False-localizing Pupil with Intracranial Hemorrhage

Unilateral Fixed Dilation of the Pupil as
a False-localizing Sign with Intracranial
Hemorrhage: Case Report and
Literature Review
Laurence A.G. Marshman, F.R.C.S.,
Charles E. Polkey, M.D., Christopher C. Penney, F.R.C.R.
Department of Neurosurgery, King’s College Hospital, Denmark Hill, London, England

OBJECTIVE AND IMPORTANCE: Although other focal signs may prove
“false localizing,” it is a neurosurgical axiom that unilateral fixed dilation
of the pupil occurs ipsilateral to a supratentorial mass.
CLINICAL PRESENTATION: A 25-year-old man collapsed with a dense right
hemiplegia and a Glasgow Coma Scale score of 6 (eye opening, 1; motor,
4; verbal, 1) after rupture of a left middle cerebral artery aneurysm
associated with an intrasylvian hematoma. Initially, both pupils had
remained equal-sized and reactive: however, within hours, the right
(contralateral) pupil became fixed and dilated (i.e., false localizing). For
some time, the left (ipsilateral) pupil remained small and reactive; at
emergency craniotomy, this also became fixed and equally dilated.
INTERVENTION: After evacuation of the clot and wrapping of the aneurysm,
both pupils rapidly became equal-sized and reactive. Twenty-four hours
later, concurrent with massive left hemispheric swelling and a midline
shift, the left (ipsilateral) pupil became unilaterally fixed and dilated (i.e.,
false localizing). Eventually, the right (contralateral) pupil also became
fixed and dilated, concurrent with cardiovascular collapse. Death occurred within 10 hours.
CONCLUSION: Unilateral fixed dilation of the pupil in patients with hemispheric mass lesions may be false localizing. Furthermore, disparate
“herniating mechanisms” can arise despite mass effect emanating from
the same side. Because such mechanisms cannot be witnessed, their
nature remains speculative. An extensive review is contained in this
article. (Neurosurgery 49:1251–1256, 2001)
Key words: False localizing, Iridoplegia

CASE REPORT

A

25-year-old Ukrainian male immigrant was found unconscious,
slumped on a toilet. His breathing was
irregular and the gag reflex was depressed. He was intubated and ventilated (without paralysis) by paramedics,
and intravenous diazepam was admin-

istered for a presumed seizure. Pulse
rate and blood pressure were 73 beats
and 116/64 mm Hg, respectively; both
pupils appeared equal in size (4 mm)
and reactive to light. Routine investigation at the local Emergency Department
revealed the only abnormality to be a
serum potassium of 2.9 mmol/L. A
loading dose of phenytoin was admin-

1251

istered in view of the presumed seizure.
Computed tomographic scanning (Fig.
1) demonstrated a large 3.5 ⫻ 5.5-cm
hemorrhage in the left sylvian fissure,
with extensive subarachnoid but modest intraventricular extension. There
was significant mass effect, but only minor midline shift. No significant change
occurred in cardiovascular or pupillary
parameters during transfer to our center, and his core body temperature was
36.8°C. The Glasgow Coma Scale score
on arrival was 6 (eye opening, 1; motor,
4; verbal, 1), with flexion to painful
stimulation on the left side, and paralysis on the right. He was sedated with
propofol and observed. Arterial blood
gases were maintained within normal
ranges, with oxygen saturations of 98 to
100% and pCO2 values of 30 to 35
mm Hg. During this time, both pupils
remained equal in size and reactive to
light (directly and consensually). Each
pupil, however, decreased to 2 mm over
the next 2 hours, concomitant with sedation (40). At this stage, the right (contralateral) pupil became unreactive to
light (directly or consensually) and progressively dilated to 6 mm over a period
of 30 minutes, with a slightly oval outline. The left pupil remained unchanged
(2 mm) and reactive. Valproate was administered in addition to intravenous
mannitol. Repeat CT scanning (Fig. 2)
showed a slight increase in mass effect
and in midline shift as a result of swelling. Immediately preoperatively, the left
pupil became fixed and dilated as well,
also with a slightly oval outline. Neither
pupil appeared to respond to mannitol.
No significant change occurred in motor
or hemodynamic parameters throughout this period and the patient remained
apyrexial.
At emergency craniotomy, without
angiography, copious clot was evacuated from the left sylvian fissure surrounding a large, ruptured, left middle
cerebral aneurysm. The aneurysm could
not be safely dissected and was
wrapped with cotton wool. Within 2
hours of surgery, both pupils became
equal in size (2 mm) and reactive to
light, directly and consensually. The left

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Marshman et al.

