Cerebral aneurysm

We report a rare case of posterior communicating artery occlusion mimicking a cerebral aneurysm. A 62-year-old man was admitted to Towakai Hospital with sudden onset of left motor weakness. He had developed thunderclap headache five days before. Computed tomographic scan and lumbar tap were negative for subarachnoid hemorrhage (SAH). Digital subtraction angiography and three-dimensional computed angiography showed aneurysmal protrusion at the junction of the right internal carotid (IC) artery and posterior communicating artery (PcomA). Because minor bleeding from IC-PcomA junction aneurysm was strongly suspected, a pterional craniotomy was performed. At surgery, there was no evidence of SAH but the PcomA was occluded at the peripheral portion. Several perforators arose from the proximal portion of the PcomA. An aneurysmal protrusion especially without a prominent PcomA does not always indicate an IC-PcomA aneurysm. In diagnosing protruding vascular lesions at the bifurcation between the IC-PcomA, not only infundibular dilatation but also occlusion of the PcomA should be considered if the PcomA is not visualized. [Neural Res 2003; 25: 543-545]

Keywords: Aneurysm; infundibular dilatation; posterior communicating artery

INTRODUCTION

We report a patient with occlusion of the posterior communicating artery (PcomA) who developed a sudden headache. In this patient, subarachnoid hemorrhage was ruled out by computed tomography (CT) and lumbar puncture. However, the occlusive site was the peripheral portion on cerebral angiography, and it was difficult to differentiate arterial occlusion from cerebral aneurysm.

CASE REPORT

The patient was a 62-year-old male, with a chief complaint of headache. A sudden severe headache with cold sweat occurred five days before consultation. However, the patient did not receive treatment. The patient consulted the Emergency Outpatient Unit of our hospital for incomplete paralysis of the left side and disturbance of consciousness.

Neurologically, consciousness was evaluated as level 8 according to the Glasgow Coma Scale (GCS). Disorientation for time and place as well as incomplete paralysis of the left side were noted. Cerebral CT showed only old lacunar infarction. There was no subarachnoid hemorrhage. Cerebrospinal fluid test findings were normal. Three-dimensional computed angiography (3D-CTA) and cerebral angiography revealed an aneurysm-like shadow protruding like a rod at the bifurcation between the right internal carotid artery and the PcomA (Figure 7). Therefore, we planned aneurysmal clipping by right frontotemporal craniotomy. Intra-operative findings did not show subarachnoid hemorrhage, thickening or adhesion. There was no aneurysm at the bifurcation between the right internal carotid artery and the posterior communicating artery. In the posterior cerebral artery-side lumen of the advanced posterior communicating artery, a black thrombus was detected under direct vision. The PcomA was occluded at this site, being the peripheral portion (Figure 2, intra-operative photograph). There was no dissection. The proximal lumen of the PcomA showed marked circumferential arteriosclerotic change. However, there was no enlargement or thinning detected in any region. Since a perforating branch bifurcated and showed patency, only exploration was performed.

After admission the left incomplete paralysis was improved. However, the patient was always somnolent, and enervation and apathy persisted at wakening. CT and magnetic resonance imaging (MRI) revealed right thalamic infarction. One month after admission, internal carotid arteriography showed occlusion of the posterior communicating artery. Only the peripheral portion was visualized. The patient was discharged, although disorientation, reduced initiative, and memory disorder persisted.

DISCUSSION

Takeuchi et al. reported that warning signs1-4 were observed in 48%-59% of patients with cerebral aneurysm prior to rupture, and that approximately 50% of patients developed sudden headache attacks that had not been previously experienced. The etiology is mainly classified into three types:

1. Minor bleeding (of cerebral aneurysms themselves).

2. Vascular origin related to dilatation of cerebral aneurysms themselves.

3. Ischemic lesion related to spasm or occlusion.

In particular, minor bleeding was observed in 20%-71% of cerebral aneurysms that caused major bleeding. Minor bleeding most commonly occurred 2-7 days prior to major bleeding. Many studies2,5-9 have reported that minor bleeding can be accurately diagnosed by CT and cerebrospinal fluid test. However, it has been indicated that intra-operative or angiographic findings show minor bleeding in some patients even when subarachnoid hemorrhage is ruled out by CT and cerebrospinal fluid test findings3,10.

