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(Stroke. 1995;26:609-613.)
© 1995 American Heart Association, Inc.

Articles

Massive Infarcts Involving the Territory of the Anterior Choroidal Artery and Cardioembolism

R. Levy, MD; C. Duyckaerts, MD, PhD J.-J. Hauw, MD

From INSERM U 360, Association Claude Bernard, Hôpital de la Salpêtrière, Paris, France.

Correspondence to Professor J.-J. Hauw, Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, 47 Blvd de l'Hôpital, 75651, Paris, Cedex 13, France.


*    Abstract
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 *Abstract
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Background and Purpose At neuropathological examination, the territory of the anterior choroidal artery is frequently found to be involved in massive infarcts of the internal carotid artery territory. The aim of our study was to analyze the clinical spectrum, the course, and the mechanism of these massive infarcts compared with the rare infarcts involving only the anterior choroidal artery territory.

Methods Retrospective clinical examination and pathological study were performed in 35 patients with cerebral infarcts affecting at least the territory of the anterior choroidal artery.

Results In no patient had the involvement of the anterior choroidal territory infarcts been recognized clinically, nor had the triad of clinical signs (hemiplegia, hemianesthesia, and hemianopsia) classically seen in infarcts restricted to this territory been found alone. Impairment of consciousness, cognitive disorders, or oculomotor palsies had been found in addition to one or more signs of the triad. This was probably related to the involvement of other territories (94%), especially the middle cerebral artery territory (68%) and the posterior cerebral artery territory (20%). The concomitant involvement of several territories was due most frequently to an occlusion of the internal carotid artery, which was found at autopsy in 74% of the patients. These occlusions were often associated with cardioembolism (54%). In contrast, artery-to-artery embolism (17%) and small-artery disease (6%) were seldom found. Only two cases of infarcts restricted to the anterior choroidal artery territory were observed.

Conclusions The involvement of the territory of the anterior choroidal artery in massive infarcts was due mainly to a cardioembolic occlusion of the internal carotid artery.


Key Words: cardioembolic stroke • carotid arteries • cerebral arteries • cerebral infarction


*    Introduction
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 *Introduction
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Ten cases of infarcts involving only the anterior choroidal artery (AChA) territory have previously been pathologically described.1 2 3 4 5 6 7 8 9 Foix et al2 (1925) recognized at autopsy an infarct restricted to the territory of the left AChA. The patient had a massive hemiplegia and sensory loss on the right side of the body accompanied by a right hemianopsia without impairment of consciousness or aphasia. Subsequent reports emphasized that the association of these three clinical signs was characteristic of infarction restricted to the AChA territory.4 5 Computed tomographic (CT) studies of such infarcts showed an area of reduced density in the posterior limb of the internal capsule.10 The pathogenic mechanism was often attributed to lipohyalinosis of the small and deep branches of the AChA.11 However, several authors have shown that the possibility of embolism from a cardiac source or from an occlusion of the internal carotid artery (ICA) should not be underestimated.12 13 14 15 16 17 18

The common experience of neuropathologists is, however, somewhat different. They frequently observe the involvement of AChA territory in massive infarcts due to the occlusion of the internal carotid artery. However, this involvement is not precisely described in many textbooks.9 19 20 21 22 We thus analyzed the clinicopathological findings in 35 cases of infarcts affecting the territory of the AChA in isolation or in association with other arterial territories to clarify the clinical signs and symptoms, the course, and the pathogenic mechanism of these strokes.


*    Subjects and Methods
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 *Subjects and Methods
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A retrospective analysis was made of 58 clinicopathological cases of ischemic stroke, involving at least the territory of one AChA. The observations were collected between 1965 and 1992 at the Salpêtrière Hospital (Paris) in the Department of Neuropathology from patients admitted to the Departments of Neurology.

