Intracranial Cerebral Artery Dissection of Anterior Circulation as a Cause of Convexity Subarachnoid Hemorrhage.

Original Paper Received: September 28, 2014 Accepted: April 27, 2015 Published online: June 16, 2015

Cerebrovasc Dis 2015;40:45–51 DOI: 10.1159/000430945

Intracranial Cerebral Artery Dissection of Anterior Circulation as a Cause of Convexity Subarachnoid Hemorrhage Kazuki Fukuma a Masafumi Ihara a Tomotaka Tanaka a Yoshiaki Morita c Kazunori Toyoda b Kazuyuki Nagatsuka a

c

Divisions of Neurology and b Cerebrovascular Medicine, Department of Stroke and Cerebrovascular Diseases, Department of Radiology, National Cerebral and Cardiovascular Center, Suita, Japan

Key Words Cerebral artery dissection · Convexity subarachnoid hemorrhage · cSAH · Antithrombotic treatment

Abstract Background: Convexity subarachnoid hemorrhage (cSAH), defined as intrasulcal bleeding restricted to hemispheric convexities, has several etiologies: reversible cerebral vasoconstriction syndrome, cerebral amyloid angiopathy, and internal carotid artery (ICA) stenosis or occlusion. However, it remains unknown whether cerebral artery dissection causes cSAH. Methods: We retrospectively investigated patients admitted to our hospital between 2005 and 2013 with ischemic stroke or transient ischemic attack caused by cerebral artery dissection. Cerebral artery dissection was diagnosed by cervical or cerebral magnetic resonance imaging (MRI) or computed tomography (CT) showing a wall hematoma. CT angiography, ultrasonography, or intra-arterial digital-subtraction angiography detected cerebral artery dissection if a double lumen, string sign, intimal flap, or dissecting aneurysm was observed at a nonbifurcation site. We used CT or MRI to detect cSAH, which was defined as blood collection

© 2015 S. Karger AG, Basel 1015–9770/15/0402–0045$39.50/0 E-Mail [email protected] www.karger.com/ced

restricted to one or few cerebral sulci without extending to the basal cisterns, ventricles, or Sylvian and interhemispheric fissures. Demographic, neuroimaging, treatment, and prognostic data were collected. Results: In total, 82 patients were diagnosed with ischemic stroke caused by cerebral artery dissection. The following arteries were affected: the ICA (9 patients), anterior cerebral artery (ACA; 12 patients), middle cerebral artery (MCA; 12 patients), vertebral artery (37 patients), basilar artery (5 patients), posterior cerebral artery (2 patients), and posterior inferior cerebellar artery (4 patients). In addition, 1 patient presented with simultaneous dissection in both the vertebral and internal carotid arteries, and 6 patients (7%) presented with cSAH (3 men and 3 women, age 39–67 years). The MCA was dissected in four cases and the ACA in two cases, with cSAH frequencies of 33 (4 of 12) and 17% (2 of 12), respectively, in those vessels. Artery dissection in the vertebrobasilar artery system was not responsible for cSAH (0 of 48). In all the MCA dissection cases, cSAH occurred in the arterial border zone between the ACA and MCA territories. Although 2 patients showed early reperfusion with temporary cSAH enlargement, cSAH was selflimiting. Antithrombotic treatment did not complicate the clinical course when used in 4 patients during acute or sub-

Masafumi Ihara, MD, PhD Department of Stroke and Cerebrovascular Diseases National Cerebral and Cardiovascular Center 565-8565, Suita (Japan) E-Mail ihara @ ncvc.go.jp

