Korean Journal of Cerebrovascular Surgery 2008;10(3):524-527.
Published online September 1, 2008.
Anterior Choroidal Artery Syndrome occurring after endovascular coiling Treatment : Report of Two Cases.
Lee, Young Han , Whang, Kum , Lee, Ji Yong , Kim, Myung Soon , Lee, Myeong Sub
1Department of Radiology, Yonsei University Wonju College of Medicine, Korea. cursor2@yonsei.ac.kr
2Department of Neurosurgery, Yonsei University Wonju College of Medicine, Korea.
3Department of Neurology, Yonsei University Wonju College of Medicine, Korea.
Abstract
Anterior choroidal artery (AChA) syndrome is widely known to be composed of a triad of hemiparesis, hemisensory loss and homonymous hemianopia. AChA syndrome is an unusual complication of aneurysmal treatment. This report documents two cases of AChA syndrome that occurred after an endovascular aneurysmal coiling procedure. Both cases showed complete recovery of the neurologic deficit at the time of discharge. To avoid this complication, meticulous caution is required to preserve the posterior communicating artery, the AChA and the various perforators during an endovascular procedure. When AChA syndrome occurs, immediate treatment is necessary, including vasodilators, thrombolytics and close observation of the patient's clinical status.
Key Words: Anterior choroidal artery infarction, Intracranial aneurysm, Interventional radiology

Introduction


  
Anterior choroidal artery (AChA) syndrome is an unusual complication of aneurysmal treatment. AChA syndrome is widely known to be composed of a triad of hemiparesis, hemisensory loss and homonymous hemianopia in its complete form. However, the clinical picture is sometimes less complete.3)8) Among the classic symptoms, hemiparesis, the most constant clinical manifestation, is caused by the interruption of the corticospinal fibers, which descend in the posterior limb of the internal capsule and the cerebral peduncle. Hemianopsia is the most variable feature of AChA syndrome, possibly because of the plethora of collateral vessels.5)8) 
   AChA syndrome induced by surgical clipping has been issued for many years.2)7)9) Most of these have concerned spontaneous AChA territory infarction or the experimental occlusion of this artery for Parkinsonism.5) Other causes are hypertensive atherosclerotic disease and diabetic-related vascular disease. Some authors suggested the possibility of thromboembolic event.4) Surgical operation for an internal carotid artery aneurysm also can be an important cause of AChA syndrome, and some reports have concerned this surgical complication.2)10) In terms of endovascular treatment, same vascular injury and ischemic infarct also can occur during the procedure. We report two cases of AChA syndrome occurring after an endovascular aneurysmal coiling procedure, and provide a brief discussion of AChA syndrome. 

Case Report 

Patient 1 
   A 43-year-old man was admitted with a seizure. A neurologic examination showed an alert mental status without motor or sensory impairment. A computed tomographic (CT) scan revealed an all-cisternal subarachnoid hemorrhage (SAH). On his angiogram, a large aneurysm (16 x 12mm in diameter) of the right distal internal carotid artery (ICA) was observed (Fig. 1A). Primitive posterior communicating artery (PCoA) and single AChA were noted near the aneurysmal sac. Aneurysmal coiling was performed well using 20 Guglielmi Detachable Coils (GDC, Target
®, Fremont, CA), total 382cm lengths with a microcatheter (Exelsior, Target®, Fremont, CA) in conjunction with microguidewire (Agility, soft tip, Cordis®, Miami, FL). A 5000 unit heparin mixed solution was administered intravenously. At the end of the aneurysmal coiling procedure, the AChA was not visualized and the PCoA was thrombosed on the angiogram (Fig. 1B). Immediate thrombolytic therapy using urokinase 300,000 units was taken through the intra-arterial microcatheter at the level of right distal ICA. After thrombolytics, the PCoA was recanalized, however AChA remained non-visualized after treatment. Clinically neurologic deficit, namely, left motor weakness (Grade I) and sensory loss developed after endovascular procedure (One hour later after GDC). The visual field defect of bilateral hemianopsia was also noted. After urokinase infusion (Fig. 1C), his motor and sensory deficits showed gradual improvement (Grade IV-/IV-, arm/leg) over the subsequent day. BASA 200mg was administered orally from post-GDC 1 day to discharge day. The neurologic deficits started to be improved, and the symptoms are nearly free on post-GDC 2 day. A CT scan was obtained a few weeks later revealed a low density area in the right posterior limb of the internal capsule. At the time of discharge (35 days later after GDC), the neurological deficits had completely disappeared. 

