The annual incidence of the intracranial dissecting aneurysms is about 1 to 1.5 per 100,000. They are a well-known cause of stroke and subarachnoid hemorrhage in young and middle-aged patients .
Intracranial dissecting aneurysms have some clinical and radiological features that differentiate them from both saccular aneurysms and non-aneurysmal arterial dissections . First, the favorable outcome of arterial dissections with medical therapy alone is not observed in dissecting intracranial aneurysms, which tend to keep growing and eventually bleed. Second, ruptured dissecting aneurysms are unstable and have a tendency to re-bleed in the acute phase with up to 70% of re-bleeds in the first 24 h thus requiring urgent treatment as the mortality rate of the re-bleeding is nearly 50% . Due to its dissecting nature, wall friability can make surgical clipping difficult and even risky. On the other hand, recanalization after coiling alone is almost certain. Therefore, deconstructive modalities of treatment like trapping or parent vessel occlusion, performed either surgically or endo-vascularly, have predominated for managing those lesions, usually with good results. However, in situations in which parent artery preservation is mandatory, the use of stent-assisted techniques may be the most adequate choice .
From an angiographic perspective, many aspects in the morphology and location of an aneurysm suggest its dissecting nature: the morphology of an aneurysm being fusiform or irregular in shape, an aneurysm rapidly changing in shape or size, an aneurysm associated with focal stenosis giving the “pearl-and-string” sign, an aneurysm arising at a distal location or from an arterial segment not from the usual bifurcation points, or an aneurysm involving the whole arterial circumference .
In our study if the patient presented with ruptured intracranial dissecting aneurysm, the aim of treatment in the acute phase is to secure the patient from re-hemorrhage, so parent artery occlusion is the main line of treatment especially in presence of good collateral supply and no major branches involved. However, in presence of poor collateral supply or major branch included within the dissected segment we tend to use artery preserving techniques, either by securing the aneurysm using coils in the acute stage followed by another step of stent deployment few weeks later to avoid dual antiplatelet in the acute stage or by loading the patient with dual antiplatelet followed by stent-assisted coiling or flow diverter stent deployment.
In subacute stage, according to the location of the aneurysm and the arterial architecture we may choose either artery preserving technique or parent artery occlusion.
If the patient presented with non-ruptured dissecting aneurysm, we tend to use artery preserving technique if it is technically feasible.
The age of the patients in our study ranged from 3 months to 61 years. The mean age of the study group was (43.5 ± 12.2) years old. This shows a relative homogeneity with the mean age of intracranial dissecting aneurysm patients published in the literature being 45.6 ± 8.7 years and a peak age of onset in the 40 s .
The sex of patients whom presented with dissecting aneurysms in the literature showed a male predominance [10,11,12]. Our study showed male predominance with male to female ratio 2.8:1, among 19 patients 14 of them were males (73.7%) versus 5 were females (26.3%).
The distribution of the intracranial dissecting aneurysms in our study was 78.9% located at the posterior circulation versus 21.1% located in anterior circulation. This is similar to that reported by  Kwak et al. who also showed that the prevalence of dissecting aneurysm was 76% in the posterior circulation .
The size of the intracranial dissecting aneurysms was also assessed in our study which showed that 52.6% of lesions were small size aneurysms, 26.3% were large aneurysms and 21.1% had giant size. This is relatively matching with Lee et al.  who showed that 68% of the lesions were small sized aneurysms.
Patients with dissecting aneurysms may present by variable presentations including headache, subarachnoid hemorrhage, neurological deficit due to mass effect or stroke. The reported incidence of SAH in the literature is similar to that of our data. In our series 13 patients (68.4%) presented by SAH. Yamaura et al. reported that the incidence of SAH was 58% (206 of 357 cases) . In a study by Mizutani, 108 out of 206 patients treated during the 23 years were admitted with SAH . Also, 86 developed SAH out of 143 patients reported by Ono et al. .
Formerly, dissecting aneurysms of the intracranial carotid circulation had been known to cause cerebral infarction in young individuals. However, recent case reports have shown that dissecting aneurysm of the intracranial carotid circulation can cause subarachnoid hemorrhage. Also, Ohkuma et al.  revealed that SAH is the dominant type of presentation in the carotid circulation. This is also matching with our results as all patients of the anteriorly located dissecting aneurysm presented with SAH.
Our study showed no statistically significant difference between the different clinical presentations regarding the treatment method. This indicates that the way of endovascular treatment doesn't depend on the presentation symptoms only but also on multiple complicated overlapping factors such as the onset of presentation (e.g. SAH in acute or subacute stage), the site of the lesion (the lesion affecting main artery or small branch, whether proximally or distally located), availability of collateral circulation and vessels condition (e.g. difficult stent deployment in small tortuous vessels).
