Stroke 1998 Mar;29(3):645-52
Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South Korea.
Background And Purpose: Correlation of MRI findings with various vascular pathologies has rarely been attempted in patients with lateral medullary infarction (LMI). The aim of the present study was to correlate the diverse MRI lesions with the vascular lesions seen on conventional cerebral angiography in LMI.
Methods: The subjects included 34 patients with LMI who underwent both MRI and conventional angiography. We analyzed the risk factors, clinical features, MRI findings, and angiography results. The size of the infarction was also measured. We attempted to correlate the MRI findings with the vascular lesions shown in the angiograms.
Results: Presumed causes for infarction were atherothrombosis in 19 patients, arterial dissection in 8, cardiogenic embolism in 3, moyamoya disease in 1, small-vessel disease in 1, and embolism of unknown source in 2. Isolated posterior inferior cerebellar artery (PICA) disease (n = 8) was usually associated with atherothrombosis and correlated with thin, round, or diagonal band-shaped lesions in the lateral-superficial area of the caudal medulla and/or dorsolateral portion of the rostral-middle medulla. Short-segment distal vertebral artery (VA) disease (n = 9) was usually due to atherothrombosis and correlated with small lateral caudal and/or medium-sized, diagonal band-shaped rostral-middle medullary lesions. There were 13 patients with long-segment VA disease sparing (n = 8) or involving (n = 5) the proximal part of the VA with concomitant occlusion of the PICA in 7 patients. This vascular lesion produced either large MRI lesions extending ventrally (n = 5; 4 were associated with VA dissection) or small lesions mimicking those produced by isolated PICA disease (n = 8; 6 were associated with atherothrombosis and 1 patient had moyamoya disease). These large MRI lesions characteristically produced bilateral or contralateral trigeminal sensory involvement. Normal angiogram (n = 4; 3 patients were presumed to have cardiac embolism, one lesion was associated with small-vessel infarction) was associated with small, round lesions that produced minor and fragmentary symptoms. Among these subgroups, the size of the infarct in the patients with long-segment VA disease due to dissection was significantly larger than that of the patients with other vascular lesions.
Conclusions: Our data suggest that the heterogeneous MRI lesions (and consequent clinical syndromes) of LMI are correlated with diverse angiographic findings, which in turn are due to different pathogenic mechanisms: etiology, location and size of the involved vessels, speed of the lesion development, and status of collateral channels. Generally, infarcts related to multiple vessel involvement, dissection, and poor collateral circulation are larger than those associated with single-vessel disease, long-standing atherothrombosis/cardiac embolism, and good collateralization.