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The Posterior Cerebral Artery Syndrome
CM. Fisher

ABSTRACT: Embolic and thrombotic infarction in the territory of the posterior cerebral artery (PCA) is described
with emphasis on the stroke and cerebrovascular features rather than special neurological syndromes. Of 47 cases of
obstruction at the distal bifurcation of the basilar artery, 43 (95%) were consistent with embolism. The clinical
categories and pathological findings are presented. Local embolism, vertebral distal-stump embolism, the dynamics
of hemorrhagic infarction and embolus-in-transit are briefly described. The prodromal manifestations of PCA
thrombotic occlusion include photopsias, hemianopic blackouts, headache, transient episodes of numbness, episodic
lightheadedness, spells of bewilderment and rarely tinnitus. Recognition of these may allow prevention of a stroke.
Prodromal photopsias did not closely resemble the scintillating displays of migraineurs. When the stroke occurred,
visual complaints ususally predominated. A sensory deficit occurred in one-third of cases. In 25 cases of memory
impairment the dominant hemisphere was involved in 24. The kinds of visual hallucinations, simple and formed, are
described.
RESUME: Le syndrome de I'artere cerebrate posterieure. L'infarctus embolique et thrombotique dans le territoire de
I'artere ceYebrale posterieure (ACP) est decrit en mettant l'emphase sur 1'ictus et les manifestations cerebrovasculaires
plutot que sur des syndromes neurologiques particuliers. Parmi 47 cas d'obstruction au niveau de la bifurcation
distale de I'artere basilaire, 43 (95%) etaient compatibles avec une embolic Nous en presentons les categories
cliniques et les constatations anatomopathologiques. Nous decrivons brievement l'embolie locale, l'embolie au
niveau du moignon distal de I'artere vertebrale, les aspects dynamiques de l'infarctus hemorragique et de I'embole en
transit. Les manifestations prodromiques de I'occlusion thrombotique de I'ACP incluent la photopsie, l'anopsie
hemianopique, la cephalee, les episodes transitoires d'engourdissement, les etourdissements episodiques, les acces
de disorientation et plus rarement le tinnitus. L'identification de ces symptomes peut permettre de prevenir un ictus.
La photopsie eprouvee comme prodrome par ces patients ne ressemble pas aux scintillements percus par les
migraineux. Quant l'ictus survient, les symptomes visuels predominaient habituellement. Un deficit sensitif etait
present chez un tiers des cas. L'hemisphere dominant etait implique dans 24 cas de deficit de la memoire sur 25. Nous
decrivons les types d'hallucinations visuelles, simples et organisees.
Can. J. Neurol. Sci. 1986; 13:232-239
The arteries of pre-eminent interest to the neuro-ophthalmologist are the ophthalmic and central retinal arteries anteriorly and the posterior cerebral artery posteriorly. While the
former receive a good deal of clinical attention, the stroke
profile of the posterior cerebral artery (PCA) is not often discussed.
Specific aspects of the PCA syndrome are singled out for special study, for example, amnesia, mesencephalo-thalamic deficits and the visual and speech disorders of the temporo-occipital
region. The more general features of PCA ischemia have been
described in several reports over the years.1"8 However, the
literature contains no comprehensive description of strokes due
to occlusive disease of the PCA. PCA strokes are rather common and my records contain notes on more than 370 cases
which had been studied with variable degrees of thoroughness.
The aim of this paper is to describe the clinical syndromes
associated with ischemic events in the PCA territory, with
emphasis on the neuro-ophthalmological aspects.

VASCULAR ANATOMY

The PCA arises from the terminal basilar artery bilaterally in
71% of cases, mainly from the internal carotid artery (ICA)
unilaterally in 22% of cases and bilaterally in 7%. In angiographic
studies a vertebral injection fills both PCAs in almost 90% of
cases. In embolism to the bifurcation of the basilar artery and
the precommunal PCAs the size of the precommunal PCAs (the
segment proximal to the posterior communicating artery) and
the size of the posterior communicating arteries will be a factor
in determining the availability of collateral flow.
The penetrating branches to the midbrain and the thalamus
according to Percheron9 are usually four in number and arise
from the proximal few mm of the PCA. They fan out in the
sagittal plane to supply a paramedian core of tissue extending in
continuity through the entire vertical extent of the midbrain,
subthalamus and posterior two-thirds of the thalamus (Figure
1). Their distribution is unusual in that a penetrator from one