After analysis of the files of these 58 patients, 21 were excluded for the lack of some clinical information and 2 others for incomplete pathological studies. Therefore, 35 patients with detailed clinical and autopsy data were selected for this study. Patient 15 has already been reported by Buge et al (1979).8 There were 18 women and 17 men. Their ages ranged from 51 to 89 years (mean age, 74.5 years). The mean age of the women (76.5 years) was slightly higher than that of the men (72 years).

Every infarct with a size over 1.5 cm and involving the anatomic territory of the AChA was included. The following areas were considered to be supplied by the AChA23 24 25 : medial segments of the globus pallidus, the posterior half of the posterior limb of the internal capsule and retrolenticular fibers of the capsule including the optic and auditory radiations, the optic tract, the tail of the caudate nucleus, the uncus, the posteromedial half of the amygdaloid complex, the anterior hippocampus and the dentate gyrus, the external half of the lateral geniculate body, and the middle third of the cerebral peduncle. Because the participation of the AChA in the irrigation of the thalamus remains controversial,26 thalamic infarcts in isolation were not included in this study. Past infarcts, dating from more than 1 month before autopsy, were distinguished from recent infarcts on clinical and pathological grounds.27

The risk factors, medical case history, clinical examination at admission and during hospitalization, results of neuroimaging, and, finally, the delay between the onset of stroke and death, the circumstances of death, and the presumed neurological diagnosis were noted in each case. Hypertension, diabetes mellitus, cigarette smoking, and hypercholesterolemia were considered to be risk factors for atherosclerosis, whereas atrial fibrillation, flutter, mitral prolapse, mitral stenosis, prosthetic valves, endocarditis, and myocardial infarction (recent or past with akinesia, mural thrombus, or aneurysm) were risk factors for cardioembolism.

Autopsy protocol included examination of the intracranial and extracranial cerebral arteries, the aortic arch, and the heart. The cervical spine and the base of the skull were removed to examine the arteries throughout their entire length. The arterial configuration and the site and extent of arterial lesions of the circle of Willis were reconstructed in a diagram (FigureDown). For technical reasons, the initial segment of the AChA could not be studied in most cases. Indeed, this small artery is subjected to numerous anatomic variations and is located in an area that is frequently disrupted by the removal of the brain at autopsy.



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  		Figure 1. Schematic diagrams show cerebral artery lesions in 35 patients. Each of the 35 cerebral artery trees of the patients included in this study are shown and numbered. The lettered diagram is a schematic representation of a cerebral artery tree. A indicates aortic arch; B, right primary carotid artery; C, left internal carotid artery; D, left primary carotid artery; E, left internal carotid artery; F, right vertebral artery; G, left vertebral artery; H, basilar artery; I, right middle cerebral artery; J, left middle cerebral artery; K, right posterior cerebral artery; L, left posterior cerebral artery; M, right anterior cerebral artery; and N, left anterior cerebral artery.

Microscopic examination was performed on brain samples taken within, and also at some distance from, the pathological tissues. To ascertain the nature of the occlusions, segments of the occluded arteries were embedded in paraffin and stained with hematoxylin-eosin and phosphotungstic acid–hematoxylin. Criteria for embolism were as follows: (1) multiple infarcts in different territories, including extracerebral infarcts; (2) hemorrhagic infarcts; (3) an arterial occlusion by a thrombus not connected to the arterial wall in recent infarcts; and (4) an arterial occlusion by an organized thrombus surrounded by a normal arterial wall in old infarcts.28 29 Criteria for cardioembolism were (1) the presence of criteria for embolism and (2) a source of cardiac embolism.


*    Results
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 *Results
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Of the 35 patients in our study, 24 (69%) had one or more atherosclerotic risk factors. Hypertension was the most frequent (16 patients); smoking was present in 5 patients and diabetes mellitus in 4. Five patients had hypercholesterolemia. Twenty-seven patients (77%) had potential sources of cardioembolism: myocardial infarctions and atrial fibrillation were the most frequent findings (26 patients had one or both). Mitral stenosis (n=2), mural thrombus in association with myocardial infarction (n=2), mitral prolapse (n=1), endocarditis (n=1), and atrial flutter (n=1) were the other cardiogenic findings. In 16 patients (45.5%), both atherosclerotic and cardiogenic risk factors were associated. Only 1 patient had no cerebrovascular risk factors.

