visual recovery” in 20 reviewed, the following conclusions regarding
patients (80%) (31). No mention was made of the therapy seem warranted:
criteria used in selecting these patients for de-
compression. Niho does state that if preoperative
vision is less than finger counting at 0.1 m, operation
should be performed within 1 week. If vision is better 1. If visual loss at the moment of impact is total, as
than this but less than 6/60 (20/200). an operation measured by visual acuity, pupillary response, or VER
should be performed within 3 weeks after head injury. testing, surgical intervention is of no value.
Fukado’s experience in 400 cases of transethmoidal
surgical decompression of the optic nerve has been
summarized. Because of the safety of the procedure, 2. If visual loss develops after impact or can be
Fukado suggested that the trcnsethmoidal approach demonstrated to be progressive with serial
may be the operative procedure of choice in optic observations (acuity, pupils, VER), optic nerve
nerve decompression (10, 11). Karnick et al. used this exploration and decompression is indicated.
surgical approach in 10 patients, operating on 3 within
a week of head trauma. 3 within a month, and 4 later
than 1 month (23). In 2 patients who sustained head
trauma within 1 month of operation, there was some 3. The use of megadose steroids is appropriate as
improvement in visual acuity. Sofferman used the an adjunct to the diagnosis and treatment of indirect
transethmoidal approach in 4 patients (43). In 2, total optic nerve injury.
blindness persisted postoperatively. In 1, vision
remained unchanged at 4/200. The 4th patient was
unconscious before operation, and his postoperative 4. The transethmoidal route for optic nerve
visual acuity was 20/30. decompression is a proven alternative to the
There are few data regarding the medical transfrontal approach.
management of indirect optic nerve trauma. Walsh did
not specifically discuss this issue, but he stated that
“cortisone and mannitol may be helpful where optic
14 KLINE et al. Neurosurgery. Vol. 14, No. 6

5. Thorough evaluation of the intracanalicular 9. Feinsod M. Auerbach E: Electrophysiological


portion of the optic nerve with bony tomography and examinations of the visual system in the acute phase
high resolution CT is essential. However, the absence after head injury. Eur Neurol 9:56-64, 1973.
of radiological abnormalities does not contraindicate 10. Fukado Y: Results of 350 cases of surgical
surgical intervention. decompression of the optic nerve. Trans Ophthalmol
Soc NZ 25:96-99, 1975.
11. Fukado Y: Results in 400 cases of surgical
6. At present, the decision to operate must be decompression of the optic nerve. Mod Prob
individualized in each case. Ophthalmol 14:474-481, 1975.
There is an obvious need for a prospective study 12. Gjerris F: Traumatic lesions of the visual pathways, in
dealing with the management and treatment of Vinken PJ, Bruyn CW (eds): Handbook of Clinical
indirect optic nerve injury. This will require the Neurology. Amsterdam. North Holland Publishing Co.
interest and availability of a team of physicians 1976. vol 24, pp 27—57.
including a neurosurgeon, an ophthalmologist, and a
radiologist. For a comprehensive study, all patients 13. Greenberg RP. Becker DP, Miller JD, Mayer DJ:
who sustain visual loss should be included. The Evaluation of brain function in severe human head
trauma with multimodality evoked potentials: Part 2.
efficacy of surgical decompression or systemic Localization of brain dysfunction and correlation with
steroids must be measured and compared to a control posttraumatic neurological conditions. J Neu- rosurg
group that receives no therapy. Surgical procedures 47:163-177, 1977.
that do not require a craniotomy are probably
preferable. The “vision salvage rate” in this specific 14. Grove AS Jr: Orbital trauma and computed tomography.
patient population must be determined. One would Ophthalmology 87:403-411. 1980.
hope that the data obtained will provide greater 15. Hammer VG. Ambos E: Das traumatische
understanding and a rational basis for the treatment of Optikusscheidenhämatom und seine operative
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159:818-819, 1971.
ACKNOWLEDGMENT 16. Hammerschlag SB, O’Reilly GVA, Naheedy MH:
The authors thank William F. Hoyt, M.D., for Computed tomography of the optic canals. AJNR
reviewing the manuscript. 2:593-594, 1981.
17. Head injury nomenclature: A glossary of head injury
Reprint requests: Lanning B. Kline, M.D., Eye including some definitions of injuries of the cervical
Foundation Hospital, 1720 University Boulevard. spine. Prepared by the Ad Hoc Committee of the
Birmingham, Alabama 35233. Congress of Neurological Surgeons. Clin Neurosurg
12:388-394, 1966.
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