Mechanism of @entity1188 in @entity1779 on XXXX .

@entity1 @entity1851 @entity32 @entity64 @entity353 @entity1188 @entity731 @entity1779 @entity385
Acute @entity1188 in @entity1779 (AMIMC) are thought to suggest the presence of cardioembolic sources or systemic hypercoagulopathy. However, the mechanism and the simultaneous occurrence of AMIMC are not well known. We reviewed 685 consecutive acute @entity385 @entity1 who underwent @entity353 ( @entity353 ) within 48 hours of onset. AMIMC was defined as multiple acute @entity353 lesions distributed in more than one cerebral circulation (i.e., 2 anterior and 1 posterior circulations). Signal intensities on apparent diffusion coefficient (ADC) maps corresponding to acute @entity353 lesions were classified as 'low', 'iso-' or 'high' signals. Blood markers obtained within 24 hours after admission were compared between @entity1 with and without AMIMC. Sixty-seven (9.8%) @entity1 had AMIMC. Frequency of cardioembolism in AMIMC @entity1 was only 29.9% (20/67), which was not different from non-AMIMC @entity1 (21.7%, p = 0.16). Large-artery @entity731 (LAA) or small-vessel occlusion (SVO) in multiple circulations or combined LAA and SVO were identified in 34.3% (23/ 67) of AMIMC @entity1 , although pure LAA and pure SVO were less frequent than in non-AMIMC @entity1 . ADC signals were purely 'low' in 38 (56.7%) and 'mixed' (low with iso- or high) in 29 (43.3%). Cardioembolism tended to be associated with 'low' ADC signals (75.0%) compared with other @entity64 mechanisms (48.9%; p = 0.062). @entity1851 was higher in AMIMC than in non- AMIMC @entity1 (p = 0.009). @entity64 mechanisms responsible for AMIMC are heterogeneous. ADC findings suggest that AMIMC commonly occur stepwise and may be useful in determining @entity64 mechanism. Systemic @entity32 may be associated with the pathogenesis of AMIMC.