The principal data concerning the neurological status of the patients at admission are shown in Table 1Down. Briefly, all but 1 patient had hemiparesis or hemiplegia (97%). Motor deficits involved the face, arm, and leg in 39.5% of these cases. One patient had only central facial paresis. There was no pure motor stroke. Sensory loss was less frequent. When noted, all modalities were involved. None of these patients had pure sensory stroke. Eleven patients (31.5%) developed hemianopsia, and of these 1 had an upper quadrantanopsia. In none of the 35 patients was the clinical triad of infarction of the AChA territory (hemiplegia, hemianesthesia, and homonymous hemianopsia) found alone. Various degrees of impairment of consciousness, ranging from decreased alertness to deep coma, were noted at admission in 63% of the patients. Aphasia and hemispatial neglect were often present (51%). Deviation of eyes and head contralateral to the sensorimotor deficit (14%), vertical and lateral conjugate gaze palsies (6%), and motor perseverations (6%) that could be related to a frontal-lobe syndrome were the other neurological signs detected at admission.


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  		Table 1. Neurological Status at Admission

CT scan was performed in 20 patients (57%). Areas of reduced density in the territory of the middle cerebral artery (MCA) were visible in each case. These infarcts always involved the deep territory of the MCA. In 16 patients they were massive, affecting the whole territory supplied by the MCA. Infarcts extending to the ipsilateral territory of the anterior cerebral artery were detected in 5 patients. In 1 patient, hypodensity was observed at the junction of the MCA and the anterior cerebral artery territories. An ipsilateral infarct in the territory of the posterior cerebral artery was seen in 1 patient. Another patient had an infarct of the posterior cerebral artery in the opposite hemisphere. CT scan showed marked cerebral swelling in 7 patients. CT scan was unable to detect the involvement of AChA territory in association with ischemic lesions of the deep MCA territory.

Aspiration pneumonia and pulmonary embolism were the major causes of death (40% and 11.5%, respectively). The delay between the onset of stroke and death ranged from 1 day to 10 months (median duration of survival, 7 days). In 14 cases (40%), death occurred in less than 5 days. In 12 of these 14 patients (85.7%), impairment of consciousness was noted at admission and at brain examination. Nine of these 14 patients had transtentorial herniation. In contrast, in the group of patients (n=21) who died after the sixth day, an impairment of consciousness at admission was noted in 10 (47.6%), and transtentorial herniation was seen only in 2.

At pathological examination, only 2 patients had infarcts restricted to AChA territory: 1 with bilateral infarcts limited to the AChA territories and 1 with a single left AChA infarct. All the other patients had infarcts involving the AChA territory combined with infarction in one or several other arterial territories (94%). Among those infarcts involving other territories, there was frequently a recent ipsilateral MCA infarct (n=24; 68%). In those patients with MCA infarcts, the deep portion of the territory was consistently involved. Recent infarcts in the territories of the ipsilateral anterior cerebral artery were combined with MCA and AChA infarcts in 6 cases. Recent infarcts of the posterior cerebral artery territory ipsilateral to the AChA lesion (and in combination with MCA infarcts) were found in 7 other cases (20%). The posterior cerebral arteries in these patients were supplied by a large posterior communicating artery, suggesting that the posterior cerebral artery flow originated from the ICA system. In 9 patients, vertebrobasilar infarcts were present, strongly suggesting embolic mechanisms.

By far the most frequent arterial pathology was the occlusion of the ICA (n=26; 74%) (FigureUp). In 15 patients (58%) it extended along the entire length of the ICA. The occlusion was restricted to the distal portion of the intracranial ICA in 11 subjects. In 10 of these patients, the occlusion extended to the initial part of the MCA. In 2 patients, the occlusion originated in the primitive carotid artery and extended to the ICA. One patient had an MCA occlusion without ICA occlusion.

