We present a series of dissecting PCA aneurysms from a single center that were treated with endovascular techniques. We describe the clinical and angiographic presentation, treatment technique, and outcomes. To our knowledge only few cases of dissecting PCA aneurysms have been described in the literature with the largest series by Lv et al. (2009
). In our case series, we have described the clinical presentations and the treatment approach that may help in deciding the optimal endovascular technique and the long-term follow-up of patients with ruptured or unruptured dissecting PCA aneurysms. Our study carries all the drawbacks of a retrospective review.
The exact definition of dissecting aneurysms is not described in the literature. They are mostly reported based on the author’s consensus of their angiographic appearance that has been described as “pearl and string” or “blow out.” The natural history of these aneurysms is also not well known. In few case reports patients were followed without any surgical or endovascular intervention and had no complications. The true incidence of risk of initial bleed or re-bleed cannot be ascertained.
The most common presentation in our case series was SAH (six out of seven) secondary to aneurysmal rupture presenting with headache and focal neurological deficits corresponding to the vascular territory of the PCA. Only one patient presented with ischemic stroke without SAH. Ischemic stroke presentation of the dissecting PCA aneurysm is infrequent in this series in line with other reported case series. Of the cases that are reported in literature 54% presented with SAH, 25% with focal neurological deficits without SAH and in 21% aneurysms were discovered incidentally (Berger and Wilson, 1984
; Pozzati et al., 1991
; Lazinski et al., 2000
; Ciceri et al., 2001
; Kiazawa et al., 2001
; Hamada et al., 2005
; Vilela and Guolao, 2006
; Nistri et al., 2007
; Renard and Milhaud, 2007
; Lv et al., 2009
; Oran et al., 2009
; Chang et al., 2010
; Maillo et al., 1991
; Hallacq et al., 2002
Most of the patients were of younger age group suggesting that these aneurysms have different etiology than a traditional saccular aneurysm. Only one patient had typical risk factors for aneurysm including hypertension and smoking. Various etiologies are suggested including infectious (syphilis, mycotic), migraine, cystic medial necrosis, fibromuscular dysplasia, homocysteinuria, mixed connective tissue disease, and trauma (Hamada et al., 2005
). There was no significant recent or remote trauma in any patient, although two of the patients had a coughing or sneezing episode before developing the headache, supporting the hypothesis of predisposition to dissection. One of the patients who presented with SAH had multiple spontaneous vessels dissection including one vertebral artery and one ICA in addition to the PCA. Almost all the aneurysm occurred in the region of P2/P3 segment, this particular part of the PCA traverses across the tentorium cerebri coursing supra-tentorialy. Stress on the vessel wall along the edges of tentorium is one possible theory to explain the development of the dissecting PCA aneurysm (Drake et al., 1996
). Concomitant vasculopathies like Moya Moya or AVM are reported to be present in some cases of intracranial dissecting aneurysms suggesting their development is both flow and development related. Berger and Wilson (1984
) in their review of dissecting intracranial aneurysm discussed the difference between the intracranial and extra-cranial dissections. The extra-cranial dissections develop between the media and adventitia layers of vessel wall while the intracranial dissections are mostly present between the intimal and media layers and are surrounded by normal adventitia. The reason for this difference is not known but suggests that a small tear in the intima, especially at the branching points can be a trigger to intracranial vascular dissections and subsequent aneurysm malformation. We noted that the majority of our patients had an enlarged P-comm, whether this contribute to high flow in the PCA territory and had role in the development of the aneurysm is unknown. Other authors have contributed these aneurysms to high flow states that in some instances is related to associated AVM’s (Ciceri et al., 2001
Although treatment of dissecting aneurysms without obliteration of parent artery has been described for aneurysms other than PCA (Lempert et al., 1998
), rarely this approach has been done for dissecting PCA aneurysm. We attempted this approach on four of the patients without sacrificing the parent artery. Neuroform™ (Boston Scientific, Natick, MA, USA) stents were used in three patients (1, 2, and 7) when crossing the aneurysm was felt to be technically feasible in order to attempt the stent-assisted coiling. In one of the patients; the PCA was supplying the dissected and occluded ICA via the P-comm and the P1 had to be preserved. The fourth patient had a very large blowout aneurysm with ability to reconstruct the artery with complex shape coils only without the need of stent.
In one case series of open surgical clipping, the aneurysm was wrapped to avoid closure of the artery. No other case series attempted in preserving the artery. Chang et al. presented 14 cases of PAO followed by occipital to PCA bypass. This was associated with significant procedural morbidity and caution was advised using this approach (Chang et al., 2010
It seems feasible to save the PCA with stent-assisted coiling if potential deficits with sacrifice are of concerns especially in a young patient that could be deprive of driving. However, the durability and safety of artery saving technique cannot be ascertained with this small series. Even in our experience of four cases that were initially had no parent artery occlusion, no re-bleeding occurred, however two of them required retreatment (50%). First one, later required occlusion of the artery due to regrowth and expansion of the aneurysm, and the second one required recoiling.
It is likely that the definitive endovascular approach to treat these aneurysms is to occlude the parent artery if the aneurysm is distal to the P2 segment. However, it is feasible and technically possible to treat without occluding the artery, if a large deficit is expected from such occlusion, or progression of thrombus to the basilar tip is of a concern. A PCA balloon test occlusion may predict deficits due to artery sacrifice; however, technical difficulty in tracking the balloon must be weighed against the benefit of the test occlusion. Only few of the reported case series described using a PCA balloon occlusion test (Hallacq et al., 2002
In our case series the final and ultimate treatment was parent artery occlusion in four out of seven (one initially had stent-assisted coiling and later complete occlusion was required), coiling only in one case and stent-assisted coiling two out of seven cases. In our cases treated with parent artery occlusion (four out of seven) none of them developed new neurological deficit following the procedure or on discharge. Although this is retrospective study and a neurological deficit is defined by a change in NIHSS. It does not encompass extensive battery of testing that can be performed for temporal and occipital lobes function. Previously reported case series had five post-procedure complications resulting in ischemic strokes in the territory of PCA, two of them developed hemiparesis. The series with occipital to PCA bypass was associated with significant complications from the bypass procedure that included epidural hematoma, occipital infarct/edema or angiographic failure of bypass (Chang et al., 2010
). In all these cases the parent artery was sacrificed either by surgical approach or endovascular technique. (Table summarizes the previously reported case series).
Previously reported PCA dissecting aneurysms.