J Neurol Neurosurg Psychiatry 1999;67:169–173

169

When the left brain is not right the right brain
may be left: report of personal experience of
occipital hemianopia
Monroe Cole

Abstract
Objectives—To make a personal report of
a hemianopia due to an occipital infarct,
sustained by a professor of neurology.
Methods—Verbatim observation of neurological phenomena recorded during the
acute illness.
Results—Hemianopia, visual hallucinations, and non-occipital deficits without
extraoccipital lesions on MRI, are described and discussed.
Conclusions—Hemianopia, due to an occipital infarct, without alexia, is not a disability which precludes a normal
professional career. Neurorehabilitation
has not been necessary.
(J Neurol Neurosurg Psychiatry 1999;67:169–173)
Keywords: occipital; hemianopia; visual hallucinations.

Department of
Neurology, Case
Western Reserve
University and
University Hospitals of
Cleveland, 11100
Euclid Avenue,
Cleveland, OH
44106–5000, USA
M Cole

Personal reports of illness, disability, and the
experience of being a patient, recorded by a
trained observer, are of use to the medical profession. None of us plan to make such personal
observations, but once the opportunity arises
advantage should be taken of it.
I am a right handed neurologist who underwent an aortic valve replacement with a St Jude
valve, as well as a double coronary artery
bypass graft, on 2 January 1997 when aged 63.
A self performed neurological examination in
the recovery room disclosed a right hemianopia. Brain MRI and neurological examination
(fig 1 and fig 2) demonstrated only a left
occipital infarct on both banks of the calcarine
fissure and the dense right hemianopia.

On the second day I became aware of visual
hallucinations. These were especially prominent between 3 January and 10 January. (They
are, however, not entirely gone after 2 years and
appear to be fixed.)
My wife suggested, and continually encouraged me, not to miss the opportunity to record
my observations.
At first, virtually all of the hallucinations
were in bright colours, but some days they were
in muted grey, brown, or yellow. These duller
colours would usually appear as swirling
drapes, always in the right visual field, but
tending to interfere with vision in general. Only
twice did I see objects in black and white.
Sometimes the colour was not quite appropriate. Often there was a pony with his head cradled in my right arm. I recognised the pony as
the one owned by my granddaughter, but the
colour was wrong.
Most of the hallucinatory material was
recognisable but, as in the example above, the
colours did not always fit the object. I saw many
horses, dogs, and an even greater number of
people, most of whom I could recognise. They
moved, danced and swirled, but their purpose
was unclear. The hallucinations were neither
horrendous nor frightening. Many hallucinations were annoying even though I realised that
they were unreal. One hallucination often
recurred. There would be a hand thrust out
towards me; it would get larger, become
distorted, and then shake in a stereotyped
manner either in the horizontal or sometimes
in the vertical plane. Although the hallucinations interfered with vision, even at their worst

Correspondence to:
Dr Monroe Cole,
Department of Neurology,
Case Western Reserve
University and University
Hospitals of Cleveland,
11100 Euclid Avenue,
Cleveland, OH 44106–5000,
USA. Telephone 001 216
844 3769; fax 001 216 844
5066.
Received 16 October 1998
and in final form
5 March 1999
Accepted 5 March 1999

Figure 1

Brain MRI. (A) Sagittal view. Note infarct on both banks of the calcarine fissure. (B) Horizontal view.

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Cole

I could continue to do some visual tasks such as
shaving.
Hallucinations did not occur during sleep
and could be diVerentiated from dreams. During dreams, visual images were bilateral—that
is, not confined to the right visual field—and
movements were not stereotyped.
In contradistinction to the hemianopic
hallucinations described by Kölmel,1 my hallucinations were (1) not motionless; (2) not colourless; (3) not smaller than normal; (4) and
not extinguished by eye movement. Finally, (5)
my hallucinations were virtually continuous
during the first few weeks.
On several occasions I saw what seemed to
be a fortification outline. Unlike my migrainous fortification scotomata, however, this did
not move across the visual field but stayed in
one spot until it disappeared. Furthermore, the
edges of the scotomata did not twirl or glisten,
as my migrainous scotomata always do.
Certain factors made the hallucinations
worse, such as tachycardia, increased heart
failure, or an arrhythmia requiring electroconversion—which occurred five times postoperatively. During at least some of these
episodes—for example, after cardioversion— I
was seen to be mildly confused. The hallucinations were more prominent as the day went on
and normally worse when I was taken to an
unfamiliar environment.
On discharge, while being driven home, I
was constantly surprised by tall, hallucinatory
objects along the right side of the road. Sometimes they would be on the right side of a bend
in the road, causing me to wonder if the road
were blocked. The further the car went,
however, the more certain I became that our
progress would not be impeded. These hallucinations were stereotyped: large tan or cream
coloured buildings reminding me of old public
buildings or churches one would see driving in
Italy. Such hallucinations persist, but only
occasionally, and are very brief and evanescent.
A further peculiarity of these roadside hallucinations are that they have only occurred while
I am heading east, as they did when I first was
driven home from the hospital. I have never
been aware of them while I am heading west—
that is, away from home. Other hallucinatory
phenomena persist, especially diagonal lines in