Downloaded by: University of Melbourne 198.143.52.1 - 1/17/2016 1:35:42 PM

a

Introduction

Convexity subarachnoid hemorrhage (cSAH) refers to bleeding in one or more cerebral sulci without extending to the basal cisterns, ventricles, or Sylvian and interhemispheric fissures. Previously, cSAH was an underdiagnosed condition but it has recently been found in stroke patients with an increasing availability of magnetic resonance imaging (MRI) modalities, such as T2*-weighted imaging. Several etiologies have been associated with cSAH, including reversible cerebral vasoconstriction syndrome (RCVS), cerebral amyloid angiopathy (CAA), severe carotid artery stenosis, posterior reversible encephalopathy syndrome, vasculitis, moyamoya disease, cortical venous thrombosis, dural arteriovenous fistula, cavernoma, and brain abscess [1–10]. However, little is known about whether cerebral artery dissection causes cSAH, and only one case of cerebral artery dissection with concomitant cSAH has been reported [8] when excluding cases accompanied by RCVS or fibromuscular dysplasia (FMD) [11]. However, the clinical information of this case is unavailable. Therefore, in this study, we reviewed the records of patients admitted to our hospital with cerebral artery dissection and imaging abnormalities indicating cSAH. In addition, we investigated the features, clinical course, and pathophysiology of cSAH.

Methods We retrospectively investigated patients admitted to our hospital between 2005 and 2013 diagnosed with ischemic stroke or transient ischemic attack caused by cerebral artery dissection (intracranial cerebral or carotid artery dissection). Cerebral artery dissection was diagnosed on the basis of an evidence of a wall hematoma on either cervical or cerebral MRI or computed tomography (CT). CT angiography, ultrasonography, and intra-arterial digital-subtraction angiography (DSA) were used to detect cerebral artery dissection if a double lumen, string sign, intimal flap, or dissecting aneurysm was observed at a nonbifurcation site. MRI studies, including diffusion-weighted imaging (DWI), fluid-attenuated inversion recovery (FLAIR) and T2*-weighted

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MRI sequences, and magnetic resonance angiography (MRA), were performed with a Siemens 1.5T Magnetom Vision MRI (Siemens Medical Solutions, Erlangen, Germany). DWI was obtained using the following parameters: repetition time, 4,000 ms; echo time, 100 ms; matrix, 128 × 128; field of view, 23 cm; section thickness, 4 mm; intersection gap, 2 mm; and b values, 0 and 1,000 s/mm2. MRA was performed using the following parameters: repetition time, 35 ms; echo time, 7.6 ms; flip angle, 20°; field of view, 200 mm; matrix, 224 × 512; and slice thickness, 0.6 mm. We included cases presenting with spontaneous cSAH. Spontaneous cSAH was defined as follows: any blood collection restricted to one or more cerebral sulci but without extension to the basal cisterns, ventricles, or Sylvian and interhemispheric fissures and that was not secondary to trauma. We considered cSAH to be indicated by hyperdensity exclusively in the cortical sulci on brain CT, hyperintensity on FLAIR, and hypointensity on T2*-weighted MRI sequences. The evolution of cSAH was intermittently monitored over time with serial imaging and was classified as full, partial, and no resolution. The follow-up period was defined as the time from the initial assessment to the full resolution or to the last follow-up without full resolution. All images were independently reviewed by a stroke neurologist (K.F.) and by expert neuroradiologists. A consensus meeting was planned with another stroke neurologist to reach an agreement in cases where discrepancies existed between initial individual readings. To assess intraobserver agreement, CT and MRI images were reassigned to the stroke neurologist (K.F.) for a second time and reevaluated under blinded conditions. Data related to demographics, medical history, symptoms, neuroimaging, and treatment were collected.

Results

Eighty-two patients were diagnosed with ischemic stroke due to intracranial cerebral artery dissection during the study period. The following arteries were affected: the internal carotid artery (ICA; 9 patients), the anterior cerebral artery (ACA; 12 patients), the middle cerebral artery (MCA; 12 patients), the vertebral artery (VA; 37 patients), the basilar artery (5 patients), the posterior cerebral artery (PCA; 2 patients), and the posterior inferior cerebellar artery (4 patients). In addition, 1 patient presented with simultaneous dissection of both the VA and ICA. Six patients (7%) were found to have cSAH on the basis of imaging studies at the time of admission. The baseline demographics of the 6 patients are shown in table 1, together with their clinical course and imaging abnormalities in figures 1 and 2, respectively. There were no discrepancies in cSAH readings between the stroke neurologist and expert neuroradiologists, with interobserver and intraobserver (K.F.) agreement for cSAH of 100% each. Fukuma/Ihara/Tanaka/Morita/Toyoda/ Nagatsuka


acute phases. All patients achieved a 3-month poststroke modified Rankin Scale of 0–2. Conclusion: Our data suggest that cSAH caused by intracranial cerebral artery dissection is not rare. Further investigations are needed to elucidate the precise mechanism underlying cSAH in cerebral artery dissection. © 2015 S. Karger AG, Basel

