Patient 2 was a 56-year-old woman with aSAH. ICP increased up to 25mmHg despite EVD, artificial ventilation, and analgosedation. She became hemodynamically unstable and required intravenous noradrenaline at a rate of 0.56 µg/kg/min. ECoG and LDF displayed 5 SDs, which induced spreading depressions of activity, spreading ischemias of up to 190-second duration (Fig A), and spreading suppressions of low-frequency vascular fluctuations. Spreading ischemia concurred with disturbed autoregulation similar to a previous report. Accordingly, ptiO2 seemed to follow the fluctuations of mean arterial pressure (MAP). The PTDDD was 102.3 minutes and occurred on day 1.\nIn addition to a large intracerebral hemorrhage (ICH) in the right temporal lobe, magnetic resonance imaging (MRI) on day 1 revealed large infarcts in the territories of both anterior cerebral arteries, the right MCA, and both posterior cerebral arteries, as well as lacunar infarcts in right thalamus and pons. On day 2, a family discussion was held and a DNR-CC order was activated. The patient was terminally extubated. Figure B shows the nonspreading depression of activity during the falling phase of ptiO2. A very slow, homogeneous DC positivity started simultaneously with the drop in ptiO2. Superimposed on this DC positivity, the terminal SD then started at electrode 3.
Patient 4, a 63-year-old man with previous myocardial infarction, hypertension, and diabetes mellitus, suffered from a CT-proven infarct of the complete right MCA territory. Decompressive hemicraniectomy was performed 37 hours after onset of the left-sided hemiparesis. On day 4, MRI additionally revealed infarcts in the vascular territories of the left MCA and right posterior inferior cerebellar artery as well as both cerebellar hemispheres. No SDs were recorded before the terminal one. A family discussion was held and a DNR-CC order was activated followed by terminal extubation on day 5. Figure B shows the nonspreading depression of activity during the falling phase of ptiO2. A very slow, homogeneous DC positivity started simultaneously with the drop in ptiO2. Superimposed on this DC positivity, the terminal SD then started at electrode 3.