The PICA is the greatest of the branches of the vertebral artery and is the causative vessel for aneurysms in the posterior fossa, which cause cerebral infarction and cranial nerve compression in many patients. The PICA is formed by six segments and two loops. The telovelotonsillar and cortical segments are its distal parts. The bifurcation of the basilar artery and the origin of the PICA are the most common sites from which giant aneurysms arise in the vertebrobasilar system. Other locations within the posterior cranial fossa are much less common. Computed tomography reveals giant aneurysms as oval-shaped lesions with surrounding edema and, frequently, calcification. Contrast enhancement is strictly dependent on intra-aneurysmal thrombosis, but it may not be sufficient to confirm the diagnosis of the nature of the lesion, because it cannot differentiate these lesions from tumors. MRI can demonstrate a well-defined mass, with peripheral signal void rim and no contrast-enhancing components. Angiography is the most important diagnostic modality for revealing the true nature of the lesion, especially when there are no signs or symptoms of subarachnoid bleeding [
5‐
7]. This exam should scan the presence of a contralateral PICA, the collateral circulatory pattern and the dominance, that are important radiological parameters, while deciding the choice of treatment. Multiple aneurysms can develop in the PICA [
1]; they can be accompanied by arteriovenous malformations in rare cases; and they have low incidence of bleeding [
2,
3]. Giant intracranial aneurysms can be distinguished when completely thrombosed. They may escape angiographic identification when not thrombosed or partially thrombosed, which are the most common types [
4‐
6]. The symptoms of ruptured PICA aneurysms are similar to those of subarachnoid hemorrhage Most patients who have unruptured PICA aneurysms present with compressive syndrome because these malformations usually appear clinically as space-occupying lesions and may occasionally be mistaken for tumors [
4,
7]. Early aneurysm treatment is necessary in patients presenting with SAH because rebleeding rates may be as high as 78%. The ideal treatment of a saccular lesion is clipping or endovascular obliteration of the aneurysm neck with preservation of the lumen. Giant aneurysms of the distal PICA are rare: to the best of our knowledge, only 14 cases of a total of 17 surgically treated patients have been reported [
1‐
14]. Surgical treatment of these aneurysms has yielded good results [
1,
5,
8,
9,
11,
13], with clinical improvement, and only one patient died after surgery [
14] (Table
1). The surgical approach for PICA aneurysms depends on the site of occurrence. For distal PICA aneurysms, suboccipital craniotomy is preferred. A different surgical option must be considered, however, when a dissection is performed, when the neck cannot be clipped without occlusion of the parent vessel or when small arteries arising from this segment pass through the brainstem. Trapping and excision of the aneurysm, as well as arterial reconstruction, performed by direct end-to-end anastomosis or insertion of an interposed arterial graft are possible treatment options [
2,
3,
8,
9,
13,
14]. An ultrasonic aspirator should be used for debulking of thrombosed or partially thrombosed aneurysms. Intra-operative fluoroangiography and Doppler ultrasonography can be very useful modalities for visualizing exclusion of the aneurysm from the circulation. Mortality can be related more to vasospasm as a result of subarachnoid hemorrhage rather than to technical aspects of surgery [
1,
2,
4,
6,
15]. Endovascular treatment of distal PICA aneurysms with parent vessel occlusion may be an option. It has a complication rate as high as 13% due to the extremely variable and tortuous course of the PICA [
7,
9].
Table 1
Reports of giant aneurysms of distal posterior inferior cerebellar artery
a
| 1 | 50/F | PFS | Trapping | Death |
Miller and Newton, 1978 [ 7] | 1 | 61/F | PFS | NR | NR |
| 1 | 72/F | PFS | Clipping | Good |
Egashira et al., 1979 [ 6] | 1 | NR | PFS | Clipping | NR |
Osenbach et al., 1986 [ 10] | 1 | NR | Ocular bobbing | Clipping | NR |
| 2 | NR | Hemorrhage | Trapping in both cases | Good |
| 3 | 37 to 66/2 M, 1 F | NR | Proximal ligation | Good |
Dernbach et al., 1988 [ 1] | 1 | 47/M | Asymptomatic | Clipping | Good |
| 1 | 11 months/M | PFS | Clipping | Good |
Richmond and Schmidt, 1993 [ 12] | 1 | 67/M | FMS | Clipping | Good |
| 1 | 69/F | Ataxia | Clipping + anastomosis (SO) | Good |
Drake and Peerless, 1997 [ 3] | 1 | 70/F | NR | Trapping | Excellent |
| 1 | 52/M | Headache | Clipping + anastomosis (SO) | Good |
| 1 | 64/F | Headache, hemiparesis | Clipping(SO) | Good |
Present case | 1 | 74/F | Headache | Clipping(SO) | Good |