Download Role of computed tomography in vertebrobasilar ischemia (1985)

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Neuroradiology (1985) 27:484-493
© Springer-Veflag 1985
Role of computed tomography in vertebrobasilar ischemia
A. BonafO, C. Manelfe ~, B. S c o t t o
1,
M.Y. Pradere 2, and A. Rascol 3
1Department of Neuroradiology (Pr. C. Manelfe), 2Department of Pathology (Pr. J. Fabre),
3Departrnent of Neurology (Pr. A. Rascol), H6pital Purpan, F-31059 Toulouse Cedex, France
Summary. Precise delineation of vertebrobasilar ischemia by computed tomography (CT) appears difficult due to the numerous variations in distribution
of the posterior fossa arterial supply. While pontine
and upper brainstem infarctions can be readily demonstrated, medullary infarction remains beyond the
scope of present CT scanners. CT findings in cases
of basilar artery occlusion include bilateral pontine
infarction or extensive brainstem ischemia, associated with cerebellar and posterior cerebral vascular
damage. Demonstration of basilar artery occlusion
using routine CT is only rarely achieved. In cerebellar ischemia, CT, in conjunction with clinical syndromes, helps in the recognition of the arterial territory involved. CT provides useful guidelines for the
treatment of cerebellar stroke, leading to surgery in
cases of massive cerebellar infarction.
Key words: Computed tomography - Vertebrobasilar
ischemia - Brainstem infarction - Basilar artery occlusio - Lacunes
Brainstem infarction results in a constellation of
signs and symptoms related to occlusion of the basilar artery or one of its branches. Computed tomography (CT) may help to define the extent and nature of
vascular damage but has little value in the management of patients with brainstem infarctions. In contradistinction, early recognition of cerebellar infarction before the advent of CT was based on precise radiological delineation of the lesion in order to guide
a posterior fossa decompression: Wood and Murphey [1] used ventriculography or pneumoencephalography; Momose and Lehrich [2] recommended carotid and vertebral angiography. Now, CT scanning
is the definitive method not only to establish the di-
agnosis but also to provide important guidelines for
the treatment of patients with cerebellar softening.
Anatomy
Developtmental variations, either in origin, course or
caliber of vessels, are so frequent that a given vertebro-basilar system will seldom, if ever, fit with an
ideal symmetrically developed embryological pattern.
Despite numerous vascular anomalies, Foix and
Hillemand [3] described three types of vessels whose
distribution can be traced down to a medullary, pontine or midbrain level: [1] paramedian, [2] short circumflex, and [3] long circumflex arteries. Paramedian and short circumflex rami originate directly from
the vertebral and the basilar arteries. They delimit a
paramedian and a basal territory. Long circumflex
arteries are represented by the cerebellar arteries.
They supply the dorsolateral territory of the brainstem.
Medullary infarction
The blood supply of the medulla derives from the
vertebral arteries. The central medulla is supplied by
perforating branches arising from the anterior spinal
artery. The basal and dorsolateral territories' vascular supply comes from the posterior inferior cerebellar artery (pica). Infarction of a wedge-shaped area
of the medulla posterior to the olive results in a Wallenberg's syndrome. On clinical examination the lateral medullary syndrome includes:
- ipsilateral paralysis of the palate, pharynx and larynx from involvement of the nucleus ambiguus, and
the exiting fibers of the ninth and tenth nerves,
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Fig. 1 a-e. Right Wallenberg's syndrome, a, b Contrast-enhanced CT: gray matter enhancement of the inferior surface of the right cerebellar hemisphere and inferior vermis, c Right vertebral artery occlusion at C2 level consistent with a spontaneous dissection, d, e Left
vertebral artery angiogram: retrograde filling of hemispheric branches of right pica via pial anastomoses (arrows)
ipsilateral ataxia of the limbs from involvement of
the inferior cerebellar peduncle,
ipsilateral loss of pain and temperature sense on
the face from involvement of the descending tract
and nucleus of the fifth nerve,
- ipsilateral Horner's syndrome from involvement of
the descending sympathetic tract,
nystagmus due to involvement of the vestibular
nuclei,
contralateral loss of pain and temperature sense on
the body due to damage of the crossed spinothalamic tract.