In the SAH group, 7 patients (53.8%) were treated by parent artery occlusion. Whereas 6 patients (46.2%) were treated via artery preserving technique. Three of them presented at the subacute stage and were treated by stenting (two were treated by stent assisted coiling and one was treated by telescopic stenting using 2 braided stents inducing flow diverter effect to avoid occlusion of the PICA that was arising from the dissected aneurysm of the V4 segment of the vertebral artery). The 3 other patients were treated by selective aneurysmal coiling in the acute stage that was followed by stent deployment few weeks later, to avoid immediate stenting and dual antiplatelet administration in the acute stage. (two of them were affecting the M1 segment of the MCA, so PAO would result in catastrophic outcome, the other one was PCA P2-3 segment small sized aneurysm with preserved normal arterial architecture proximal and distal to it).
Placing coils inside a dissecting aneurysmal sac is not considered alone as a long-term efficient and safe technique. In our study, the 3 patients for whom coils were deployed in the aneurysmal sac at the acute stage, were treated in another session by stent-deployment few weeks later. It was shown in the literature that selective aneurysmal coiling alone in dissecting aneurysms may lead to re-bleeding event as described by Krings and Choi  due to the weak diseased arterial wall that will lead to aneurysmal regrowth. Hence treatment of a dissecting aneurysm should be performed either by total occlusion of the dissected segment or by stent deployment across the dissected arterial segment to induce endothelialization over the stent mesh, causing healing of the arterial wall.
Among the patients in the non-SAH group; 4 patients representing 66.66% of the cases were treated by parent artery occlusion, as the aneurysmal size was giant or large, being associated with loss of the normal arterial architecture distal to the dissected segment. One patient (16.66%) was treated by artery preserving technique. One patient (16.66) had a vertebro-basilar junction dissecting aneurysm that was treated by combined technique; flow diverter stent was deployed from right vertebral artery to basilar artery then left vertebral artery was occluded distal to the origin of the left PICA to stop the in-flow filling of the aneurysm located at the junction of both vertebral arteries with the basilar artery.
Regarding the complication events in our study, among 11 patients treated with parent artery occlusion, 8 patients showed no significant disability, whereas 3 patients developed post-procedural cerebral infarction. One of them was procedure-related and the 2 other events were sequelae of vasospasm related to the initial subarachnoid hemorrhage. At 3 months follow up only 1 patient kept a mild disability (mRs = 2).
Among 7 patients managed by artery preserving techniques, 5 patients showed no significant disability, whereas 1 patient developed mild symptoms and 1 patient developed moderate disability related to the subarachnoid hemorrhage. At 3 months follow up 2 patients had a mild disability (mRs = 2).
None of our cases who were treated with stent assisted coiling or flow diverter stent showed procedure-related thromboembolic events or delayed aneurysmal rupture. No other technical adverse events occurred such as coil herniation or aneurysmal dome perforation.
Our results show that the final outcome not only depends on the method of treatment whether deconstructive or reconstructive but, it also depends on the neurological hazards related to the presenting insult which in our study was worse within the reconstructive group as some patients developed neurological deficits related to the subarachnoid hemorrhage not to the endovascular management..
Or results are almost matching with the published endovascular studies by Jin et al. , Mohammadian et al. , Li et al.  and Debette et al. . In contrast to the endovascular outcome; Kitanaka et al. reported that the long-term outcome of surgically treated lesions was somehow favorable, but there was a very high rate of postoperative neurological complications, and the major causes of disability were attributable to lower cranial nerve palsy and associated events in half of the patients with poor outcome .
Two patients showed partial aneurysmal recurrence at 6 months angiographic follow up. One of them has been treated by parent artery occlusion by coils packed inside a P2 segment dissecting aneurysm of a PCA. Despite packing the whole aneurysmally dilated segment, the dissecting aneurysm showed minimal refilling by retrograde flow from leptomeningeal collaterals to the PCA. The patient was still complaining of headache but no interventional treatment was possible as no endovascular route was amenable to reach the aneurysm again. The patient was kept for symptomatic treatment and follow up. This case showed that in case of parent artery occlusion, deploying coils inside the dissecting aneurysm with parent artery occlusion may be insufficient and it is preferrable to extend the coils to the segment of the parent artery distal to the aneurysm, to avoid back-door refilling of the dissected segment.
The other patient developed partial recurrence of the MCA aneurysm that has been initially treated by stent-assisted coiling. The follow up angiogram showed partial aneurysmal refilling within the pack of coils which necessitated another endovascular session passing the microcatheter through the stent struts to add more coils within the aneurysmal sac.