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 7 was a 57-year-old male who was found at the base of a stairway. The patient neurologically deteriorated in the field, with decline in the GCS from 13 to 8, was intubated in the emergency department, and was admitted to the neuroscience intensive care unit. CT scans showed hemorrhagic contusions, subdural hematoma, and traumatic SAH. ICP, ptiO2, and rCBF probes, and intraparenchymal depth electrodes were placed in the right frontal lobe and continuous scalp DC/AC-EEG was monitored using Ag/AgCl-electrodes. Five SDs were observed on day 2, and elevated ICP at >40mmHg became intractable despite administration of muscle relaxants, pentobarbital, and 3% saline. Per discussions with family, a DNR-CC order was placed on day 5 and the patient was terminally extubated. Approximately 10 minutes thereafter, a slow, homogeneous DC shift was observed on intraparenchymal DC/AC-ECoG and scalp DC/AC-EEG electrodes in synchrony with the decline in oxygen saturation and PtiO2, a final ICP spike, and declining cerebral perfusion and respiratory arrest. Nonspreading depression was observed across intraparenchymal and scalp electrodes during the falling phase of ptiO2. Asystole for 20 seconds began 3 minutes later, only 13 seconds before the start of terminal SD (Fig ).