FIGURE 1. A and B,
serial CT scans at
presentation where
both pupils were
equal and reactive to
light. There is extensive hemorrhage
spreading around the
left sylvian fissure
and into the adjacent
left temporal lobe.
There is also considerable, and widespread, subarachnoid hemorrhage, with a small amount of intraventricular hemorrhage. Moderate mass effect is apparent with minor midline shift to the right.

FIGURE 2. A and B,
serial CT scans at the
first deterioration
where fixed dilation
of the contralateral
pupil was false localizing. Extensive hemorrhage remains in
relation to the left
sylvian fissure and
the left temporal
lobe. An underlying
middle cerebral
artery aneurysm is probably visible. Local edema is apparent with mass effect distorting the left lateral ventricle; however, only minor midline displacement (particularly subfalcine) is apparent to the right. Despite this, right ventricular distention
suggests that some degree of obstruction has occurred at the contralateral foramen
of Monro. The left ambient cistern is clearly patent, which implies that gross ipsilateral uncal herniation has not occurred yet.

arm and leg continued to flex to painful
stimuli; the right side remained hemiplegic. Clinical parameters remained
stable for approximately 24 hours, after
which the left (ipsilateral) pupil gradually became fixed (directly and consensually) and dilated (6 mm). No concomitant change occurred in motor or
hemodynamic parameters, and the right
pupil remained small (2 mm) and reactive. CT scanning demonstrated low attenuation in left middle and partial posterior
cerebral
arterial
territories,
consistent with infarction (Fig. 3). There
was considerably increased mass effect
with distortion of the upper brainstem.
However, there was no evidence of significant further hemorrhage. Despite the
administration of intravenous mannitol,

the left pupil remained fixed and dilated;
no further clinical deterioration was apparent for more than 20 hours. After this
time, however, the right pupil also became fixed and dilated (5 mm). The mean
arterial pressure fell to 65 mm Hg, with a
central venous pressure of 11 cm H2O,
despite fluid challenge and inotropic support. Cardiovascular collapse became inexorable, and the patient died 10 hours
later. The patient’s family refused postmortem examination.

DISCUSSION
Localizing signs with supratentorial
masses, in particular contralateral hemiparesis, were known to the ancient
Egyptians (1). The localizing value of

the pupil, however, was not specified
until the 19th century, despite pictorial
evidence from 16th century woodcuts
(7, 15, 30). In 1830, Bright (2) was the
first to describe a case of unilateral iridoplegia, along with bradycardia and
depressed consciousness, associated
with an ipsilateral extradural hematoma. Macewen (25) later described similar cases in a patient series with skull
fractures. Cushing (8) noted, in 1908,
that miosis briefly preceded progressive
mydriasis with hemispheric compression. Hutchinson (19) in 1867, specifically correlated ipsilateral iridoplegia
and intracranial hemorrhage with ipsilateral oculomotor compression. Although Meyer (27) later identified uncal
herniation with hemispheric compression, Reid and Cone (32) specifically
correlated this with oculomotor distortion and iridoplegia. Despite concern by
Jefferson (20) that iridoplegia related to
brainstem distortion rather than the oculomotor nerve, he is credited with the
modern concept of the “tentorial pressure cone.”
Between 1953 and 1958, Sunderland
(38, 39) extensively studied normal anatomic relationships at the tentorial hiatus. He found considerable variation in
the size of the brainstem-tentorial aperture available for uncal herniation. The
widest apertures occurred in older subjects, where atrophy prevailed. Because
uncal-oculomotor contact was frequently noted in Sunderland’s specimens, he proposed that ipsilateral uncal
compression of the superolateral oculomotor nerve, where parasympathetic
pupilloconstrictor fibers coursed, was
the first event in tentorial coning. Initially this “irritated” the fibers, causing
transient ipsilateral miosis (as Cushing
had observed); paralysis ensued, with
serial mydriasis. Further compression
ultimately affected more resilient somatic fibers, leading to complete ipsilateral oculomotor paralysis (38, 39). This
sequence has since become established
neurosurgical dogma and has been confirmed clinically in cases of intracerebral
hemorrhage (34, 35). In these studies,
loss of light reflex was the first ocular
sign; complete oculomotor paralysis
was delayed, in exact agreement with
Sunderland (38, 39).

Neurosurgery, Vol. 49, No. 5, November 2001

False-localizing Pupil with Intracranial Hemorrhage
FIGURE 3. A and B,
serial CT scans at the
second deterioration
where fixed dilation
of the ipsilateral
pupil was true localizing. Extensive low
attenuation in the left
middle (and part of
the left posterior)
cerebral artery territories suggests infarction in these regions.
This is associated with significantly increased mass effect and midline displacement
to the right, with distortion of the upper brainstem and compromise of the contralateral quadrigeminal cistern. Both the recent craniotomy and the evacuation of
the left-sided hematoma are clearly evident.

