Diagnosis of cerebrovascular diseases by 3.0 T magnetic resonance susceptibility-weighted imaging

Abstract

Objective To investigate the effect of using 3.0 T magnetic resonance susceptibility-weighted imaging (SWI) in the diagnosis of cerebrovascular diseases. Methods A total of 261 patients with cerebrovascular diseases admitted to our hospital between January 2017 and January 2019 were included in the study, including 69 of cerebral infarction, 78 of cerebrovascular malformation, 11 of moyamoya disease, 54 of cerebral hemorrhage and 49 of cerebral hemangioma. All patients underwent T1WI, T2WI and SWI imaging. The SWI features of cerebrovascular abnormalities, cerebral infarction, spontaneous and traumatic cerebral hemorrhage were analyzed. The results of T1WI, T2WI and SWI cavernous hemangioma were compared. Results All 89 patients with cerebrovascular abnormalities were confirmed by surgery or clinical data. There were 78 cases of vascular malformations, including 50 of cavernous hemangioma, with a total of 163 lesions; 23 of arterial malformations (including 2 of multiple lesions) , with a total of 6 lesions; 5 of venous malformations (including 3 of temporal lobe disease and 2 of cingulate gyrus disease) . The remaining 11 cases were Moyamoya disease. There were 69 cases of cerebral infarction. Acute non-hemorrhagic cerebral infarction showed slightly long signals on T1WI and T2WI, or peripheral edema. Acute hemorrhagic cerebral infarction showed equal or low signal on T2WI, but there was no significant change on T1WI. Old cerebral infarction caused by cystic changes or softening of infarction location showed long signals on T1WI and T2WI. Acute infarction showed high signal on SWI, old infarction showed slightly low or equal signal, and those with hemorrhage showed low signal. Acute and hyperacute cerebral hemorrhage showed no abnormal signal or low signal on T1WI, low signal on T2WI, and no obvious peripheral edema. In the subacute phase, T1WI and T2WI showed high signals and peripheral edema. In the chronic phase, there was a linear low signal ring between the hematoma and peripheral edema, which was caused by hemosiderin aggregation. The hematoma showed long signals on T1WI and T2WI, and no peripheral edema. The detection rate of SWI in the hyperacute phase of cerebral hemorrhage was 100% (12/12) . In subacute and chronic phase of cerebral hemorrhage, the detection rates of SWI, T1WI and T2WI reached to 100%. Conclusion 3.0 T magnetic resonance SWI clearly shows vascular lesions and missed lesions in routine sequences, which may provide more data support for clinical differential diagnosis. Key words: 3.0 T magnetic resonance susceptibility-weighted imaging; Cerebral vascular malformation; Cerebral infarction; Cerebral hemorrhage