Arteriosclerosis in the carotid system was present in 15 patients (43%) and was severe in 1 case. In 4 of these 15 patients, the ICA was not occluded. Ulcerated plaques of the aortic arch were present in 3 cases, in association with cardiac sources of embolism. Small-vessel disease (arteriolosclerosis) limited to the territory of deep perforator arteries and associated with small and deep infarcts was noted in 2 cases (6%). Both these patients also had atherosclerosis of the ICA, and 1 of them had cardioembolism. Last, no vascular lesions were seen in 3 patients.

The causes of these strokes are summarized in Table 2Down. Embolic mechanism was detected in 77% of the patients. A cardiac source was the main cause of embolism (54%). This was probably the cause of the unilateral infarct affecting the AChA territory in isolation, which occurred together with an embolus in the ipsilateral humeral artery. In this case, there was a recent thrombus and a mild stenosis (20%) both located at the origin of the ICA and at its most distal part. An artery-to-artery mechanism was responsible for 17% of these cases. In the last 2, the origin of the arterial embolism remained uncertain, and it could have resulted either from a cardiac source or from an artery-to-artery migration. Atherosclerotic thrombosis of the ICA was probably responsible for two strokes (patients 7 and 26). Lipohyalinosis of branches of the AChA was suspected in the patient with bilateral infarcts restricted to the AChA territory (patient 15), already reported by Buge et al (1979).8 Another patient had a dissecting aneurysm of the ICA with an occlusion extending to the first few centimeters of the MCA. In 4 patients (11%), neither arterial pathology nor any other cause of infarction was found.


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  		Table 2. Presumed Etiology


*    Discussion
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 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 *Discussion
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When present, the triad of clinical signs of an AChA infarct (hemiplegia, sensory loss, and hemianopsia contralateral to the lesion)2 was always associated with other neurological signs or symptoms. Impairment of consciousness and eye and head deviation contralateral to the clinical deficit, which were frequently associated with this clinical triad, indicated that the strokes were massive and extended beyond the territory of AChA. The aphasia found in 12 patients was not interpreted as being related to subcortical lesions. Although subcortical language disorders are observed in left AChA infarctions,10 30 31 in our patients such disorders could be explained by concurrent infarcts in the territory of the left MCA.

In fact, even in patients with an infarct restricted to the AChA territory, the clinical triad is rare and has been documented previously in only 4 cases.2 4 5 31 An occlusion of the AChA might even be asymptomatic, as suggested by the studies of Cooper32 (1954) who performed surgical ligatures of this artery in Parkinson's disease. In our study, the patient with a left unilateral AChA infarct in isolation (patient 19) had hemiplegia with loss of consciousness. The infarct affected the medial segment of the globus pallidus, the posterior half of the posterior limb of the internal capsule, and the uncus. The mechanism of the loss of consciousness in this patient remains obscure. However, it should be mentioned that lethargic states have been previously described in 2 similar cases.10 Patient 15 of our study, who had bilateral involvement of the AChA territory, exhibited a pseudobulbar syndrome and paralysis of the vertical gaze. These clinical signs were explained by destruction of both corticobulbar tracts, whereas the corticospinal tracts were spared.8

In studies providing CT scan imaging, infarction restricted to the AChA territory was revealed by an area of reduced density in the posterior limb of the internal capsule, sparing the thalamus medially but encroaching on the globus pallidus laterally.10 11 17 31 In our study, this pattern was not found in the 20 patients who underwent CT scan because the AChA infarcts were always combined with an infarction in the deep territory of the ipsilateral MCA. This may explain why the possible involvement of the AChA territory had not been raised before postmortem examination.