-
-
-
-
Although Wallenberg's syndrome is known as that of
the pica, according to Fisher et al. [4], and Escourolle
et al. [5] it generally results from a distal vertebral artery occlusion not necessarilly including the ostium
of the pica. Toole [6] reported a 75% incidence of intracranial vertebral artery occlusion and 10% of pica
occlusion. Salamon and Huang [7] in a series of 100
anatomic dissections demonstrated that a unique
feeder supplying the retro-olivary region is rare
(20%). The vascular supply of the lateral medullary
fossa includes multiple sources which originate
mainly from the basilar artery, anterior inferior cer-
486
ebellar (aica), vertebral artery, and to a lesser degree,
from the pica.
However the lateral medullary syndrome is the
commonest brainstem ischemic syndrome but its CT
presentation has received little attention. Among our
7 patients presenting with Wallenberg's syndrome
and explored by CT none was suggestive of a dorso-
Fig.2a and b. Left Millard-Gubler syndrome, a, b Contrast-enhanced CT scan: enhancing lesion in the base of the pons extending toward the floor of the fourth ventricle without crossing the
midline (paramedian infarction of the pons)
lateral infarction, four were indicative of ischemic
changes in the pica territory (Fig. 1) and one correlated with vascular infarction in the territory of the anterior inferior cerebellar artery (aica). Two CT done
in a subacute stage (7 days; I month) were negative.
Hinshaw et al. [8] reported 2 cases with infarction
in the territory of the pica, lower pons, and medulla
but did not elaborate on the capabality of CT in delineating the precise extension of the ischemic lesions at a lower brainstem level.
Puns
Direct perforating and short circumferential
branches originate from the dorsal surface of the
basilar artery and penetrate into the belly of the
pons. They supply the paramedian and lateral ponfine territories where they irrigate the corticobulbar,
corticospinal, corticopontine fibers, the medial lemniscus, and the VI and VII nerves nuclei; they reach
the subependymal layer of the floor of the fourth
ventricule and provide blood supply to the medial
longitudinal fasciculus. The dorsolateral pontine territory is part of the aica vascular supply.
Pontine infarction results from unilateral occlusion of basilar penetrating branches. Occlusion of a
single paramedian or circumferential arterial branch
results either from an atheromatous deposit at the
origin of the penetrating vessel or extension of an
atheromatous plaque over the ostium of the basilar
branch [9]. Paramedian infarction at a lower pontine
level causes a Millard-Gubler syndrome (VI and
VII nerve palsies, contralateral hemiplegia) (Fig. 2).
At an upper pontine level, the association of a direct
lateral gaze palsy and a contralateral hemiplegia including the face constitutes a Foville's syndrome.
Among our 17 patients with a paramedian and/
or a lateral pontine infarction investigated by CT,
14 cases demonstrated brainstem ischemic changes
at the expected level. In one case the lesion extended
upward into the base of the peduncle. Three cases
had negative CT posterior fossa exploration.
According to Hinshaw et al. [8] while combined
brainstem and cerebellar infarction were common,
isolated brainstem infarcts were rare and predominated at the level of the pons (4 out of 49 cases explored by CT) or encompassed midbrain and pons
(1 case).
Midbrain and thalamus
Intrinsic midbrain and thalamic branches originate
from the basilar bifurcation and the proximal portion of the posterior cerebral arteries.
