Hemiplegia in
posterior cerebral artery occlusion
M. Hommel, MD; G. Besson, MD; P. Pollak, M I P. Kahane, MD; J.F. Le Bas, MD; and J. Perret, MD

Article abstract-We report 4 patients with hemiplegia due to a posterior cerebral artery occlusion. Associated clinical signs
were aphasia, alexia or a neglect syndrome, hemianopia, and hemisensory loss. Hemiplegia was due to infarction in the lateral
midbrain. The level of the occlusion in the posterior cerebral artery may be located distal to the junction with the posterior
communicating artery.
NEUROLOGY 1990;40:1496-1499

The occlusion of a posterior cerebral artery (PCA)
causes a spectrum of manifestations, including homonymous visual field defects, abnormal visual perception, and neuropsychological signs a n d symptoms.
Usually, there is little or no weakness.' Two reported
cases of hemiplegia with PCA territory infarction were
not verified with imaging studies or autopsy.2 Only the
case of Caplan et a13had anatomic verification; it was a
lateral midbrain infarct. We report 4 patients with
hemiplegia associatedwith infarction in the territory of
t h e PCA.
Case reports. Patient 1. A 66-year-old man with a history
of cigarette smoking was admitted for sudden right hemiplegia. On admission, there was complete right hemiplegia
affecting face, arm, and leg, with a Babinski sign, right hypoesthesia, and right homonymous hemianopia. The head and
eyes were turned toward the left. He was aphasic with impaired comprehension, loss of repetition, and he was able to
perseverate only in rare, stereotyped, poorly articulated
phonemes. CT without contrast injection 3 days after the
onset showed a hypodensity in the left posterior thalamus and
left occipital and temporal lobes (figure1A). MRI 24 days after
the stroke (CGR magniscan with a 0.5 Tesla superconducting
magnet in joined axial T,-weighted images [TE = 60, 120
msec; TR = 2,000msec] of 9-mm thickness, from the medulla
to the vertex) confirmed CT and also showed an infarction in
the anterolateral part of the left cerebral peduncle (figure 1B).
The patient did not improve, remained bedridden, and died 7
months later.

Patient 2. A 58-year-old hypertensive man with a history of
myocardial infarction and valvular aortic stenosis complained
of left temporal cephalalgia for 3 days. He then developed a
right ataxia. He was admitted on the 4th day with a right
hemiplegia affecting the face, arm, and leg, and a Babinski
sign. He had a right anesthesia and right homonymous hemianopia. Upward gaze was limited. The eyes and head were
turned toward the left. He was dysarthric, fluency was de-

creased, and semantic paraphasia, neologisms, and perseverations were present in spontaneous speech. Comprehension
was severely impaired. He was alexic. CT, performed without
contrast injection on the 4th day after the stroke, showed a
hypodensity affecting the thalamus and the occipital and the
inferior part of the temporal lobes. An MRI study on the 12th
day, in axial T,-weighted images of 10-mm thickness with
contiguous slices, confirmed the CT findings and also showed
an infarct in the left ventral peduncle (figure2). One year later,
sensory perception had improved, and he was able to walk
slowly, but was dependent in all activities of daily living. He
remained alexic and aphasic with decreased fluency and voice
volume. Comprehension, however, had recovered, repetition
was normal, and the paraphasia, neologisms, and dysarthria
had disappeared.

Patient 3.A 76-year-oldright-handed woman with a history
of hypertension and myocardial infarction was admitted for
heart failure. On the next day, she was found with a complete
right hemiplegia affecting the face, arm, and leg, and a
Babinski sign. The head and eyes were turned toward the left,
and she had a right homonymous hemianopia. She was alert
but mute and did not respond to verbal orders. Painful stimuli
elicited normal reactions on the left side but stereotyped extensor responses on the right. Pupil size and reactivity, as well
as ocular movements, were normal. CTwithout contrast injection on the same day showed a hypodensity affecting the left
midbrain, posterior thalamus, occipital lobe, and the inferior
and medial part of the temporal lobe (figure 3). She died from
cardiogenic collapse 4 days later. No autopsy was obtained.