Case 1 Case 2 Case 3 Case 4 Case 5 Case 6

Fig. 1. Clinical courses of 6 patients with

cerebral artery dissection complicated by cSAH before and after the onset of neurological symptoms.

0 (Onset of neurological symptom) Headache

Admission

10

Recurrence of infarction

day Heparin

Aspirin

Table 1. Baseline demographics of the 6 patients with cerebral artery dissection complicated

Case

1

2

3

4

5

6

Age, sex

39 M

62 F

67 F

49 M

53 F

47 M

History

Smoking

HT, HL

HT, HL, DM

HT, HL, smoking, HT Rt. ACA dissection

HT, smoking, tuberculosis

cSAH

Rt. frontal and parietal sulci

Rt. frontal sulci

Lt. frontal and posterior sulci

Lt. frontal sulci

Rt. frontal sulci

Bi. frontal and parietal sulci

Site of infarction

Rt. MCA territory

Rt. MCA territory

Lt. BG, CR, Lt. M2 territory

Lt. MCA territory

Rt. ACA territory

Lt. ACA territory

Angiography on admission

Rt. ICA top-M1 Rt. M1 stenosis, stenosis Rt. M2 occlusion

Lt. M1 stenosis, Lt. M2 occlusion

Lt. M1 stenosis, Lt. M2 occlusion

Rt. A2 stenosis

Lt. A1–A3 stenosis

Evidence of dissection

Intramural hematoma

Intramural hematoma

Intramural hematoma

Intimal flap

Pearl and string Intramural signs hematoma

BP on admission, 136/72 mm Hg

195/115

172/92

153/108

160/80

173/126

Early reperfusion (+)

(−)

(−)

(−)

(−)

(+)

Initial therapy

Edaravone

Edaravone, IV AHD

Heparin, edaravone, IV AHD

Heparin, edaravone

Oral AHD

Edaravone, IV AHD

Neurological deterioration

(−)

(−)

2 h after admission

(−)

(−)

(−)

Recurrence of infarct

16 days after admission

(−)

(−)

2 days after admission

(−)

(−)

Prevention

Cilostazol

Aspirin

Aspirin, clopidogrel

Aspirin

None

None

Intracranial Cerebral Artery Dissection of Anterior Circulation as a Cause of cSAH


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HL = Hyperlipidemia; DM = diabetes mellitus; Lt. = left; Rt. = right; A1–A3 = segment of ACA; M1–M2 = segment of MCA; BG = basal ganglia; CR = corona radiata; IV = intravenous; AHD = antihypertensive drug; BP = blood pressure; HT = achieved hypertension.

a

b

c

Fig. 2. Imaging study findings of Cases 1–6. a CT scans on admission showing cSAH (arrows). b FLAIR (b1–4 and b6) or T2*weighted MRI (b5) on admission showing cSAH (arrows). c Dif-

fusion-weighted MRI on admission showing acute infarction. d Conventional angiography showing dissection lesions (red arrowheads).

DSA showed that the MCA and the ACA were responsible for four and two cases of dissection, respectively. Therefore, the corresponding cSAH frequencies in each vessel were 33 (4 of 12) and 17% (2 of 12), indicating that all patients with cSAH presented with abnormalities in the anterior cerebral circulation. In Cases 2–6 (table 1), hypertension had been controlled before hospitalization, but high blood pressure was observed at presentation and substantially fluctuated for several days after admission. Four of these patients required mild antihypertensive medication. The median duration of systolic blood pressure elevation greater than 150 mm Hg was 11.2 (range 7–16) days. The median age of the 6 patients (3 men and 3 women) was 49 (range 39–67). Five of the 6 patients experienced

headaches but did not describe the classical thunderclap headache, and the temporal onset of neurological symptoms and headache varied between patients (fig. 1). Moreover, there were no reports of transient focal sensory or motor symptoms preceding their cSAH. Two patients had elevated red blood cell levels in their cerebrospinal fluid, but none of the patients had autoantibodies related to vasculitis, imaging findings suggestive of RCVS or FMD, or evidence of multiple microbleeds indicative of CAA or carotid artery stenosis. Case 1 was a 39-year-old man who experienced a transient headache 4 days before admission. He presented with a recurrence of headache associated with neurological symptoms and normal blood pressure. Imaging re-

