Introduction

Midbasilar artery aneurysms are defined as aneurysms that involve the basilar artery trunk below the superior cerebellar arteries and above the vertebrobasilar junction. These lesions are rare, comprising less than 1% of all aneurysm encountered in some series, and can be one of the most treacherous aneurysms to treat. Historically, these lesions were treated via surgical means with significant morbidity and mortality. With recent advances, endovascular therapy has become increasingly promising, yet controversy remains as to when to treat and the ideal treatment for these lesions.

Major controversies in decision making addressed in this chapter include:

1. 
   

   Whether or not treatment is indicated.

   
   
2. 
   

   Open versus endovascular treatment for midbasilar artery aneurysms.

   
   
3. 
   

   Management of unruptured midbasilar artery aneurysms causing mass effect and thromboembolisms.

   
   
4. 
   

   Role of flow diverters in midbasilar artery aneurysms.

Whether to Treat

The decision to treat a basilar trunk aneurysm is similar to the decision process for all intracranial aneurysms. One must weigh the natural history of a lesion, the presence and severity of symptoms, and the risk of treatment. Balancing these factors in a way that is personalized for the patient and the lesion to be treated is vital to make appropriate clinical decisions. Aneurysms of the midbasilar can present with many different symptoms including rupture with subarachnoid hemorrhage (SAH), mass effect on the brainstem or cranial nerves, and stroke due to thromboembolism ( 1 , 2, 3 in algorithm ).

As with any intracranial aneurysm, rupture of the aneurysm portends a terrible natural history and would in almost all cases necessitate treatment ( 4–10 in algorithm ). The exceptions to this might be, as with other aneurysm, cases where the patient′s likely outcome is so poor due to poor aneurysm grade, advanced age, or medical comorbidities.

The decision to treat unruptured aneurysms in this region is more nuanced. In general, asymptomatic midbasilar aneurysms thought to have a significant rupture risk per standard aneurysm criteria (size, growth on serial imaging, aggressive morphology, history of previous rupture, etc.), basilar aneurysms symptomatic due to mass effect on the brainstem or cranial nerves, and giant aneurysms presenting with ischemia and thromboembolic events should be considered for treatment ( 4–7 in algorithm ).

Anatomical Considerations

The basilar artery directly supplies the brainstem via pontine perforators and the posterior fossa via its major branches—anterior inferior cerebellar arteries (AICA), superior cerebellar arteries (SCA), and posterior cerebral arteries (PCA). The midbasilar artery is defined as the basilar artery beginning at the vertebrobasilar junction and ending at the paired SCA origins (▶ Fig. 38.1 ). It is an approximately 3 cm segment of the artery running in the median groove along the anterior surface of the pons. Some anatomical variation exists in this segment′s course with patients occasionally having quite tortuous basilar arteries. Ectasia of the midbasilar can sometimes be so extreme that it can cause compressive symptoms on paramedian structures such as cranial nerves (▶ Figs. 38.2 – 38.4 ).

This segment of the basilar artery gives rise to the paired AICAs. These course laterally from their origin at the basilar artery and provide blood supply to the lateral pons, cerebellopontine angle, and petrosal surface of the cerebellum. Additional branches originating from the midbasilar artery include a number of perforators that can be divided into two groups—median pontine branches and transverse pontine branches. The numerous median pontine branches arise from the posterior surface of the basilar and enter the pons directly. The larger and less numerous transverse pontine branches arise from the lateral basilar artery, course along the surface of the pons wrapping around the brainstem, and provide multiple perforators to the pons′s lateral regions.

The middle third of the basilar artery is one of the most surgically inaccessible locations intracranially. The selection of surgical approaches to the midbasilar artery depends heavily on individual variation of skull base anatomy and the location of the pathology in relation to the petrous bone. Many approaches have been described to this area including transpetrosal approaches, far lateral approaches and extreme lateral variations, posterior supra- and infratentorial combined approaches, and in select cases extended anterior transylvian approaches or anterior transclival approaches.

Pathophysiology/Classification

Aneurysms of the midbasilar artery can be classified in many ways. The most straightforward way when discussing a treatment algorithm is morphology—saccular versus fusiform.

Saccular aneurysms have been described at all branch points along the basilar including the AICAs and the midbasilar perforators. These tend to be true aneurysms with all layers of the vessel dysplastically expanded. Saccular aneurysms can also arise directly from the trunk of the basilar. The pathophysiology of aneurysm formation in these cases can also involve a contained dissection with the dome of the aneurysm lacking intima.

Fusiform aneurysms of the basilar trunk can be divided into dolichoectatic and dissecting aneurysms. Dolichoectatic fusiform aneurysms are the consequence of disease of an entire segment of vessel circumferentially, usually as a result of atherosclerosis. The affected vessel becomes dysplastic, tortuous, elongated, and dilated. This process can be progressive leading to neurological deficits from compression on adjacent structures, intraluminal thrombus formation and thromboembolic events or perforator infarcts, hydrocephalus from mass effect, and rupture from weakness in this wall.

Dissecting fusiform aneurysms of the basilar artery trunk, however, arise secondary to intimal damage and the creation of a false lumen along the basilar artery. This is usually related to atherosclerotic damage to the vessel but can be spontaneous or traumatic as well. The false lumen can fill with blood or clot and result in symptomatic thromboembolism, perforator infarcts, and also rupture.

Workup

Related posts:

37 Vertebral Artery Aneurysms 39 Basilar Artery Apex Aneurysms 41 Superior Cerebellar Artery Aneurysms 42 Anterior Inferior Cerebellar Artery Aneurysms 46 Dissecting Intracranial Aneurysms of the Posterior Circulation 44 Giant Aneurysms of the Posterior Circulation

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