Neuroradiology (1985) 27:484-493 Neareradinlegy © 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 1 Department 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 is- chemia by computed tomography (CT) appears dif- ficult due to the numerous variations in distribution of the posterior fossa arterial supply. While pontine and upper brainstem infarctions can be readily dem- onstrated, 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, associat- ed with cerebellar and posterior cerebral vascular damage. Demonstration of basilar artery occlusion using routine CT is only rarely achieved. In cerebel- lar ischemia, CT, in conjunction with clinical syn- dromes, helps in the recognition of the arterial terri- tory 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 oc- clusio - Lacunes

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 verte- bro-basilar system will seldom, if ever, fit with an ideal symmetrically developed embryological pat- tern.

Despite numerous vascular anomalies, Foix and Hillemand [3] described three types of vessels whose distribution can be traced down to a medullary, pon- tine or midbrain level: [1] paramedian, [2] short cir- cumflex, and [3] long circumflex arteries. Paramedi- an 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 brain- stem.

Brainstem infarction results in a constellation of signs and symptoms related to occlusion of the basi- lar artery or one of its branches. Computed tomogra- phy (CT) may help to define the extent and nature of vascular damage but has little value in the manage- ment of patients with brainstem infarctions. In con- tradistinction, early recognition of cerebellar infarc- tion before the advent of CT was based on precise ra- diological delineation of the lesion in order to guide a posterior fossa decompression: Wood and Mur- phey [1] used ventriculography or pneumoencephal- ography; Momose and Lehrich [2] recommended ca- rotid and vertebral angiography. Now, CT scanning is the definitive method not only to establish the di-

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' vascu- lar supply comes from the posterior inferior cerebel- lar artery (pica). Infarction of a wedge-shaped area of the medulla posterior to the olive results in a Wall- enberg's syndrome. On clinical examination the lat- eral medullary syndrome includes: - ipsilateral paralysis of the palate, pharynx and lar- ynx 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 cere- bellar 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 spinothalam- ic 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 ar- tery occlusion not necessarilly including the ostium of the pica. Toole [6] reported a 75% incidence of in- tracranial 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-

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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-en- hanced CT scan: enhancing lesion in the base of the pons extend- ing 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 correlat- ed with vascular infarction in the territory of the an- terior 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 de- lineating the precise extension of the ischemic le- sions 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 pon- fine territories where they irrigate the corticobulbar, corticospinal, corticopontine fibers, the medial lem- niscus, 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 ter- ritory is part of the aica vascular supply.

Pontine infarction results from unilateral occlu- sion 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 in- cluding 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 predomi- nated at the level of the pons (4 out of 49 cases ex- plored 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 por- tion of the posterior cerebral arteries.

The paramedian branches form the retro-mam- millary 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 Con- trast-enhanced CT: enhancement of paramedian thalamic areas

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Fig.4 Right sided Weber's syn- drome. Low attenuation change in the fight peduncle (arrow); lateral in- farction of the mesencephalon

Fig.5a and b. Parinaud's syn- drome, 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 retro- mammillary pedicle enter the brain through the pos- terior perforated substance, interpeduncular fossa and medial cterebral peduncles, and supply the ante- rior and part of the posterior thalamus, hypothala- mus, subthalamus, substantia nigra, red nucleus, oculomotor and trochlear nuclei, oculomotor nerve, mesencephalic reticular formation, pretectum, ros- tromedial floor of the fourth ventricle and the poste- rior portion of the internal capsule [l 1].

Short circumferential arteries arise from the proximal portion of the posterior cerebral and supe- rior cerebellar arteries. They supply the lateral por- tion of the corticospinal tract; substantia nigra, red nucleus, and the lateral tegmentum.

Long circumferential arteries arise from the pos- terior 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 mes- encephalon depends on an arterial network formed over the quadrigeminal bodies by the superior cere- bellar artery and two distinct branches of the posteri- or cerebral artery: the choroidal and the quadrigemi- nal arteries.

Occlusion of the retro-mamillary pedicle results in a thalamopeduncular infarct, or it may dissociate and cause a unilateral or bilateral paramedian tha- lamic infarction (diencephalic group) or a paramedi- an midbrain infarction (mesencephalic group). Ac- cording to Percheron [12] the arterial configuration of the retro-mammillary pedicle varies considerably from paired and symmetrically distributed dience- phalic and mesencephalic arteries, to a unique, uni- lateral vessel with a bilateral distribution. Thala- mopeduncular infarctions are associated, in about 20% of the cases, with occlusion of the upper third of the basilar artery [13]. Unilateral or bilateral parame- dian thalamic infarction presents with transient co- ma, followed by hypersomnia, memory, and vertical gaze disturbances. In this group of patients [14] CT scanning has been very uniform, showing low densi- ty lesions in one or both medial thalami with or with-

out contrast enhancement (Fig. 3). According to Bar- bizet 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 originat- ing from the apex of the basilar artery causes para- median and basal infarction of the cerebral pedun- cle. 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 ab- normal 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 brain- stem 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 syn- drome combined a peduncular infarct and an is- chemic lesion in the territory of the superior cerebel- lar 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 basi- lar artery 3 times as often as the upper third. Athero- sclerosis is the common cause of proximal basilar ar- tery 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 pene- trating branches leading to bilateral ventral pontine infarction. Symptomatology not only depends upon

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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 infarc- tion (arrow). d-f Post-rnortem examination (axial sections at corresponding levels). Loyez staining method, d Right inferior cerebellar pe- duncle 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 an- terograde or retrograde thrombosis. Prognosis is gen- erally poor [19, 20] but long term survival with mod- erate disability in cases of proved basilar artery oc- clusion [21] strongly advocate the need for an early diagnosis.

