The posterior cerebral artery (PCA) is involved in approximately 30% of moyamoya disease (MMD) cases. Symptomatic PCA regression following anterior revascularization was predominantly found in children and young adults. Occipital artery-middle cerebral artery (OA-MCA) bypass can be used as one of the option for revascularization in the posterior portion of the brain. OA-MCA bypass demonstrates a several advantages over conventional OA-PCA bypass. Technical points are described in this chapter.
Keywords: moyamoya disease, OA-PCA bypass, OA-MCA bypass, posterior cerebral artery, revascularization
Occlusive lesions in the posterior cerebral artery (PCA) are observed in 26 to 43% moyamoya disease (MMD) patients at the initial diagnosis, which is associated with disease advancement and poor prognosis.1 Although majority of the patients with PCA involvement is asymptomatic, revascularization in the anterior circulation occasionally advances PCA involvement in certain patients.2 PCA regression causes several clinical issues such as follows: (1) additional PCA lesions can cause extensive cerebral ischemia beyond the territory of the PCA, (2) ischemic injury to frontoparietal connection fibers potentially impairs cognitive function, and (3) surgical treatment involves more complex procedures. Nevertheless, revascularization in the posterior portion of the brain is generally difficult. While source for blood supply through indirect procedure is limited in the posterior portion of the head, the direct anastomosis may be less competent than the superficial temporal artery-middle cerebral artery (STA-MCA) bypass. Previous literatures describe indirect methods for revascularization in the posterior half of the brain3,4 as well as occipital artery-posterioer cerebral artery (OA-PCA) bypass for the direct anastomosis in the posterior circulation.5 Alterative approach such as OA-MCA bypass is described.
We consider that anterior revascularization as the first treatment choice at the time of diagnosis, regardless of the PCA involvement. Accordingly, patients who persistently demonstrated ischemic symptoms attributable to PCA lesions or “delayed” PCA involvement following the anterior revascularization is selected as candidates for posterior revascularization. Hemodynamic compromise is evaluated such as using single-photon emission computed tomography (SPECT) and acetazolamide test. Symptomatic occlusive lesions in PCA territories were identified by their decreased cerebrovascular reserve, an avascular area on a cerebral angiogram, or hyperintense vessels on fluid-attenuated inversion recovery (FLAIR).6
OA-MCA bypass procedure is not commonly used. However, it can be effective when posterior part of the brain requires additional source of blood supply. OA-MCA bypass does not require prone position and may be effective when combined with indirect procedure. Although source of indirect procedure is limited, a large craniotomy may facilitate neovascularization from the dura matter. Pericranial flap is also available.
OA-MCA bypass can effectively alleviate recurrent ischemia due to PCA involvement.2 Furthermore, improving cerebral perfusion in the posterior portion of the brain may ultimately lead to improved revascularization in the anterior circulation territory as well.7 Furthermore, surgical revascularization in the posterior portion of the brain may not only be effective in stroke prevention, but also potentially improve cognitive outcomes by preventing ischemic injury in frontoparietal association fibers.8
Patency rate might not be comparable as in the STA-MCA bypass because of its technical difficulty.
Symptomatic PCA lesions are the target of OA-MCA bypass. Considering the symptoms as well as the distribution of cerebral infarctions, the area susceptible to ischemia due to PCA lesions is not only confined to the visual cortex, but also extends to adjacent cortices beyond the watershed zone.
Recipient artery may not be competent as to allow direct anastomosis. Indirect procedure should always be considered as an alternative of OA-MCA bypass.
OA-MCA bypass should be avoided in patients who had demonstrated delayed wound healing in anterior revascularization, as harvesting OA could cause further damage to blood flow supply the scalp.
In order to select optimal surgical candidates, multimodal neuroimaging studies are employed, which can ascribe ischemic symptoms to the advanced PCA lesions. However, there is a poor correlation between the PCA regression and the hemodynamic compromise, as detected by SPECT.9 Hyperintense vessels on FLAIR (or ivy signs) may serve as a marker for critical ischemia.10
In addition to complications due to standard craniotomy, wound necrosis as well as difficulty of direct anastomosis should be mentioned for informed consent.
Patient is placed in semi-supine position with general anesthesia.
Patient is placed in semi-supine position in revascularization via OA-MCA anastomosis. A skin incision is made along the lateral branch of the OA. The OA is then dissected from the subcutaneous tissue. The subcutaneous tissue flap is made by the periosteal and loose areolar connective tissue. The OA is anastomosed to the cortical branch of the MCA located in the parietal lobe, such as the distal segment of angular artery. The dural flaps are inverted and placed on the surface of the brain. The subcutaneous tissue flap muscle is sutured to the edge of the dura mater. (See Fig. 11.1).
It may be difficult to find competent artery for the direct anastomosis. Distal segment of angular artery may be optimal site for the anastomosis. At the distal segment of the OA, the size of the artery diminishes abruptly as the OA runs through the subcutaneous fat layer. In addition, a relatively long pedicle necessary for reaching recipient arteries would reduce the rate of long-term patency.
It is necessary to use indirect procedure when direct anastomosis is not successful. Wide craniotomy, particularly in the anterior portion, would facilitate indirect revascularization from middle meningeal artery via the transdural anastomosis.
Anterior revascularization is the first option of the treatment, even if radiological examinations indicate additional PCA involvement. We consider that prophylactic revascularization to the PCA territory may not be necessary given that majority of the PCA fall-off after the anterior revascularization remains asymptomatic. PCA involvement can be detected either at the time of initial diagnosis or in follow-up examinations, following anterior revascularization. PCA lesions progress for several years, or even a decade, after initial revascularization.2,5,11 Therefore, we consider that continuous scrutiny is neces
sary in outpatient basis in patients with a prior history of anterior revascularization.
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