Natural Course of Dissecting Vertebrobasilar Artery Aneurysms without Stroke

Management Strategy and Clinical Findings

Reports of incidentally found DVBAs are rare, but the detection of DVBAs is rising due to increased and improved screening by brain imaging. Therapeutic management of patients with DVBA who are asymptomatic or present only with pain remains controversial and is not well-established.^2,3 DVBA with pain is considered a critical condition predictive of stroke, for which either a surgical or endovascular approach is the treatment of choice.^4⇓–6 Rabinov et al⁷ reported on 28 patients with DVBA who were treated surgically or endovascularly; 2 patients presented with pain only, of whom 1 was surgically treated and rated a score of 3 on the modified Rankin Scale. Ahn et al⁵ reported their endovascular treatment of 14 patients with DVBA, of whom 5 presented with headache only. In our series, none of the patients who presented with pain only at diagnosis had a hemorrhagic or ischemic stroke during observation. On the basis of our results, aggressive interventional treatment may not be necessary for patients with DVBA presenting with pain only.

The establishment of optimal medical management is also controversial. Kim et al⁸ reported their large series of 191 patients with unruptured vertebrobasilar artery dissections, including ischemic and nonischemic symptoms, in which 81 patients presented with headache only. All were treated either endovasculary (n = 46) or by medical therapy with anticoagulation (n = 49), antiplatelet therapy (n = 48), or analgesics (n = 48). The necessity for anticoagulation or antiplatelet therapy remains unclear; our results, at least, do not prove the necessity for anticoagulation or antiplatelet therapy for patients presenting with pain only.

We did not use any antiplatelet or anticoagulation therapy during observation. One patient who presented with mass effect at diagnosis had a brain stem infarction during observation and was admitted to another hospital. The patient received anticoagulation therapy and subsequently experienced SAH. Some similarities can be found with Tsutsumi et al,⁹ who reported a vertebral artery dissection causing SAH in a similar patient who had initially presented with infarction and had received antiplatelet agent therapy. Thus, pain management and blood pressure control are recommended for patients presenting with pain only or ischemic symptoms.

Yasui et al¹⁰ reported their histopathologic findings of incidentally detected fusiform vertebrobasilar aneurysms, which demonstrated intimal thickening, disruption of the internal elastic lamina, and degeneration of the media. They concluded that an incidental fusiform vertebrobasilar aneurysm has the potential to develop into a dissecting aneurysm. In our series, only 1 patient with an incidentally found DVBA experienced clinical deterioration and aneurysm growth during observation.

Morphologic Changes

Observation with serial radiologic examinations should be performed on patients with unruptured DVBAs. Most of the DVBAs in group 1 did not show morphologic findings in the vessel wall. Sato et al¹¹ showed that disrupted internal elastic lamina, covered with intimal thickening, is commonly found at postmortem examination in normal intracranial vertebral arteries of patients who died of causes other than intracranial lesions. Most of the incidentally detected lesions occurred silently or with minor headache and vessel wall healing occurred silently.

Ahn et al¹² reported the difference in the morphologic evolution of the lesion; 25 of 34 symptomatic intracranial vertebrobasilar dissections with dilation without stenosis had no change compared with their initial shape. Pozzati et al¹³ described cases of spontaneous resolution of fusiform aneurysm in the vertebrobasilar system proved by angiography. Naito et al¹ reported that angiographic features of vertebral artery dissection changed for 12 of 20 patients (60%) and that deterioration of features was seen in 4 cases (20%). Nakagawa et al¹⁴ reported serial angiographic changes in 88.2% of unruptured vertebral artery dissections. In our series, morphologic changes were observed in 22 of 113 patients (19.5%) and 5 (4.4%) had DVBAs that enlarged. As for DVBAs having the possibility of changing morphologically, we suggest serial radiologic follow-up for nonstroke DVBAs.

Mizutani¹⁵ reported on 44 patients who presented with nonischemic unruptured dissections in the vertebrobasilar system, of which 10 DVBAs improved, 4 enlarged, and 1 ruptured during observation. Mangrum et al¹⁶ reported that enlargement of nonsaccular intracranial aneurysms correlated significantly with median aneurysm diameter and symptomatic compression at diagnosis. Flemming et al¹⁷ reported that the annual prospective risk of hemorrhage from a vertebrobasilar artery nonsaccular intracranial aneurysm is 0.9% and that an aneurysm diameter of at least 10 mm is strongly indicative of future rupture. In our series, aneurysms of <10 mm had a favorable clinical outcome, but aneurysms of >10 mm with symptoms due to mass effect had a risk of clinical deterioration and enlargement. In such cases, surgical or endovascular intervention should be considered.

Limitations of the Study

This study has several limitations. First, the radiologic examination findings were not the same for all patients. The diameter of the aneurysm was different between CTA and MRA. Nevertheless, the goal of this study was not to compare the differences in the devices but to evaluate the changes in findings with the same method. Each patient was evaluated with either CTA or MRA TOF only. Second, we defined “DVBA” as a nonsaccular aneurysm located at a nonbranching site of the vertebrobasilar artery; however, it is sometimes difficult to determine whether an incidental asymptomatic fusiform aneurysm may have resulted from spontaneously healed dissections or other underlying vascular abnormalities, especially with only CT. Third, intramural hematoma was significantly associated with a change of vertebrobasilar dissection on follow-up in a previous report.¹² In this study, most imaging was performed with CT angiography. CTA has limitations in detecting an intramural hematoma. Fourth, in this study, mean follow-up was 2.9 years. This time is relatively short to evaluate the natural history of these lesions. In this study group, 3 patients demonstrated relatively good clinical outcome, though these patients showed significant risk of enlargement. This discrepancy may be due to lack of long-term follow-up. Fifth, in some cases, follow-up was discontinued, and these patients might have experienced SAH or infarction and might have been admitted elsewhere. Finally, we have a small number of patients with nonstroke DVBA who were treated with endovascular therapy; they do not entirely reflect the results of the study, but this small number will have a negligible effect on the natural course of nonstroke DVBA for the whole group. Although the study has these limitations, the results may provide important information for the treatment and further investigation of nonstroke DVBA.