Most early deaths (<5 days) in this study resulted from massive infarcts involving a large part of the ICA territory and causing clinical symptoms such as impairment of consciousness secondary to transtentorial herniations. The rate of early death (40%) was unusually high among the 35 patients. Reports on infarctions involving other territories, including one report from our neuropathology department, have shown that 15% to 23% of patients died within 4 days of the stroke.33 34 35 36 In the present study, the patients who died within 4 days of the stroke presented more severe vigilance disorders than those who died on or after day 5. This may be explained in part by the transtentorial herniation often noted at brain examination. Furthermore, in these cases there was a massive stroke affecting at least three arterial territories, always including that of the MCA. These massive and rapidly fatal strokes often resulted from cardioembolic occlusions of the ICA (86%). A previous study has also shown a higher early mortality rate after cerebral embolism from a cardiac source (25% to 30%) compared with the percentage (10% to 25%) after atherothrombotic stroke.37

AChA infarcts were usually combined with other infarcts in one or several other territories of the main branches of the ICA. If the participation of the AChA territory has not been explicitly stated yet in the literature, it should not be underestimated: previous work from our laboratory found its involvement in 33% of the patients from an autopsy series of subjects with massive infarcts of the ICA territories.38 The MCA territory was by far the most frequently involved. The frequent association of AChA infarcts with infarcts in the other territories of the ICA can be explained by the occlusion of the ICA proximal to the ostia of the main branches, which occurred in 74% of our patients. Indeed, the AChA usually originates from the ICA 2 to 4 mm distal to the posterior communicating artery, but it can arise from the MCA or from the posterior communicating artery and even anastomose with either the posterior communicating artery or the posterior cerebral artery.39 40 41 The latter point might partly explain the combination of infarcts in the AChA and posterior cerebral artery territories. Such an explanation is supported by the fact that these posterior cerebral arteries were supplied by the ICA flow. This suggests that these infarcts resulted from embolism into the carotid system alone rather than into both the vertebrobasilar and carotid systems.

Embolic occlusion, either from a cardiac source or from artery to artery, seems to be by far the most frequent cause. A cardiac source was the most frequent in this study; 19 (54%) of the 35 patients had patent sources of cardioembolism, and in 8 other patients (23%) a potential source was present. The rate of cardioembolism was clearly higher in this study than that previously reported in epidemiological studies.42 43 44 In contrast, artery-to-artery embolism was rare. However, since large infarcts resulting from cardioembolism are seen more frequently at autopsy, smaller infarcts involving the AChA territory (especially those from atherosclerosis) should not be underestimated. Small-artery occlusive disease (lipohyalinosis) is the most common cause of infarcts restricted to the AChA territory: it was probably involved in at least 11 of the 30 cases previously reported.1 2 3 4 5 6 7 8 10 11 14 It was found in 2 cases of this series, but this mechanism could be ascertained in only 1 of them. However, Leys et al17 (1994) found only 1 case of small-artery occlusion and 4 cases of cardioembolism in a study including 16 patients with AChA infarcts. In this study, lipohyalinosis of small arteries was the cause of the bilateral infarcts restricted to the AChA territory, whereas the unilateral infarct limited to the AChA territory resulted from cardioembolic occlusion, and no lipohyalinosis was found.


*    Acknowledgments
 
We thank Drs P. Brunet, A. Buge, P. Castaigne, C. Derouesné, J.C. Gautier, D. Laplane, F. Lhermitte, M. Poisson, G. Rancurel, M. Serdaru, and J.L. Signoret for providing the clinical files of the reported cases; Nick Barton for reviewing the English of the manuscript; and C. Raiton, N. Fenoy, J. Despert, and P. Mielle for technical assistance.

Received October 17, 1994; revision received January 12, 1995; accepted January 14, 1995.


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 *References
 

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Which patient fares worse after early deterioration due to swelling from hemispheric stroke?
Neurology, December 14, 2004; 63(11): 2142 - 2145.
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G. A. Lammie, P. A. G. Sandercock, and M. S. Dennis
Recently Occluded Intracranial and Extracranial Carotid Arteries : Relevance of the Unstable Atherosclerotic Plaque
Stroke, July 1, 1999; 30(7): 1319 - 1325.
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