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 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 ).