Patient 3, a 78-year-old woman, showed large bifrontal ICH in addition to aSAH. She had 12 SDs on days 2 and 3, and 1 on day 10. One SD was a spreading convulsion. The others were classified as spreading depressions. The PTDDD was 144.1 minutes and occurred on day 2. Her past medical history was significant for liver cirrhosis of unknown etiology. During her clinical course, she developed a hepatorenal syndrome with progressive failure of liver, kidneys, lungs, and circulation. A family discussion was held and a DNR-CC order was activated followed by terminal extubation on day 11. As shown in Figure A, the ECoG showed a deviation from the 2 previous cases because the terminal SD started in electrode 3 at 7 minutes before the circulatory arrest. In this moment, spontaneous brain activity was still present. Accordingly, the terminal SD induced spreading depression at electrode 3. From electrode 3, the SD spread to the other electrodes. Finally, nonspreading depression rendered the remaining spontaneous brain activity isoelectric while the terminal SD was still propagating. Presumably, the last SD originated from the rim of the previous ICH. The circulatory arrest then converted this SD into a terminal one.
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.