J Neurol (1992) 239 : 162-164

Journal of

Neurology
© Springer-Verlag 1992

Bilateral anterior cerebral artery territory infarction
in the differential diagnosis of basilar artery occlusion
A . Ferbert 1 and A . Thron 2
1Abteilung ftir Neurologie and 2Abteilung ftir Neuroradiologie, RWTH, Pauwelsstrasse, W-5100 Aachen, Federal Republic of Germany
Received February 7, 1991 / Received in revised form April 15, 1991 / Accepted June 19, 1991

Summary. Two patients with bilateral anterior cerebral
artery (ACA) territory infarction are presented whose
initial d i a g n o s i s was b a s i l a r a r t e r y occlusion. B o t h h a d
t e t r a p a r e s i s ; in o n e it was a s y m m e t r i c a l . B o t h h a d t h e i r
e y e s o p e n a n d d i d n o t r e s p o n d to c o m m a n d e x c e p t t h a t
a f t e r a d e l a y t h e y f o l l o w e d with t h e i r eyes a s m o o t h l y
m o v i n g o b j e c t ; this was t h e o n l y sign of a w a r e n e s s . O n e
p a t i e n t h a d a c l e a r v e r t i c a l gaze p a l s y in t h e u p w a r d a n d
downward direction unaccompanied by pupillary abnorm a l i t i e s . C o m p u t e d t o m o g r a p h y r e v e a l e d fresh b i l a t e r a l
A C A i n f a r c t i o n in b o t h p a t i e n t s ; o c c l u s i o n in t h e h i n d
b r a i n c i r c u l a t i o n was e x c l u d e d b y a n g i o g r a p h y in o n e .
B o t h p a t i e n t s s u f f e r e d f r o m a t r i a l f i b r i l l a t i o n , so c a r d i a c
e m b o l i s m was t h e m o s t l i k e l y cause o f t h e s t r o k e . W e
conclude that bilateral ACA territory infarction should
b e c o n s i d e r e d in t h e d i f f e r e n t i a l d i a g n o s i s of b a s i l a r
a r t e r y o c c l u s i o n , e v e n if a c c o m p a n i e d b y v e r t i c a l gaze
palsy.

Key words: B i l a t e r a l a n t e r i o r c e r e b r a l a r t e r y i n f a r c t i o n Akinetic mutism - Vertical gaze palsy

Introduction
T h e m a j o r f e a t u r e o f a s t r o k e in t h e f o r e b r a i n h e m i s p h e r e s is a s e n s o r i m o t o r h e m i p a r e s i s t h a t m a y show
b r a c h i a l o r c r u r a l p r e d o m i n a n c e d e p e n d i n g o n t h e territ o r y i n v o l v e d . T e t r a p a r e s i s a n d an a l t e r e d l e v e l of consciousness at t h e o n s e t of t h e s t r o k e a r e h i g h l y suggestive
o f i s c h a e m i a in t h e h i n d b r a i n c i r c u l a t i o n , unless t h e
p a t i e n t a l r e a d y h a s a m a j o r i n f a r c t i o n in o n e h e m i s p h e r e
a n d t h e r e is r e c e n t i s c h a e m i a of the o p p o s i t e h e m i s p h e r e .
I n t h e f o l l o w i n g w e r e p o r t two p a t i e n t s w i t h b i l a t e r a l ant e r i o r c e r e b r a l a r t e r y ( A C A ) o c c l u s i o n w h o w e r e initially d i a g n o s e d as suffering f r o m b a s i l a r a r t e r y occlusion.
Offprint requests to: A. Ferbert

Case reports
Case 1
This 65-year-old patient noticed sudden onset of weakness in his
arms and legs which improved so that on admission 3 h later he had
only a right hemiparesis with crural predominance as well as sensory disturbance in the right leg. Computed tomography (CT) was
normal. Electrocardiography revealed atrial fibrillation. There
was no previous history of diabetes, smoking, or hypertension but
blood pressure on admission was 220/120 mmHg. Twenty-four
hours after the onset he experienced a sudden deterioration with
severe tetraparesis. Plantar responses were extensor bilaterally.
On request he could follow the examiner's finger with his eyes in
the horizontal plane but not in the vertical plane. This finding
could be reproduced several times in spite of some delay before
the execution of pursuit movements. Smooth pursuit was often
overlaid by catch-up saccades. On passive head movement to the
left and to the right as well as in the vertical plane, oculocephalic
reflexes could be obtained. Optokinetic responses could not be elicited with a small striped drum. Stimulation with a broad or fullfield optokinetic stimulus was not possible; tetraparesis prevented extensive testing in the electro-oculographic laboratory. The
pupils were medium-sized and promptly reacted to light. He did
not open his mouth on command. Facial muscles were activated to
painful stimuli. Corneal reflexes were normal. A sensory examination was not possible because the patient could not respond. There
were some spontaneous random saccades of low amplitude in
the horizontal plane. Saccades to verbal command were not performed either in the horizontal or in the vertical plane. When we
tried to elicit visually guided saccades by sudden repetitive movements of the examiner's fingers, the patient would only occasionally gaze towards the target. Doppler ultrasonography of the extracranial brain-supplying arteries was normal. Vertebral angiography was performed because there was a suggestion of a basilar
artery thrombosis, but the appearances were normal. The next day
the patient deteriorated in consciousness and had to be provided
with a tracheal tube. CT 3 days after the first signs showed a lowdensity area in the territory of the A C A bilaterally (Fig. 1). Over
the next 3 weeks the condition was unchanged with minor fluctuation in wakefulness. The only spontaneous activity was opening
the eyes and sometimes looking around. No communication via
blinking or eye movements was ever possible.
Case 2
This 68-year-old female had been found unresponsive on the floor
of her flat and was admitted to our hospital. Two weeks earlier she

