doi: 10.1161/01.STR.0000013564.73522.05
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(Stroke. 2002;33:941.)
© 2002 American Heart Association, Inc.
Original Contributions |
Dissecting Aneurysms of Intracranial Carotid Circulation
From the Department of Neurosurgery, Hirosaki University School of Medicine, Hirosaki, Japan.
Correspondence to Hiroki Ohkuma, MD, Department of Neurosurgery, Hirosaki University School of Medicine, 5 Zaifu-Cho, Hirosaki, 036-8216 Japan. E-mail ohkuma{at}cc.hirosaki-u.ac.jp
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Abstract |
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Background and Purpose— Clinical features of nontraumatic dissecting aneurysms of intracranial carotid circulation remain unclear because investigation of this disease has been limited to case reports. The aim of this study was to investigate the clinical features of this disease through the use of cooperatively collected cases.
Methods— The cases diagnosed as dissecting aneurysms of intracranial carotid circulation on the basis of clinical signs and neuroradiological findings in 46 stroke centers from 1995 through 1999 were collected, and their clinical features were analyzed.
Results— Forty-nine cases of dissecting aneurysms of intracranial carotid circulation were collected. Thirty-two patients presented with subarachnoid hemorrhage (SAH), and 17 presented with cerebral ischemia. The ratio of this disease to all intracranial dissecting aneurysms treated in the same institutes for the same period was 19.1%, and the ratio of SAH resulting from this disease to SAH of unverified origin treated in the same institutes for the same period was 6.2%. The predominant site of lesion was the internal carotid artery in 18 of 32 patients (56%) with SAH and the anterior cerebral artery in 13 of 17 patients (76%) with cerebral ischemia. The predominant angiographic findings were that stenosis with dilatation occurred in 20 of 32 patients (63%) with SAH and stenosis without dilatation was seen in 11 of 17 patients (65%) with cerebral ischemia. Poor prognosis was seen in 21 of 32 patients (66%) with SAH, which was due largely to rebleeding seen preoperatively, during operation, and even postoperatively when clipping or wrapping of the aneurysmal bulge was performed.
Conclusions— Nontraumatic dissecting aneurysm of intracranial carotid circulation is not as rare as expected. It seems to be one of the important causes of SAH of unverified origin.
Key Words: aneurysm • cerebral aneurysm • cerebral ischemia • dissection • subarachnoid hemorrhage
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Introduction |
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Nontraumatic dissecting aneurysm or arterial dissection has been known to occur in both the intracranial portion of the carotid circulation and vertebrobasilar circulation. Recent studies have focused mainly on those occurring in the vertebrobasilar circulation, and its pathogenesis, clinical features, neuroradiographic findings—including angiographic findings, histopathology, and treatment—have been evaluated in many reports.1–10
On the other hand, nontraumatic dissecting aneurysms of the intracranial carotid circulation have been investigated as case reports. From case reports published in English, we could collect 38 cases in which angiographic and/or histopathological findings were presented and a clinical course was described in detail.11–37 Formerly, dissecting aneurysms of the intracranial carotid circulation had been known to cause cerebral infarction in young individuals.11–13,15–20 However, recent case reports have shown that dissecting aneurysm of the intracranial carotid circulation can cause subarachnoid hemorrhage (SAH).31–37 The real clinical features remain unclear because reports regarding dissecting aneurysm of the intracranial carotid circulation have been limited to the case reports. Of 38 reported cases, 20 (53%) were reported after 1990,22–28,31–37 which suggests that the number of reported cases has increased with the recognition of this disease and the advance of diagnostic procedures and that dissecting aneurysm in the intracranial carotid system might not be as rare as originally thought. Therefore, the clinical features of dissecting aneurysm of carotid circulation should be investigated in detail through the use of collected cases. The aim of this study was to evaluate the clinical and epidemiological features of dissecting aneurysms in the intracranial carotid circulation by analyzing cases cooperatively and retrospectively collected from 46 stroke centers in the Tohoku district in Japan during 5 years (1995 through 1999).
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Subjects and Methods |
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The Tohoku district is located in the northern part of the main island of Japan and consists of 6 prefectures; its population is 9 813 000 according to the 1995 census population data of Japan. In this district, 46 institutes, which are the main stroke centers in each region and treat two thirds of the patients with stroke in the district, belong to the Study Group of Association of Cerebrovascular Disease in Tohoku and participated in this study.