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Fukuma/Ihara/Tanaka/Morita/Toyoda/ Nagatsuka


d

vealed cSAH of the right frontal and parietal lobes in the arterial border zone accompanied by infarction in the right MCA region (fig. 2). The right proximal M1 segment was occluded on MRA; however, at the time of DSA, there was reperfusion, irregular stenosis from the top right ICA to the proximal M1 segment, and collateral blood vessels had developed from the ACA and PCA to the MCA region. On day 2 of hospitalization, cSAH enlarged with dilatation of the right MCA suggestive of hyperperfusion on MRA. Consequently, antithrombotic therapy was initially avoided, although heparin treatment was initiated on day 16 following exacerbation of the right M1 stenosis with infarction. Cilostazol (200 mg/day), an antiplatelet agent, was administered for secondary prevention, and recurrence was not observed until 90 days after the onset. In Cases 2–4, each patient had cerebral infarction and cSAH in the ACA/MCA border zone. None of these patients showed early reperfusion. In Case 2, antithrombotic agents were avoided in the acute phase because of cSAH, but the patient ultimately received heparin and then aspirin in the subacute phase without consequences. In Cases 3 and 4, antithrombotic agents were used for the initial treatment without the cSAH enlarging and without further bleeding. However, Case 3 experienced worsening of their hemiparesis 2 h after the initiation of the heparin treatment; therefore, treatment was discontinued to minimize the effects of cerebral bleeding. Case 4 experienced an exacerbation of their stenosis with an embolic infarction on day 2 of hospitalization. Increasing their heparin dose and adding aspirin on day 4 was sufficient to prevent further stroke recurrence. In Cases 5 and 6, both patients presented with cerebral infarction in the ACA territory. Case 5 had cSAH in the ACA/MCA border zone and hemorrhage was observed not only in the sulcus but also in the infarcted area, suggesting hemorrhagic infarction. Thus, antithrombotic agents were avoided. Case 6 had cSAH in the ACA/PCA border zone, with early reperfusion and no collateral blood vessel formation on their admission on DSA. Follow-up CT scans on day 2 of hospitalization showed enlargement of the cSAH in Case 6. The temporal changes in CT, FLAIR, and T2*-weighted MRI imaging abnormalities are summarized in online supplementary table 1 (for all online suppl. material, see www.karger.com/doi/10.1159/000430945). All patients achieved a modified Rankin Scale of 0–2 (Case 5 = 0; Cases 2 and 6 = 1; and Cases 1, 3, and 4 = 2) at 3 months poststroke.

