PMC9479518_01
On admission, the expansion of the left chronic subdural hematoma was observed (b), compared to the finding 2 years before (a). Diffusion-weighted images showed the left watershed infarction between the anterior and middle cerebral arteries (c), which was resulted from the severe left carotid stenosis (d) with a T1 hyperintense plaque (e; arrowhead). Note that the contralateral carotid artery was also highly stenotic in the same degree. Intracranial large-vessel stenosis or occlusion was not present (f).
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Head computed tomography showed the expansion of the left CSDH over 2 years [Figures 1a and b]. Magnetic resonance (MR) imaging revealed multiple brain infarctions in the left cortical border zone between the anterior and middle cerebral arteries [Figure 1c]. Subsequent MR angiography demonstrated the severe stenosis with an unstable plaque in the bilateral cervical internal carotid artery (ICA) (85% in the left, North American Symptomatic Carotid Endarterectomy Trial method), to which the brain infarctions were attributed [Figures 1d-f].
After the evacuation of chronic subdural hematoma (CSDH), the left middle meningeal artery (MMA) embolization was conducted. Angiography showed stains of the hematoma membrane and two frontal branches of the MMA were identified as feeders: one running anteriorly (1) and another superiorly (2). The former was embolized with platinum coils since the anastomosis to the internal carotid artery (ICA) through the ophthalmic artery was present (a), whereas the latter was treated with n-butyl-2-cyanoacrylate (b). The stains completely disappeared after embolization (c). Afterward, the left CAS was performed using a distal balloon protection device (d and e). Computed tomography scans over time showed the gradual expansion of the left CSDH in 2 months since the surgical drainage (f and g).
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Furthermore, to avoid hematoma recurrence after upcoming carotid artery stenting (CAS) with long-term antiplatelet therapies, we conducted the left middle meningeal artery (MMA) embolization with platinum coils and n-butyl-2-cyanoacrylate (NBCA) 13 days after the evacuation [Figures 2a-c]. Then, 7 days after MMA embolization, the left CAS was successfully performed under dual antiplatelet therapy (DAPT) with aspirin and clopidogrel [Figures 2d and e]. The left CSDH, though still asymptomatic, gradually expanded in 2 months [Figures 2f and g].
Diffusion-weighted images on the second admission showed acute cerebral infarction in the right middle cerebral artery territory (a). Magnetic resonance angiography revealed the right internal carotid artery occlusion and collateral circulation through the anterior communicating artery (b). The emergency right carotid artery stenting was necessary the next day (c and d), resulting in the flow restoration in the right cerebral hemisphere (e).
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However, 2 months later, he presented with the left transient hemiparesis, and MR imaging on admission revealed the occlusion of the right ICA [Figures 3a and b]. The emergency right CAS was required [Figures 3c-e].