Embolic occlusion of the rostral basilar artery re- sults in an admixture of mesencephalic, thalamo- subthalamic, and occipital syndromes, named ac- cording to Caplan, "top of the basilar" syndrome [22]. Occlusion of the basilar bifurcation and proxi- mal segments of posterior cerebral arteries cause thalamic and ventral mesencephalic infarction and unilateral or bilateral temporo-parieto-occipital in- farctions. The "top of the basilar" syndrome includes an array of visual, oculomotor, and behavioral ab- normalities often without prominent motor dysfunc- tion. Rostral basilar artery occlusion is generally ac- companied by severe depression of the level of con-

sciousness resulting from the destruction of the peri- aqueductal reticular formation.

CT findings in cases of basilar artery occlusion include bilateral pontine infarction, thalamo-pe- duncular infarction or extensive brainstem ischemia associated with cerebellar and posterior cerebral ar- terial vascular damage. Direct assessment of throm- boembolism of the main arterial trunks may occa- sionally be achieved by plain CT when the incrimi- nated 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 re- quires dynamic CT but at times may be achieved by comparison of plain and enhanced CT: "If the atten- uation value of a given part of the basilar artery re- mains unchanged on post-contrast scan in compari- son with the pre-contrast scan, while the other struc- tures opacify, the diagnosis of occlusion is definite" (Fig.6).

Demonstration of occlusion of the lower two- thirds of the basilar artery by means of CT remains difficult. Extensive brainstem and cerebellar ische-

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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 (ar- row). 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 subarach- noid cisterns of the posterior fossa and prevents cor- rect visualisation of vascular structures. In more be- nign cases, congenital variations in basilar artery lev- el of origin and erratic course on the ventral surface on the pons [7] makes the diagnosis of proximal basi- lar 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 pontomes- encephalic junction, or the absence of the posterior vascular pillar in the interpeduncular fossa is posi- tively correlated with upper third basilar artery oc- clusion (Fig. 7).

Lacnnes

Lacunes are small ischemic brain infarcts in the terri- tory of deep penetrating arteries in patients with arte- rial hypertension. Segmental arterial disorganization with lipohyalinotic changes represents the underly- ing vascular lesion [25]. Several lacunar syndromes have been identified: pure motor hemiplegia, dysar- thria, clumsy hand syndrome, and ataxic hemipare- sis are the most frequent syndromes encountered in the vertebrobasilar territory [26]. While in the neuro- pathological study of Fisher [25] pontine lesions ac- counted 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 la- cunar infarctions [28], at the level of the posterior fos- sa it may help in distinguishing deep penetrating ves- sel 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 presenta- tion of a pica infarction is a lateral medullary infarc- tion in about 20% of the cases. In approximately 80% of the patients the clinical features of an acute cere- bellar infarction uncomplicated by brainstem infarc- tion consists of vertigo, nausea or vomiting, and trun- cal ataxia. In 50% of the cases of chronic healed cer- ebellar infarction no past medical history of posteri- or fossa cerebrovascular disease could be retrieved. In Sypert and Alvord series [30] asymptomatic cere- bellar infarction was constantly associated with in- volvment of the posterior inferior aspect of the cer- ebellum.

On a basis of CT the demonstration of a pica in- farction remains questionable in many instances. Pri- marily the pica is the commonest site of posterior fossa arterial variation: the vessel being hypoplastic or absent in about 25% of the cases. Furthermore an- atomic studies demonstrate considerable overlap- ping in the areas supplied by the pica and aica over the postero-inferior surface of the cerebellum.

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Fig.8a and b. Pontomedullary infarction (aica syndrome), a, b Precontrast CT: low attenuation area adjacent to the right cere- bello-pontine angle (dorsolateral infarction of the lower pons)

Among the hemispheric branches (internal, mid- dle and external), the internal is the most constant. Salamon and Huang [7] found the internal branch present in 91% of the hemispheres studied. The ex- ternal branch was the less consistent of the hemi- spheric branches, its territory over the biventer and the inferior semilunar lobules being inversely related to the area supplied by the aica and the superior cer- ebellar artery (sca).

Infarction of the inferior vermis and infero-medi- al surface of the cerebellum as demonstrated by CT indicates, according to anatomical studies, a pica oc- clusion.