The cases of nontraumatic dissecting aneurysms in the intracranial carotid circulation diagnosed by stroke specialists in each institute on the basis of clinical and neuroradiological findings from 1995 through 1999 were submitted to the Study Group of Association of Cerebrovascular Disease in Tohoku. The study group reviewed medical records and all neuroradiological images of the submitted cases, and the cases that fulfilled the following criteria were registered in this study. The first criterion was sudden onset of ischemic or hemorrhagic symptoms; the second was that cerebral angiography show characteristic findings of arterial dissection,3,8–10 which were divided as follows, and additional criteria were required according to the angiographic findings to confirm arterial dissection: (1) the double-lumen sign (the presence of false lumen or an intimal flap) was used as a reliable finding of arterial dissection1,7,38; (2) stenosis with dilatation (the pearl and string sign) was also used as a reliable finding of arterial dissection1,9,38–40; (3) dilatation without stenosis required an additional definition to confirm arterial dissection (Discoloration of the affected artery around the aneurysmal dilatation, which was considered to be due to intramural hematoma, should have been seen during operation); and (4) stenosis without dilatation (the string sign) or occlusion (tapered occlusion) also required additional definitions. Stenosis was not segmental but extensive on initial angiography, and resolution of stenosis or occlusion should be seen on follow-up angiography, which has been considered to be a reliable angiographic sign of arterial dissection.40–42 In addition, discoloration of the affected artery considered to be due to intramural hematoma should have been seen during operation. The third criterion was that these findings of arterial dissection exist in the intracranial portion on cerebral angiography, and the fourth was that no obvious atherosclerotic changes were found in other intracranial arteries on cerebral angiography. Finally, the findings of cerebral angiography were to be consistent with the clinical symptoms.
Three observers of the study group independently judged the submitted cases using the above diagnostic criteria. If agreement among the 3 observers was reached, the patient was enrolled in this study.
The following clinical parameters were evaluated and compared: age, sex, lesion site, prodrome, type of onset, angiographic findings, other neuroradiographic findings, treatment, risk factors, clinical course, and prognosis. Headache that occurred before onset that was neither sudden nor severe like the headache caused by SAH was evaluated as a prodrome.1,7–9 In the patients presenting with signs of bleeding, the clinical condition on admission was evaluated by use of the Hunt and Hess grade, and the SAH grade on CT scan was evaluated with Fisher classification. Rebleeding was evaluated to investigate vulnerability of bleeding of this lesion. An episode of prehospitalization rebleeding was defined as unusual sudden headache with loss of consciousness or sudden deterioration of consciousness level occurring after the initial SAH and before admission, after exclusion of other causes such as epileptic seizure from the clinical course.43,44 Posthospitalization rebleeding was confirmed on CT scan compared with that taken on admission. Patients were considered to have symptomatic vasospasm when ischemic neurological deficits such as disturbance of consciousness or motor and speech impairment occurred from days 4 to 14 after SAH, after exclusion of other causes for neurological deficits such as rebleeding, hydrocephalus, surgical complications, metabolic disturbances, hypoxia, or seizure.45,46 Prognosis was evaluated at 1 month, 3 months, and 1 year after the ictus by use of the Glasgow Outcome Scale (GOS).47 Poor prognosis was defined as severe disability, vegetative state, or death on the GOS.
In addition, the numbers of patients with whole SAH, SAH caused by rupture of intracranial saccular aneurysms, and dissecting aneurysm of the vertebrobasilar circulation treated in the same institutes during the same period were reported to estimate the comparative incidence of dissecting aneurysm of the intracranial carotid circulation.
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Results |
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During the 5 years between 1995 and 1999, 56 patients were treated as dissecting aneurysms of the intracranial carotid circulation in the 46 institutes and were submitted to the study group. Of these 56, 7 were excluded because the dissection originated from the extracranial carotid artery in 3, the dissection was found incidentally without symptom in 2, and obvious atherosclerotic changes were found in other intracranial arteries in 2. Therefore, 49 patients were registered as having dissecting aneurysms of the intracranial carotid circulation (Table 1). Of the 49 cases, SAH was detected on the initial CT scan in 36 cases.