The paramedian branches form the retro-mammillary pedicle and are divided into two groups~ I)
thalamoperforating (or diencephalic); and 2) mes-
Fig.3 a-c. Bilateral paramedian
thalamic infarction, a Precontrast
CT: low attenuation lesions of both
antero-medial thalami, b, c Contrast-enhanced CT: enhancement of
paramedian thalamic areas
487
Fig.4 Right sided Weber's syndrome. Low attenuation change in
the fight peduncle (arrow); lateral infarction of the mesencephalon
Fig.5a and b. Parinaud's syndrome, a Precontrast CT: discrete
low attenuation in the fight superior
colliculus (arrow). b Post contrast:
enhancement in the right superior
colliculus
encephalic arteries [10]. The branches of the retromammillary pedicle enter the brain through the posterior perforated substance, interpeduncular fossa
and medial cterebral peduncles, and supply the anterior and part of the posterior thalamus, hypothalamus, subthalamus, substantia nigra, red nucleus,
oculomotor and trochlear nuclei, oculomotor nerve,
mesencephalic reticular formation, pretectum, rostromedial floor of the fourth ventricle and the posterior portion of the internal capsule [l 1].
Short circumferential arteries arise from the
proximal portion of the posterior cerebral and superior cerebellar arteries. They supply the lateral portion of the corticospinal tract; substantia nigra, red
nucleus, and the lateral tegmentum.
Long circumferential arteries arise from the posterior cerebral and the superior cerebellar arteries.
They supply the quadrigeminal plate, spino-thalamic
tract, and superior cerebellar peduncle.
The vascular supply of the tectum of the mesencephalon depends on an arterial network formed
over the quadrigeminal bodies by the superior cerebellar artery and two distinct branches of the posterior cerebral artery: the choroidal and the quadrigeminal arteries.
Occlusion of the retro-mamillary pedicle results
in a thalamopeduncular infarct, or it may dissociate
and cause a unilateral or bilateral paramedian thalamic infarction (diencephalic group) or a paramedian midbrain infarction (mesencephalic group). According to Percheron [12] the arterial configuration
of the retro-mammillary pedicle varies considerably
from paired and symmetrically distributed diencephalic and mesencephalic arteries, to a unique, unilateral vessel with a bilateral distribution. Thalamopeduncular infarctions are associated, in about
20% of the cases, with occlusion of the upper third of
the basilar artery [13]. Unilateral or bilateral paramedian thalamic infarction presents with transient coma, followed by hypersomnia, memory, and vertical
gaze disturbances. In this group of patients [14] CT
scanning has been very uniform, showing low density lesions in one or both medial thalami with or with-
out contrast enhancement (Fig. 3). According to Barbizet et al. [15] the infarcted area involved the ventral
anterior nuclei, dorsal medial nuclei, intralaminar
nuclei, and mammillo-thalamic tracts.
Occlusion of deep penetrating mesencephalic
branches and short circumferential arteries originating from the apex of the basilar artery causes paramedian and basal infarction of the cerebral peduncle. The resulting signs include an ipsilateral third
nerve palsy and a contralateral hemiplegia (Weber's
syndrome). Damage to the red nucleus interrupts the
dentato-rubro-thalamic tract and causes severe abnormal movements in the upper limb, opposite to the
third nerve palsy (Benedikt's syndrome).
CT studies of isolated midbrain infarction have
been limited to a few case reports [16]. Hinshaw et al.
[8] in a retrospective study of 49 patients with brainstem and cerebellum infarctions did not discover any
case of isolated ischemic midbrain lesion.
We examined 3 cases of Weber's syndrome and
found evidence of paramedian or lateral midbrain
infarction in two (Fig. 4). One case of Benedikt's syndrome combined a peduncular infarct and an ischemic lesion in the territory of the superior cerebellar artery.
Occlusion of the quadrigeminal artery results in a
vertical gaze palsy (Parinaud's syndrome) caused by
an infarction of the posterior commissure (Fig. 5).
Basilar artery occlusion
Thrombosis affects the lower two-thirds of the basilar artery 3 times as often as the upper third. Atherosclerosis is the common cause of proximal basilar artery occlusion. Distal occlusion results from heart
disease or intra-arterial embolism (atherosclerotic
plaques proximally located on the parent vessel or
the distal vertebral artery) [17].