Figure 2

Visual fields by Goldmann perimetry. A. od 3 May 1997; B. os 3 May 1997.

the right visual field, noted mostly inferiorly.
These are not annoying but occasionally
distract me while I am reading.
Generally, I am unaware of my hemianopia
unless I attend to it or strike things on my right
side. I may start a line of writing on the wrong
line above if the left side of the line is blank,
since I may be unaware of writing on the right
side of the line.
On a few occasions illusions were noted. At
the end of my hospital bed there was a clamp
which, when I first began looking at it, seemed
to be a telescope on a military gunsight. After I
saw what this actually was, I never had this
problem again. Much more unusual were
several episodes of false perception of colour.
On one such occasion I painted an outdoor
chair white. A few weeks later the house was
professionally stained white, and a deck was
stained battleship grey. I looked at the chair,
which was some distance from the house, and
wondered to myself why the painters had bothered to repaint my chair the same grey. I walked
over to inspect it carefully and found that it was
as white as the day I painted it.
I never read throughout my stay in
hospital—the first time I ever remember
passing time without reading. In fact, I noted,
as did observant visitors, that I usually kept my
eyes closed. I found vision bothersome although I never had diplopia. The exact quality
which bothered me is diYcult to analyse. I
simply found it uncomfortable to see. After
discharge I was constantly encouraged to read
and was given a novel with large print. My
enjoyment of reading was limited but rapidly
improved, so that after the first book was completed I began to read for real pleasure. Medical literature came rapidly thereafter. I had difficulty reading in a moving car, mainly because
I would lose the line in which I was reading, but
after some weeks I could and would read constantly in a car.
Discussion
Hemianopic hallucinations occur in about an
eighth of hemianopic patients.1
In some patients the hemianopic hallucinations occur at the onset of the ictus—for example, case 8 of Lance2—but usually there is a
latent period before onset. Most hallucinations

171

When the left brain is not right the right brain may be left

consist of familiar people, animals, or objects;
some have no obvious familiarity. Lance2 states
that hallucinations consist of people and things
rather than landscapes and scenes.
WHERE IN THE BRAIN ARE HEMIANOPIC
HALLUCINATIONS ORGANISED?

They obviously do not arise from destroyed
visual cortex. I would predict that they arise
from remaining visual cortex or, more likely,
from extrastriate cortex.3 Manford and
Andermann4 have recently reviewed various
putative mechanisms of visual hallucinations.
The physiological cause could be irritable cortex adjacent to the lesion, the original idea of
Seguin5 in 1886. As Lance noted,2 “the concept
of spontaneous discharge of neuronal circuits
in ischemic cortex is attractive.” In one of his
patients (case 9) in whom the clinical description does not suggest an epileptic disorder, hallucinations were reduced or abolished by anticonvulsant therapy. Weinberger and Grant6,
however, concluded that visual hallucinations
“are not due to cortical excitability but are psychological phenomena involving the total integrative activities of the mind.” Cogan7 concluded that episodic hallucinations represent
irritative phenomena, while continuous nonstereotyped ones are better explained as a
“release phenomenon” by loss of normal
control by “higher centers”. Brust and
Behrens8 and Fisher9 both support this
interpretation. I am unaware of definite data to
answer this question.
My original hallucinations were virtually, but
not absolutely, continuous, and often recurred
in a stereotyped manner. My present hallucinations, which are both simple (diagonal lines)
and complex (roadside buildings), do not seem
to represent seizures, as they last only seconds
and have no other features of seizures, such as
an aura, alteration of consciousness, or postictal confusion. Furthermore, the complex, or
formed visions only occur under one
condition—that is, riding in a car.
IS THE VISUAL FIELD, AS PLOTTED BY PERIMETRY
OR CAMPIMETRY, AN ARTIFACT?
Most neurologists accept the fact of a precise
retinotopic projection to certain parts of the
visual cortex—namely V1, V2, and V3—which
correspond to Brodmann’s areas 17,18, and
the posterior part of 19.
The retinotopic map was originally deduced,
mainly by Holmes and Lister10 and Holmes11–14
studying wounded soldiers. By carefully correlating the site of the entrance wound, sometimes supplemented by radiography, with
perimetry Holmes, and Riddoch15 were able to
describe the retinotopic organisation of the
visual cortex. In these investigations they
corroborated the work of Inouye in the RussoJapanese war and also the papers of Marie and
Chatelin,16 Axenfeld,17 Dimmer,18 and UthoV19
(see also Symonds20 and Spalding21). Holmes’
map was revised by Horton and Hoyt22.
In certain respects the visual field, as
demonstrated by perimetry or campimetry, is
an artifact of the method used: monocular or
binocular, static or dynamic, fixation or gaze.