The concept of false-localizing signs
with intracranial mass lesions, first categorized by Collier (6) in 1904, was later
epitomized by Kernohan and Woltman
(22) in 1929. Kernohan and Woltman
showed that hemiparesis could be ipsilateral when, as a result of lateral brainstem shift, contralateral peduncular
notching occurred at the tentorial edge.
In similar fashion, other signs, such as
hemianopia, could also prove false localizing; depending on brain shifts (14,
20, 31). How true localizing, then, is
Hutchinson’s pupil? Pevehouse et al.
(31) found a larger contralateral pupil in
9 (9%) of 101 patients with acute or
chronic subdural hematomas with
anisocoria. More significantly, Brower
(4) found a larger contralateral pupil in
29% of 132 patients with acute or
chronic subdural hematomas and anisocoria. Gassel (14), in 250 patients with
intracranial meningiomas, found the
larger pupil to be false localizing in as
many as 12 (80%) of 15 patients with
anisocoria. Unfortunately, all of these
studies were essentially retrospective,
with little or no mention of temporal
pupil reactivity, and with heterogeneous case-mixes, including both acute
and chronic herniations. Furthermore,
anisocoria is present in up to 20% of a
normal population (40). However,
Schwartz and Rosner (37) found a larger
contralateral pupil with invariable loss
of light reflex in 9 (50%) of 18 patients
with space-occupying lesions and anisocoria. More recently, Chen et al. (5) de-

scribed a case in whom unilateral iridoplegia occurred contralateral to an acute
frontal intracerebral hemorrhage.
An important advance in determining
the mechanism of mass-induced iridoplegia came from the experiments of
Jennet and Stern in 1959 (21). In contrast
to Reid and Cone (32), Jennet and Stern
showed that unilateral hemispheric balloon compression could cause rapidly
reversible iridoplegia without significant uncal herniation and oculomotor
compression (21). Moreover, the contralateral pupil was larger in 12% (without obvious explanation at postmortem). An initial, transient miosis was not
commented upon in any animal studied; while electrical conduction studies
implicated the oculomotor nerve as the
site of dysfunction. Questioning Reid
and Cone’s mechanism, Jennet and
Stern envisaged oculomotor nerve “impingement” against “unyielding structures” as etiological. However, they also
cited Thompson and Malina’s (41) concept of “dynamic axial brainstem distortion,” where supratentorial pressure
causes the brainstem to buckle during
its descent as a result of its caudal tethering by way of the first dentate ligament. Oculomotor dysfunction could
therefore also relate to brainstem dysfunction, as Jefferson (20) had stated.
Weintraub (44) and, later, Hassler (17)
elaborated this concept by postulating
descent-induced traction of vulnerable
paramedian brainstem arteries; this occurred as a result of their rostral tether-

1253

ing by the circle of Willis. Such traction
resulted in brainstem ischemia and,
with rupture in extreme cases, midbrain
hemorrhages, a key pathological feature
of terminal coning (28, 42). Although
some have since dismissed brainstem
descent as merely a late epiphenomenon
(12, 13), others have clearly shown that
it is both acute and proportional to the
size of the supratentorial mass (43). Furthermore, abnormal pupillary responses
have been correlated with critically reduced brainstem blood flow clinically
(33).
The precise pathophysiology of iridoplegia with supratentorial mass lesions,
necessarily speculative in any one case
(5, 12, 34, 35), may clearly be either “peripheral” (oculomotor nerve [19, 21, 23,
32, 38, 39, 44]) or “central” (brainstem
[12, 13, 17, 18, 30, 33]). Postmortem evidence, lacking in our case and in the
recent case of Chen et al. (5), casts light
mainly on terminal events (13). The
presence of oval pupils does not localize
the compressive focus to any particular
region (11, 26). The uniqueness of our
case relates to the fact that lateralization
of initial iridoplegia differed completely
between two clinical scenarios, despite
mass effect emanating from the same
side. In the first deterioration, the contralateral pupil became fixed and dilated long before any abnormality occurred in the ipsilateral pupil. In this
instance, mass effect related to left sylvian fissure hemorrhage (Figs. 1 and 2).
After decompressive surgery, both pupils regained normal size and reactivity,
a situation remained for 24 hours. In the
second clinical deterioration, the ipsilateral pupil dilated first. Mass effect here
related primarily to hemispheric swelling as a result of left middle and partial
posterior cerebral arterial infarction
(Fig. 3). Clearly, two distinct herniating
mechanisms had occurred with two,
temporally distinct, but unilateral
pathologies.
Lateral brainstem movement in the
transverse plane slackens the nerve in
the direction of translation (i.e., the contralateral oculomotor nerve) (35, 38, 39,
44). Simultaneously, it pulls taut the ipsilateral nerve, bowstringing it around
the posterior clinoid process (35, 38, 39,
44). A low brainstem oculomotor origin
(39, 44), with each nerve coursing up-

