Cerebral thrombosis

Complete thrombosis followed by recanalization of giant aneurysms is an infrequent process that has been exceptionally mentioned in relation to nongiant saccular aneurysms. A 25-year-old male presented with a right temporal hematoma and associated subarachnoid hemorrhage. Cerebral angiography revealed a small blister-like dilatation at the right middle cerebral artery bifurcation. The cerebral hematoma was surgically removed and a large thrombosed aneurysm was discovered and was wrapped. Follow-up angiography revealed complete recanalization of the aneurysm with preservation of all the arterial branches and the aneurysm was then completely occluded with detachable coils. This case provides insight into the wellknown but poorly understood dynamic process of thrombosis and recanalization of cerebral aneurysms. The possible role of a cerebral hematoma in the pathogenesis of this process is discussed. [Neurol Res 2003; 25: 857-859]

Keywords: Cerebral aneurysm; thrombosis; recanalization; embolization

INTRODUCTION

Partial thrombosis of giant aneurysms is not uncommon in the natural history of cerebral aneurysms, however complete angiographie occlusion occurs less frequently1,2. Giant thrombosed aneurysms are considered unstable lesions that may either grow, recanalize, bleed, compress or give rise to thromboembolic events3-7. Therefore, it has been suggested that the presence of intra-aneurysmal clot in giant aneurysms has little prognostic significance and does not alter the management or outcome after treatment8.

In nongiant aneurysms, the process of thrombosis and recanalization has been only exceptionally described and in general, is poorly understood9. Several factors (i.e., geometrical configuration of the aneurysm neck and fundus, hemodynamic, biological) have been implicated to interact in the delicate balance between thromboeenesis and thrombolysis within the aneurysm2,9-13.

We describe here a case of thrombosis and recanalization of a nongiant saccular aneurysm and we discuss possible pathogenic mechanisms.

CASE REPORT

A 25-year-old male was brought to the emergency room with a two day history of sudden onset severe headache and left arm weakness. On admission, the patient was alert and oriented, alternating excitation and confusion, with pupils equal and responsive to light, marked nuchal rigidity, left facial palsy, moderate left arm paresis and mild leg paresis (GCS 15). On noncontrasted head computed tomography, a right frontotemporal hematoma with moderate mass effect and associated subarachnoid hemorrhage was diagnosed (Figure 1). Digital subtraction cerebral angiography revealed a small (1 mm diameter) blister-like dilatation at the right middle cerebral artery (MCA) bifurcation (Figure 2). For the next three days, the patient's condition stabilized and he improved neurologically, he was alert and oriented with hemiparesis and moderate headache. A routine follow-up CT revealed an increased mass effect and the patient was brought to the operating room for hematoma removal. Through a right extended pterional approach, the cerebral hematoma was surgically removed and a large completely thrombosed MCA aneurysm was discovered. The aneurysm body was stiff and its residual neck was short. Clipping was performed several times but the clip slipped and occluded the frontal MCA branch and thus, wrapping with gauze was performed. The patient evolved satisfactorily and improved the hemiparesis. he was able to walk independently and a mild arm paresis persisted. Twenty days after surgery a follow-up angiography revealed complete recanalization of the aneurysm and preservation of all the MCA branches (Figure 3). Subsequently, endovascular embolization was performed and the aneurysm was then completely occluded with detachable coils (Figure 4). The patient evolved favorably and was transferred to a short-term rehabilitation facility two days after the procedure. After two weeks, the patient returned to work.

DISCUSSION

Spontaneous intra-aneurysmal thrombosis is a welldocumented phenomenon that has been noted in approximately 50% of giant intracranial aneurysms8. The incidence of complete thrombosis in giant aneurysms is significantly lower and ranges between 1 3% and 20%1. The occurrence of these phenomena in nongiant (large or small) aneurysms has been reported exceptionally9.

Morley and Barr14 defined giant intracranial aneurysms arbitrarily as those greater then 25 mm in diameter and those lesions have increasingly been recognized as a special clinical and surgical entity. Giant aneurysms are believed to derive from smaller saccular aneurysms15, and must be regarded as dynamic lesions with respect to their growth, intraluminal thrombosisrecanalization phenomena and their subsequent risk of bleeding, development of mass effect or thromboembolic events3-8.

The high incidence of thrombus formation in giant aneurysms has been related mainly to the ratio between aneurysmal volume and aneurysmal neck size; in aneurysms with a relatively small neck, intraluminal thrombosis may occur7,10. Other biophysiological parameters such as the age of the aneurysm, hemodymanics in the parent artery, direct distortion of the parent artery by the aneurysmal sac, endothelial damage due to intrasaccular turbulent flow, and the angiographie procedure itself have been also proposed2,9,12.

In the presented case, the dome size of the MCA aneurysm was about 13mm and the neck size was 3 mm, thus the volume:orifice ratio was relatively large. In addition, we considered that a main factor for thrombosis was the tamponade effect exerted by the parenchymal bleeding that surrounded the aneurysm. This compressing effect progressively increased during the first days with the development of hematomaassociated-edema, thus promoting conditions for thrombosis. Theoretically, such extraluminal pressure may have modified not only the ratio between aneurysmal volume/neck but also other mentioned factors, especially the hemodynamics in the MCA secondary to external compression, arterial distortion or transient acute vasospasm.

On the other hand recanalization may be another event of the dynamic process described. The mechanism of recanalization is poorly understood however; liquefaction of the thrombus and subsequent intrathrombotic dissection by blood flow could be a possible explanation12. In the presented case, recanalization was observed in close time-relation to surgical removal of the cerebral hematoma and wrapping of the aneurysm. Minimal manipulation of the aneurysm was required and inadvertant dislodgement of intraluminal clots was considered theoretically possible but very improbable; due to the fact that no new neurological deficit or new CT infarction were assessed postoperatively. Moreover, the patient's neurological condition (i.e., headache, vomiting, weakness) improved after clot removal. Again, the same theoretical considerations regarding the direct and indirect effects of the hematoma (triggering/causative factor) promoting thrombosis may be applied to recanalization when this factor is suppressed by removal.

Thrombosis and recanalization may thus be considered opposite processes in relation to their pathogenesis. No consensus exists regarding management of thrombosed aneurysms, but mass effect lesions are currently decompressed and clipped. This case illustrates the unstable balance between prothrombotic and thrombolytic phenomena into the aneurysm sac and thus, the need of close neuroimaging follow-ups for patients harboring thrombosed aneurysms; even complete thrombosis may not be a final stage.

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Jose E. Cohen*[dagger], Gustavo Rajz*, Felix Umansky* and Sergey Spektor*

*Department of Neurosurgery, [dagger]Department of Endovascular Neumsurgery and Interventional Neuroradiology Hadassah University Hospital, Jerusalem, Israel

Correspondence and reprint requests to: Jose E. Cohen, MD, Kiryat Hadassah, POB 12000, 91120 Jerusalem, Israel. [jcohenns@yahoo.com] Accepted for publication June 2003.

Copyright Forefront Publishing Group Dec 2003
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