br Discussion br Acknowledgments br Introduction br

Discussion
Acknowledgments
Introduction
Case report A man 68 years of age was admitted to our hospital on April 3, 2006, because of progressive weakness on the right side and dysarthria. On March 30, 2006, the patient had begun to feel weakness of the right upper and lower limbs. Neurologic examination revealed a right central-type facial palsy, right upper limb weakness (Grade 1), and right lower limb weakness (Grade 3). His past history showed vascular risk factors such as hypertension, hyperlipidemia, smoking, and diabetes. The results of laboratory studies were normal. Electrocardiography showed sinus tachycardia. Carotid ultrasonography showed mild atherosclerotic changes common carotid arteries, carotid bifurcations, and internal carotid chenodeoxycholic acid on both sides. Brain computed tomography (CT) showed presence of infarction involving the left internal capsule region (Fig. 1). Thus an impression of left cerebral infarction was made. Brain magnetic resonance imaging (MRI) performed on April 4, 2006, confirmed the diagnosis of acute infarction involving the left internal capsule region, mainly in the anterior choroidal artery (AChA) territory (Fig. 2). Sudden loss of consciousness was noted on April 5, 2006. The Glasgow Coma Scale (GCS) dropped to E1V1M4, and an emergent brain CT revealed subarachnoid hemorrhage (SAH) with intraventricular hemorrhage and acute hydrocephalus (Fig. 3). A neurosurgeon was called in for emergency consultation. The patient then underwent emergent external ventricular drainage. The clinical condition improved after surgery and the GCS became E3VeM5 on April 10, 2006. Carotid angiography was performed on April 10, 2006, and it revealed a saccular-type aneurysm with pseudoaneurysm formation in the left internal carotid artery (ICA)- posterior communicating artery (PcomA) region (Fig. 4). The left AChA was not visualized. The patient underwent craniotomy for clipping of the aneurysm on April 12, 2006. The operative findings consisted of a 0.5 × 0.6 × 0.8 cm saccular-type aneurysm and a pseudoaneurysm (1 × 1.5 × 2 cm) in the left ICA-PComA region (Fig. 5). Besides that, an occluded left AChA was found tightly compressed by the aneurysm. The patient was kept in the intensive care unity for postoperative care. After surgery, the GCS was still E3VeM5. The clinical course was uneventful.
Discussion Previous studies suggested that intracranial aneurysms can act as sources of distal embolization. A spontaneous thrombus can be observed within the aneurysm sac, presumably because of turbulence and slow flow. This thrombus formation can lead to embolization in the distal vascular distribution, which can clinically manifest as transient ischemic attacks or cerebral infarctions. In 1968, Taptas and Katsiotis reported a patient with late hemiplegia after subarachnoid hemorrhage, and they proposed embolism from the aneurysm sac as the causative mechanism. Qureshi and colleagues stated that ischemic strokes attributable to embolization from the aneurysmal sac were observed in 9 of 269 patients (3.3%) with unruptured aneurysms. A Mayo Clinic series reported that even aneurysms smaller than 1 cm presented cerebral ischemia and became symptomatic. Another possible mechanism for the cause of cerebral infarction is mechanical obstruction of the cerebral artery by a neighboring lesion. A neoplasm may cause cerebral arterial occlusion by tumor embolism or arterial encasement. Meningioma has been reported to cause of occlusion of the carotid artery. Direct invasion into the arterial wall is the commonly accepted mechanism of infarction. In the present case, the left AChA was occluded by mechanical compression from the PComA aneurysm, which resulted in hemodynamic cerebral infarction. To our knowledge, this is the first case of an aneurysm causing neighborhood arterial occlusion by compression mechanism. The AChA is the first branch distal to the PComA. The AChA does not have any collateral supply from its cisternal or plexal segments. Occlusion of the AChA could be a likely cause of ischemic events. Of aneurysms arising from the internal carotid artery, 30% are from the PComA, 6% from the internal carotid bifurcation, and 4% from the AChA. Ischemic episodes as a presenting feature of intracranial aneurysms could be an indicator of poor prognosis. Our case suggests that evaluation for aneurysms should be considered in certain stroke patients. We have also pointed out a mechanism of aneurysm-related cerebral infarction by compression but not by thromboembolism, which has probably not attracted enough attention in the past.