Watershed infarction on computed tomographic scan. An unreliable sign of hemodynamic stroke.

We identified three patients with computed tomography-defined infarctions that were partly or exclusively located in watershed territories; clinical evaluation and cerebral angiography suggested that the infarcts were of embolic origin. In two patients, arteriography demonstrated minimal carotid plaque without evidence of significant stenosis. The third patient did have high-grade stenosis of the petrous portion of the ipsilateral internal carotid artery, but arteriography demonstrated a branch artery occlusion corresponding to the territory of the infarction. Although most authors suggest that watershed territory infarctions arise from hemodynamic events, cerebral embolization may be a common cause.

Transcranial Doppler ultrasonography in the determination of brain death.

Transcranial Doppler (TCD) ultrasonography was used to perform multiple examinations of 24 patients who sustained cranial injuries, 23 of whom progressed to death. In the 20 of these 23 patients for whom an adequate TCD signal could be obtained, a characteristic reverberating wave form pattern was observed, with an associated net flow velocity of less than 10 cm/sec in all cases. In the last patient in our study group, a reverberating pattern was also identified, however, a net flow velocity of greater than 20 cm/sec was associated with functional recovery. Correlations of neurological function, TCD tracings, and net flow velocities permitted identification of characteristic hemodynamic changes that preceded cerebral circulatory arrest. Early changes included decreased flow velocity as well as an increase in pulse pressure. Late changes consisted of a persistent increase of pulse pressure with the appearance of retrograde flow velocities during diastole. In the end stage, complete diastolic retrograde flow velocities were found. These gave rise to the characteristic reverberating pattern mentioned earlier. Identification of flow velocity reversal alone, however, proved to be inadequate for making the diagnosis of brain death. Evaluation of net flow velocity (calculated at bedside) was found to be a more sensitive determinant of brain death and closely paralleled the patients' neurological function.

Transcranial Doppler monitoring of cerebral flow velocities during surgical occlusion of the carotid artery.

Transcranial Doppler (TCD) was used to assess collateral flow and to quantitate perfusion velocity changes in a group of 18 patients requiring temporary or permanent surgical occlusion of the internal carotid artery for treatment of their cerebrovascular lesions. Velocity measurements were correlated with times of occlusion and neurological outcome in order to assess safe vessel occlusion times and the need for an intraoperative shunt. These data were used to calculate a perfusion velocity index (PVi), which indicated that values greater than 2 were well tolerated, and values of less than 1 were associated with ischemic signs. In addition, preoperative TCD examinations were combined with compressive maneuvers of the carotid artery in the neck to evaluate the feasibility of carotid clamp ligation for the treatment of giant intracranial aneurysms deemed unsuitable for direct clipping. When maintenance of neurological function and intracranial vessel flow velocities were found to be normal, with aneurysmal flow velocities of zero, ligation of the carotid artery could safely be undertaken. Finally, TCD allowed continuous surveillance of cerebral hemodynamics, which gave immediate assurance of postoperative ICA patency, as well as the ability to identify high velocity states associated with hyperperfusion syndromes, which occurred in two patients.

A method for evaluation of brain tumor growth using implantable diffusion chambers.

Major drawbacks associated with in vitro assays for sensitivity of brain tumors to specific chemotherapeutic drugs include uncertainty of end-point validity, the need for large tissue samples, and cost. Furthermore, these assays do not address the question of conversion of the drug to active moeities by metabolic pathways in the host or alteration of drug activity by binding to plasma protein. We propose to develop a technique for growth and quantitation of tumor cells in small-pore diffusion chambers that contain the tumor cells and protect them from the immune system of the immunologically unrelated host. These chambers, fabricated from acrylic rings and membranes of 0.22 microns pore size, are sterilized, filled with a precisely quantitated inoculum of tumor cells, and implanted in the peritoneal cavity of rats. Replication of the cells is determined by enzymatic digestion of the supporting matrix of the cells within the chamber and counting the single cell suspension with a hemocytometer or automated cell counter. Precise comparison can thus be made between different drugs regarding their effect on cell growth in the host. This assay can be performed with the basic equipment and personnel available in most cell culture laboratories and requires a small number of tumor cells. Mass production of the diffusion chambers may make the assay less costly and faster than assays that do not involve exposure of tumor to drug in a living host. In addition, the assay should permit screening of new chemotherapeutic agents against human tumors under physiologic conditions.