This paperwas presented at theToronto Academy of Medicine in June 1985 as part of a special lecture in honourof the late Dr. J. L. Silversides. Part I of the 1985
Silversides lecture appeared in the February 1986 issue of the journal.
From the Neurology Service, Massachusetts General Hospital, Boston. Massachusetts.
Reprint requests to: C. Miller Fisher. M.D., Neurology Service. Massachusetts General Hospital, Fruit Street. Boston, Mass., U.S.A. 02114

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Ischemia in the PCA territory is associated with a great many
neurological abnormalities any one of which could in itself be
the topic of a separate lecture. On this occasion our main
interest is in the characteristics of the stroke process, rather
than an analysis of complex neurological phenomena, and
therefore, it must suffice to merely enumerate the various
symptoms and signs from which the syndromes are derived
(Table 1). The main feature, of course, isahemianopiaorother
visual field defect which in most instances localizes the process
and the other manifestations are largely subsidiary.

THE VASCULAR PROCESS

Figure I — Diagram ofbranches to mesencephalon and thalamusfrom PCA.
A = Inferior and superior mesencephalic paramedian artery; B = Posterior subthalamo-thalamicparamedian artery;C ~ anterior subthalamothalamic paramedian artery.

PCA may divide to supply the medial part of the midbrain
tegmentum bilaterally and the medial part of each thalamus
bilaterally, occlusion producing a so-called butterfly infarct. In
about 50% of cases the penetrating arteries arise predominantly
from one PCA in the form of a pedicle giving rise to a leash of
small vessels and the presence or not of this arrangement will
again influence the effect of occlusion of the proximal PCA.
The structures supplied include in the midbrain the mesencephalic periaqueductal gray matter, nucleus and fibers of the
third nerve, raphe nuclei, Edinger-Westphal nucleus, median
reticular nuclei, medial longitudinal fasciculus, pars compacta
of the substantia nigra, superior cerebellar peduncles and their
decussation, and the medial third of the base of the peduncles.
In thalamus and subthalamus the paramedian structures most
often involved are the intralaminar and parafascicular nuclei,
inferior median nucleus, medial anterior central nucleus and
the superior internal pole of the red nucleus. The entire midbrain is supplied from the PCAs and not directly by branches
from the basilar artery.
The long and short peduncular branches of the PCA — some
six in number— supply the cerebral peduncles. More posteriorly there arise successively from the PCA, the posterior choroidal arteries, medial and lateral, running to the superior part
of the thalami, the thalamogeniculate vessels to the posteroventral
thalamus, including the sensory nucleus, the branches to the
hippocampus, the anterior and posterior temporal branches to
the inferior surface of the hemisphere, the parieto-occipital
branch to the medial occipital surface, the splenial branch to
the corpus callosum and finally the calcarine branch to the
visual cortex and its association areas.
When an occluded PCA arises from the ICA, a lateral thalamic deficit occurs without the midbrain-medial thalamic syndrome while on the other hand, when a vestigial precommunal
PCA unilateral or bilateral is occluded, the latter syndrome
occurs in the absence of a hemianopia and other hemispheric
signs.

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The two main vascular occlusive processes are embolism and
thrombosis, just as they are in the other cerebral arteries. The
PCA is unusual, however, in that it is the special site of another
important process, namely migraine. In patients with classical
migraine accompaniments, the visual system is involved in 90%
of cases either by itself or along with other accompaniments
(paresthesias, aphasia, etc.). So fundamental is the relationship
of migraine to the PCA territory that one might say the PCA is
the artery of migraine. The interpretation of visual symptoms,
seemingly arising as the result of PCA ischemia, is regularly
complicated by the possibility that the migraine process is
operative; and this is not true to the same extent of the other
cerebral arteries.
Postcommunal occlusion of the PCA in which the clinical
picture is limited to deficits arising in the hemisphere and lateral
thalamus is some seven times as frequent as precommunal
occlusion in which the territory of the entire PCA is involved
and midbrain and medial thalamic deficits are added to the
postcommunal syndrome. The stupor coma or abulia of midbrainmedial thalamic origin so dominates the clinical picture that the
hemispheral deficits may not be recognizable. In this regard the
syndromes due to precommunal and postcommunal occlusion
are really quite distinct and separate.

