Journal of Neurology, Neurosurgery, and Psychiatry 1985;48:1179-1181

Short report

Syndrome of the mesencephalic artery: report of a
case with CT and necropsy findings
M SETH HOCHMAN, JORGE J SOWERS, JOCELYN BRUCE-GREGORIOS
From the Departments ofNeurology, Radiology and Pathology, University ofMiami School of Medicine and
Mercy Hospital, Miami, Florida, USA

SUMMARY The syndrome of the mesencephalic artery refers to the clinical constellation of akinetic mutism and third nerve palsy which results from occlusion of one or more of the posterior
thalamoperforating arteries that arise from the proximal posterior cerebral artery. A patient with
this syndrome is described in whom a bilateral paramedian midbrain infarct was shown by
computed tomography and confirmed pathologically. To our knowledge, this is only the second
reported case of mesencephalic infarct shown by computed tomography and the first in which the
CT findings have been corroborated by pathological examination.
The syndrome of the mesencephalic artery' is the
clinical constellation of akinetic mutism and third
nerve palsy which results from occlusion of one or
more of the posterior thalamoperforating arteries of
Percheron:23 these are the anterior and posterior
thalamo-subthalamic paramedian and superior and
inferior mesencephalic paramedian arteries. All of
these penetrating branches arise from the proximal
three or four millimeters of each posterior cerebral
artery which has been variously named the basilar
communicating artery and the mesencephalic
artery.' The resulting infarct involves the midbrain,
subthalamus and/or the thalamus and typically has a
butterfly shape because a penetrating branch from
one mesencephalic artery may supply both paramedian areas.
The syndrome of the mesencephalic artery is not
well-known to neurologists, in part because of the
rarity of the infarct, but also because of the difficulties of diagnosis. According to Fisher,3 infarcts in the
distribution of the mesencephalic artery are not usually disclosed on CT scan. We now describe a patient
with the syndrome of the mesencephalic artery in
whom a bilateral paramedian midbrain infarct was
documented by computed tomography and
confirmed pathologically. To our knowledge, this is
Address for reprint requests: M Seth Hochman, MD, 3661 South
Miami Avenue, Miami, Florida 33133, USA.

Received 4 January 1985 and in revised form 1 March 1985.
Accepted 8 March 1985.

only the second reported case of mesencephalic
tegmental infarct demonstrated by computed
tomography and the first in which the CT findings
have been corroborated by the post-mortem examination.
Case report
The patient is a 69-year-old white male who was brought
to the Emergency Room after having been found unresponsive on the floor of the office building in which he
worked. Initially, the patient appeared comatose with
5 mm diameter mid-position fixed pupils which did not
react to light directly or consensually and closed eyes which
did not open spontaneously or on verbal command. Eyes
were maintained at the extremes of lateral gaze. No change
in the position of either eye was noted after unilateral and
simultaneous bilateral ice water caloric irrigation in the
head-hanging and 300 head-elevated positions. No vocalisation, spontaneous speech or extremity movements were
noted. However, on external stimulation, the patient was
observed to move his extremities. An axial CT scan of the
brain, before and after contrast-enhancement with routine
consecutive 10 mm sections of the posterior fossa were
considered normal, although considerable artifact-induced
image degradation was present. Repeat routine CT scan
performed one week following admission was again normal. A third CT scan performed three weeks following
admission with 5 mm contiguous sections of the brain stem
revealed a well-defined butterfly-shaped area of decreased
absorption coefficient within the tegmental area of the
upper and lower mesencephalon (fig 1). During eight
weeks in hospital the patient manifested a low level of
intermittent response to sensory stimuli. Although he
remained akinetic and mute, rarely following repeated

1179

Hochman, Sowers, Bruce-Gregorios

1180

upward to form cavitary lesions in the posterior medial
thalamus. Small bilateral relatively symmetrical infarcts
were seen in the intralaminar thalamic areas. Microscopically, the central tegmental area of the mid-brain at the
level of the pretectal region showed a large organising
slightly haemorrhagic infarct extending ventrally to the
involved red nucleus bilaterally, as well as the medial portion of the cerebral peduncles. Some outline of the ventral
tegmental tracts remained in the central portion of the
infarct. Exiting oculomotor nerve tracts showed extensive
Wallerian degeneration.

