Hypertensive Bilateral Thalamic Hemorrhage: Distribution of Ruptured Blood Vessels and Hematoma and Considerations on the Mechanism of Vascular Rupture

The ruptured blood vessels of a 57-year-old Japanese man who had died 5 days after bilateral hypertensive thalamic hemorrhage (HTH) were investigated by preparing 9 paraffin-embedded tissue blocks, all containing the hematomas. Each block was cut serially into 6-μm-thick sections. The first of every 18 sections was stained with Victoria blue and hematoxylin-eosin, the second with elastica-Goldner, and the third with phosphotungstic acid-hematoxylin. Several additional stainings, including immunostaining for α-smooth muscle actin and synaptophysin, were performed as necessary. In the large hematoma on the right, 18 cross-sections of ruptured blood vessels, comprising 12 arteries and 6 veins, were observed in the area supplied by the thalamoperforate arteries, thalamogeniculate arteries, and some of the posterior choroidal arteries. With an anteroposterior distribution, these ruptured vessels were observed in the middle third to posterior third of the thalamus, with arteries especially concentrated in the middle third. The small hematoma on the left was distributed mainly in the internal capsule. Two cross-sections of ruptured arteries, one of which had ruptured on the internal capsule side, were observed in the lateral part of the ventral posterolateral nucleus of the thalamus. In the hematomas, degeneration of medial smooth muscle cells due to arteriolosclerosis was observed in 14 cross-sections of ruptured arteries encountered, one of which showed a ruptured dissecting aneurysm. Microaneurysm or lipohyalinosis was not evident in any of them as well as the other non-ruptured arteries within the hematomas. The arteries surrounding the hematomas showed fibrinoid degeneration, lipohyalinosis, disruption of the internal elastic lamina, and degeneration and loss of smooth muscle cells in the media. Even though serial sections were examined at the rupture sites, no aneurysm-like structure was found. We concluded that HTH essentially arises from arterial wall fragility due to hypertension, and that aneurysm formation may not be essential.