LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES

Bilateral Homonymous Hemianopia
with Sparing of Central Vision After
Subdural Hematoma
Marco Soza, Patricio Tagle, Trevor Kirkham and Jaime Court

ABSTRACT: A patient with bilateral homonymous hemianopia with preservation of the central vision, spatial
disorientation and memory deficits secondary to bilateral occipital and mesial temporal infarctions, is presented. The
cerebral damage followed a subdural hematoma with tentorial herniation and compression of both posterior cerebral
arteries.
RESUME: Hemianopsie homonyme bilaterale epargnant la vision centrale a la suite d'un hematome sous-dural Nous
rapportons le cas d'un patient presentant une hemianopsie homonyme bilaterale avec preservation de la vision
centrale, disorientation spaciale et deficit de la memoire secondaires a des infarcissements occipitaux et mesiotemporaux bilateraux. Les dommages cerebraux sont survenus a la suite d'un hematome sous-dural avec hernie
tentorielle et compression des deux arteres cerebrales posterieures.
Can. J. Neurol. Sci. 1987; 14:153-155

Bilateral homonymous hemianopia from cerebral infarction
is a rare occurrence. 1,2 Most reported patients present with a
visual field defect that is partial and recovers spontaneously. 1 ' 3
In some cases there is concomitant optic atrophy" which makes
it difficult to interpret the visual field defects; in others, the
presence of occipital infarction has not been sufficiently documented either by computerized tomography or by postmortem
examination of the brain. The most common causes appear to
be occlusions of the posterior cerebral arteries secondary to
atheroma, emboli or migraine. 3,5 Bilateral homonymous hemianopia with sparing of central vision is even less frequent.' 5 , 6
In autopsy material, tentorial herniation of the hippocampal
gyrus of the temporal lobe has been clearly correlated with
occipital infarction, due to compression of the posterior cerebral arteries. 7 However, clinical reports of bilateral homonymous
hemianopia with sparing of the central vision after tentorial
herniation are rare. 4,7,8
In this paper, we present the case of a patient who developed
a permanent and complete bilateral homonymous hemianopia
with preservation of central vision after transtentorial herniation
secondary to subdural hematoma. In addition, he developed
severe anterograde and retrograde amnesia and spatial disorientation. Computerized tomography of the brain revealed
bilateral occipital infarctions.

CASE REPORT

A 38 year old, previously healthy man presented with progressive
headache, nausea and blurring of vision. Two months prior to admission,
he had suffered a head injury which had left him unconscious for
approximately two hours. Examination revealed bilateral papilledema,
spatial disorientation and amnesia; he was unable to recall any of the
events of the past two months. There were no signs of focal neurologic
deficits, and the general physical examination was unremarkable. Twenty
hours after his admission, the patient developed convulsive seizures
involving his right extremities and a persistent right hemiparesis. The
pupils became dilated, the right more than the left, and both were
unresponsive to light. Babinski sign was present bilaterally. An EEG
showed bursts of bilateral and synchronous delta waves over both
frontal lobes. Blood pressure was 170/110, pulse 80/min. and regular. A
right carotid angiogram, through femoral catheterization, showed a
large right frontal subdural hematoma and bilateral tentorial herniation.
After surgical evacuation of the hematoma, the hemiparesis, pupillary abnormalities and papilledema rapidly resolved, but a severe defect
in the visual fields was noted, consisting of bilateral homonymous
hemianopia with sparing of the central 10° of vision in both eyes (Figure
I). The patient behaved as if he were blind, but he could recognize a
small pin on the floor.
The spatial disorientation persisted and despite having spent many
days in hospital, the patient never learned to go from his room to the
bathroom. Furthermore, while in his room, he was unable to find his
own bed. When offered a chair, he sat with the chair back to his side or
even in front of him. On several occasions, the patient tended to sit
beside the chair. Often we observed him trying to get into bed from the
foot of the bed instead of from the side near the pillows.

From the Department of Neurology and Neurosurgery of Catholic University of Chile, Santiago (Drs. Soza. Tagle, Court) and from McGill University. Montreal, Quebec
(Dr. Kirkham)

Received December 10, 1985. Accepted infinalform January 19, 1987
Reprint requests to: Dr. Marco Soza, Departamento de Neurologia, Hospital Universidad Catolica, Marcoleta 347. Santiago, Chile

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Figure I — Visualfields showing bilateral homonymous hemianopia with preservation of central vision in both eyes.