We reviewed the clinical courses of patients with cerebral infarction caused by intracranial cerebral artery dissection accompanied by incidental findings of cSAH. The affected blood vessels were intracranial arteries of the anterior circulation in all patients. In particular, it is noteworthy that cSAH developed in one-third of cases with MCA dissection and one-sixth of those with ACA dissection, but in no cases with arterial dissection of the posterior circulation. Thus, cSAH tended to occur in the arterial border zone between ACA/MCA or ACA/PCA territories; in such cases, arterial dissection should be suspected. RCVS and CAA are believed to be the major causes of cSAH. Kumar et al. evaluated 29 patients with cSAH and demonstrated that RCVS was a common cause of cSAH in patients aged ≤60 years, while CAA was more common in those aged >60 years [11]. RCVS may accompany carotid or VA dissections; for instance, carotid artery dissection was observed in 8% (7 of 89) of patients with RCVS [12]. There are contrasting hypotheses for this phenomenon: (1) arterial dissection causes RCVS and (2) RCVS makes arteries more likely to tear [10]. In addition, several other mechanisms may be involved in cSAH development, such as fissure formation caused by leptomeningeal vessel vasculopathy and bleeding from leptomeningeal vessels caused by reperfusion injuries associated with vascular spasm [13]. However, no reports have claimed that cSAH occurs because of intracranial cerebral artery dissection in the absence of RCVS or FMD. Our study, which investigated 82 consecutive cases of cerebral artery dissection over a 9-year period, showed that cerebral artery dissection is not a rare cause of cSAH. Several reports have attributed cSAH to symptomatic ICA stenosis or occlusion [14–17]. In an investigation of 15 patients (median age 65 years) with cSAH, Geraldes et al. demonstrated that the predominant etiology of cSAH was atherosclerotic stenosis of the ipsilateral ICA (5 patients, 33%), suggesting that carotid artery lesions represent the most common etiology of cSAH in the elderly [14]. Two mechanisms have been proposed for cSAH associated with atherosclerotic carotid artery stenosis. The first is the rupture caused by acute changes in the hemodynamics of unstable collateral blood vessels dilating in the arterial border zone [14–16]. The second is the necrosis or rupture of the peripheral vessel caused by embolism from the stenotic lesions to the hypoperfused vessel [17]. Consistent with these mechanisms and suggestive of rap-



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Discussion

idly changing hemodynamics, 5 of the 6 patients in our review had high blood pressure on admission and two had evidence of early reperfusion. Other possible mechanisms underlying cSAH specific to arterial dissection also warrant discussion, such as damage to the internal elastic lamina and media or vasa vasorum [18, 19]. Pathological studies have shown that multiple or tandem dissections occur not only in the ruptured artery but also in other intracranial arteries [20]. Therefore, in Case 4, different arteries were probably subjected to dissection at different times (table 1), suggesting that the latent arterial vulnerability involves both the intracranial artery affected by dissection on neuroimaging studies and other arteries that seem intact. Thus, latent vulnerability in the leptomeningeal artery distal to the dissection site may be attributable to cSAH. Intriguingly, pathological evidence of FMD can exist in the leptomeningeal arteries without involving the larger arteries [21], suggesting that latent pathology can exist and cause cSAH in these arteries. We assume that cSAH in cases with dissection is caused by the interaction of several mechanisms, as described earlier, but hemodynamic change probably plays the most significant role. Our study was notable for its finding that no cases of cSAH arose from the posterior circulation. A plausible explanation for this is that dissection in a unilateral VA does not lead to hemodynamic derangement in the posterior circulation because paired VAs unite to form the basilar artery. From a treatment perspective, 4 of the 6 patients did not initially receive antithrombotic treatment. However, 3 patients experienced neurological deterioration or

stroke recurrence. This suggests that even in patients with artery dissection whose conditions are complicated by cSAH, antithrombotic agents should be considered during the subacute phase at the latest, particularly when accompanied by stenosis with a high risk of ischemic stroke. Notably, the use of antithrombotic agents in 4 patients during the acute or subacute phase did not complicate their clinical courses and cSAH was ultimately self-limiting. There was no relationship between the persistence of cSAH and the duration of systolic blood pressure elevation greater than 150 mm Hg. cSAH findings resolved in the order CT, FLAIR, and T2*-weighted MRI. Hypointensity on T2*-weighted MRI persisted for >3 months in Cases 2 and 3 who received antiplatelet treatment without consequences. Thus, prolonged evidence of cSAH on T2*-weighted MRI sequences may not always imply a risk for bleeding. There were several limitations to this study. The small sample size will necessitate comprehensive testing with a larger sample. Thus, the interpretation of this case series should be viewed as a hypothesis-generating study that will need to be followed by larger prospective studies that are specifically designed to elucidate the underlying mechanisms. In conclusion, although RCVS, CAA, and ICA stenosis and occlusion are considered the major causes of cSAH, associations of intracranial cerebral artery dissection of the anterior circulation with cSAH are not rare. However, further investigations are needed to elucidate the precise mechanism underlying cSAH in intracranial cerebral artery dissection.

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