EMBOLISM TO THE POSTERIOR CEREBRAL ARTERY

Embolism is discussed first because it is pertinent to the
aforementioned important matter of precommunal versus
postcommunal occlusion. When an embolus is small, it enters
one or other PCA and depending on its size is arrested somewhere along the course of the artery producing an infarct of
corresponding size. When the embolus is large, it lodges at the
top of the basilar artery, where it may block one or both PCAs
in their precommunal segment. Differences in the size of the
two PCAs along with the configuration of the bifurcation will
help to determine the path, the final resting place and the effect
of the embolus. In this so-called "top o' the basilar syndrome,"
all deficits are usually confined to PCA territory, but occasionally extend slightly into the uppermost pons or the adjacent
cerebellum since paramedian arteries to the pons and the superior cerebellar arteries arise only I or 2 mm away.
Precommunal occlusion of one or both PCAs is by no means
rare and comes to the attention of the neuro-ophthalmologist
because of pupillary abnormalities and disorders of eye movement.
The typical upper brainstem lesion associated with precommunal
occlusion is the butterfly infarct. Forthis presentation I reviewed
47 cases of obstruction in the region of the basilar bifurcation.

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Table 1: Signs and Symptoms of Ischemia in Posterior Cerebral Territory

VISUAL

NON-VISUAL

PROXIMAL
Third nerve palsy, Parinaud's syndrome, vertical gaze paresis, paralysis of downward gaze,
bilateral ptosis, oval pupils, blepharospasm,
retraction nystagmus, tucking of eyelids, anterior
internuclear ophthalmoplegia, pseudo-paralysis
of 6th nerve, decreased or absent spontaneous
blinking with retained reflex blink to light and
sound, absence of slow roving eye movements,
absence of horizontal saccades, delayed eye
closure on falling asleep, ocular tremor.

DISTAL
Hemianopia, unilateral and bilateral; Anion's
syndrome, alexia without agraphia, coloranomia,
dyschromatopsia, hallucinations: simple, complex, formed and unformed. Central photophobia, visual perseveration, polyopia, tilted vision,
visual spread. Migraine: scintillations, blindness
and blurring. Prosopagnosia, topographic agnosia, visual agnosia, peduncular hallucinosis,
checkerboard fields, metamorphopsia.

Abulia, drowsiness, brief wake-sleep cycles,
coma, dementia, tachyphemia, hemiparesis, decerebrate posture, Horner's syndrome, cerebellar ataxia, rubral tremor, Weber's syndrome,
Claude's syndrome, Benedikt's syndrome, hemiballismus, asterixis, Cheyne-Stokes respiration.

Sensory deficit, Dejerine-Roussy thalamic
pain, choreoathetosis, confusion, agitation, impairment of memory, anomia for proper names,
isolated dysgraphia, unsteadiness or lightheadedness, hemorrhagic infarction secondary to brain
herniation.

including 24 studied pathologically. In 44 of the 47 cases (94%)
the evidence favored embolism as the vascular process rather
than thrombosis. It can be asserted, therefore, that almost all
strokes involving the bifurcation of the basilar artery are embolic.
In this preliminary analysis, the pathological findings in 24
cases showed the midbrain involved in 19 cases and the distal
PCA in 12 cases. The distribution of lesions is shown in Table 2.
The broad clinical categories in the 47 cases are listed in Table
3. Stupor and coma occurred in 35 cases, the neurological
deficits were minor in 3 cases and the remaining cases had
deficits of intermediate severity.
Since a penetrating branch from one PCA may supply the
midbrain and thalamus bilaterally it may be difficult to determine clinically if an embolus has blocked one or both PCAs
precommunally. Rarely, a small embolus enters an artery of
Percheron (0.3 to 0.5 mm in diameter) and gives rise to an
isolated small infarct in the midbrain or thalamus.
Embolism to the postcommunal PCA accounts for at least half
of all postcommunal infarcts, thrombosis and migraine accounting for the rest. The neurological deficits due to embolism are
similar to those associated with thrombosis of the postcommunal

Table 2: Structures involved in embolism to distal bifurcation of the
basilar artery
Number
of Cases
Midbrain, thalamus, peduncle, PCA occipital
Midbrain, thalamus, peduncle, PCA occipital, SCA
Midbrain, thalamus, peduncle, PCA occipital, pons
Midbrain, thalamus, peduncle, pons
Midbrain, thalamus, peduncle
Midbrain, thalamus, SCA
Midbrain, thalamus, SCA, pons
Midbrain, peduncle
Midbrain, SCA
Midbrain tegmentum
Thalamus
Thalamus, peduncle, PCA, SCA
PCA, pons

5
4
1
1
1
1
2
1
1
1
4
1
_J^
24

Table 3: Clinical features associated with embolism to the distal bifurcation of the basilar artery
Number
of Cases
Rapid onset of coma
Minor neurological deficits
Stupor with neurological deficits
intermediate in severity between 1 and 2
Cortical blindness
Amnesia
Alteration of Behavior
Deficits produced by embolus-in-transit

