Posterior Cerebral Artery Stenosis
Michael S. Pessin, MD," Eddie S. Kwan, MD,? L. Dana DeWitt, MD," Thomas R. Hedges 111, MD,S
Daniel Gale, MD,? and Louis R. Caplan, MD"

We analyzed the clinical features of symptomatic posterior cerebral artery (PCA) stenosis in 6 patients selected from 15
patients with angiographically documented PCA atherostenosis occurring during a 7-year period. Transient ischemic
attacks (TIAs) were the major presentation in 5 patients. A homonymous visual field defect was present in 2 patients.
TIA symptoms were predominantly visual or sensory, or both. The most common visual symptom was difficulty seeing
to one side. One patient saw flashing lights. Sensory spells were always paresthetic, usually involving the arm and hand
and occasionally the face and leg. Three patients had visual and sensory spells together. Two patients with a visual field
defect had calcarine infarcts found by computed tomography. All patients were treated with warfarin. During followup (4 months to 4 years), no patient had a new stroke in the PCA territory, and only one continued to have TIAs. PCA
atherostenosis is rarer than PCA embolic occIusion. In contrast to those with PCA embolism, our patients with PCA
atherostenosis had more TIAs and fewer infarcts. The clinical features of PCA stenosis-preponderance of visual and
sensory TIAs-distinguish this vascular lesion from stenosis of the middle cerebral artery.
Pessin MS, Kwan ES, DeWitt LD, Hedges TR 111, Gale D, Caplan LR:
Posterior cerebral artery stenosis. Ann Neurol 2 135-89, 1987

Infarction in the posterior cerebral artery (PCA) territory is commonly caused by embolism, either cardiogenic o r from a more proximal vertebrobasilar intraarterial or unknown source C1, 4, 7, 91. In contrast,
PCA atherostenosis is an uncommon lesion [l, 91
whose clinical course and angiographic features have
not been reported. T o clarify the clinical features of
PCA stenosis, we retrospectively analyzed 6 symptomatic patients with PCA atherostenosis and compared
them to our previous series 191 of patients with PCA
embolism.

Methods
Patients were selected by reviewing the angiographic log
book for the 7-year period, 1978 through 1985. Fifteen patients with atheromatous PCA stenosis were identified, but
review of the medical records showed that only 6 had related
symptoms. We report the clinical and angiographic features
in these 6 patients. Patients with a recognized cardiac embolic source were excluded.
All angiograms were performed through the transfemoral
route and were reviewed in detail by a neuroradiologist
(E. S. K.). Information noted included the degree of PCA
stenosis as measured directly from the angiogram and compared to an adjacent section of normal artery; the location
and extent of the stenosis; associated stenosis in the vertebrobasilar circulation; and any hemodynamic effects evidenced by slow flow through the stenotic region or shifts
in the collateral vessels of the adjacent border zone. Computed tomographic (CT) scans were reviewed in all patients

From the Departments of 'Neurology, ?Radiology, and tOphthalmology, Tufts-New England Medical Center, Boston, MA.
Received May 12, 1986. Accepted for publication June 18, 1986.

for areas of infarct in the PCA territory as well as in the
brainstem and cerebellum.
All patients were examined by one of the authors, and the
medical records were reviewed in detail for all pertinent
information. Neuroophthalmological examination was carried out in 4 of the patients.

Results
Angiographic and CT Findings
The angiographic and CT data are presented in Table
1. Five patients had unilateral symptomatic PCA stenosis and 1 patient had bilateral disease. Based on anatomical segments of the PCA described by Margolis
and co-workers IS], the stenosis affected the more
proximal (perimesencephalic) portion of the PCA in
all patients. In the 5 patients with unilateral PCA disease, the site of stenosis was the peduncular segment
in 2 , ambient segment in 2, and quadrigeminal segment in 1. The patient with bilateral symptomatic PCA
stenoses had involvement of the peduncular and ambient segments. There were single areas of stenosis in
4 patients and multiple areas in 2. The length of
stenotic areas varied from 2 to 5 mm. The degree of
stenosis ranged from 50 to 80%. Antegrade flow
through stenoses was present in all patients and there
was no angiographic evidence of slowing or other hemodynamic effects. Intraluminal thrombus or distal
embolization was not present. In 4 patients, both
PCAs arose from the basilar artery, and in the 2 other

Address reprint requests to Dr Pessin, Department of Neurology,
Tufts-New England Medical Center, 171 Harrison Ave, Boston,
MA 02'''.