Takeuchi et al.3 reported that cerebral aneurysms were detected in 52 of 562 patients (9.3%) with sudden headache in whom subarachnoid hemorrhage was ruled out by CT findings and lumbar puncture, and that localized subarachnoid hemorrhage was detected in 8 of 46 patients who underwent surgery. Therefore, they concluded that cerebral aneurysm should be aggressively investigated in patients with sudden headache.

In the present patient, subarachnoid hemorrhage was ruled out by CT and cerebrospinal fluid test findings. However, a sudden severe headache occurred five days before consultation, causing incomplete paralysis of the left side and consciousness disorder. Therefore, cerebral angiography was performed, considering tar dive ischemic attack and cerebral thrombus formation related to cerebrovascular convulsion following subarachnoid hemorrhage. Although neither stenosis nor occlusion was detected in the trunk artery, an aneurysm-like shadow protruding like a rod was observed at the bifurcation between the right internal carotid artery and the posterior communicating artery. Therefore, surgery was performed under a diagnosis of minor aneurysmal bleeding at the site.

Endo et al.11,12 reported surgical findings in 34 patients with protruding vascular lesions at the bifurcation between the internal carotid artery and the PcomA that did not meet the standard criteria for infundibular dilatation on cerebral angiography. Ten patients had cerebral aneurysms, while 24 patients had infundibular dilatation without wall abnormalities. In one of these patients, occlusion of the PcomA was observed. In our investigation, only Endo et al, reported that occlusion of the PcomA was visualized like an aneurysm, making differentiation difficult. In their series, they indicated that the developmental grade of the posterior communicating artery was a clue to evaluating protruding vascular lesions at this site. When the PcomA is advanced, the possibility of aneurysm or pre-state is suggested. In contrast, when the PcomA is immature, simple infundibular dilatation is suggested. This is useful for differentiating aneurysms from infundibular dilatation. However, when the PcomA is not visualized on pre-operative cerebral angiography, not only infundibular dilatation but also occlusion of the PcomA should be considered, as reported in the present patient and by Endo et al.

CONCLUSION

We report a patient with occlusion of the PcomA in whom the occlusive site was the peripheral portion on cerebral angiography and it was difficult to differentiate the lesion from cerebral aneurysm. In diagnosing protruding vascular lesions at the bifurcation between the internal carotid artery and the PcomA, not only infundibular dilatation but also occlusion of the PcomA should be considered if the PcomA is not visualized.

REFERENCES

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9 Wijdicks EFM, Kerkhoff H, van Gijin J. Long-term follow-up of 71 patients with thunderclap headache mimicking subarachnoid haemorrhage. Lancet 1988; 11: 68-70

10 Day JW, Raskin NH. Thunderclap headache: Symptom of unruptured cerebral aneurysm. Lancet 1986; II: 1247-1248

11 Endo S, Furuichi S, Takaba M, Hirashimo Y, Nishijima M, Takaku A. Clinical study of enlarged infundibular dilation of the origin of the posterior communicating artery. J Neurosurg 1995; 83: 421-425

12 Furuichi S, Endo S, Nisijima M, Takaku A. Dilated lesion at internal carotid artery posterior communicating artery junction. No Shinkei Geka 1993; 21: 605-609

Masahiro Kawanishi, Ichiro Sakaguchi and Hiroji Miyake

Department of Neurosurgery, Towakai Hospital, Osaka Medical College

Correspondence and reprint requests to: Masahiro Kawanishi, MD, Department of Neurosurgery, Ijinnkai Takeda General Hospital, 28-1, Ishidamoriminamimachi, Hushimiku, Kyoto, Japan.

[masahiro.kawanishi@nifty.ne.jp] Accepted for publication November 2002.

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