Patient 4. A 69-year-old man had a history of cigarette
smoking, hypertension, and, 13 years before the stroke, a left
trigeminal neuralgia attributed to a fusiform aneurysmal vertebral artery kink demonstrated with angiography. He was
admitted for the progressive 3-day evolution of a left hemiplegia. On examination, the hemiplegia affected the face, arm,
and leg, with a head and eyes deviation toward the right. There
was no Babinski sign. Hypoesthesia for fine discrimination,
light touch, joint position, pain, and temperature was ob-

From the Departmentof Clinical andBiologica1Neurosciences,Stroke Unit and Magnetic Fksonance Unit, Centre HospitalierUniversitairede Grenoble,Grenoble,
France.
Received January 23,1990. Accepted for publication in final form April 3,1990.
Addreas correspondenceand reprint requests to Dr. Marc Hommel, Clinique Neurologique,Centre Hospitalier Universituire de Grenoble, BP 217 X 38043, Grenoble,
Ceder, France.
1496 NEUROLOGY 40 October 1990

A

Figure 1. (A) Patient 1. CT
showing a left thalamic
(single arrow) and
occipital (double arrows)
infarct. (B) Patient 1. MRI
i n T,-weighted sequences
showing the left midbrain
infarct (arrows).

Figure 2. Patient 2. MRI showing the left mdbrain (single
arrow) and occipital (double arrows) infarct.
served on the left side. Visual fields were normal. There was a
disorientation for time but not for place. After 7 days, the
disorientation had disappeared, and a left spatial neglect syndrome was observed. CT without contrast on day 4 after the
stroke showed a hypodensity in the posterior part of the right
thalamus. An MRI study, performed on day 35 after the stroke
in T,-weighted axial images, also showed an infarct in the
right midbrain (figure 4).During the follow-up, he had a deep
venous thrombosis, pneumonia, and an acute cholecystitis.
Sensory perception fully recovered, but he had a residual
hemiparesis. Six months later, he needed minimal help in
daily activities, and some left motor neglect remained.

Discussion. A 3rd nerve palsy with crossed hemiplegia, Weber’s syndrome, is a well-known midbrain
syndrome. When due to infarction, the arterial occlusion is located at the origin of the PCA, where the
paramedian branches supplying the 3rd nerve nucleus
and fascicles, and the short circumferential branches
supplying the lateral part of the midbrain, have their
rigi in.^ None of our cases had a 3rd nerve palsy or
tegmental signs or symptoms indicating a midbrain
lesion, with the exception of an upgaze paresis in patient 2.

Figure 3. Patient 3. CT showing the left midbrain, temporal,
and occipital infarct.

Sometimes, in PCA occlusion, paresis and sensory
loss occur. There are 2 proposed hypotheses:
Johanssonb suggested, in a CT study, possible involvement of the pyramidal tract in the internal capsule, or
associated lacunes in the corona radiata. Benson and
Tomlinson2 suggested midbrain infarction in 2 cases
with neuropsychological signs and symptoms of PCA
territory involvement and radioisotope brain-scanning
evidence. Caplan et a1,3 in an anatomic case, showed
infarction in the lateral midbrain. In each of our cases,
the hemiplegia was associated with an infarct in the
midbrain. In 3 patients, the sensation could be assessed
and was decreased or abolished. This loss could have
been due to either thalamic involvement or midbrain
lemniscal system infarction.6
Conjugate deviation of the head and eyes toward the
side of the lesion is not common in PCA occlusion. Case
1 described by Caplan et a13 had the same anatomic
lesions as ours, and as observed in our 4 cases, a contralateral head and eye deviation.
October 1990 NEUROLOGY 40 1497

I

I

PCoA

I

Figure 4. Patient 4. MRIshowing the infarct in the right
midbrain (arrow).