85

Table I , Angiographic and Computed Tomographic Findings in 6 Patients with Posterior Cerebral Artery Stenosis
Patient
No.

Site of Stenosis

Percent
Stenosis

CT Findings"

Other Lesions

3
4

Peduncular segment
Quadrigeminal segment
Peduncular segment
Ambient segment

80
63
50
75

Negative
Calcarine infarct
Negative
Calcarine infarct

5

Ambient segment

80

Negative

bb

Left ambient segment
Right peduncular segment

72
50

Negative
...

...
...
Left ICA occlusion
Left MCA stenosis, right calcarine
branch stenosis
Diffuse VB atheroma, asymptomatic
right PCA stenosis
...
...

1
2

"CT findings in symptomatic PCA territory only.
bBilateral symptomatic PCA stenoses.

CT = computed tomography; VB = vertebrobasilar; ICA = internal carotid artery; MCA = middle cerebral artery; PCA = posterior cerebral
artery.

patients one PCA arose from the internal carotid artery and one from the basilar artery. Associated lesions
included diffuse atheromatous changes in the vertebrobasilar system in 1 patient, including severe asymptomatic PCA stenosis; stenosis of the middle cerebral
artery (MCA) and calcarine artery branch in 1, and
occlusion of the internal carotid artery in 1.
CT scans showed calcarine infarcts corresponding to
the symptomatic PCA in 2 patients, and a calcarine
infarct in the territory of an asymptomatic PCA stenosis in 1 other patient. One patient had a small cerebel-

lar infarct, one had a thalamic lacuna, and one had
bilateral capsular lacunae.

Clinical Featlcres
Table 2 presents the clinical findings. There were 5
men and 1 woman, ranging in age from 63 to 7 9 years.
Hypertension was present in 2 patients and one also
had diabetes mellitus. O n e patient had mitral valve
prolapse and another had coronary artery disease. The
left PCA was symptomatic in 3 patients, the right in 2,

Table 2. Clinical Features i n 6 Patients with Posterior Cerebral Artery Stenosis
Patient
No.

Sex, Age
(Yr)

1

M, 6 8

2

M, 7 9

3

M. 64

M, 69

M, 63
F, 78

Number and Nature of TIAs

Stroke Features

Treatment and Follow-up

Two over 2 mo; in one, black loss
of vision to right, clumsy
involuntary movements in right
arm, and garbled speech, 2-3
hrs; right hand weakness
None

None

Asymptomatic on warfarin for 4
mo; then death from intracranial
hematoma after head injury

Left hemianopia

Many over 6 wk; loss of vision to
right, pins-needles in right fingers
moving up arm with occasional
speech difficulty, 2 min
Three over 4 mo; loss of vision to
left, once tingling left hand-face;
a few min to 45 min
Many over 2 mo; tingling, pinsneedles in right cheek, armhand, occasionally leg, 5 min
Four over 9 mo; bilateral visual loss
or flashing lights-gray vision,
gray loss of vision to right, bright
red-white lights, sometimes leg
numbness and lightheadedness,
10 min

None

Asymptomatic on warfarin for 14
mo
TIAs continued on warfarin for 4
mo

TIA = transient ischemic attack; M = male; F = female.

86 Annals of Neurology Vol 21

N o 1 January 1987

Left superior
quadrantanopia
None (old left
hemiparesis)
None

Asymptomatic on warfarin for 4 yr,
then death due to left hemisphere infarction
Asymptomatic on warfarin for 5 mo
One episode left visual blurring on
warfarin, died at 9 mo

and one had bilateral symptoms localized to both PCA
territories.
The presenting problem in 5 patients were PCA
territory transient ischemic attacks; the 1 remaining
patient had an established homonymous hemianopia
without warning TIAs. One of the patients with TIAs
(no. 4 ) had a left superior quadrantanopia on Goldmann perimeuy. The 2 patients with homonymous visual field deficits both had appropriate calcarine infarcts shown by CT.
The TIAs were brief and multiple. Three patients
had two, three, and four TIAs, respectively, and 2
patients had “many” over 6 weeks to 9 months. TIAs
lasted 2 to 10 minutes, the longest 2 to 3 hours. Four
of the 5 patients with TIAs had visual symptoms as
part of their attacks. The features included visual loss
to one side, sometimes described as black or gray. One
patient with bilateral PCA stenoses experienced unilateral or bilateral visual symptoms of flashing lights, redwhite lights, or gray vision. All patients with visual
spells also had other simultaneous symptoms, including clumsiness and involuntary movements of an arm,
migrating pins and needles sensations in the arm and
hand with speech difficulty, tingling of the face and
hand, and lightheadedness with leg numbness. One
patient had only sensory TIAs consisting of tingling
and pins and needles sensation of the cheek, arm,
hand, and occasionally the leg.
Treatment and Follow-up

