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PubMed2004

Bithalamic infarcts: embolism of the top of basilar artery or deep cerebral venous thrombosis?

Bithalamic infarcts are usually attributed to thromboembolism of the top of the basilar artery. However, in some cases, deep cerebral venous thrombosis and thrombosis of cerebral venous sinuses was proved to be the cause. The case of a 47-year-old female with ischemic thalamic and mesencephalic lesions is reported, that was attributed to thrombosis of internal cerebral veins. In cases of bithalamic infarcts, apart from the top of the basilar artery syndrome, deep cerebral venous thrombosis should be taken into consideration. Neuroimaging findings such as generalized cerebral edema, multiple infarcts or hemorrhages, hyperdense appearance of cerebral sinuses or veins and filling defects in the cerebral venous sinuses in contrast-CCT, can lead to the proper diagnosis.

Basilar Artery↗
PubMedDate not supplied

The effect of intravenous tissue-type plasminogen activator in a rat model of embolic cerebral ischemia.

Thrombolytic agents may be useful in the treatment of cerebral ischemia caused by arterial thrombosis or embolic occlusion. A trial of intravenous human tissue-type plasminogen activator (rt-PA) was carried out in seven male Sprague-Dawley rats subjected to embolic cerebral ischemia, with eight control animals. One-hour-old autogenous blood clot was injected into the internal carotid artery. A 30-minute infusion of 10 micrograms/kg/minute of rt-PA or saline followed. Areas of ischemia at two hours post-embolization were assessed by digital image processing of serial iodo-14C-antipyrine autoradiographic images. The volumes of "no-flow" (NF) and "low-flow" (LF) regions were calculated. One animal in each group suffered no detectable ischemia; the remainder had well-defined regions of middle and posterior cerebral artery ischemia. No animal sustained a hemorrhagic lesion. Treatment produced no noticeable effect on the patency of cervical vessels. Total NF and LF volumes were less for the treated group but did not reach statistical significance by t-test. In middle cerebral distribution sections, however, LF volume was significantly less (p less than 0.05) for treated animals (150 vs. 191 mm3), primarily due to a more significant decrease in LF volume in the anterior-middle cerebral overlap zone (47 vs. 90 mm3; p less than 0.025). Fibrinogen levels were not altered by drug treatment (p greater than 0.30).

Animals↗