Patient 2 
   A 49-year-old man was admitted with a sudden headache. He was alert without focal neurologic deficits, but a SAH was identified on a CT scan. Cerebral angiography revealed a about 9 x 10 mm sized large aneurysm originating from the right distal ICA and diffuse vasospasm involving the right distal ICA and its distal branches (Fig. 2A). Total 6 GDC(GDC, Target
®, Fremont, CA), 78cm, and 3 Detachable Coils (Detach Coil System (DCS), CookÁ, Copenhagen, Denmark), 40cm, were used to obliterate the aneurysmal sac with a microcatheter (Exelsior, Target®, Fremont, CA) in conjunction with microguidewire(Agility, soft tip, Cordis®, Miami, FL). A 5000 unit heparin mixed solution were administered intravenously. The result was good without remaining residual aneurysmal sac on his angiogram (Fig. 2B). At the end of the procedure, papaverine 300mg was infused using an intra-arterial microcatheter to relieve the diffuse vasospasm. Postoperative angiogram showed improvement of the diffuse vasospasm of the ICA compared with the initial angiogram (Fig. 2C). However, left hemiparesis (Grade I/II-III, arm/leg) and hemisensory loss developed during the immediate postoperative period (a half hour later after GDC). Visual symptoms were absent. BASA 100mg was administered orally from post-GDC 2 day to discharge day. Symptoms are gradually improved, and the symptoms are nearly free on post-GDC 3 day, and no abnormal neurologic deficit was evident at the time of discharge (27 days later after GDC). MR images of brain obtained 3 weeks after aneurysmal coiling showed a brain infarct in the AChA territory (Fig. 2D). 

Discussion 

   Endovascular treatment of an intracranial aneurysm using a detachable coil was first introduced by Guglielmi et al. in 1991. Although endovascular treatment is an excellent modality for aneurysmal treatment, various complications can lead to serious results1). Thromboembolic events related to the use of coil embolization are relatively common complications, especially in wide-neck or large aneurysms. In the case of anterior choroidal artery (AChA) aneurysms, the diameter of artery is very small, and thus it is very difficult to perform the coiling whilst observing the relationship between the AChA and the aneurysm. Saccular aneurysms of AChA are very important clinically because they usually have a broad and thin neck and hence demand extremely careful neurosurgical treatment.5)6)10) 
   Thus, the procedure always carries the risk of parent artery occlusion and a thromboembolic event. In our cases, we thought that thromboembolic event and accompanying AChA occlusion had caused the AChA syndrome. In first case reported here, we used thrombolytics to recanalize the occluded vessel, but only the posterior communicating artery was recanalized. In the second case, we thought diffuse vasospasm was the one of cause of the thromboembolic event. We used papaverine to relieve the vasospasm, but it couldn't prevent the AChA territory infarction. 
   The AChA is located within an arcuate zone between the striatum anterolaterally and the thalamus posteromedially,8) and supplies penetrating branches from its proximal segment to the optic tract and to the medial segment of the globus pallidus.5)6) Occlusion of the cisternal segment of the AChA and/or its perforators may cause hemiparesis, ataxia, hemisensory loss, hemianopsia, and certain cognitive disorders6)8)9) In our cases, all patients showed hemiparesis, but only one patient had a visual symptom. Hemisensory loss can be caused by an abnormality of sensory radiation in the posterior limb of the internal capsule. We observed hemisensory loss in both described cases. Since the AChA is known to have rich anastomosis with the posterior communicating artery and the posterior cerebral artery, these findings may reflect the variable development of this collateral circulation.8) 
   In terms of surgical cases, progressive improvement of neurologic deficit after the development of AChA syndrome has been reported.2)7)9) Both our cases showed complete recovery of neurologic deficit at the time of discharge. We believe that this was due to fortuitous collateral vessels supply to the AChA territory. However, when symptoms appear, patients always show dense hemiparesis, and there is a possibility of symptom aggravation. Thus, due care should be exercised during the coiling procedure to avoid vascular compromise. So interventionists prevent compromise of parent artery by avoding excessive coiling and should administer thrombolytics such as urokinase and tPA to the patient or recanalize as soon as possible when thrombosis develop. 

Conclusion 

   Anterior choroidal artery (AChA) syndrome is a rare complication that can occur during the endovascular treatment of a distal ICA aneurysm. Meticulous caution is required to preserve the posterior communicating artery (PCoA), AChA, and various perforators. However, it is not easy to preserve them, especially in those with a large aneurysm. When AChA syndrome occurs, immediate treatment with thrombolytics or vasodilators and close observation of patient's clinical status are necessary. 


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