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Nils Hecht, Johannes Woitzik, Jens P. Dreier and Peter Vajkoczy


Currently, reliable low-cost and noninvasive techniques to assess cerebral perfusion in the operating room are not available. The authors report on their first clinical experience with laser speckle contrast analysis (LASCA) as a complementary imaging tool for the noninvasive and dynamic assessment of cerebral blood flow (CBF) during neurovascular surgery. The purpose of this preliminary study was to address the general feasibility of LASCA in terms of handling and image quality and to provide an example of its clinical implications.


Laser speckle contrast analysis was performed in patients undergoing cerebral revascularization procedures for the treatment of hemodynamic compromise and complex aneurysms. The portable LASCA device was centered over the surgical field, and continuous 5-minute recordings of relative CBF were obtained. In the case of flow augmentation for hemodynamic compromise, CBF monitoring was performed before and after completion of the anastomosis. In the case of flow replacement for parent artery sacrifice, CBF monitoring was performed during consecutive 30-second test occlusions of the radial artery graft after proximal internal carotid artery sacrifice and the subsequent initiation of blood flow through the bypass.


In all cases, the authors achieved good visualization of relative CBF in addition to flow imaging in both the bypass graft and the cortical vasculature. During a sudden CBF decrease after test occlusion of the radial artery graft and subsequent flow initiation through the bypass, LASCA allowed immediate visualization and measurement of relative CBF in excellent spatiotemporal resolution.


In this study LASCA offered noninvasive and rapid intraoperative assessment of relative CBF, which can be used for optimizing neurovascular procedures.

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Andrew P. Carlson, C. William Shuttleworth, Sebastian Major, Coline L. Lemale, Jens P. Dreier and Jed A. Hartings

The authors report on a 57-year-old woman in whom progression to brain death occurred on day 9 after aneurysmal subarachnoid hemorrhage without evidence of significant brain edema or vasospasm. Neuromonitoring demonstrated that brain death was preceded by a series of cortical spreading depolarizations that occurred in association with progressive hypoxic episodes. The depolarizations induced final electrical silence in the cortex and ended with a terminal depolarization that persisted > 7 hours. To the authors’ knowledge, this is the first report of terminal spreading depolarization in the human brain prior to clinical brain death and major cardiopulmonary failure.

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Jens P. Dreier, Natalie Ebert, Josef Priller, Dirk Megow, Ute Lindauer, Rolf Klee, Uwe Reuter, Yoshinori Imai, Karl M. Einhäupl, Ilya Victorov and Ulrich Dirnagl

Object. The pathogenesis of delayed ischemic neurological deficits after subarachnoid hemorrhage has been related to products of hemolysis. Topical brain superfusion of artificial cerebrospinal fluid (ACSF) containing the hemolysis products K+ and hemoglobin (Hb) was previously shown to induce ischemia in rats. Superimposed on a slow vasospastic reaction, the ischemic events represent spreading depolarizations of the neuronal—glial network that trigger acute vasoconstriction. The purpose of the present study was to investigate whether such spreading ischemias in the cortex lead to brain damage.

Methods. A cranial window was implanted in 31 rats. Cerebral blood flow (CBF) was measured using laser Doppler flowmetry, and direct current (DC) potentials were recorded. The ACSF was superfused topically over the brain. Rats were assigned to five groups representing different ACSF compositions. Analyses included classic histochemical and immunohistochemical studies (glial fibrillary acidic protein and ionized calcium binding adaptor molecule) as well as a terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling assay.

Superfusion of ACSF containing Hb combined with either a high concentration of K+ (35 mmol/L, 16 animals) or a low concentration of glucose (0.8 mmol/L, four animals) reduced CBF gradually. Spreading ischemia in the cortex appeared when CBF reached 40 to 70% compared with baseline (which was deemed 100%). This spreading ischemia was characterized by a sharp negative shift in DC, which preceded a steep CBF decrease that was followed by a slow recovery (average duration 60 minutes). In 12 of the surviving 14 animals widespread cortical infarction was observed at the site of the cranial window and neighboring areas in contrast to findings in the three control groups (11 animals).

Conclusions. The authors conclude that subarachnoid Hb combined with either a high K+ or a low glucose concentration leads to widespread necrosis of the cortex.