Consider, for example, some of the research on
macular sparing or splitting. Holmes11 14
showed that the central 10° of the visual field is
projected to the most posterior part of the striate cortex, including that part of the posterolateral occipital tip. Cogan7 indicated that macular sparing is more common with parietal or
parieto-occipital lesions and less common with
temporal or occipital lesions. He also states that
macular sparing is absent with “paracentral
scotomas from lesions in the occipital pole.”
But cases 14, 15, and 19 of Holmes and Lister10
show just such sparing. Cogan,7 however,
seems to accept the idea that macular sparing
or splitting may be an artifact of testing.
Williams23 showed that macular splitting
demonstrated by fixation could be converted
by having the subject gaze at a second stimulus
about 5° from the fixation stimulus. He
emphasised the factor of attention, or relative
lack of it, to the fixation point as the primary
artifact of macular sparing or splitting.
VerhoeV24 also thought that macular sparing
was only apparent and hypothesised that with
occipital lesions it was due partly to instability
of fixation and partly to the establishment of an
eccentric fixation point—a so called pseudofovea (see also Gray et al25).
I find that preservation of my temporal crescent is helpful20 when examining confrontational visual fields. As my stimulus enters my
preserved temporal crescent, it provides better
orientation to the stimulus position than simply
“knowing” where the stimulus is by position
perception.
FORMED VERSUS UNFORMED VISUAL
HALLUCINATIONS

Probably most neurologists (see Kennedy’s
discussion in Cushing26 and Weinberger and
Grant6 for reviews) consider that complex
visual hallucinations are more likely found with
temporal lobe lesions, and that simple ones,
such as photopsias, are of occipital origin.
Horrax27 strongly supported this view, as did
Cushing. Horrax and Putnam28 state more
strongly that “formed figure hallucinations are
not produced by occipital tumors.” (Their
material consisted entirely of tumours.)
A number of observers (for example, Weinberger and Grant6) have concluded that
formed or unformed, simple or complex, visual
hallucinations may arise anywhere from the
retina to the visual cortex. It should be recalled
that the first description of hemianopic hallucination by Seguin5 in 1886 described the hallucinations as “simple,” but they consisted of
chairs and chickens. It behoves us to be more
specific when discussing visual hallucination.
The visual hallucinations of hemianopia, delerium, or seizure are likely to have diVerent
mechanisms.4 How they relate to one another is
less certain.
EYE MOVEMENTS

I am possibly the only person who has ever
been tested for eye movements, preoccipital
and postoccipital lesion. Before the lesion,
hypometric and hypermetric saccades were
recorded, and were considered normal for age,

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Cole

when I was tested at the age of 62. Postlesion,
the hypometric and hypermetric saccades were
greater in degree, reaching a “staircase”
pattern. Furthermore, when I searched for a
stimulus in the blind hemifield, the strategy of
an overshoot saccade, as described by Meienberg et al,29 was used, thus placing the stimulus
in the seeing field.
“BLINDSIGHT” AND THE RIDDOCH SYNDROME
The perception of movement is thought to be
organised in the middle temporal area comprising anterior area 19 and part of posterior
area 37 (V5). (see Symonds,20 Douglas et al,30
and Barton and Sharpe31 for discussion of striate and extrastriate cortical organisation.)
“Blindsight” is thought to occur if this area is
intact. “Blindsight” is used by most authors to
mean the ability to identify movement or
orientation of stimuli without conscious awareness of having seen the stimulus.
“Blindsight” diVers in certain respects from
the so called Riddoch15 syndrome. Riddoch’s
patients were consciously aware of movement
in the blind hemifield, but not of shape or colour. His patients probably had sparing of V5.32
I have been tested by Drs Lea AverbuchHeller and John Stahl, by the magnetic search
coil technique, for both “blindsight” and the
Riddoch phenomenon and demonstrate neither, suggesting that V5 is lesioned. However,
Barton and Sharpe31 conclude that survival of
V5 is not suYcient for “blindsight”. My MRI
does not indicate a lesion in V5.

tions in addition to those which are more specifically dependent on the region damaged.”
Further, “...in any brain damage one may
expect to find disturbances in function which—
according to current views—are not primarily
served by the damaged part.”
VISION IPSILATERAL TO THE LESION