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The third remarkable deficit was a complete loss of memory for
recent events. Despite the fact that he was able to recall the first and
middle names of his thirteen brothers and sisters, and to give many
details of his marriage ten years ago, he could not remember that he had
been examined just 30 minutes previously.
These severe neurologic deficits remained essentially unchanged
during a four year follow-up period. The visual fields of both eyes
remained constricted although visual acuity was 20/20 bilaterally. No
pupillary abnormalities, oculomotor deficits, alexia or visual agnosia
were encountered. The fundi were normal, as well as optokinetic
nystagmus. A formal psychometric study revealed severe impairment
both in spatial orientation and in memory for recent events, with
relative preservation of intellectual functions.
Two years postoperatively, a computerized tomography of the brain
showed bilateral occipital infarctions, as well as slight dilation of the
left Sylvian cistern consistent with discrete atrophy of the left temporal
lobe (Figure 2A, 2B).
DISCUSSION

In the case presented here, a right subdural hematoma caused
bilateral tentorial herniation as documented by the signs of
midbrain dysfunction and by carotid angiography. As the
hippocampal gyrus herniates through the tentorial incisura, it
presses the ipsilateral posterior cerebral artery against the tentorial
edge. The contralateral posterior cerebral artery can also be
pulled against the tentorial edge by the downward displacement
of the brainstem. 4 The obvious result of bilateral posterior
cerebral artery occlusion is bilateral occipital infarction, as well
as damage in the basomesial surface of both temporal lobes.
These lesions were confirmed in our patient by computerized
tomography.
The cerebral insult suffered by our patient resulted in a
remarkable clinical picture consisting of bilateral homonymous
hemianopia with sparing of the central vision, spatial disorientation and amnesia. These changes remained almost unaltered
after more than four years of follow-up.
The bilateral homonymous hemianopia in the case reported
here is of special interest because of its completeness, which
has been seldom reported, 9 and because of the full preservation
of central vision with normal visual acuity in the 10-20 degrees
in the center of the fields of both eyes. The sparing of central

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vision in posterior cerebral artery occlusions is due to the fact
that the occipital pole derives its blood supply from terminal
branches of the middle cerebral artery. 1,3 It is worth noting as
well that our patient did not develop optic atrophy (as in many
cases in the literature) 4 indicating that no major damage to the
pre-geniculate visual pathways occurred. The preservation of
optokinetic nystagmus is also in agreement with an occipital
origin of the visual field defects.
Symonds and MacKenzie' found that among 58 cases with
bilateral homonymous hemianopia collected from the literature
and from their own experience, they encountered only 11 with
circular sparing of central vision. In their cases in which postmortem confirmation of bilateral occipital infarction was available,
arterial thrombosis or emboli were identified as the cause.
McAuley and Ross-Russell 5 encountered only one case with
preservation of central vision among 39 subjects with visual
defects secondary to vascular lesions of the posterior visual
pathways. Their cases were correlated with CAT scans. Nepple
et al2 reported three patients who after subdural hematomas
developed extensive visual defects with relative sparing of
central vision. However, the only visual field shown in their
paper is a combination of a right homonymous hemianopia with
a left quandrantanopia.
Bilateral occlusion of the posterior cerebral arteries may
produce severe amnesia, l0 as in our case. In these circumstances,
the critical area for memory impairment seems to be the subcortical temporal white matter or temporal stem. I0 In our patient, in
addition to bilateral occipital infarctions, the CT scan showed
evidence of atrophy at least of the left temporal lobe.
Another remarkable deficit in our patient was his spatial
disorientation. It is rarely encountered in the literature as a
consequence of posterior cerebral artery occlusions.' It has
been described in bilateral parieto-occipital lesions." Nevertheless, in our patient, we can not rule out that the spatial
disorientation might have been due to direct right parietal lobe
compression and damage by the subdural hematoma itself.
Other signs occasionally reported in patients with occipital
infarctions such a visual agnosia, alexia, or denial of the visual
deficit, were not present in the case reported here.

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A

B

Figure 2 — A) CTscan showing bilateral occipital infarctions. B) CT scan at a lower level than Figure 2A showing anatomical preservation of both occipi

ACKNOWLEDGEMENTS

This work was supported by the Gildemeister Foundation. The authors
express their thanks to Drs. S. Carpenter and G. Karpati for reviewing
the manuscript and to Mrs. M. Erdelyi for secretarial assistance.

REFERENCES

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Kaul SN, Du Boulay GH, Kendall BE, et al. Relationship between
visual field defect and arterial occlusion in the posterior circulation.
J Neurol Neurosurg Psychiatr 1974; 37: 1022-1030.

Volume 14, No. 2 — May 1987
https://doi.org/10.1017/S0317167100026299 Published online by Cambridge University Press

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