Thrombosis of the lower third and mid portions
of the basilar artery causes occlusion of direct penetrating branches leading to bilateral ventral pontine
infarction. Symptomatology not only depends upon
488
Fig.6a-f. Mid portion basilar artery occlusion, a-cContrast-enhancedCTscanattheleveloftheponto-medullaryjunction(a),pons(b),
and mesencephalon (c). a Opacification of the lower basilar artery (arrowhead); paraventricular white-matter low attenuation in the fight
cerebellar hemisphere (arrow). b Absence of opacification of the basilar artery. Right sided paraventficular low attenuation sparing the
cerebellar cortical mantle (arrows). e Opacification of the tip of the basilar artery; questionable fight mesencephalic paramedian infarction (arrow). d-f Post-rnortem examination (axial sections at corresponding levels). Loyez staining method, d Right inferior cerebellar peduncle infarction: watershed infarction? (arrow). e Right paramedian pontine infarction (arrow). f Bilateral mesencephalic paramedian
infarction (arrows)
the occlusion site but also on the adequacy of surface
collateral flow and rheological and hemodynamic
factors [18]. A stagnation thrombus may progress
caudad and occlude the intracranial portions of the
vertebral arteries, or cephalad and reach the basilar
bifurcation. Cerebellar ischemia will result from anterograde or retrograde thrombosis. Prognosis is generally poor [19, 20] but long term survival with moderate disability in cases of proved basilar artery occlusion [21] strongly advocate the need for an early
diagnosis.
Embolic occlusion of the rostral basilar artery results in an admixture of mesencephalic, thalamosubthalamic, and occipital syndromes, named according to Caplan, "top of the basilar" syndrome
[22]. Occlusion of the basilar bifurcation and proximal segments of posterior cerebral arteries cause
thalamic and ventral mesencephalic infarction and
unilateral or bilateral temporo-parieto-occipital infarctions. The "top of the basilar" syndrome includes
an array of visual, oculomotor, and behavioral abnormalities often without prominent motor dysfunction. Rostral basilar artery occlusion is generally accompanied by severe depression of the level of con-
sciousness resulting from the destruction of the periaqueductal reticular formation.
CT findings in cases of basilar artery occlusion
include bilateral pontine infarction, thalamo-peduncular infarction or extensive brainstem ischemia
associated with cerebellar and posterior cerebral arterial vascular damage. Direct assessment of thromboembolism of the main arterial trunks may occasionally be achieved by plain CT when the incriminated vessels course in the axial section plane. Gfics
et al. [23] demonstrated an occlusion of a middle
cerebral artery and circumpeduncular segment of a
posterior cerebral artery. Vonofakos et al. [24] stated
that proper assessment of basilar artery occlusion requires dynamic CT but at times may be achieved by
comparison of plain and enhanced CT: "If the attenuation value of a given part of the basilar artery remains unchanged on post-contrast scan in comparison with the pre-contrast scan, while the other structures opacify, the diagnosis of occlusion is definite"
(Fig.6).
Demonstration of occlusion of the lower twothirds of the basilar artery by means of CT remains
difficult. Extensive brainstem and cerebellar ische-
489
Fig.7a-e. Occlusion of the basilar artery, a Precontrast CT: left low attenuation lesion at the
base of the pons? (arrow). Contrast-enhanced CT: b "Lacunar infarction" in the left thalamus (arrow). eAbsence of opacification of the tip of the basilar artery, d, e Left vertebral angiogram:
proximal occlusion of the basilar artery with partial distal reconstitution via cortical anastomoses
between pica and aica on the right (arrows)
mia causes mass effect that compresses the subarachnoid cisterns of the posterior fossa and prevents correct visualisation of vascular structures. In more benign cases, congenital variations in basilar artery level of origin and erratic course on the ventral surface
on the pons [7] makes the diagnosis of proximal basilar artery occlusion questionable. Enhanced CT is
more effective in demonstrating upper third basilar
artery occlusion. The absence of opacification of the
tip of the basilar artery at the level of the pontomesencephalic junction, or the absence of the posterior
vascular pillar in the interpeduncular fossa is positively correlated with upper third basilar artery occlusion (Fig. 7).