Rizzo and Robin36 have studied vision in the
hemifield ipsilateral to a V1 lesion and
concluded that it is impaired. The authors
hypothesised that the deficit was either on the
basis of diaschisis, or due to a lesion of V2,
which has a strong transcallosal projection—at
least in monkeys. The diaschisis impairs transcallosal connections to the opposite hemisphere from V2, V4, and V5. Furthermore,
they hypothesised that visual attention or vigilance is impaired. Such an attention deficit is
not measured by usual perimetry but a method
thought to demonstrate its eVect was devised
by Williams.23
This deficit may best be described in the
words of Rizzo and Robin36 as “complaints of
tired eyes, things looking diVerent, blurred or
funny.” I do not find that I shun visual tasks
such as reading, even under diYcult conditions. I do need a great deal of light on any
subject. For example, looking for something
underneath a shelf or table is particularly diYcult. Furthermore, I suspect that my visual
attention is impaired as I often look for something, and fail to see it.
LIVING WITH A HEMIANOPIA

IMBALANCE

Riddoch15 also reported in his case that when
there is any remaining vision in the blind hemifield, vision may actually increase the diYculty
of ordinary life, as the disparity of the two half
fields is “frequently suYcient to aVect...equilibrium in walking.”
I too have inconstant imbalance. This was
worse early in the course and soon after
discharge from hospital. It was notably worse in
unfamiliar environments and when vision was
less clear. It still persists in unfamiliar environments, with decreased vision—for example, in
reduced light, and also with fatigue. Usually it
is not a problem, but in certain circumstances,
such as going down stairs, I try to go more
slowly and to hold onto the railing. The imbalance cannot in my case be ascribed to any type
of “blindsight,” as noted above. Magnetic resonance imaging shows no lesion in the cerebellum, brainstem, or anywhere else to explain it.
Examination of vestibular function demonstrated no abnormality.
This postural disturbance was well discussed
by Rondot et al.33 They pointed out that imbalance, or as they suggested “visual ataxia”,
which is to be diVerentiated from optic ataxia,34
occurs often in patients with homonymous
hemianopia. The defect is not of labyrinthine
origin, but may be a recentring of the centre of
gravity in relation to the spared visual field.
Brodal,35 in discussing certain otherwise unexplainable symptoms after his stroke, concluded
“...destruction of even a localised part of the
brain will cause consequences for several func-

The prognosis for recovery of an occipital
hemianopia depends entirely on the nature of
the causative lesion. One might be hopeful of
some recovery after closed head trauma, haemorrhage, infection, or inflammation. When the
lesion is an infarct, (the most frequent cause of
of an occipital hemianopia), there is probably
little chance of recovery, depending on the
extent of actual infarction with regard to the
ischaemic penumbra.
Of more importance is the disability caused
by such a hemianopia. Even intelligent patients
often are surprised when a hemianopia is demonstrated, despite the fact that it has been so
demonstrated on numerous examinations (see,
for example, case 1 of Williams and Gassel37).
Insight into the existence of a hemianopia generally relates to the ability to function in life
situations.37 Compensation for the visual field
defect probably is due to the deployment of
“gaze vision”—that is, not attending to a
fixation point; the use of searching saccades;
and possibly to development and use of a pseudofovea. I personally am unaware of my hemianopia unless I take pains to fixate. I also find
that unless specifically informed, my colleagues, patients, friends, and people I meet are
unaware of my deficit.
I am more bothered by an intermittent
hallucination of diagonally placed, thin blue
lines at 30–40° below the horizontal meridian
and 25–35° to the right of the vertical
meridian. Even this is only annoying if I am
reading, but does not hinder me in doing so. I
have to be careful not to run into people on my

When the left brain is not right the right brain may be left

right, or worse, to ignore them. I have already
alluded to my generalised diYculty with vision
and some imbalance.
Somewhat more vexing to me is the search
for objects. I interpret this problem to be a
deficit of visual attention rather than of vision.
Refractive correction has made no diVerence
and the searched for object is not necessarily in
the hemianopic field.
My only real handicap is being unable to
drive. I do not drive because I think it is too
dangerous and also because it is illegal. Being
unable to drive in the modern world is a mixed
blessing. However, for the person who lives
alone and is unable to arrange for a driver, the
handicap could be severe.
Some programmes of visual rehabilitation,
including the use of Fresnel prisms,38 have been
tried to improve the function of the hemianopic
patient. I have little use for this approach. Nor
do I think that so called neurovisual rehabilitation (see KerkhoV et al39)—that is, saccadic
training— is of much use as spontaneous
adaptation occurs without “treatment”. A
good, randomised control study would be necessary to change my opinion. What is more
important is that the patient slows down to
make certain that saccades are directed,
actually overdirected, into the hemianopic
field. I would say to a patient who has an
occipital hemianopia without alexia, “count
your blessings and reflect on how bad it might
have been.”
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