12
3
23
2
2
1
4
47

PCA, a subject to be discussed under that heading. Small
emboli may enter a PCA branch, either penetrator or superficial,
causing a very limited deficit. Minute embolic particles may
cause multiple microinfarcts in the calcarine cortex leading to
vague unexplained visual symptoms.
The diagnosis of infarction in PCA territory was revolutionized by the invention of CT scanning; and magnetic resonance
scanning is adding another whole dimension of sensitivity especially in studies of the brainstem and thalamus.
Clinically the diagnosis of embolism is favored when the
stroke has occurred in the absence of prodromal TIAs and
particularly in the presence of an embolic source such as atrial
fibrillation. The possibility of migraine may be raised, but embolism never produces the visual display with "build-up" characteristic of migraine. An embolus typically undergoes migration
and lysis and a patent artery by angiography signifies embolism
— or migraine. However, angiography in the first 48 hours may
show an embolic plug that will have disappeared later. Symptomatic thrombosis always has associated with it tight stenosis
or occlusion.
Two aspects of PCA embolism warrant further comment.
(I) Vertebral distal-stump embolism When a vertebral artery
undergoes thrombosis, thrombus building up in the distal stump,
may become disloged and pass along the basilar artery to enter
one or other PCA. 10 Clinically, such cases are probably not
infrequent, although proving the source of an embolus is always

PCA syndrome — Fisher
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LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
virtually impossible. The results of a pathological study of
"local embolism"" (artery-to-artery embolism) in the basilar
system are shown in Table 4. It will be noted that "local
embolism" had occurred in 25% of vertebrobasilar cases and
the infarcts were in the PC A territory in 17 of 18 cases making
distal-stump embolism particularly relevant to our present subject.
In a recent case (Figure 2) a man aged 61 developed a left
PCA syndrome including impaired gaze upwards, a slight right

Table 4: Characteristics of infarcts in 18 patients with local embolism
in the vertebrobasilar systems
Number
of Cases
Vessel Involved
Basilar
Bilateral vertebral
Unilateral vertebral
Regions of Infarction
Calcarine unilateral
Calcarine bilateral
Superior cerebellar
Calcarine and cerebellar

14
2
1
I

Age of Infarcts
Old
Recent
Old and recent

13
2
3

being free of thrombus. In the absence of any other source of
embolism it was inferred that emboli had arisen in the stump of
the occluded left vertebral artery. It is conceivable that timely
anticoagulant therapy would prevent such a complication.
(2) The dynamics of embolism and hemorrhagic infarction in the
vertebrobasilar territory Embolic infarcts may be pale or hemorrhagic or mixed. Hemorrhagic infarcts are usually embolic and
probably the result of the migration, fragmentation and lysis of
emboli allowing the restoration of arterial flow to the infarcted
tissue. Infarcts in which the embolus is found blocking the
artery of supply, usually remain pale. When a large embolus
passes along the vertebral artery and then along the basilar
artery, it may leave in its wake hemorrhagic infarcts that are a
sign of what is called an "embolus-in-transit". Figure 3 portrays the pathological findings in a case of embolism in which

EMBOLUS

HEMORRHAGIC
INFARCT

PALE INFARCT

EMBOLUS

Figure 3 — Diagram of hemorrhagic and pale infarction left in wake of
embolus passing through vertebral artery and basilar artery to reach
left PCA where embolic plug was found in artery just proximal to pale
infarct.
there were hemorrhagic infarcts in cerebellum, pons, midbrain
and thalamus and the main embolus was found lodged in the left
PCA proximal to a pale infarct. As the embolus moved along
the basilar artery, it may have temporarily blocked the mouths
of the penetrating arteries or given rise to a small embolic
particle as it did in the posterior inferior cerebral artery. The
PCA is a common site of hemorrhagic infarction (Figure 4).
A lively topic of discussion is just when does an infarct
become hemorrhagic if it is going to do so. It has been my
impression that it occurs early, perhaps in the first 24 hours, but
recently there came to my attention a case of PCA infarction in
which the infarct was bland by CT on day 9 and very hemorrhagic
Figure 2 — Diagram of left verbetral artery occlusion with evidence of distal
on day 17 in the absence of therapy.
stump embolism to PCA and SCA.

hemiparesis, right homonymous hemianopia and alexia without dysgraphia. He died suddenly 2'/2 months later and pathologically there was occlusion of the left vertebral artery with
distal extension of the thrombus and infarcts in the territory of
the left PCA and right superior cerebellar artery, both arteries