All patients were treated with warfarin and followed
from 4 months to 4 years (Table 2). While taking warfarin, 4 patients remained asymptomatic, one (no. 3)
continued to have TIAs, and one (no. 6) had only one
TIA during a 9-month follow-up period. No patient
had a new infarction in the PCA territory. Three patients died while being treated with warfarin with prothrombin times that showed therapeutic levels; one
had an intracranial hematoma after head injury, one
died of a new infarction in the left hemisphere (MCA
territory), and one was found dead with no cause determined.
Patient Histories
The following patient histories illustrate the typical
clinical course.
Patient 1

A 68-year-old man had two TIAs over a 2-month period.
While giving a sermon, he felt weak and lost vision to the
right side as if something had blackened it out. His right arm
became clumsy, with involuntary movements, and his speech
was garbled. The attack lasted 2 to 3 hours. On another
occasion he had weakness of his right hand. Neurological
findings were normal. Bilateral carotid and left vertebral artery angiography demonstrated severe stenosis of the proxi-

Fig 1. Antemposterior view of a selective left vertebral angiogram
with simultaneous compression of the lejit carotid arteq. There is
a high-grade stenosis (arrow) in the proximal left posterior cerebral artery just distal to its junction with the left posterior communicating artery. Compression of lejit carotid artery eliminated
the possibility dj%wartifact created by non-opacifed blood from
the anterior circulation.

mal portion of the left PCA, just distal to the posterior
communicating artery (Fig 1). Both carotid bifurcations had
only mild atheroma.
Neuroophthalmological findings were normal. Routine
laboratory studies yielded normal results, including complete
blood count, platelet count, electrocardiogram, and echocardiogram. The patient remained symptom free for 4 months
while taking warfarin. One night he fell in the bathroom,
striking his head on the bathtub. On the way to the hospital
he lost consciousness and died in 6 hours. Postmortem examination showed a parenchymatous hemorrhage in the right
hemisphere.
Patient 3

A 64-year-old man had many TIAs over a 6-week period.
The attacks usually consisted of a 2-minute episode of loss of
vision to the right side, pins and needles sensation of the
right fingers that moved up the arm, occasionally accompanied by speaking difficulty and weakness of the right arm.

Pessin et al: Posterior Cerebral Artery Stenosis 87

Fig 3. Lateraluieu, of a right common carotid angiogram demonstrates a long iweguhr beaded appearance in the ambient segment of the rtght posterior cerebral artery (double arrows).

Fig 2. Anteroposterior view of a left subclavian angiogram.
Moderate stenosis is identifed at the junction of the peduncular
and ambient segments of the posterior cerebral artety (arrow).

He had a history of hypertension, mild renal insufficiency,
and peripheral vascular disease.
Neurological findings were normal. Bilateral carotid and
left vertebral artery angiography demonstrated occlusion of
the left internal carotid artery at its origin, with a normal
right carotid system. Stenosis was present at the proximal left
PCA (Fig 2). Routine laboratory findings were normal except for a blood urea nitrogen level of 53 mg/dl and a
creatinine concentration of 1.6 mgldl. The patient was
started on warfarin therapy but his TIAs continued during a
4-month follow-up.
Patient 4
A 69-year-old man had three TIAs during a 4-month period.
His attacks were stereotyped and consisted of visual loss to
the left side, lasting a few minutes to 45 minutes. During one
of these episodes he also noted tingling of the left hand and
face. His past history was noteworthy for peripheral vascular disease. Neurological examination revealed only a left
superior quadrantanopia on Goldmann perimetry. Bilateral
carotid and a left brachial angiogram demonstrated that the
right PCA filled from the carotid injection and showed several areas of irregular stenosis (Fig 3). Minor atheroma of the
carotid bifurcation was present. CT showed a right occipital
enhancing infarct. Routine laboratory studies including an
electrocardiogram were normal. Warfarin therapy was begun
and the patient remained asymptomatic during a 4-year follow-up. H e then died of a new infarction in the left hemisphere while he was still taking warfarin.

