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Reversible Cerebral Vasoconstriction Syndrome with Cortical Subarachnoid Hemorrhage due to Acute Cortical Infarction Beneath the Sulcus:A Case Report Yuho EBATA 1 , Yutaka FUKUDA 2,3 , Hikaru NAKAMURA 1,2 , Genki CHIKAMATSU 1,2 , Eri SHIOZAKI 1,2 , Tomoya MORITSUKA 2 , Takeshi HIU 2 , Ichiro KAWAHARA 2 , Tomonori ONO 2 , Wataru HARAGUCHI 2 , Ryujiro USHIJIMA 2 , Keisuke TSUTSUMI 2 1Residency Program, Department of Neurosurgery, National Hospital Organization Nagasaki Medical Center 2Department of Neurosurgery, National Hospital Organization Nagasaki Medical Center 3Fukuda Neurosurgical Hospital Keyword: reversible cerebral vasoconstriction syndrome , RCVS , cortical subarachnoid hemorrhage , cSAH , acute cortical infarction , hemorrhagic infarction , ischemia-reperfusion injury pp.1073-1079
Published Date 2019/10/10
DOI https://doi.org/10.11477/mf.1436204076

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  • Abstract
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 We report a rare case of reversible cerebral vasoconstriction syndrome(RCVS)with cortical subarachnoid hemorrhage(cSAH)associated with a fresh cortical infarction beneath the sulcus with thick cSAH.

 A 34-year-old woman presented with history of thunderclap headache. She was transferred to our hospital for further examination of a cSAH in the left frontal lobe. Results of the cerebrospinal fluid examination were unremarkable, but three-dimensional rotational angiography revealed multiple instances of narrowing of the cortical branches of the anterior and middle cerebral arteries, suggesting the diagnosis of RCVS. Diffusion weighted imaging(DWI)demonstrated a small cortical area with high-signal intensity around the sulcus , where a thick cSAH clot was observed. This cortical lesion appeared as low-signal intensity on the apparent diffusion coefficient maps, and the follow-up T2-weighted images(obtained 3 months after onset)demonstrated a residual lesion that was smaller than the initial DWI abnormality with high-signal intensity;thus indicating the presence of a coincident fresh cortical infarction. The position of the infarct next to the thickest portion of cSAH suggested that it was the bleeding source of the cSAH. Ten days after onset, the cerebral blood flow and volume in the cortex around the cSAH increased as compared to the same area on the contralateral side.

 These findings suggested that at least one of the bleeding mechanisms of the cSAH was related to the hemorrhagic infarction or subpial hemorrhage resulting from the “ischemia-reperfusion injury” due to the acute disturbance of the pial vessel microcirculation with subsequent rapid resolution of the blood flow during the early phases of RCVS. These dynamics could not be demonstrated with contemporary angiographic imaging.


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電子版ISSN 1882-1251 印刷版ISSN 0301-2603 医学書院

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