I
Within the 1st few days after the stroke, the neuropsychological features in our patients (aphasia, alexia,
and neglect), the presence of hemiplegia, hemisensory
loss, hemianopia, head and eyes deviation, and verbal
language difficulty make it difficult to distinguish main
trunk middle cerebral artery from PCA occlusion on
clinical grounds alone. In the more chronic period, we
were not able to distinguish a specific right PCA syndrome in patient 4.Patient 2 remained aphasic with a
pattern of reduced fluency and voice volume, normal
repetition, and absence of dysarthria, often described in
thalamic aphasia.7 But we have difficultiesin ascertaining, on this criterion and in 1patient only, whether a
specific left PCA syndrome may exist.
Foix and Hilleniand4described the paramedian and
circumferentialarteries, originating from the top of the
basilar artery, supplying the 3rd nerve nucleus and fascicles, and the pyramidal tract in the ventral-lateral
midbrain. According to their study, a hemiplegia without a 3rd nerve palsy did not seem possible. Zeal and
Rhoton: in an anatomic study of 50 brains, divided the
PCA into 3 parts: PI from the origin in the basilar artery
to the posterior communicating artery; P2 (mean
length, 50 mm) was divided into an anterior (P2A) and
posterior half (P2P), with P2A beginning at the posterior communicating artery and coursing around the
peduncle, and P2P beginning at the posterior margin of
the posterolateral midbrain and terminating at the posterior aspect of the midbrain within the ambient
cystern; P3 proceeds posteriorly from the level of the
pulvinar in the lateral aspect of the quadrigeminal
cistern and ends at the anterior limit of the calcarine
fissure. The average length of the P3 segment is 20 mm
(figure 5). The thalamoperforating arteries arise from
P1 and supply the anterior part of the posterior
thalamus, hypothalamus, subthalamus, substantia
nigra, red nucleus, oculomotor nucleus and nerve. The
short circumflex arteries, present in 66% of brains,
originate in 86%of the cases from P1, pass only a short
distance around the brainstem before entering the
brain, and send branches to the cerebral peduncle, contributing to the blood supply of the corticospinal tract.
The corticobulbar and corticospinal pathways are also
1498 NEUROLOGY 40 October 1990

Figure 5. Axial diagram of the midbrain. BA = basilar
artery; PCoA = posterior communicating artery; PI = P1
part of the posterior cerebral artery (PCA); P2a = anterior
segment of the P2 part of the PCA; P2p = posterior
segment of the P2 part of the PCA; P3 = P3 part of the
PCA; TPA = thalamoperforating arteries; TGA =
thalamogeniculate arteries; SCA = short circumflex
arteries; PPA = peduncular perforating arteries; PMA =
paramedian arteries; CST = corticospinal tract in cerebral
peduncle; SN = substantia nigra; RN = red nucleus; IIIrd
= oculomotor nucleus.

supplied by the perforating branches originating from
P2A in 94% of the cases and from P2P in the remaining
6%. The thalamogeniculate arteries have their origin at
the P2A level. An arterial occlusion of the end of P1 or
beginning of P2A could induce a midbrain infarction
with hemiplegia and anesthesia without a 3rd nerve
palsy. As the thalamogeniculatearteries have the same
origin, an occlusion may also cause a posterior thalamic
infar~tion.~J*
Our 4 cases had an infarction in the lateral midbrain involving the pyramidal tract and the
posterior thalamus supplied by the thalamogeniculate
arteries. Three patients also had an occipital and temporal infarction in the more distal territories of P3.
These findings suggest that the occlusion was located at
the P2A portion of the PCA in our patients.

References
1. Caplan LR. Posterior cerebral artery syndromes. In: Vinken PJ,
Bruyn GW, Klawans HL, Toole JF, eds. Handbook of clinical
neurology, vol53. Vascular diseases Part I. Amsterdam: Elsevier,
1988409-415.
2. Benson DF, TomlinsonEB. Hemiplegic syndromeof the posterior
cerebral artery. Stroke 1971;2:559-564.
3. Caplan LR, De Witt LD, Pessin MS, Gorelick PB, Adelman LS.
Lateral thalamic infarcts. Arch Neurol1988;45959-964.
4. Foix C, Hillemand P. Les &res de l’axe enchphalique jusqu’au
diencbphale inclusivement.Rev Neurol (Paris) 1925;6:705-739.
5. Johansson T. Occipital infarctions associated with hemiparesis.
Eur Neurol1985;24276-280.
6. Duvernoy HM. Human brainstem vessels. Berlin: Springer, 1978.
7. Cambier J, Graveleau Ph. Thalamic syndromes. In: Vinken PJ,
Bruyn GW, Klawans HL, Frederiks JAM, eds. Handbook of clinical neurology, vol 45. Clinical neuropsychology. Amsterdam:

Elsevier, 1985:87-98.
8. Zeal AZ, Rhoton AL. Microsurgical anatomy of the posterior
cerebral artery. J Neurosurg 1978;48534-559.
9. Hayman LA,Berman SA, Hinck VC. Correlation of CT cerebral
vascular territories with function: 11. Posterior cerebral artery.

AJR 1981;137:13-19.
10. Takahashi S, Goto K, Fukasawa H, Kawata Y, Uemura K,
Yaguchi K. Computedtomography of cerebralinfarctionalongthe
distribution of the basal perforating arteries. Radiology
1985;155119-130.