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Marshman et al.

ward through the interpeduncular cistern, also predisposes to nerve bowstringing during brainstem descent.
Moreover, since the basilar artery is
tethered to the brainstem, each nerve is
increasingly slung around its corresponding posterior cerebral artery as
coning proceeds (44). Sunderland (38,
39) found that the upper surface of the
normal oculomotor nerve was frequently grooved by either the posterior
cerebral artery or the posterior communicating artery. Conversely, the lower
surface was often grooved by an elevating superior cerebellar artery of high
basilar origin (38, 39). More recently,
Lang (24) showed that the oculomotor
nerve may even be pierced at its origin
by a posterior cerebral arterial branch in
up to 14% of autopsies. Such normal
variants clearly suggest a predisposition
to oculomotor nerve tethering that
could be incurred during even the mildest of brain shifts, a concept clearly compatible with Jennet and Stern’s experimental findings (21). Kerr and
Hollowell (23) demonstrated that the oculomotor nerve is the most pressuresensitive intracranial structure to correlate with mydriasis; the fact that
complete oculomotor paralysis is infrequently seen with mass lesions (13) may
instead implicate traction as the
mydriasis-evoking stimulus (21).
Other mechanisms are also possible.
For example, the contralateral oculomotor nerve may become wedged against
its adjacent tentorial edge by the posterior cerebral-superior cerebellar arterial
angle during “midline shift” (23, 38, 39).
This mechanism, possibly in evidence in
Figure 2A, could adequately account for
the contralateral iridoplegia detailed in
one of the patients described by
Schwartz and Rosner (37). However,
brainstem rotation may also occur with
hemispheric mass lesions in the sagittal,
coronal, or axial plane. For example, it is
possible that axial rotation may occur
such that the contralateral brainstem
moves posteriorly (38, 39). If so, then this
would pull taut the contralateral nerve
while relaxing the ipsilateral nerve. Such
axial rotation, combined with a low oculomotor origin, could explain the occurrence of contralateral iridoplegia before
the effects of ipsilateral uncal herniation
in the first of our patient’s deteriorations.

Weintraub (44) noted cases of proximal
oculomotor bruising, the presumed result
of posterior cerebral artery descent and
compression, that were also inexplicably
more marked on the contralateral side. It
should be noted that stimulation of the
ipsilateral hippocampus (such as may occur with herniation) also elicits contralateral mydriasis (16, 23).
It is difficult to explain why the ipsilateral pupil dilated first in the patient’s
second deterioration. One possibility is
that, should ipsilateral uncal herniation
have eventually ensued in the first deterioration, a partial herniation is likely
to have persisted despite oculomotor recovery (21). This, and the fact that a
nerve previously distorted possesses a
lower threshold for a second insult (38,
39), would encourage earlier ipsilateral
oculomotor dysfunction with reherniation. Most likely, a more important factor was that the second deterioration
related to hemispheric edema rather
than sylvian fissure hemorrhage. Jefferson (20) thought that, in view of the
inferolateral tentorial slope, downward
compression would initially encourage
medial temporal lobe movement away
from the tentorial edge (“. . . its tentlike
form . . . protects the midbrain”). This
could explain delayed ipsilateral uncal
herniation in the first deterioration. In
contrast, ipsilateral uncal herniation
was considered far more likely with
hemispheric edema because expansion
would be radial (20, 36). Thus, a residual
medially displaced left uncus, along
with a process more likely to encourage
its herniation anyway, could conceivably account for earlier ipsilateral iridoplegia in the second deterioration. Partial left posterior cerebral artery
infarction (Fig. 3) suggests that left uncal
herniation had ultimately occurred
here. Alternating asymmetries in brainstem blood flow (33), however, are not
likely to explain both deteriorations (29).
Furthermore, gross hemodynamic fluctuations, a tenet of “dynamic axial
brainstem distortion” (34, 39), were not
observed in either acute deterioration
(but only, instead, terminally with bilaterally fixed and dilated pupils). Consistent contralateral hemiplegia throughout both deteriorations is probably
explained by vertical straightening of

