ENDOVASCULAR

                                   ANEURYSMS

1.Twin aneurysms

M1, M1 bifurcation, ACoM, ..

2. Tandem Aneurysms

Tandem aneurysms are rare vascular lesions that denote the presence of two or more aneurysms in close proximity to each other on the parent vessel. No particular systemic disease such as Marfan syndrome, Ehlers-Danlos syndrome or polycystic kidney disease has been associated with the development of tandem aneurysms despite their propensity for increased risk of multiple intracranial aneurysms. Tandem aneurysms present unique challenges for treatment both via surgical or endovascular strategies. Endovascular management of tandem aneurysms has traditionally been performed utilizing stent-assisted coiling when wide necked. The need for multiple catheterizations or several interventions for the treatment of separate aneurysms, and the potential need for more than a single stent based on the inter-aneurysm distance, add complexity to these procedures. We sought to assess our experience using PED for treatment of tandem intracranial aneurysms.

3.Mirror Aneurysms

Incidence of mirror aneurysms is 5-12% of overall intracranial aneurysms. Mirror aneurysms can occur in any vascular segments of the intracranial arterial system, however, it predominates in the middle cerebral artery followed by the posterior communicating artery. Intracranial mirror aneurysms are uncommon and their management is a neurosurgical challenge. Till date, the best therapeutic option for such cases is highly controversial and debated.

4.Clipped Aneurysm

During microsurgical clipping, a small metal clip is used to stop blood flow into the aneurysm. A craniotomy is performed to create an opening in the skull to reach the aneurysm in the brain. The clip is placed on the neck (opening) of the aneurysm to obstruct the flow of blood, and remains inside the brain.

5.Kissing Aneurysm

Kissing’ aneurysms were initially described and defined by Jefferson. They are special types of multiple aneurysms defined as two adjacent aneurysms arising from identical or different arteries with separate origins and partially adherent walls. Cases of ‘Kissing’ aneurysms make up <1% of all intracranial aneurysms. Due to ‘kissing’ aneurysms occurring in arteries sharing adherent walls, they may be misdiagnosed as a single aneurysm, resulting in patients undergoing the wrong treatment, which may lead to the subsequent rupture of the aneurysms. Fortunately, 96.8% of reported cases had a favourable prognosis with only one case having an unknown prognosis. ‘Kissing’ aneurysms are commonly located in the proximal of the internal carotid artery following fenestration deformity. Notably, ‘kissing’ aneurysms of bilateral distal anterior cerebral arteries (DACAs) are rare and, to date, only 3 cases of DACA ‘kissing’ aneurysms have been reported prior to the current case.

6. Blister Like

Blood blister-like aneurysms (BBAs) include arterial lesions from non-branching sites (dorsal or anterior wall) on the internal carotid artery (ICA) . Although there have been descriptions of BBAs located at other sites within the intracranial circulation , the initial and most classic definition of a BBA is restricted to the ICA. They are particularly rare, representing approximately 0.9–6.5% of all ICA aneurysms , 1% of all intracranial aneurysms,  and 0.5–2% of all ruptured aneurysms . These lesions were first described in the late 1970s , but the term “blister” was introduced in 1988 by Takashi. Patients typically present with acute subarachnoid hemorrhage (SAH), and the affected population is younger than patients with saccular aneurysms . Some authors have reported a female predominance, a right-sided ICA predominance and an association with hypertension . The classical morphology is small, hemispherical-shaped and bulging from non-branching sites on the ICA . They are typically diagnosed after a bleed because their small size allows them to be frequently missed on the first computed tomography angiogram (CTA) or even on the first digital subtraction angiogram (DSA). Special attention must be paid to the radiological evolution of a BBA after rupture because its progression to a saccular shape can be seen up to several days after the bleed.

7.   Giant Aneurysms

Giant intracranial aneurysms have always been, and remain, among the most difficult cerebrovascular lesions to treat. Surgical therapy has evolved with refinement of microsurgical technique, improvements in instrumentation, application of skull base surgical techniques, and application of anesthetic techniques like hypothermic circulatory arrest and cerebral protection. Despite these advances, combined surgical morbidity and mortality have remained in the 20% - 30% range for many years, partly due to inherent treatment risks and partly due to merciless pathological anatomy, like wide aneurysm necks, complex arterial branches, intraluminal thrombus, atherosclerotic degeneration of arterial tissues, and adherent perforating arteries. Persistent morbidity with surgical therapy and steady advances in endovascular therapy have encouraged attempts at coiling of giant aneurysms, with or without adjunctive techniques like stents or balloon assistance. In addition to coiling techniques, flow diversion and endoluminal reconstruction with devices like Pipeline have been utilized with promising early results, particularly with giant aneurysms located along petro cavernous and paraclinoid segments of the internal carotid artery (ICA), and along the basilar trunk.

8. Aneurysm presenting with cranial nerve palsies (2-3-6 etc)

Most of unruptured intracranial aneurysms (UIAs) remain asymptomatic. But, some patients with UIAs may present with cranial nerve palsy. Oculomotor nerve palsy (ONP) is a well-known symptom associated with intracranial aneurysm commonly co-existing with posterior communicating artery (P-com) aneurysm. The most common cause of secondary ONP is diabetic neuropathy, and another common cause is compression of the nerve by an intracranial aneurysm1. The incidence of ONP associated with intracranial aneurysm is reported to be about 13.8%. The possible mechanisms of

ONP secondary to intracranial aneurysm are;

1) Direct compression of oculomotor nerve by an aneurysmal mass,

2) Pulsating effect of the aneurysm,

3) Irritation by subarachnoid hemorrhage,

4) A combination of the above mechanisms

ONP caused by intracranial aneurysm compromises the patient's quality of life, and it also may be a warning sign of impending rupture of aneurysm. Thus, the unruptured intracranial aneurysm with

ONP necessitates immediate treatment measures