Lacnnes
Lacunes are small ischemic brain infarcts in the territory of deep penetrating arteries in patients with arterial hypertension. Segmental arterial disorganization
with lipohyalinotic changes represents the underlying vascular lesion [25]. Several lacunar syndromes
have been identified: pure motor hemiplegia, dysarthria, clumsy hand syndrome, and ataxic hemiparesis are the most frequent syndromes encountered in
the vertebrobasilar territory [26]. While in the neuropathological study of Fisher [25] pontine lesions accounted for 16% of all the lacunes, only a few cases
have been reported with positive CT findings [27].
This discordance may be explained by the small size
of these lacunar infarcts which are unresolved by
present CT scanners.
As at the supratentorial level where CT provides
an efficient delineation between subcortical and lacunar infarctions [28], at the level of the posterior fossa it may help in distinguishing deep penetrating vessel infarction from lacunes [27].
Cerebellar infarction
Posterior inferior cerebellar artery (pica)
About 85% of symptomatic cerebellar infarcts occur
in the territory of the pica [29]. The clinical presentation of a pica infarction is a lateral medullary infarction in about 20% of the cases. In approximately 80%
of the patients the clinical features of an acute cerebellar infarction uncomplicated by brainstem infarction consists of vertigo, nausea or vomiting, and truncal ataxia. In 50% of the cases of chronic healed cerebellar infarction no past medical history of posterior fossa cerebrovascular disease could be retrieved.
In Sypert and Alvord series [30] asymptomatic cerebellar infarction was constantly associated with involvment of the posterior inferior aspect of the cerebellum.
On a basis of CT the demonstration of a pica infarction remains questionable in many instances. Primarily the pica is the commonest site of posterior
fossa arterial variation: the vessel being hypoplastic
or absent in about 25% of the cases. Furthermore anatomic studies demonstrate considerable overlapping in the areas supplied by the pica and aica over
the postero-inferior surface of the cerebellum.
490
Anterior inferior cerebellar artery (aica)
Fig.8a and b. Pontomedullary infarction (aica syndrome), a,
b Precontrast CT: low attenuation area adjacent to the right cerebello-pontine angle (dorsolateral infarction of the lower pons)
Among the hemispheric branches (internal, middle and external), the internal is the most constant.
Salamon and Huang [7] found the internal branch
present in 91% of the hemispheres studied. The external branch was the less consistent of the hemispheric branches, its territory over the biventer and
the inferior semilunar lobules being inversely related
to the area supplied by the aica and the superior cerebellar artery (sca).
Infarction of the inferior vermis and infero-medial surface of the cerebellum as demonstrated by CT
indicates, according to anatomical studies, a pica occlusion.
The vascular territory of the aica varies greatly and is
subdivided in 3 categories [7]: short, terminating at
the flocculus (41%); intermediate, supplying the flocculus and part of the biventer and anterior quadrangular lobules (35%); long, supplying part of all the
territory of the pica including the posterior inferior
surface of the cerebellar hemisphere and the inferior
vermis (24%). Ischemia in the distribution of the aica
usually results in infarction of the dorsolateral pontomedullary region and the inferolateral cerebellum
(Fig. 8). Since the labyrinthine artery arises from the
aica in approximately 80%, vestibular infarction accompanies cerebellar dysfunction. Signs and symptoms include vertigo, ipsilateral hearing loss, facial
weakness, nystagmus away from the side of the lesion, and cerebellar asynergy. In addition, ipsilateral
loss of pain and temperature sensation of the face
from involvement of the trigeminal nucleus, and
controlateral decreased pain and temperature sensation on the body from involvement of the crossed
spino-thalamic tract, are usually present. The clinical
course is that of an acute onset followed by gradual
improvement over a variable period of time.