88

Annals of Neurology Vol 21 N o I January 1987

Discussion
PCA atheromatous stenosis, like MCA stenosis, is an
uncommon vascular lesion, given that we identified
only 15 patients in a 7-year angiographic review. During the same approximate time, we identified 80 patients and reported on 35 with presumed embolism of
the PCA territory {9]. Among 22 patients with necropsy-proved disease of the PCA main stem or
branch, only 2 had atherothrombotic occlusion [11.
Other studies 11, 4, 71 have corroborated that embolism, either cardiac or local, is the major mechanism
in ischemia and infarction of the PCA territory. We
could not find other reports that systematically analyzed angiographically proved PCA stenosis. The small
number of patients in the present study may reflect in
part our predominantly white patient population; intracranial vertebrobasilar atheroocclusive disease may be
more common in blacks {S].
The proximal portion (perimesencephalic segments)
of the PCA was the major site of stenosis, as shown by
angiography-a finding similar to the stenosis found in
MCA disease affecting the main stem. Hemodynamic
changes and the distal effects of embolism are the presumed mechanisms for production of symptoms, although we were unable to document their presence on
angiography .
TIAs were the major presentation in 5 of our patients. TIA features were distinctive, with visual symptoms predominant, often associated with sensory complaints. These features help distinguish PCA territory
TIAs from those associated with MCA stenosis, in
which motor and speech disturbances are common and
visual symptoms absent {b}.The TIAs were often multiple and stereotyped, features consistent with an

atherothrombotic-hemodynamic mechanism. The simultaneous occurrence of 2 or more TIA symptoms
was the rule. In contrast, only 3 of 35 previously reported patients with presumed embolism of the PCA
territory had warning TIAs 191, and all had infarcts of
the PCA territory, most of sudden onset.
At first glance, the visual and sensory TIA features
in our patients with PCA stenosis resemble migrainous
accompaniments. However, absence of headache, lack
of a build-up in the visual disturbance, and absence of
gradual progression or transition from one symptom to
another help distinguish TIAs originating in the PCA
territory from migrainous events 12, 31.
All of our patients were treated with warfarin, but
the small numbers and lack of controls preclude endorsement of any specific therapy. During follow-up,
no patient had further infarction in the territory of the
PCA stenosis, yet 3 patients fared poorly, dying of
other causes. Recognition of the clinical features of
PCA stenosis may help identify more patients with this
condition and lead to appropriate study of various
medical treatments.

References
1. Castaigne P, L'Hermitte F, Gautier JC, et al: Arterial occlusions
in the vertebro-basilar system. A study of 44 patients with postmortem data. Brain 96:113-154,1973
2. Fisher CM: Migraine accompaniments versus arteriosclerotic
ischemia Trans Am Neurol Assoc 93:211-213, 1968
3. Fisher CM: Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks. Can J Neurol Sci 7:9-17,
1980
4. Fisher CM, Karnes WE: Local embolism. J Neuropathol Exp
Neurol 24:174, 1965
5. Gorelick PB, Caplan LR,Hier DB, et al: Racial differences in the
distribution of posterior circulation occlusive disease. Stroke
16~785-790, 1985
6. Hinton RC, Mohr JP, Ackerman RH, et al: Symptomatic middle
cerebral artery stenosis. Ann Neurol 5:152-157, 1979
7. Koroshen WJ, Ropper AH: Local embolism as a cause of stroke
in the posterior circulation. Neurology 35(suppl 1):214, 1985
8. Margolis MT, Newton TH, Hoyt WF: The posterior cerebral
artery: Part 11. Gross and roentgenologic anatomy. In Smith JL
(ed): Neuro-Ophthalmology Symposium of University of Miami
and the Bascom Palmer Eye Institute. Hollandale, FL, Huffman,
1970, pp 161-192
9. Pessin MS, Lathi ES, Cohen MB, et al: Clinical features and
mechanism of occipital infarction in the posterior cerebral artery
territory. Ann Neurol 18:123, 1985

Pessin et al: Posterior Cerebral Artery Stenosis

89