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THROMBOSIS OF THE POSTERIOR CEREBRAL ARTERY

Thrombosis of the PCA is usually the result of atherosclerosis,
which has a predilection to form in the circumpeduncular or
ambient segment of the postcommunal part of the artery rather
than the precommunal. One can predict the site of thrombosis

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numbness of the tongue, the right side of the chin and right hand lasting
a few seconds. On Warfarin sodium the spells ceased.
Case 2 — A man aged 67 in one month had five spells of striped vision
in the right visual field likened to looking through a Venetian blind
placed on its side. There were approximately 15 stripes. They lasted 10
to 15 seconds and seemed to occur when he looked at a bright landscape
or seascape. Aspirin was prescribed. One year later he reported five
spells of numbness of the right cheek, hand, forearm and leg, each spell
lasting about four minutes. Angiography showed tight stenosis of the
left PCA.
Case 3 — For six months the patient experienced TIAs consisting of
bright, moving circles before her eyes lasting 5 to 10 seconds. They
revolved counterclockwise and the patient called them "pieces of
electricity". At first they occurred one or twice a month, increased to
once or twice a week and on the day preceding the onset of a persistent
left homonymous hemianopia, the display occurred three times in one
day.
Case 4 — Fourteen days and eight days before the onset of a left
hemianopia the patient lost vision for five minutes associated with a
flash or ball of light "like the sun".
Case 5 — On each of the three days before the onset of a, left
hemianopia, a purple blob appeared in the left visual field associated
with a lightning bolt of different colors shooting out of it like Halley's
comet.
These brief descriptions illustrate the many variations in the
photopsias reported by patients with disturbances of the visual
system, such as transient monocular blindness with or without
carotid disease, migraine, transient ischemic attacks in the
PCA territory, and occipital lobe seizures. The number of
different patterns that a few basic ingredients can assume is
truly remarkable. Perhaps they are visualized away from central vision where they cannot be seen clearly, causing a vagueness in description. It seems to be impossible to develop an
experience with them that is of practical use clinically. Perhaps
Figure 4 — HemorrhagicinfarctionoftherightPCAterritoryandboththalami
if studied more diligently, they would make more diagnostic
in embolism.
sense, but that day has not arrived. It is even conceivable that
there with some regularity and hence in thrombosis the clinical
analysis would provide information about the nature of the
manifestations are almost always those of the postcommunal
underlying processes. The subject of photopsias has an additerritory sparing the midbrain. (While midbrain-medial thational unfortunate aspect, namely, the undue amount of time
lamic deficits are here being assigned almost automatically to
and space it takes to describe them. Worse still, there is no
embolism rather than thrombosis, it should be pointed out that
framework in which to classify them and one is unable to
there is no record of a detailed pathological study of Percheron's
remember for long the patient's account.
arteries in such a case.) The results of thrombotic occlusion are
As already mentioned, episodic photopsias were not comvariable and unpredictable since collateral blood flow to the
mon as TIAs in PCA thombosis. Two further patients had
distal PCA from the middle cerebral artery and anterior cereprodromal transient hemianopic blackouts.
bral artery via the meningeal anastomoses are different from
patient to patient. Total occlusion is occasionally asymptomatic.
Case 6 — For one week there occurred three to five spells daily of
Whether the blockage is precommunal or postcommunal, emboblank vision out to the right side lasting for a couple of minutes. On the
lism occurs suddenly and usually without warning, whereas
seventh day a spell was combined with numbness of the right hand and
thrombosis is frequently associated with prodromal headache
angiography showed tight stenosis of the left PCA.
and transient ischemic attacks (TIAs) consisting of numbness
Case 7 — For twelve hours, while awake, the patient had blackouts of
the central part of the right visual field interrupted by a return of vision
of the face and arm, or face, arm and leg on the opposite side.
for a second or two three times a minute. After 24 hours the seeing and
non-seeing periods each lasted 10 seconds and were occurring three
Prodromal TIAs
times a minute. There were no scintillations. There was a deep headache in the left forequarter of the cranium. The spells ceased four hours
From the standpoint of the neuro-opthalmologist the occurafter Heparin therapy was begun.
rence of prodromal photopsias would be important since early
More frequently, patients had less well-defined transient
diagnosis would provide an opportunity to intervene and previsual complaints in the day or two before the stroke — blurring
vent a full PCA stroke. However, such herald photopsias were
uncommon and were recorded in only 5 of 150 cases.
of vision, trouble focusing, difficulty seeing words, or a vague
interference with vision lasting a few seconds up to one hour.
Case 1 — Floaters, hexagons and octagons came and went in a flash
It is surprising that there was no example of prodromal visual
and were seen far temporally in the right visual field. When the patient
spells
closely resembling the scintillating phenomena described
looked in their direction, they disappeared. After two weeks, there
by migraineurs. In none of the cases was there a shimmering
appeared a light chocolate-colored spot in central vision, also coming
and going. In the next two weeks he had frequent TIAs consisting of
brightness and it may be a useful rule that the scintillating visual

