Artikel
Spatiotemporal propagation of spreading depolarization on the human cerebral cortex after malignant hemispheric stroke
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Veröffentlicht: | 4. Juni 2012 |
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Objective: Experimental evidence suggests that spreading depolarization (SD) is a key-phenomenon for infarct progression. Its recent detection after human brain damage in high incidence and in association with poor outcome has gained much attention. However, little is known about the spatiotemporal propagation of spreading depolarization over the human cortex and its impact on progressive brain damage.
Methods: In the present study we used laser speckle technology to intraoperatively monitor the spatiotemporal propagation of SDs in patients with malignant hemispheric stroke undergoing hemicraniectomy. We characterized the type of cerebral blood flow alterations and investigated associated changes of the intrinsic optical signal. During the postoperative period, we recorded SDs by subdural electrocorticography and assessed infarct progression by serial magnetic resonance imaging.
Results: In 7 of 20 patients 19 spreading depolarizations were observed with up to 5 in a single patient during a 20-minute period. The propagation area ranged from 0.1 to 4.8 cm2 and the propagation velocity from 1.7 to 9.2 mm/min. Thirteen SDs were associated with an increase of cerebral blood flow, 4 with a decreased and 2 with a biphasic response. During the postoperative period, frequent SDs were assessed by electrocorticography. The mean stroke volume determined by the MRI directly after surgery was 281 ± 68 cm3. Two patients had no infarct progression while in the remaining patient, a median infarct progression of 28 cm3 (range 12 to 48 cm3) occurred.
Conclusions: We present the first study describing spatiotemporal changes of cerebral blood flow associated with SDs in patients with malignant hemispheric stroke. In contrast to experimental findings that observed larger SDs more or less propagating over the entire hemisphere, we found multiple rather small SDs with both hyper- and hypoemic blood flow responses. The data suggests involvement of SD in delayed infarct maturation.