Vertebral Dissecting Aneurysms

The natural history of dissecting vertebral artery aneurysms (DVAA) is not well described; however, once the artery is ruptured with SAH, high morbidity and mortality rates have been reported (68). DVAA are often caused by a shearing injury at the origin of the meningeal branch of the VA. Indeed, one study reported that 69% of patients rebled before they reached therapy; of these, 57% rebled within 24 hr, with a mortality rate of 46.7% (69). Other investigators have shown SAH with isolated vertebrobasilar dissection to have a rebleed rate of 30% to 70% within hours to weeks, including a fatality rate of approximately 50% (70-77). A recent study of endovascular management of vertebrobasilar dissecting aneurysms found the mortality rates in a treated group to be approximately 20% and, in the untreated group, approximately 50%

(78). Thus, although these lesions are complicated and often treacherous, their high rebleed mortality rate warrants urgent aggressive management. These lesions can be complicated, requiring collaborative, often creative and innovative strategies, integrating the talents of the entire neuroscience team.

The first step in DVAA evaluation is a careful, selective 4-vessel cervicocerebral angiog-raphy to confirm abnormalities, including irregular and tapered luminal narrowing (secondary to the hematoma) with dilated segments, fusiform dilatation, ripple "wavy" dilations, delayed contrast flow/occlusion, and retention of contrast in the vessel wall or intimal flap (79). Importantly, associated multivessel dissections of the carotid or contralateral VA are found in up to two-thirds of VA dissections (80). Correlation of findings with CT and/or magnetic resonance imaging is mandatory to identify associated signs of brain stem infarct (lateral medullary syndrome), focal hematoma adjacent to the basilar artery in the prepontine cistern, or other posterior fossa abnormalities.

It is useful to review the histopathology of DVAA, because it helps to explain why aSAH can result from two different patterns of VA dissection, i.e., those isolated to the intradural V4 segment and those originating in the extradural cervical segment, extending into the intradural segment

(79). The wall of the intradural V4 segment shows thin adventitial and muscular layers, absence of external elastic lamina and thicker internal elastic lamina, as compared to the extradural cervical segment of the VA (69,75,80-83). Thus, a subadvential dissection of the cervical VA is the culprit when VA dissection is associated with localized posterior fossa aSAH.

Surgical repair of these lesions is now rarely performed. Endovascular therapy depends on the location of the lesion. Most often, this requires a deconstructive trapping procedure, sacrificing the parent vessel of the aneurysm. However, the decision to use this procedure depends upon the lesion location, configuration, dominant VA, collateral circulation, adjacent branch involvement [posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA)], anterior spinal artery, or basilar artery), time of presentation, and, if possible, results of a BTO prior to permanent occlusion of the injured vessel to simulate the effects of permanent occlusion (78). Typically, if the disrupted segment is proximal to the origin of the PICA, the VA can be occluded proximal to PICA, such that flow is maintained to PICA from the contralateral VA via retrograde filling of the distal VA. If the disrupted segment is distal to the origin of the PICA, the VA is occluded distal to the PICA, and flow is maintained to the PICA from the ipsilateral VA.

Reconstructive procedures in DVAA are rarely indicated, but parent-vessel sparing has been safely performed, with variable success, combining stents and coils (56,84-89), stent-within-a-stent (90-92), and stent-grafts (93,94 ).

It is difficult to angiograpically determine the dissected length of the injured VA. In fact, postmortem histology of the distal intracranial segment of an acute DVAA shows the wall to be primarily composed of clot (95). Thus, if reconstruction is attempted, it is important to remember that the healing process of the intradural VA is unpredictable, in part, because of the previously described normal histologic fragmentation of this segment. Furthermore, it is unknown if normal structural integrity will return. Thus, frequent imaging is warranted to monitor for interval regrowth or contained disruption (56).

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