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Corneal reflexes were normal, The right arm was severely paretic.
She did not move her left arm on request but could withdraw it to
painful stimuli. There was tremor at rest in the left arm. Both legs
showed extensor rigidity. Plantar responses were extensor. Facial
muscles contracted bilaterally to painful stimuli. CT revealed an
old small cortical-subcortical infarction in the territory of the left
middle cerebral artery (MCA). As she had aspirated on her way to
the hospital, she had to be intubated and ventilated immediately.
Brain-stem auditory evoked potentials were normal on the left and
showed signs of peripheral hearing loss on the right side. A repeat
CT on the following day showed a bilateral infarction in the whole
territory of the A C A in addition to the old lesion (Fig. 2).
Over the following days, the patient could then open her eyes
on request but only with a significant delay. No further reactions
could be evoked. Thus, extensive testing of oculomotor functions
including optokinetic stimulation could not be performed. However, oculocephalic responses on passive head turning in the horizontal and vertical plane (doll's eyes phenomenon) was always
present. Communication via eye movements or blinking was not
possible. Her condition did not improve over the next 2 weeks and
she was transferred to a local hospital for further care after having
undergone another CT which showed haemorrhagic transformation of the infarctions.

Discussion

Fig.1. Case 1. Three days after the first clinical signs CT shows
bilateral anterior cerebral artery infarction including the corpus
callosum with the size of the infarction being larger on the left side
(left side of the figure is right side of the patient)

Fig. 2. Case 2. CT 1 day after the occurrence of the tetraparesis
shows bilateral anterior cerebral infarction that extends from the
corpus callosum to the convexity (left side of the figure is right of
the patient)

had experienced a transient hemiparesis with full recovery. Her
previous history revealed a stroke 10 years previously, from which
she had totally recovered, as well as atrial fibrillation. There was
also a previous history of rest tremor in the left arm. On admission
she was anarthric but followed a light with her eyes on request with
some delay as the only sign of responsiveness. There were no signs
of infranuclear oculomotor disturbances nor was there spontaneous or gaze-evoked nystagmus. Visually guided saccades could not
be elicited presumably because of the patient's limited ability to
cooperate. Pupils were small, of equal size and reacted to light.

T h e m a i n clinical f e a t u r e s o f o u r p a t i e n t s w e r e a s y m m e t r i c a l t e t r a p a r e s i s a n d a state t h a t can b e d e s c r i b e d as
a k i n e t i c m u t i s m . T h e r e was also v e r t i c a l gaze p a r e s i s in
o n e p a t i e n t . T e t r a p a r e s i s o r t e t r a p l e g i a is a c o m m o n sign
in b a s i l a r a r t e r y o c c l u s i o n a n d was f o u n d in a b o u t half of
t h e 85 p a t i e n t s p r e v i o u s l y r e p o r t e d f r o m o u r d e p a r t m e n t
[61.
T h e m o r e c o m m o n m o t o r sign in b i l a t e r a l A C A i n - .
f a r c t i o n is p a r a p l e g i a c o r r e s p o n d i n g to the c r u r a l p r e d o m i n a n c e in t h e u n i l a t e r a l A C A i n f a r c t i o n [5]. It has
b e e n a t t r i b u t e d to distal A C A o c c l u s i o n , w h e r e a s in
proximal ACA occlusion brachial predominance of
h e m i p a r e s i s m a y b e o b s e r v e d , p r e s u m a b l y d u e to inv o l v e m e n t o f the i n t e r n a l c a p s u l e s u p p l i e d b y the r e c u r r e n t a r t e r y of H e u b n e r [12]. T e t r a p a r e s i s o r t e t r a p l e g i a
h a v e also b e e n d e s c r i b e d as the result o f such lesions in
t h r e e cases b y F r e e m o n [9], b u t two of t h e t h r e e p a t i e n t s
a d d i t i o n a l l y h a d a c u t e large M C A i n f a r c t i o n . A c u t e
c o m a a n d t e t r a p a r e s i s is far f r o m u n c o m m o n in p a t i e n t s
with an old, l a r g e a n d d e m a r c a t e d i n f a r c t i o n in o n e
h e m i s p h e r e a n d acute i s c h a e m i a o f t h e o p p o s i t e h e m i s p h e r e , e.g. t h r o u g h an M C A s t e m occlusion. I n such a
case, the o l d l e s i o n can b e s e e n o n C T a n d can give an
i m p o r t a n t hint t o w a r d s t h e u n d e r l y i n g c o n d i t i o n e v e n
w h e n t h e a c u t e i n f a r c t i o n o f t h e o p p o s i t e h e m i s p h e r e is
n o t y e t visible on CT.
L a c k of m o v e m e n t s was d e s c r i b e d [2] in a b i l a t e r a l
c i n g u l a t e gyrus lesion, b u t t h e r e a d e r is left with the
q u e s t i o n as to w h e t h e r this was p a r t o f the a k i n e t i c
m u t i s m . B i l a t e r a l m o t o r signs h a v e b e e n d e s c r i b e d in
o n e p a t i e n t with b i l a t e r a l b o r d e r z o n e i n f a r c t i o n s s p a r i n g
the c o r e t e r r i t o r y o f the A C A [8]. T h e fact t h a t t h e r e was
m a r k e d a s y m m e t r y of the t e t r a p a r e s i s in o n e p a t i e n t a n d
b i l a t e r a l B a b i n s k i signs in b o t h p a t i e n t s shows t h a t t h e r e
was d e f i n i t e p a r e s i s in o u r p a t i e n t s w h i c h c a n n o t b e attrib u t e d to m u t i s m .
A k i n e t i c m u t i s m has b e e n d e s c r i b e d as a t y p i c a l feature o f b i l a t e r a l A C A t e r r i t o r y i n f a r c t i o n [2, 4, 9]. A