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During the same period, 5520 cases of SAH, 4940 cases of SAH caused by ruptured saccular cerebral aneurysms, and 208 cases of dissecting aneurysms of the vertebrobasilar artery were treated in the same institutes. Calculation of these figures revealed that the ratios of SAH caused by dissecting aneurysm of the intracranial carotid circulation to whole SAH and to nonaneurysmal SAH were 0.65% and 6.2%, respectively. The ratio of SAH caused by dissecting aneurysm of the intracranial carotid circulation to ruptured saccular cerebral aneurysms was 0.73%. The ratio of dissecting aneurysm of the intracranial carotid circulation to all intracranial dissecting aneurysms was 19.1%.
According to the clinical presentation of onset, 49 patients were divided into the bleeding and ischemic groups (Table 1). Of 36 patients for whom the initial CT scan showed SAH, 4 were categorized into the ischemic group because they presented with obvious ischemic symptoms at the time of onset without sudden headache despite very slight SAH detected on the initial CT scan.
For all patients, age ranged from 10 to 83 years (mean, 51 years). The predominant sex was female, and the predominant lesion sites were the internal carotid artery (ICA) and anterior cerebral artery (ACA). Lesions existed in the ICA in 18 of 32 patients (56%) in the bleeding group and in the ACA in 13 of 17 patients (76%) in the ischemic group.
All patients underwent initial cerebral angiography within 1 month of onset, and 47 underwent initial angiography within 2 weeks of onset. Of 32 patients in the bleeding group, the initial cerebral angiography was performed within 48 hours of onset in 30 patients. Several angiographic findings are shown in Figure 1. When the double-lumen sign was accompanied by other findings, the case was categorized in both findings (Table 1). Of 15 cases with double-lumen sign, the findings were accompanied by other findings such as stenosis without dilatation (the string sign) in 7 cases and stenosis with dilatation (the pearl and string sign) in 4 cases. Stenosis without dilatation was seen in 15 patients, and as additional definitions for confirmation of arterial dissection, resolution of stenosis was seen on follow-up angiography in 4 cases, and discoloration of the affected artery considered to be due to intramural hematoma was seen during operation in 4 cases. The other 7 cases showed both stenosis and the double-lumen sign.
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) with dilatation (
) in the ACA. B, Lateral (left) and anteroposterior (right) views of right carotid angiogram showing stenosis (
) at the fusiform dilatation.In the bleeding group, stenosis with dilatation was a dominant finding and was seen in 20 of 32 cases (63%). Stenosis with or without dilatation, seen in 24 patients in the bleeding group, was considered not to be due to cerebral vasospasm because angiography was performed within 48 hours of onset in all patients. Dilatation without stenosis (dilatation only) was seen in 3 patients presenting with SAH, and discoloration of the affected artery around the aneurysmal dilatation, which was considered to be due to intramural hematoma, was seen during operation in all patients. In the ischemic group, stenosis without dilatation was dominant and seen in 11 of 17 patients (65%).
In terms of risk factors, hypertension was seen in 21 patients (43%). Of 17 patients in the ischemic group, 5 (29%) were cigarette smokers. As a prodrome, headache, which occurred from 6 hours to 10 days before onset, was seen in 8 patients (16%). Prognosis evaluated at 3 months after the ictus with the GOS revealed that 21 of 32 patients (66%) in the bleeding group showed poor prognosis, whereas only 2 of 17 patients (12%) of the ischemic group showed poor prognosis.
In the bleeding group (Table 2), poor clinical grade on admission classified as grade IV or V by the Hunt and Hess score were seen in 12 patients (38%), and severe SAH on CT scan classified as groups 3 and 4 by Fisher’s classification was seen in 26 patients (81%) on admission (Figure 2). Rebleeding was frequently seen preoperatively, during operation, and postoperatively. Operation for aneurysm was performed in 23 patients, and several operative procedures were used. Among the operative methods, postoperative bleeding was seen in 3 of 5 patients undergoing neck clipping of the aneurysmal bulge and in 2 of 8 patients undergoing wrapping of the aneurysmal bulge. In terms of poor prognosis, rebleeding after admission was causative in 14 patients (67%).