Discussion

Fig 1 CT S mm contiguous axial section, before
injection of contrast, at caudal mesencephalic level.
Note the well-defined bilateral paramedian tegmental
areas of low absorption coefficient corresponding to
the ischaemic infarct, adjoining each other at the
midline.
verbal commands, he would move his extremities and
when asked to open his eyes, at times, contract the frontalis
muscle. Occasionally, he would utter unintelligible vocalisations when his tracheostomy tube was occluded. The
patient was discharged to a nursing home where he died
four weeks later.

Neuropathological findings
Gross appearance of the carotid and vertebrobasilar arterial system showed moderate atherosclerosis. No site of
local occlusion could be identified. Focal leptomeningeal
fibrosis, mild cortical atrophy and slight ventricular
enlargement were present. The major pathology was seen
in the mid-brain: (fig 2) within the central tegmental area,
there was a well-defined organising infarct which extended
throughout the entire length of the mid-brain. The focus of
necrosis and cavitation was contiguous with an organising
haemorrhagic lesion in the left pretectal region extending

cm

2

Fig 2

2

Paramedian mesencephalic infarct.

Although our patient occasionally would utter unintelligible vocalisations and rarely move his
extremities following repeated verbal commands
and at times contract the frontalis muscle when
asked to open his eyes, for most of the time he
satisfied the criteria for the hypersomnolent type of
akinetic mutism set forth by Plum and Posner.9
Akinetic mutism in humans has been observed with
lesions in the walls of the third ventricle and following bilateral brain damage to the anterior cingulate
gyri, globus pallidus and paramedian diencephalic
and mesencephalic reticular formation as in the
present case. Biller and colleagues4 have recently
described a patient in whom a mesencephalic tegmental infarct was shown radiographically by highresolution computed tomography. Clinically their
patient exhibited bilateral ptosis, internuclear ophthalmoplegia and somnolence which occurred
immediately following percutaneous transluminal
coronary artery angioplasty. A cranial CT scan
obtained several hours following onset of symptoms
was normal. Repeat CT with 2 mm sections of the
upper brain stem at a 300 angle to the orbital meatal
line 96 hours after onset of symptoms revealed a
non-enhancing focal area of lucency consistent with
infarction in the rostral mesencephalic dorsal tegmentum in the area of the oculomotor nuclear complex and the median longitudinal fasciculus.
Whether a CT scan with contiguous thin sections of
the mid-brain, subthalamus and thalamus would
show small circumscribed paramedian infarcts in the
first hours following the onset of the syndrome of
the mesencephalic artery cannot be answered. Only
routine 10 mm sections were obtained on the first
negative CT scan performed on our patient on the
first hospital day and also on the second CT scan one
week later. The fact that on the third scan the infarct
was noted on only two contiguous 5 mm slices
suggests that contiguous thin-section technique is
important in demonstrating these infarcts. Thin sections will reduce the partial volume effect and the
induced artifacts resulting from the dense osseus and
air-contrasting structures at the base of the skull.5

Syndrome of the mesencephalic artery
Increase in milliamperage and scanning time will
reduce the quantum noise inherent in these thin sections. Special scanning plane6 (minus 150 to the
infra-orbital meatal line) will further reduce boneinduced artifacts and better demonstrate mesencephalic anatomy.' The reported sensitivity of CT in
detecting ischaemic cerebral infarcts has ranged
from as low as 10% during the first 48 hours to as
high as 84% after this period of time has elapsed
following the onset of symptoms.8 It is possible,
then, that even with careful CT scanning technique,
demonstration of the syndrome of the mesencephalic artery may be delayed. Therefore, if there is
evidence of fluctuating or incomplete neurological
deficit in the distribution of the branches of the
mesencephalic artery and no infarct or haemorrhage
is demonstrated on contiguous thin sections of the
vascular territories of these branches, anticoagulation may be warranted in attempt to prevent
further ischaemic infarction. Care must be taken not
to confuse the normal low density of the decussation
of the superior cerebellar peduncles with an infarct
within the caudal mesencephalon.' The low density
of the superior cerebellar peduncular decussation
does not extend to the rostral mesencephalic level.
Although there was no pathological confirmation
that the area of mid-brain lucency in the case of
Biller etal was the anatomical site of an infarct,
nonetheless, the fact that this abnormality was
limited to the rostral mesencephalon clearly distinguishes it from the normal low attenuation decussation of the superior cerebellar peduncles. In our own
case, the areas of low attenuation involved both the
upper and lower mesencephalon and extended to

1181
the midline (fig 1). As the low density of the
superior cerebellar peduncular decussation does not
extend to the midline, this subtle but important differential point helped in defining the lower limits of
the infarct radiographically. Post-mortem examination confirmed that the infarct extended throughout
the entire length of the midbrain.
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