J Kim1, H-Y Choi, H S Nam, J Y Lee, J H Heo. 1. Department of Neurology, National Core Research Center for Nanomedical Technology, Yonsei University College of Medicine, Seoul, Korea.
Abstract
BACKGROUND AND PURPOSE: The tuberothalamic artery (TTA), one of the arteries supplying the paramedian thalamic area, is peculiar because it originates from the posterior communicating artery (p-comA), which connects the vertebrobasilar and carotid systems. METHODS: From Stroke Registry, 23 consecutive patients with an acute infarction involving the TTA were selected. We investigated the mechanism of TTA infarction. RESULTS: Fourteen of 23 patients (61%) had coexisting infarctions outside the TTA territory (carotid in three, vertebrobasilar in seven, and both carotid and vertebrobasilar arteries in four patients). Coexisting lesions were most common in the posterior thalamoperforating arterial territory (seven patients). Eleven out of 14 patients (79%) with coexisting lesions had embolic sources from the heart or proximal atherosclerotic arteries, and cardioembolism was the most common mechanism. However, eight of the nine patients with isolated tuberothalamic lesions were classified as small vessel occlusions. More patients with embolic sources had visible p-comA or fetal-type posterior cerebral arteries. The vertebrobasilar arterial system played a more dominant role in developing tuberothalamic infarction than the carotid arterial system. CONCLUSIONS: Isolated TTA infarctions are rare and mostly because of small vessel occlusion. Patients with coexisting infarctions outside TTA territory usually have an embolic source, predominantly vertebral artery atherosclerosis.
BACKGROUND AND PURPOSE: The tuberothalamic artery (TTA), one of the arteries supplying the paramedian thalamic area, is peculiar because it originates from the posterior communicating artery (p-comA), which connects the vertebrobasilar and carotid systems. METHODS: From Stroke Registry, 23 consecutive patients with an acute infarction involving the TTA were selected. We investigated the mechanism of TTA infarction. RESULTS: Fourteen of 23 patients (61%) had coexisting infarctions outside the TTA territory (carotid in three, vertebrobasilar in seven, and both carotid and vertebrobasilar arteries in four patients). Coexisting lesions were most common in the posterior thalamoperforating arterial territory (seven patients). Eleven out of 14 patients (79%) with coexisting lesions had embolic sources from the heart or proximal atherosclerotic arteries, and cardioembolism was the most common mechanism. However, eight of the nine patients with isolated tuberothalamic lesions were classified as small vessel occlusions. More patients with embolic sources had visible p-comA or fetal-type posterior cerebral arteries. The vertebrobasilar arterial system played a more dominant role in developing tuberothalamic infarction than the carotid arterial system. CONCLUSIONS: Isolated TTA infarctions are rare and mostly because of small vessel occlusion. Patients with coexisting infarctions outside TTA territory usually have an embolic source, predominantly vertebral artery atherosclerosis.