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LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
aura of migraine is not the forerunner of atherothrombosis of
the PCA. However, it will be recalled that two patients had
prodromal episodes of a blank hemianopia and it is my experience that migraine can produce the same phenomenon. Another
feature was the brevity of the episodes of photopsia which
lasted 3 to 15 seconds unlike the usual migrainous spell. The
question is sometimes raised as to whether stenosis of a cerebral artery associated with a low pressure distally predisposes
to attacks of migraine. From this group of cases, the answer
appears to be " n o " . An analogous question is whether migraine
spells occurring distal to a stenosis precipitate infarction, and
again the main evidence is in the negative. There was one
unusual case, however, which speaks to this point. A man,
aged 78, had had recurrent typical scintillating zigzags for at
least 25 years associated with "build-up", occurring about
once a month and lasting 15 to 30 minutes. One day the scintillations appeared, but this time continued, and after eight hours,
the right side of the face and right hand began to tingle and he
became confused. Within 24 hours he had developed a severe
precommunal PCA stroke, including a right hemiplegia. The
possibility existed that events might have represented a persistent migrainous deficit, but pathological examination showed
atherosclerosis and superimposed thrombosis of the left PCA
in the precommunal segment. This might well be an example of
a migrainous spell precipitating infarction in a compromised
territory distal to arterial stenosis, but when the patient was
first seen, he could no longer give the details of the onset.
From this account, the opportunity will not often come to the
neuro-ophthalmologist to recognize incipient occlusion of the
PCA and possibly prevent a stroke.
The initial TIA symptoms in the PCA territory, were more
often spells of numbness coming and going, in face and arm, arm
and leg, or all three. Approximately one-third of the PCA
thrombotic cases noted prodromal spells of numbness lasting
for a few seconds up to 30 minutes, for one day, or for as long as
several months before the next symptom. There were sometimes one or two spells, other times as many as 100 before the
visual symptoms were added. Spells of isolated numbness of
this type can arise as a result of atherosclerosis of the PCA itself
or as a result of lipohyalinosis of the small penetrating artery
branch supplying the posteroventral nucleus of the thalamus.
Differentiating the two possibilities is at times impossible. It is
our experience that in PCA cases before a persistent stroke
occurs, there will always be transient symptoms of another
type than sensory, for example, visual disturbance, headache
or confusion to indicate that the true site of the disease is in the
main PCA rather than a branch and that prophylactic therapy is
in order.
Transient weakness or hemiparesis was rare as a TIA and
reflected involvement of the precommunal segment of the artery.
Weakness combined with sensory deficit may result from ischemia in the territory of the thalamogeniculate penetratingartery
(thalamo-capsular lacunar infarct) but no such case was
recognized.
Headache could be an important prodromal symptom and
preceded the stroke by days or weeks. The headache of PCA
thrombosis was most often situated above the ipsilateral eye or
in the anterior forequarter of the cranium. There could also be
associated pain in the occipital region. Occasionally the headache was referred solely to the upper parietal region ipsilaterally,
a somewhat unexpected finding. The headache was throbbing