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In the ischemic group (Table 3), infarction was confirmed in 16 patients on CT scan and/or MRI. Multiple infarctions, seen in both the peripheral territory of the affected vessels and the area of perforating arteries originating from the affecting vessels, were seen in 4 patients (Figure 3A). MRI was performed in 12 patients, and semilunar hyperintensity around signal void of lumen was seen in 6 (Figure 3B). MR angiography was performed in 14 patients, and findings corresponding to the findings on cerebral angiography were seen in all patients (Figure 4). Ischemic signs improved without aggravation in 11 patients and improved after temporary aggravation in 4 patients, which resulted in good recovery or moderate disability according to the GOS at 3 months. Ischemic signs were fixed without improvement in 2 patients, which resulted in severe disability as assessed by the GOS at 3 months. Of 4 patients with dissecting aneurysm of the ICA or middle cerebral artery, 3 were teenagers.
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Discussion |
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This study revealed that the ratio of dissecting aneurysm of the intracranial carotid circulation to all intracranial dissecting aneurysms was 19.1% and that the ratio of SAH resulting from this disease to nonaneurysmal SAH was 6.2%, which suggested that dissecting aneurysms of the intracranial carotid circulation was not as rare as expected. As recognition of this disease increases, the reported incidence of the disease will increase.
Angiographic findings of dissecting aneurysms of the vertebrobasilar circulation have been investigated in many reports, and several characteristic findings have been reported.1,3,7–10,38–40 This study showed that stenosis with dilatation is dominant in SAH cases, and stenosis without dilatation is dominant in ischemic cases, which corresponds to the results from studies on dissecting aneurysm of vertebrobasilar circulation.2,5,6,8–10 These angiographic findings appear to correspond to the histopathological findings. Histopathological studies on dissecting aneurysms of the vertebrobasilar circulation6 have revealed that the plane of dissection in cases with SAH is mainly subadventitial and is confined to the vertebral artery, which corresponds to fusiform dilatation on angiography, whereas the plane of dissection in cases with ischemia is mainly subintimal and extends to the basilar artery, which corresponds to the string sign on angiography.
Recent studies of dissecting aneurysm of the vertebrobasilar circulation have revealed that the findings on MR angiography correspond with the findings on cerebral angiography,3 which was also confirmed in this study. Therefore, MR angiography can be a substitute for cerebral angiography when repeated estimation is necessary. Semilunar hyperintensity around signal void was seen on MRI in half of the patients in this study. This hyperintensity was considered to be due to intramural hemorrhage because its margins were sharp.48 However, hematoma adjacent to the arterial lumen cannot necessarily be ruled out on the basis of MRI alone. Besides, previous studies of vertebrobasilar dissecting aneurysms have indicated that the rates of intramural hematoma shown on MRI have ranged from 32% to 100%,1,3,49 depending on the timing of MRI. Therefore, hyperintensity suggesting intramural hematoma on MRI cannot be a substitute for cerebral angiography in diagnosis.1
Regarding the presentation of symptoms, it has been known that dissecting aneurysms of the vertebrobasilar artery often cause SAH.5–7,9,10 On the other hand, dissecting aneurysms of the carotid circulation have been known to cause cerebral ischemia.11–13,15–20 This study revealed that SAH is also a dominant type of presentation in the carotid circulation. In 38 reported cases, 24 patients presented with ischemia11–28 and 14 presented with SAH.29–37 However, in 20 cases reported after 1990,22–28,31–37 11 patients presented with SAH.31–37 Nakatomi et al50 showed that stenotic lesions in the carotid circulation seen on angiography were detected in 6 of 30 patients with SAH of unverified origin, and the dissection was confirmed in 3 of those 6 patients. Mizutani32 reported that dissecting aneurysms were confirmed by operation or autopsy in 4 of 5 patients with SAH associated with stenotic or occlusive lesions in the carotid circulation seen on angiography. These findings suggest that dissecting aneurysms of the intracranial carotid circulation had formerly been missed as a cause of SAH of unknown origin because of less recognition of this disease.