the ipsilateral peduncle as a result of
localized mass effect (38, 39).
Other alternative causes of anisocoria
should be acknowledged in this discussion. The possibility of corneal contamination with iris-active drugs is currently an ever-present risk in intensive
care units (40). Spontaneous variations
in pupil size and reactivity, reflecting
balance variations in autonomic tone,
may occur physiologically (3, 40) or as a
result of migraines (40). Furthermore,
autonomic innervation may itself be
fundamentally asymmetric in head and
neck structures (9). In all of these examples, the simultaneous loss of light reflex would be unusual. Nonconvulsive
status epilepticus could also explain the
clinical findings; however, a full loading
dose of phenytoin and valproate had
been administered, in addition to intravenous diazepam. One final differential
diagnosis could be that of a “Behr pupil.” This phenomenon relates to prolonged (often persistent) contralateral
mydriasis after an ipsilateral cerebrovascular accident (18). The pathology is
presumed to be cortical, or subcortical,
in the contralateral hemisphere and not
within the optic nerve or tract, as Behr
had originally postulated (18). Importantly, rapid recovery of normal pupillary size and function after surgical decompression, by definition, excludes
this possibility, as indeed, it effectively
excludes all others (18). It could be,
however, that some of the excess falselocalizing pupils witnessed in an earlier
series related to this (or other) variants.

CONCLUSION
Unilateral fixed dilation of the pupil
with hemispheric mass lesions can be
“false localizing.” More than one “herniating” mechanism can occur in the
same patient despite mass effect emanating from the same side.
Received, June 6, 2000.
Accepted, July 5, 2001.
Reprint requests: Laurence A.G. Marshman,
F.R.C.S., Department of Neurosurgery,
King’s College Hospital, Denmark Hill,
London SE5 9RS, England. Email: l.a.g.
marshman@btinternet.com

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False-localizing Pupil with Intracranial Hemorrhage
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COMMENTS
This is a good review of the mechanisms of pupillary dilation secondary to
herniation. As reported from the Traumatic Coma Data Bank (1) and from the
Medical College of Virginia (2), it is not
uncommon for pupillary dilation to
serve as a false-localizing sign of an intracranial hematoma. Hence, its occurrence per se is not surprising. What remains enigmatic, however, is the
mechanism by which this phenomenon
occurs. Marshman et al. have reviewed
the proposed explanations nicely. However, I must confess that I still do not
clearly picture in my mind how these
mechanisms actually work.
Raj K. Narayan
Philadelphia, Pennsylvania
1. Chesnut RM, Gautille T, Blunt BT, Klauber MR,
Marshall LE: The localizing value of asymmetry
in pupillary size in severe head injury: Relation
to lesion size and location. Neurosurgery 34:840–
846, 1994.
2. Ritter AM, Muizelaar JP, Barnes T, Choi S,
Fatouros P, Ward J, Bullock MR: Brain stem
blood flow, pupillary response and outcome in
patients with severe head injuries. Neurosurgery
44:941–948, 1999.

This article provides a nice review of
pupillary inequality as a false-localizing
sign. It is important to realize that mass
lesions can be heralded by contralateral
pupil dilation in up to 10% of cases.
With the advent of near universal access
to rapid computed tomographic scanning, this is not as great a problem as in
prior decades; however, there are still
cases where even the time taken for a
fast computed tomographic scanning is
inappropriate and the surgeon must
rely on clinical localizing findings. This
article will heighten awareness of this
possibility. A sidelight is the clinical
management of this patient which, I
suspect, might vary in other centers.

Neurosurgery, Vol. 49, No. 5, November 2001

Charles J. Hodge, Jr.
Syracuse, New York

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Marshman et al.

Marshman et al. have provided an
interesting and well written review regarding the localizing value of the pupil
in the assessment of intracranial masses.
They concentrate in particular on the
possible causes for ipsilateral versus

contralateral compression. They present
a case report of a patient who developed
both ipsilateral and contralateral papillary dilation. Unfortunately, in the absence of postmortem examination, it is
impossible to determine whether the

speculation as to the causes in this patient is correct.
Steven E. Feldon
Neuro-ophthalmologist
Los Angeles, California

Examples of bony destruction of the vertebral column. From, Jean Cruveilhier, Anatomie pathologique du corps humain, ou
Descriptions, avec figures lithographiées et coloriées, des diverses altérations morbides dont le corps humain est susceptible.
Paris, Baillière, 1829–1842, vol. 1. (Courtesy, Rare Book Room, Norris Medical Library, Keck School of Medicine, University
of Southern California, Los Angeles, California.)

Neurosurgery, Vol. 49, No. 5, November 2001