Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add filters








Language
Year range
1.
Chinese Journal of Nervous and Mental Diseases ; (12): 488-492, 2016.
Article in Chinese | WPRIM | ID: wpr-502892

ABSTRACT

Objective To investigate the clinical features and TCD-detected microembolic signals in patients with hypercoagulability related multiple acute cerebral infarcts within non-single arterial territories, and to explore the possi?ble underlying mechanisms. Methods A retrospective review was conducted on all clinical, laboratory, radiological and TCD monitoring records from patients with hypercoagulability related multiple acute cerebral infarcts within non-single arterial territories, who admitted to the neurology department in our hospital. Results The data from twenty-two cases were finally included in this study. All patients presented with acute-onset localized neurological dysfunction, e.g. hemi?paresis, aphasia, hemiparesthesia, dysarthria, hemianopsia and cortical blindness. Their hypercoagulability related diseas?es included 10 cases of systemic malignancy, 5 moderate to severe hyperhomocystynemia (HCY>50μmol/L), 2 nephrot?ic syndrome, 2 antiphospholipid syndrome, 1 ulcerative colitis, 1 polycythemia vera,1 paroxysmal nocturnal hemoglobin?uria. In 18 cases, the hypercoagulability related diseases were diagnosed after their initial stroke onset. DWI showed mul?tiple disseminated acute cerebral infarcts in non-single arterial territories involving bilateral anterior or anterior plus pos?terior cerebral circulation simultaneously. Foci involved lobar cortex/subcortex of cerebral hemisphere in 22 cases, deep cerebral hemisphere in 12 cases, cerebellum foci in 10 cases,brainstem foci in 2 cases. TCD revealed microembolic sig? nals in ten of 22 patients monitored. Conclusions Patients with multiple acute cerebral infarcts involving non-single arte?rial territories, should be screened for hypercoagulability as in that hypercoagulability and microembolism might be in?volved in the etiology of cerebral infarction.

SELECTION OF CITATIONS
SEARCH DETAIL