In a comparison of the bleeding group of this study with patients with SAH caused by saccular cerebral aneurysms, differences were seen in lesion site, vulnerability of rebleeding, and prognosis. The most predominant lesion site was the ICA in the bleeding group of this study, whereas an international cooperative study of aneurysmal SAH51 showed that the ICA was the site of saccular cerebral aneurysm 29.8% of the time. Vulnerability of rebleeding was noted in the bleeding group of this study. Rebleeding before admission in aneurysmal SAH was reported to be 14%,44 whereas it was 44% in the bleeding group of this study. Therefore, early operation for dissecting aneurysms of the vertebrobasilar circulation has been recommended.5 However, bleeding was seen even postoperatively in this study when clipping or wrapping of the aneurysmal bulge was performed. For dissecting aneurysm of the vertebral artery, proximal occlusion or trapping of the parent artery has been thought to be the only possible effective surgical procedure.5,7,9 The results of this study suggested that proximal occlusion or trapping of the parent artery, which should be accompanied by bypass surgery if necessary, may also be the surgical procedure of choice whenever possible for dissecting aneurysm of the carotid circulation. Poor prognosis was reported to be 33% in aneurysmal SAH, whereas it was 66% in the bleeding group of this study, largely because of rebleeding.
Of patients presenting with cerebral ischemia in this study, 3 were teenagers, which corresponds to the previous idea that dissecting aneurysms of the carotid circulation cause cerebral ischemia in young individuals.11–13,15–20 Clinical survey of ischemic cerebrovascular disease in children and young adults has been performed by the Study Group of Association of Cerebrovascular Disease in Tohoku among the same institutes as this study for 10 years (1984 through 1993), and 58 patients <20 years of age were collected (unpublished data). Despite the difference in study periods, those figures suggest that dissecting aneurysm of carotid circulation is one of the important causes of cerebral ischemia in young individuals. However, in this study, the most predominant location of dissecting aneurysm in the patients presenting with ischemia was the ACA, which is consistent with a rising number of recent case reports.25–28 This study and these case reports suggest that dissection of the ACA in patients presenting with ischemia shows good prognosis. All of the patients with ischemia showed neither recurrent ischemia nor bleeding attack at a 1-year follow-up, regardless of the types of drugs used. However, use of anticoagulant or fibrinolytic drugs requires circumspection because 4 cases were accompanied by SAH at the onset and because recurrent hemorrhagic attacks were reported in patients using such drugs.4,9
Because this is the first report investigating nontraumatic dissecting aneurysms of the intracranial carotid circulation that is based on a large number of collected cases, the findings of this study should be confirmed by further study.
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Appendix |
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Study Group of the Association of Cerebrovascular Disease in Tohoku, Japan
Akita University, Iwate Medical University, Tohoku University, Fukushima Medical University, Hirosaki University, Yamagata University, Aomori Rosai Hospital, Hatinohe Municipal Hospital, Towada Municipal Hospital, Kuroishi Municipal Hospital, Noheji Hospital, Iwate Prefectural Central Hospital, Iwate Prefectural Kuji Hospital, Morioka Red Cross Hospital, Iwate Prefectural Miyako Hospital, Iwate Prefectural Iwai Hospital, Izumi Hospital Iwate, National Miyagi Hospital, Iwate Prefectural Fukuoka Hospital, National Iwate Hospital, Iwate Prefectural Daitoh Hospital, Higashi Hatimantai Hospital, Heiwadai Hospital, National Sendai Hospital, Kohnan Hospital, Izumi Hospital Sendai, National Miyagi Hospital, Ishinomaki Red Cross Hospital, Senseki Hospital, Miyagi Prefectural Cancer Research Center, Sendai Tokusukai Hospital, Tohoku Koseinenkin Hospital, Iwaki Kyoritu Hospital, Masukinen Hospital, Watari Hospital, Haramachi Municipal Hospital, Fukushima Medical Clinic, Takeda General Hospital, Shirakawa Kosei Hospital, Yamagata Prefectural Central Hospital, Yamagata Municipal Saiseikan Hospital, Yonezawa Municipal Hospital, Sakata Municipal Hospital, Yamagata Prefectural Kahoku Hospital, Akita Prefectural Cerebrovascular Research Center, and Akita Red Cross Hospital.
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Acknowledgments |
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We express our gratitude to the members of the 46 institutions composing the Study Group of the Association of Cerebrovascular Disease in Tohoku (see Appendix) for kind enrollment of their cases.
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Footnotes |
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The institutions that participated in the Study Group of the Association of Cerebrovascular Disease in Tohoku, Japan, are listed in the Appendix.
Received August 14, 2001; revision received November 14, 2001; accepted December 3, 2001.
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