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Neuroradiology Case of the Week

Case 215

Igor Mikityansky, MD, MPH and Barbara Germin, MD

Clinical Presentation: A 70 year-old male initially presented with four-day history of headaches, dizziness, double vision and right more than left lower extremity weakness. The patient reported falling down several times without injuring to his head or loss of consciousness. He was found to have 3 cm diameter basilar artery aneurysm. This was confirmed by the cerebral angiogram  five days later.  Two days later he had a seizure with apnea, tachycardia, and unresponsiveness. He was intubated. The CT demonstrated subarachnoid and intraventricular hemorrhage. A ventriculostomy was placed. However, given low likelihood of recovery his family withdrew the ventilator support, after which patient has expired.

Radiological Findings: Head CT: Intraventricular hemorrhage into the third, lateral and fourth ventricles. Blood is in perimesencephalic and quadrigeminal cisterns. The rounded mixed density structure with peripheral calcifications in the prepontine cystern, representing partially thrombosed aneurysm of the basilary artery. The aneurysm was deforming the pons, predominantly on the left.
     Cerebral angiogram: Fusiform aneurysm of the basilar artery from vertebrobasilar junction to mid basilar artery, measuring 3cm in diameter. The left vertebral is small.

Diagnosis:   Ruptured atherosclerotic giant fusiform basilar artery aneurysm with subarachnoid hemorrhage

Discussion: The fusiform aneurysm is defined as long segment irregular fusiform or ovoid arterial dilatation [1]. It is more common in vertebrobasilar than in carotid circulation [1]. The aneurysm over 2.5 cm in diameter are called giant [1]. Fusiform aneurysms comprise only 1% of vertebrobasilar aneurysms, but it is the most common shape of giant aneurysms of the basilar artery [2]. In the older adults, atherosclerosis is the most common cause of the fusiform aneurysm in the basilar artery [1]. It is usually associated with atherosclerotic changes in other vessels. Nevertheless, overall, it is less common than vertebrobasilar dolichoectasia or saccular aneurysm [1]
     The atherosclerotic fusiform aneurysm usually presents with vertebrobasilar transient ischemic attacks and less commonly with cranial neuropathies in the patients in their seventh or eights decades [1].
      On non-enhanced CT the aneurysm appears hyperdense, frequently with calcifications. Contrast demonstrates lumen enhancement, while intraluminal clot appears as a filling defect. The computed tomographic arteriogram demonstrates focal fusiform or saccular enlargement [1]. The MRI demonstrates variable signal on T1 weighted images, hypointense lumen and clot on T2, and strong enhancement of residual lumen on post-contrast T1. The precontrast  3D-TOF is suboptimal due to flow saturation and phase dispersion [1]. Therefore, a dynamic contrast-enhanced 3D-TOF MRA or CTA are the studies of choice.
     The differential of atherosclerotic fusiform aneurysm includes atherosclerotic dolichoectasia, giant serpentine aneurysm, nonatherosclerotic fusiform vasculopathy, and dissecting aneurysm. The dolichoectasia does not have a focal dilatation. The serpentine aneurysm is practically indistinguishable from the atherosclerotic fusiform aneurysm on imaging and appears as a large, partially thrombosed dilatation without definable neck.  Nonatherosclerotic fusiform aneurysms usually occur in younger patients with underlying vasculopathy or immune disorders. The dissecting aneurysm does not have associated atherosclerotic changes in other vessels [1].
     The fusiform aneurysm usually progressively enlarges [1]. Up to 80 % of patients with symptomatic and untreated giant aneurysm develop complications or die within 5 years since diagnosis [2]. The complications include brainstem compression, ischemia, and rupture [2-3].
     The management of fusiform aneurysms is difficult due to their morphology [2]. Occlusion of the parent arteries, “Hunterian ligation,” has been advocated as preferred method of treatment [2,4]. The “Alskock Test” is usually performed to evaluate patency of the posterior communicating (PCOM) arteries by compressing the cervical carotid artery during the injection of vertebral artery. The PCOM greater than 1 mm can be visualized and suggests possibility of collateral flow after occlusion of the vertebrobasilar system [2]. Another study reported that patients with two PCOMs greater than 1 mm diameter had better outcomes than those with one [5]. Tc99m-hexamethylpropylenamine oxime qualitative single photon emission computerized tomography (Tc99m-HMPAO SPECT) evaluation of posterior arterial territories during temporary balloon occlusion is hypothesized to be a better predictor of patient’s ability to withstand complete vertebrobasilar occlusion [5]. A two-staged proximal occlusion at the level of distal vertebral arteries has been reported to result in the thrombosis and shrinkage of the aneurysm [2]. However, the reported mortality with ligation of vertebral arteries is 30-35% [5].
     Endovascular occlusion of basilar and vertebral arteries with balloons and coils have been used in nonatherosclerotic fusiform aneurysm cases with good results [5]. Nevertheless, the treatment was associated with temporary post-procedural neurologic deficits in all patients, which resolved within several weeks with heparinization. It is explained by the thrombus formation with associated edema. There are reports of successful treatment of ruptured basilar aneurysms with stent-graft placement specifically in the location from the vertebrobasilar junction to the midbasilar artery [6]. The bare stent is used for precise anchoring in both aneurismal necks with subsequent intrastent placement of a shortest possible stent-graft occluding inflow into the aneurysmal sack.  However, both stent-graft placement and embolization carry the risk of occlusion of perforating vessels originating from the basilar artery [5-6]. In fact, the length of the basilar artery involvement was noted to correlate with likelihood of brainstem infarct after occlusion [4]. Furthermore, the older patients with atherosclerotic aneurysms are considered to be more prone to infarctions after vertebrobasilar occlusion [4].

References:

1. Osborn AG, et al. Diagnostic Imaging: Brain. Altona, Manitoba, Canada: Amirsys, 2004.
2. Omahen DA, Findlay JM. A giant fusiform basilar aneurysm treated by bilateral vertebral artery occlusion. J Clin Neurosci 2004; 11:324-328. [Medline]
3. Yasui T, Komiyama M, Iwai Y, Yamanaka K, Nishikawa M, Morikawa T. Evolution of incidentally-discovered fusiform aneurysms of the vertebrobasilar arterial system: neuroimaging features suggesting progressive aneurysm growth. Neurol Med Chir (Tokyo) 2001; 41:523-527; discussion 528. [Medline]
4. Drake CG, Peerless SJ. Giant fusiform intracranial aneurysms: review of 120 patients treated surgically from 1965 to 1992. J Neurosurg 1997; 87:141-162. [Medline]
5. Hassan T, Ezura M, Takahashi A. Treatment of giant fusiform aneurysms of the basilar trunk with intra-aneurysmal and basilar artery coil embolization. Surg Neurol 2004; 62:455-462; discussion 462. [Medline]
6. Islak C, Kocer N, Albayram S, Kizilkilic O, Uzma O, Cokyuksel O. Bare stent-graft technique: a new method of endoluminal vascular reconstruction for the treatment of giant and fusiform aneurysms. AJNR Am J Neuroradiol 2002; 23:1589-1595. [Medline]