Abstract
In this symposium entitled “Treatment of the Thrombosis”, the authors presented and discussed about five topics concerning the pathophysiology and management of the cerebral thromboembolism based upon 40 clinical materials and the experimental “no-reflow state” in cerebral ischemia produced by elevating intracranial pressure in dogs.
1) PATHOPHYSIOLOGY AND TREATMENT OF “ACUTE AND FATAL CEREBRAL THROMBO-EMBOLISM”: Thrombosis of the internal carotid artery and it's territory had a wide clinical spectrum ranging from TIA to a rapid fatal apoplectic stroke and it is essential to delineate three distinct clinical groups; (1) recurrent attacks with reversible neurologic deficit (2) acute apoplectic progressing stroke and (3) slowly progressing neurological deficit. Of 40 cases, there were 6 apoplectic stoke, 1 slowly progressing type and 33 with recurrent attacks. The acute apoplectic type showed that of acute intracranial space-taking lesion both in clinical and pathological pictures with fatal midbrain hemorrhage due to transtentorial herniation (Fig. 1A, 2A). Of interesting to note, an autopsy case treated with emergency decompressive craniectomy and expired one month later with multiple peptic ulcerations revealed no evidence of brain stem damage (Fig. 1B, 2B). The emergency decompression preventing the herniation proved to be a treatment of choice in cases with the “apoplectic and progressing stroke” of cerebral thrombo-embolism.
2) SOME REMARKS FOR USE OF UROKINASE AND HEPARIN IN THE TREATMENT OF CEREBRAL THROMBOEMBOLISM: Seventeen cases were treated with Urokinase with or without Heparin and the following remarks were obtained. (1) Thrombolytic therapy, to be effective, must be instituted before organized (non-soluble) thrombus and before the cerebral infarction occure, i.e. before 72 hours after the onset. (2) Coexistence of heart valve deseases, intracranial aneurysm, moderate to severe diabetes mellitus and operative wound, especially tracheostomy wound may constitute contraindication. (3) Partial occlusion-mural thrombus may be more effectively solved than complete occlusion of the artery.
3) SUPERFICIAL TEMPORAL AND MIDDLE CEREBRAL (STA-MCA) ANASTOMOSIS (Fig. 3, 4, 5): This was done in 18 cases with occlusive lesion in the carotid arterial system and the follow-up (6 to 22 months) results were reported (Table 1). Indication and contraindication of the procedure were discussed: TIA and RIND with demonstrable lesions sufficient to explain the attacks are good indication, while the acute apoplectic type is contraindication. Although severe neurological deficit is said to be contraindicated, 8 of 12 cases with moderate to severe neurlogical deficits showed limited but favorable results in our series.
4) CAROTID-VERTEBRAL ANASTOMOSIS: This anastomosis offered an additional soure of blood to the cerebral circulation in patients with vertebral artery occlusion or stenosis and was done in three cases. With 5 to 11 months follow-up, beneficial results were obtained in two cases. (as to surgical technique, refer Brain & Nerve 22: 1125∼1138, 1970)