Rubenstein et al. [31] reported 7 patients admitted with acute vertigo mimicking a peripheral labyrinthine disorder. Three out of seven patients had associated unilateral hearing loss suggesting partial
Fig.9a-e. Left superior cerebellar
artery occlusion. Contrast-enhanced
CT: gyral enhancement of the
anterior (b) and superior (c) surface
of the left cerebellar hemisphere
extending downward into the
inferior semilunar lobule (a)
Fig.lOa-c. Left acute massive cerebellar infarction. Non-contrast
CT: a, b Low attenuation change in
the infero-medial surface of the left
cerebellar hemisphere with displacement of the fourth ventricle, cObstructive hydrocephalus
491
Table 1. Correlations between C T findings a n d onset o f s y m p t o m s : ( - ) negative a n d ( + ) positive C T (plain a n d e n h a n c e d ) findings for
brainstem a n d cerebellar ischemia
CT
(-)
(+)
Less t h a n 48 H
48 H to 7 days
7 to 21 days
More t h a n 3 weeks
(-)
(+)
(-)
(+)
(-)
(+)
(-)
(+)
5
1
10
7
15
3
5
7
-
6
Brainstem n = 46
Cerebellum n = 28
-
brainstem involvement. Based on CT examination
there were one hemorrhagic and 6 nonhemorrhagic
cerebellar infarctions. In four documented cases the
vascular damage involved an area adjacent to the
cerebellopontine angle, lateral to the fourth ventricle.
The lesions were felt to be consistent with an acute or
a subacute infarction in the distribution of the aica.
Superior cerebellar artery (sca)
The superior cerebellar artery (sca) is the most constant branch of the infratentorial arteries. It arises
from the basilar artery or the posterior cerebral artery as a single or a duplicated vessel. The sca gives
off central, vermian, and hemispheric branches. Central rami vascularize the quadrigeminal area (long
circumflex arteries) and the deep cerebellar nuclei
(precerebellar arteries) [32]. Vermian branches arise
from the rostral trunk and supply the superior vermis. Occasionally vermian branches on one side are
hypoplastic and their area is supplied by branches of
the controlateral sca. Hemispheric branches arise
from the rostral and caudal trunks and are subdivided into internal, middle, external and marginal
branches. The internal, middle, and external
branches course over the superior surface of the cerebellum and vascularise the anterior and posterior
quadrangular lobules and, to a variable extent, the
superior and inferior semilunar lobules. The marginal branch is present in 62% of the hemispheres studied, and supplies the anterior surface of the cerebellum adjoining the petrosal fissure. Its area of supply
is inversely related to the area supplied by the aica
(Fig. 9). Occlusion of the sca may produce a distinctive clinical picture resulting from infarction of the
cerebellum, dentate nucleus, brachium conjunctivum, and long sensory pathways in the tegmentum
of the rostral pons. The clinical picture consists of ipsilateral Homer's syndrome, ataxia, choreiform
movements, and complete loss of sensation on the
opposite side of the body including the face. CT
findings in cases of sca occlusion may include paraventricular (dentate nucleus), superior vermian, and
hemispheric infarction involving the superior and
anterior surfaces of the cerebellum.
11
4
Massive cerebellar infarction
The clinical presentation [33] of a purely cerebellar
infarction may progress from a seemingly benign
condition mimicking an acute labyrinthitis to a lifethreatening posterior fossa mass lesion. The early
manifestations include dizziness, nausea, vomiting,
inability to stand or walk, and nystagmus. At an intermediate stage, as cerebellar swelling increases, it
results in hydrocephalus and causes the patient's level of consciousness to deteriorate. As the mass effect
progresses, brainstem compression signs appear (lateral gaze and peripheral facial palsies, Homer's syndrome, long tract deficits) and the patient passes
from a stuporous condition into a deep comatose
state [29].
Sypert and Alvord in 1975 [30] reviewed the
pathological features and the retrospective clinical
causes of 28 cases of acute massive cerebellar infarction. These authors stressed that the infarcts predominantly involved the postero-inferior half of one cerebellar hemisphere and that the arterial distribution
of the infarcted area was consistent with an occlusion of the pica.