Anterior inferior cerebellar artery (aica)

The vascular territory of the aica varies greatly and is subdivided in 3 categories [7]: short, terminating at the flocculus (41%); intermediate, supplying the floc- culus and part of the biventer and anterior quadran- gular 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 pon- tomedullary region and the inferolateral cerebellum (Fig. 8). Since the labyrinthine artery arises from the aica in approximately 80%, vestibular infarction ac- companies cerebellar dysfunction. Signs and symp- toms include vertigo, ipsilateral hearing loss, facial weakness, nystagmus away from the side of the le- sion, 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 sensa- tion 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 admit- ted with acute vertigo mimicking a peripheral laby- rinthine disorder. Three out of seven patients had as- sociated 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 cer- ebellar infarction. Non-contrast CT: a, b Low attenuation change in the infero-medial surface of the left cerebellar hemisphere with displace- ment of the fourth ventricle, cOb- structive hydrocephalus

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Table 1. Correlations between C T findings and onset o f symptoms: ( - ) negative and ( + ) positive C T (plain and enhanced) f indings for bra ins tem and cerebellar ischemia

C T Less than 48 H 48 H to 7 days 7 to 21 days More than 3 weeks

( - ) (+) ( - ) (+) ( -) (+) ( - ) (+) ( - ) (+)

Brainstem n = 46 5 1 10 7 15 3 5

Cerebel lum n = 28 - 7 - 6 11 4

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 con- stant branch of the infratentorial arteries. It arises from the basilar artery or the posterior cerebral ar- tery as a single or a duplicated vessel. The sca gives off central, vermian, and hemispheric branches. Cen- tral 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 ver- mis. 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 subdi- vided into internal, middle, external and marginal branches. The internal, middle, and external branches course over the superior surface of the cer- ebellum and vascularise the anterior and posterior quadrangular lobules and, to a variable extent, the superior and inferior semilunar lobules. The margi- nal branch is present in 62% of the hemispheres stud- ied, and supplies the anterior surface of the cerebel- lum 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 distinc- tive clinical picture resulting from infarction of the cerebellum, dentate nucleus, brachium conjuncti- vum, and long sensory pathways in the tegmentum of the rostral pons. The clinical picture consists of ip- silateral 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 parav- entricular (dentate nucleus), superior vermian, and hemispheric infarction involving the superior and anterior surfaces of the cerebellum.

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 life- threatening posterior fossa mass lesion. The early manifestations include dizziness, nausea, vomiting, inability to stand or walk, and nystagmus. At an in- termediate stage, as cerebellar swelling increases, it results in hydrocephalus and causes the patient's lev- el of consciousness to deteriorate. As the mass effect progresses, brainstem compression signs appear (lat- eral gaze and peripheral facial palsies, Homer's syn- drome, 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 infarc- tion. These authors stressed that the infarcts predom- inantly involved the postero-inferior half of one cer- ebellar hemisphere and that the arterial distribution of the infarcted area was consistent with an occlu- sion of the pica.

The symptomatology and the temporal profile of cerebellar infarction is indistinguishable from that of a cerebellar hemorrhage. CT scanning is the defini- tive method of diagnosis as it will demonstrate all cerebellar hemorrhage of clinical significance. By means of CT, cerebellar infarction will be caracter- ised 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, displace- ment or obliteration of the fourth ventricle and sub- arachnoid 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 hydroce- phalus develops. Consequently, the indication for in- tervention is the presence of hydrocephalus". As CT cannot accurately differentiate a purely cerebellar

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from an associated cerebellar and brainstem infarc- tion it strongly supports the less aggressive surgical procedure. Ventricular drainage appears as the procedure of choice in the treatment of hydrocepha- lus accompanying massive cerebellar infarction.

Discussion

Although a specific clinical syndrome may result from pica, aica or sca occlusion [38] it must be em- phasized that in the posterior fossa a given area of parenchyma cannot be as predictably allotted to a specific vessel as in the supratentorial circulation be- cause of the extensive anatomoses over the cerebel- lum and the variation in arterial distribution. In con- tradistinction to the supratentorial level, CT in arteri- al occlusive disease of the posterior fossa often can- not precisely relate a cerebellar infarction to a given vertebrobasilar branch.

Rodda in 1971 [39] described a watershed infarc- tion of the cerebellum located at the junction of the pica and sca territories. This type of cerebellar in- farction represented more than 75% of the 21 patho- logical cases reviewed. Hinshaw et al. [8], and Green- berg 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 cer- ebellum 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 terri- tory. In our series of 74 patients with acute complet- ed or evolving strokes, 63 (85%) had a positive CT consistent with vascular occlusive disease in the pos- terior fossa. Thirty five out of 46 patients (75%) with clinically diagnosed brainstem infarction demon- strated ischemic lesions in the pons and/or the mes- encephalon. c) the time interval between CT and onset of symp- toms: 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 be- fore the earliest changes can be visualized on a non- contrast CT. In the period from 1 to 7 days, positive CT findings (essentially low attenuation and infre- quently petechial or hemorrhagic lesions) of ische- mia in the vertebrobasilar territory, matching at least the clinical presentation (lacunar strokes being ex- cluded), 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 attenua- tion can be visualized by CT without injection in 78% of the cases. Conversely, 22% of brainstem in- farctions appear isodense with normal brain. Con- trast injection did not give any additional finding and CT scanning failed to confirm a definite, clin- ically 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