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or steady and several patients reported exacerbation of the
headache on coughing or shaking the head.
Another prodromal symptom, not rare, was episodic lightheadedness, giddiness, dizziness, or unsteadiness. It sometimes
occurred alone, at other times it accompanied the visual
symptoms. The patient was often at a loss to characterize the
sensation accurately and the neurological nature of the symptom is unclear.
Occasionally, there was a prodromal transient brief spell of
bewilderment, confusion or "not knowing where I was for a
moment", a symptom that was probably linked to involvement
of the hippocampus of the dominant hemisphere.
Two patients reported hearing a sound at the onset of the
stroke, possibly an indication of involvement of the ipsilateral
medial geniculate body. In one, it was described as the hissing
of escaping steam.
The Stroke
Now we turn to the neurological features of the stroke itself.
Visual complaints predominated in the form of a full or partial
hemianopia. A sensory deficit occurred in only one-third of
cases. It is a good rule — although not an infallible one — that in
a PCA stroke, the patient is aware of the field defect, whereas
with an occipito-parietal lesion in the middle cerebral territory,
the patient is unaware of the field defect. Also, in a left or
non-dominant occipital hemianopia central vision is not shifted
far to the right as in non-dominant parietal lesions. This abnormality is revealed by having a patient read a newspaper headline — a test which should be routine.
The PCA visual symptoms included: poor vision, not seeing
out to one side, blurred vision, bumping into things, seeing half
of things or only parts of words, difficulty seeing, focusing or
reading and spots in front of the eye. In other words, a patient's
symptoms directed attention to the true nature of the stroke.
When the lesion was confined to the calcarine visual cortex, a
hemianopia constituted the entire stroke. An occasional patient
found later to have a hemianopia reported temporary blindness
or dim vision for Vi to 4 hours at the onset of the stroke. This
event which suggests that a sudden unilateral insult may have a
bilateral effect occurred only in cases of embolism or migraine
not thrombosis. Opticokinetic nystagmus is characteristically
preserved in calcarine hemianopia. Rarely a hemianopia was
due to a lesion of the lateral geniculate body, 12 in which case a
Wernicke-type hemianopic pupil may be present.
The sensory deficit, when present, varied in severity from
slight to virtually complete anesthesia of face, arm and leg,
involving all modalities. There may be an anesthetic pseudoparalysis in which the limbs appear paralyzed, but move with
good force when the paralyzed limb is held under visual control
in the seeing half-field. Parietal lesions in the territory of the
middle cerebral artery occasionally produce such severe sensory loss, but neighborhood signs such as aphasia, elements of
Gerstmann's syndrome, or visuo-spatial disorders provide the
clue to the correct localization.
Confusion and impaired memory occurred when the hippocampal
region of the dominant hemisphere was involved. 1314 In 70
PCA cases, most of them studied only clinically, there were 25
instances of memory impairment and in 24 the dominant hemisphere was involved. Of the 45 cases with preserved memory
and orientation the dominant hemisphere was involved 13 times,
the non-dominant hemisphere 32 times. From a clinical point of

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view, it is certain that the hippocampal regions of the two
hemispheres are not equivalent. When a PCA patient became
agitated and delirious, it was almost always the dominant hemisphere that was affected. In dominant lesions, the clinical history may be unreliable because of the patient's memory
impairment, which may be inobvious.
Depression and obsessive thinking were prominent in several
patients with involvement of the dominant hemisphere. This
may be a reaction to the greater functional deficit associated
with dominant lesions compared with non-dominant, but search
for a specific relationship is warranted.
Dyslexia without dysgraphia occurred with left hemispheric
lesions. 1215 Anomia for proper names and color anomia were
present in dominant lesions. 12 Topographic agnosia has been
reported with a lesion of the lingual and fusiform gyri of the
non-dominant hemisphere. 16 Visual perseveration*1 or "sticky
vision" was common, as was metamorphopsia in which objects
appeared misshapen.
Headache could be a prominent symptom and was localized
as already described. It was related to involvement of the PCA
in its proximal 3 to 4 cm but did not correlate with the presence
or not of confusion or sensory deficit. Headache also occurred
in 7 of 25 cases of PCA embolism, but was prominent in only 2
cases.
Visual hallucinations or photopsias which were uncommon as
a prodome were more frequent once the stroke occurred. The
following are examples: flickering yellow lights in the affected
visual field and dancing pinpoints of light sometimes moving in
circles, more prominent with the eyes open; (in the following
descriptions, the field referred to will be the hemianopic field
unless stated); kaleidoscopic brilliant multicolored snowflakes
or shaved icechips carried down like a frozen mist; flashing
kaleidoscopic lights of beautiful colors in the upper quadrant
and unformed patterns far out in the visual fields; gold and
silver shooting stars in the half-field; a red ball and a blue ball
drifted across the field of vision from left to right every minute
(right hemianopia); shimmering in the half-field for several days;
flickering or shimmering dots of lights; episodes of shimmering
spots and wavy lines, sometimes colored, tending to pass in
front from left to right diagonally downward (right hemianopia);
lights like a pinwheel with firecrackers; a flash of lightning
across vision at the onset; flickering and billowing waves of
blurring; colors rotating before the eyes while looking at brightly
colored objects; blurry, blinking waviness with a sort of linear
movement in the upper part of the half-field; dancing brilliant
multicolored scotomas in the half-field. Displays of this type
usually ceased in about one week, but occasionally they lingered for one month.
Can these descriptions be arranged to fit into a simple format?
Although it would be a gross simplification, the displays might
be divided into two categories — discrete foci and lines. The
foci were of various sizes — sparks, lights, spots, etc. The
elements were bright and often colored. Flickering, shimmering,
dancing, moving and waviness were common terms. In the
photopsias just described colors were particularly prominent (8
of 14, 57%), which is in contrast with the photopsias associated
with transient monocular blindness of which only 3 of 20 (15%)
were multicolored.
Complex formed hallucinations are a well known phenomenon
in PCA infarction 1819 and are more common when the nondominant hemisphere is involved. Afewexamples must suffice:

238
https://doi.org/10.1017/S0317167100036337 Published online by Cambridge University Press

Case 1 — a well formed horse's head, brown, shiny with fine looking
harness, many tall buildings, some of which were recognizable. The
hallucinations were situated 18" from the eye on an angle of 30 degrees
to the left of center.
Case 2 — colorful, well formed fish of all sizes, moving about, shiny,
shimmering, dark red, green, brown, light blue, yellow, copper and
gold. Also, clouds and trees, etc.
Case 3 — three banks of vivid vertical lines with illuminated pips
running up the lines a variable distance and breaking into colors on
coming to a halt—the highest became red while the lower siles of arrest
were yellow, blue or green, in that order.
Case 4 — scenes consisting of streets, buildings, cars and children on
looking to the left. The scenes constantly changed. When Phenytoin
sodium was prescribed, the scenes continued in the upper part of the
field, while in the lower part of the field jungle scenes appeared with
alligators, panthers, tigers, snakes, etc.
Case 5 — a multicolored oriental rug hanging on the wall of the right
side of the room.
Case 6 — various patterns (octagons, target rings) in many bright
colors, orange, yellow, green. A transparent German shepherd dog
walked across the room. The patient's father appeared as afigure4 to 5"
tall standing on a coffee table in the left visual field. A ghost stood in the
library looking at a knitting book.
Case 7 — five to seven purple flowers resembling tulips.
Case 8 — all kinds of colored things and patterns moving in the visual
fields — street scenes, cars falling into trenches, etc., no people or
animals.
Case 9 — black and white zebra stripes on the floor and tufts of hair
growing out of objects.
Case 10 — a little face like a smokescreen off to one side.
These hallucinations came and went all day long and were
always recognized as unreal. There was no narrative action or
emotional content such as might occur in a dream. The hallucinations usually persisted for 3 to 14 days, in one case for 7
weeks. The prominence of vivid colors was again notable. The
right cerebral hemisphere was involved in ten of 14 adequately
described cases, the left hemisphere in four.
The Prognosis
Full recovery from a hemianopia was rare, especially after
the deficit had lasted two weeks. Often relatively better vision
was restored to one quadrant, usually the inferior quadrant. A
deficit in the inferior quadrant was a distinct handicap compared with a superior defect. Impairment of reading greatly
curtailed the enjoyment of life. Persistent sensory symptoms
were usually not troublesome, but in about 1% of cases a
thalamic pain syndrome developed. Orientation and memory
were nearly always restored, but damage to one hippocampus
probably reduces the margin of safety as the deterioration of
old age develops. Hallucinations, visual perseveration and
metamorphopsia were temporary. Central glare was a rare
persistent complaint. 20
FURTHER ASPECTS OF PCA

ISCHEMIA

The subjects discussed so far include embolism to the distal
basilarbifurcation, PCA embolism, localembolism, hemorrhagic
infarction, and PCA thrombosis with its prodromal and stroke
manifestations. There are a number of other aspects of PCA
ischemia, which will be summarized briefly.
1. Migraine. As already mentioned, the PCA is par excellence
the artery of migraine. The visual accompaniments, transient,
prolonged, and permanent, are of unending variation and are
beyond the scope of this presentation. However, a small group
of cases with unusual vascular events in the PCA suspected of

PCA syndrome — Fisher

LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
being migrainous and for which the term "catastrophic" or
"cataclysmic" migraine has been suggested are reported
separately.21
2. The amaurosis-amnesic syndromefollowing angiography.2223
So regularly are the alarming deficits in this reaction reversible
within 24 to 72 hours that it is probably premature to ascribe the
symptoms to ischemia.
3. Compression of the PCA in temporal lobe herniation. The
manifestations are usually buried in the stupor and coma caused
by brainstem compression. The resultant infarction is always
hemorrhagic, a circumstance which should provide a clue to
the mechanism of the process.
4. Bilateral PCA infarction.2*2526 Several syndromes are
recognized depending on the severity and extent of the damage
to each PCA territory. When embolism to the distal bifurcation
of the basilar artery is responsible, mesencephalo-thalamic
symptomatology will dominate the picture, as previously
described.

ACKNOWLEDGEMENT

This work was supported by the Freed Foundation, Washington,
D.C.

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