Capsular genu syndrome
Julien Bogousslavsky, MD, and Franco Regli, MD

Article abstract-We report 5 patients with unilateral infarct and 1 with hemorrhage limited to the genu of the internal
capsule. The most prominent finding was contralateral facial and lingual hemiparesis with dysarthria. Three patients also
showed unilateral mastication-palatal-pharyngeal weakness, and 1had unilateral vocal cord paresis. Mild limb involvement was
limited to hand weakness in 4 patients. Our findings suggest that the majority of motor corticopontine and corticocobulbarfibers
are located in the genu of the internal capsule. The faciolingual syndrome and its variants are highly suggestive of capsular genu
stroke.
NEUROLOGY 1990;40:1499-1502

In his 1902 thesis, Ferrand' mentioned that partial
forms of hemiparesis could occur in patients with lacunes in the internal capsule. The occurrence of partial
forms of motor hemiparesis from capsular stroke depends upon the location of the lesion with reference to
the topography of the motor representation of the head,
upper limb, trunk, and lower limb within the internal
capsule.2Previous reports suggested that predominant
facial weakness from capsular stroke was related to
involvement of the most rostral part of the posterior
limb in the internal capsule.3
We studied 6 patients with acute stroke limited to
the genu of the internal capsule on one side, as identified
on CT following templates developed by one of us.3 All
of them had contralateral faciolingual-and to a lesser
extent masseter-palatal-pharyngeal-laryngeal-weakness contrasting with limb involvement limited to only
mild hand weakness.
Patients. There were 5 men and 1woman, aged 43 to 84 years.
The clinical and CT characteristics in these patients are summarized in the table. All patients had unilateral lower facial
and tongue weakness, 5 had dysarthria, 3 had dysphagia,3 had
unilateral masseter weakness, 2 had unilateral palatal weakness, and 1had unilateral vocal cord paresis. No patient had
sternomastoid or trapezius weakness. The cranial nerve findings contrasted with only mild to moderate upper limb involvement in 4 patients, which was usually limited to
unilateral fingers or hand weakness. Two patients had no
dysfunction in the limbs. Standard neuropsychologicalexamination findings were normal in all patients. Extracranial
Doppler ultrasonography was unremarkable in all patients.
All patients were discharged within 3 weeks of admission,
after they had made a good to complete recovery.

Case reports. Patient 1. A 68-year-old man was admitted
because of acute dysarthria with right facial drooling and
weakness in the right hand. He smoked 12 cigarettes per day
but had no medical history. On admission, blood pressure was
160/90 mm Hg with a regular pulse. On neurologic examination, he showed severe inferior facial weakness and moderate
weakness of eye closure on the right. He had marked dysarthria with slurred speech. He complained of dysphagia, and
masseter and posterior palatal weakness was present on the
right. The tongue markedly deviated to the right on protrusion and it could not push against resistance toward the left
side. Facial and buccal sensation were normal. Corneal reflex
was symmetric. The rest of the cranial nerves were normal,
includingtrapezius and sternomastoid contraction. No abnormality was present in the limbs except for moderate weakness
of the fingers on the right, involving mainly flexion movements. Styloradial tendon reflex was slightly more brisk on
the right than on the left. Standard neuropsychologicalexamination findings were normal, Extracranial Doppler ultrasounds and ECG were normal. CT 3 days later showed a small
infarct involving the genu of the internal capsule on the left.
Recovery was complete within 2 weeks except for right facial
asymmetry and slight deviation of the tongue to the right on
protrusion.

Patient 2. A 63-year-old man with intermittently treated
arterial hypertension was admitted after he acutely experienced severe dysarthria and dysphagia. On examination, he
showed moderate facial paresis on the right predominating in
the inferior part, and had a tendency to drool. The speech was
so slurred that only a few words could be understood. Closure
of the mouth and masseter contraction were weak on the right.
There was a slight right posterior palatal ptosis with hypomotility. The tongue deviated markedly to the right on protrusion attempts. Laryngeal examination showed hypotonia and

From the Department of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Received January 26,1990.Accepted for publication in final form March 29,1990.
Addma correspondenceand reprint requests to Dr. J. Bogodavsky, Department of Neurology, CHUV, 1011 Lausanne, Switzerland.

October 1990 NEUROLOGY 40 1499