The symptomatology and the temporal profile of
cerebellar infarction is indistinguishable from that of
a cerebellar hemorrhage. CT scanning is the definitive method of diagnosis as it will demonstrate all
cerebellar hemorrhage of clinical significance. By
means of CT, cerebellar infarction will be caracterised either by a low density, isodense or hyperdensity
change, according to the amount of hemorrhage into
the infarcted tissue (hemorrhagic infarction occurs in
about 25% of the cases), or by indirect signs of a
space occupying lesion (hydrocephalus, displacement or obliteration of the fourth ventricle and subarachnoid cisterns) (Fig. 10). CT provides useful
guidelines for the treatment urging either to posterior
fossa decompression [34, 35] or ventricular shunting
[36, 37]. According to Shenkin and Zavala [37] "the
most important determining factor in the survival of
patients with cerebellar stroke is whether hydrocephalus develops. Consequently, the indication for intervention is the presence of hydrocephalus". As CT
cannot accurately differentiate a purely cerebellar
492
from an associated cerebellar and brainstem infarction it strongly supports the less aggressive surgical
procedure. Ventricular drainage appears as the
procedure of choice in the treatment of hydrocephalus accompanying massive cerebellar infarction.
Discussion
Although a specific clinical syndrome may result
from pica, aica or sca occlusion [38] it must be emphasized that in the posterior fossa a given area of
parenchyma cannot be as predictably allotted to a
specific vessel as in the supratentorial circulation because of the extensive anatomoses over the cerebellum and the variation in arterial distribution. In contradistinction to the supratentorial level, CT in arterial occlusive disease of the posterior fossa often cannot precisely relate a cerebellar infarction to a given
vertebrobasilar branch.
Rodda in 1971 [39] described a watershed infarction of the cerebellum located at the junction of the
pica and sca territories. This type of cerebellar infarction represented more than 75% of the 21 pathological cases reviewed. Hinshaw et al. [8], and Greenberg et al. [16] demonstrated by CT, in a few patients,
"border zone" infarction between or crossing the sca
and pica distributions.
The major factors affecting the efficiency of CT
in identifying infarctions are the following:
a) size: lesions less than 2 cm are usually missed [40];
b) location: infarctions of lower brainstem and cerebellum are consistently missed. Kingsley et al. [411
found that only 43% of clinically diagnosed infarcts
or strokes in evolution demonstrated CT changes
consistent with infarction in the vertebrobasilar territory. In our series of 74 patients with acute completed or evolving strokes, 63 (85%) had a positive CT
consistent with vascular occlusive disease in the posterior fossa. Thirty five out of 46 patients (75%) with
clinically diagnosed brainstem infarction demonstrated ischemic lesions in the pons and/or the mesencephalon.
c) the time interval between CT and onset of symptoms: the CT appearance of infarction is considered
in three temporal stages [42, 43]. In the acute stage
there is a time lapse of 8 to 12 h after infarction before the earliest changes can be visualized on a noncontrast CT. In the period from 1 to 7 days, positive
CT findings (essentially low attenuation and infrequently petechial or hemorrhagic lesions) of ischemia in the vertebrobasilar territory, matching at least
the clinical presentation (lacunar strokes being excluded), were recorded in 28 out of 29patients
(Table 1). Contrast infusion may produce gray matter
enhancement due to blood brain barrier breakdown
and increased vascular permeability.
In the subacute stage, areas of decreased attenuation can be visualized by CT without injection in
78% of the cases. Conversely, 22% of brainstem infarctions appear isodense with normal brain. Contrast injection did not give any additional finding
and CT scanning failed to confirm a definite, clinically established brainstem infarction in those
7 cases.
In the chronic stage (21 days to 2 months) CT
provides either retrospective evidence for cerebellar
infarction when it shows cerebellar atrophy with an
arterial distribution, or nonspecific information in a
large number of brainstem infarctions, showing only
global atrophy [41].
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Prof. C. Manelfe
Department of Neuroradiology
H6pital Purpan
Place Baylac
F-31059 Toulouse Cedex
France