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communication via a code of eye blinking and vertical
eye m o v e m e n t s like in the locked-in syndrome [11] was
not possible in our patients. With akinetic mutism no
reaction on c o m m a n d can be evoked even though the
patients have their eyes open and seem to fixate. Our
patients were not totally akinetic, as they could follow
the examiner's finger with their eyes. However, this
reaction was the only one and as it could be only
achieved with much effort by the investigator in some of
several trials, and with delay, we think that the t e r m
akinetic mutism is the most appropriate for our patients.
Such variations of a classical syndrome have also b e e n
described for the locked-in syndrome [3] and it is likely
that they also exist for akinetic mutism.
A further sign misleading us initially towards the
diagnosis of basilar artery occlusion was a vertical gaze
palsy in our first patient. Such a sign has not previously
b e e n described in A C A infarction. Basilar artery occlusion leading to a ventral pontine syndrome often produces horizontal gaze palsy with preserved vertical eye
movements. In patients with occlusion of the u p p e r basilar artery there may be vertical gaze palsy but always in
combination with pupillary abnormalities. Pure supranuclear vertical gaze palsy can be observed in vascular
midbrain lesions [7, 10], but the lesion must then be relatively restricted, not being compatible with tetraparesis.
One has to consider that the vertical gaze palsy was the
result of disturbed function of the infarcted tissue in the
A C A territory. Thalamic or midbrain areas that would
m o r e easily explain the eye m o v e m e n t abnormality are
usually not supplied by the A C A and were not infarcted
on CT in our patients. Alternatively, instead of regarding vertical gaze palsy as direct sequelae of the A C A infarction, it could be that vertical gaze in our patient was

m o r e susceptible to his attention deficits than horizontal
gaze. Further observations will be needed to clarify this
issue.

References
1. Baptista A (1963) Studies on the arteries of the brain. The
anterior cerebral artery: some anatomic features and their clinical implications. Neurology 13 : 825-835
2. Barris RW, Schuman HR (1953) Bilateral anterior cingulate
gyrus lesions. Syndrome of the anterior cingulate gyri. Neurology 3 : 44-52
3. Bauer G, Gerstenbrand S, Rumpl E (1979) Varieties of the
locked-in syndrome. J Neurol 221:77-91
4. Bogousslavsky J, Regli F (1990) Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Arch Neurol
47:144-150
5. Critchley MD (1930) The anterior cerebral artery, and its syndromes. Brain 53 : 120-165
6. Ferbert A, Brtickmann H, Drummen R (1990) Clinical features of proven basilar artery occlusion. Stroke 21 : 1135-1142
7. Ferbert A, Mtillges W, Biniek R (1990) Fascicular third nerve
palsy with decreased vertical saccade velocity of the contralateral eye. Neuro-ophthalmology 10 : 33-38
8. Fisher M, McQuillen JB (1981) Bilateral cortical borderzone
infarction. A pseudobrainstem stroke. Arch Neurol 38 : 62-63
9. Freemon FR (1971) Akinetic mutism and bilateral anterior
cerebral artery occlusion. J Neurol Neurosurg Psychiatry 34:
693-698
10. Heide W, Fahle M, Koenig E, Dichgans J, Schroth G (1990)
Impairment of vertical motion detection and downgaze palsy
due to rostral midbrain infarction. J Neurol 237 : 432-440
11. Plum F, Posner JB (1980) Diagnosis of stupor and coma.
Davis, Philadelphia
12. Webster JE, Gurdjian ES, Lindner DW, Hardy WG (1960)
Proximal occlusion of the anterior cerebral artery. Arch
Neurol 2 : 19-26