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Open access

Development and natural course of lateral posterior choroidal artery aneurysms arising from fragile choroidal collaterals in moyamoya disease: illustrative cases

Tomoaki Suzuki, Hitoshi Hasegawa, Kouichirou Okamoto, Kazuhiro Ando, Kohei Shibuya, Haruhiko Takahashi, Shoji Saito, Makoto Oishi, and Yukihiko Fujii

BACKGROUND

Choroidal collaterals are a risk factor for hemorrhagic stroke, even in the nonhemorrhagic hemisphere, among patients with moyamoya disease (MMD). Peripheral choroidal aneurysms rupture in fragile collaterals; however, the development and natural course of these aneurysms remain elusive.

OBSERVATIONS

A 51-year-old woman, who had experienced a right cerebral hemorrhage 3 years earlier, presented with asymptomatic minor bleeding from a left lateral choroidal artery aneurysm in a predeveloped choroidal anastomosis. Although the aneurysm spontaneously thrombosed within 2 months, the choroidal collaterals persisted. After bypass surgery, the choroidal anastomosis regressed, and neither a de novo aneurysm nor a hemorrhagic stroke occurred. A 75-year-old woman with MMD, who had experienced a left frontal infarction 6 years earlier, experienced recurrent right intraventricular hemorrhage from a ruptured lateral choroidal artery aneurysm that developed in the choroidal anastomosis. The aneurysm spontaneously regressed 3 days after the rebleeding with no recurrence over the following 7 years.

LESSONS

Choroidal artery aneurysms may develop in the choroidal anastomosis and rupture in the nonsurgical or contralateral hemispheres. Patients with MMD who have a history of hemorrhagic or ischemic stroke and impaired cerebral blood flow require careful observation. Although aneurysms may rapidly regress spontaneously, bypass surgery can stabilize hemodynamic stress and prevent further hemorrhage.

Open access

Repeated cerebellar infarction in the affected nondominant vertebral artery distribution with reversible vertebral artery occlusion elicited by head tilt: illustrative case

Takanori Nozawa, Kouichirou Okamoto, Shinji Nakazato, Kunio Motohashi, Tomoaki Suzuki, Kotaro Morita, Hideki Tashi, Kei Watanabe, Hitoshi Hasegawa, Masato Watanabe, Hiroyuki Kawashima, and Yukihiko Fujii

BACKGROUND

Bow hunter’s syndrome or stroke (BHS) is characterized by rotational vertebrobasilar insufficiency elicited by rotation of the neck. It is caused by dynamic and reversible occlusion of the vertebral artery (VA). Reversible symptoms of rotational vertebrobasilar insufficiency are described as bow hunter’s syndrome, although brain infarction is rarely reported as bow hunter’s stroke.

OBSERVATIONS

A 70-year-old man experienced repeated cerebellar infarctions three times in the posterior inferior cerebellar artery (PICA) distribution of the nondominant right VA connecting the basilar artery. The onset of symptoms indicating cerebellar infarcts and the patient’s head position changes were unrelated. Dynamic digital angiography (DA) revealed that the nondominant right VA was occluded by an osteophyte from the C4 vertebral body, and the right PICA branches were shown to be passing through the distal right VA from the left VA. These findings were observed when the patient’s head was tilted to the right. An arterio-arterial embolic mechanism was suggested as the cause of repeated cerebellar infarctions.

LESSONS

Transient nondominant VA occlusion has been rarely reported as a cause of BHS when the head is tilted. To confirm the diagnosis of BHS, additional head tilt is recommended when performing dynamic DA in patients with a cervical osteophyte.