Abstract / Description of output
Background: Focal brain damage after aneurysmal subarachnoid haemorrhage (aSAH) results from intracerebral haemorrhage (ICH), and early (ECI) and delayed (DCI) cerebral ischaemia.
Aim: We investigated whether spreading depolarisation (SD) variables correlate to focal damage.
Method: Consecutive patients who required neurosurgery were enrolled in six university-hospitals from 09/2009 to 04/2018. Subdural electrodes were implanted.
Results/Conclusions: Longitudinal magnetic resonance images, and computed tomography studies, if clinically indicated, revealed that 162/180 patients developed focal damage during the first two weeks. During 4.5 years of cumulative recording, 6777 SDs occurred in 161/180 patients and 238 electrographic seizures in 14/180. Ten patients died early; 90/170 developed delayed infarction ipsilateral to the electrodes. Primary objective was to show that a 60-min cutoff for the peak total SD-induced depression duration of a recording day during delayed neuromonitoring (PTDDDdelayed) predicts delayed infarction with sensitivity >0.60 and specificity >0.80. Primary analysis was significant regarding sensitivity [ = 0.756 (95% confidence interval: 0.654–0.840), P = 0.0014] but specificity was 0.588 (0.472–0.696), i.e. lower than 0.80 (P < 0.0001). Nevertheless, the area under the receiver operating characteristic curve of PTDDDdelayed was 0.758 (0.685–0.831, P < 0.0001) for delayed infarction and 0.878 (0.814–0.941, P < 0.0001) for DCI (delayed neurological deficit and/or ipsilateral infarction). In secondary analysis, a new cutoff value of 180min indicated delayed ipsilateral infarction with a targeted sensitivity of 0.622 and specificity of 0.825, and the prespecified 60-min cutoff indicated DCI with a sensitivity of 0.740 and specificity of 0.815. The results suggest that PTDDDdelayed not only indicates impending infarction but also transitory neurological deficits.
Aim: We investigated whether spreading depolarisation (SD) variables correlate to focal damage.
Method: Consecutive patients who required neurosurgery were enrolled in six university-hospitals from 09/2009 to 04/2018. Subdural electrodes were implanted.
Results/Conclusions: Longitudinal magnetic resonance images, and computed tomography studies, if clinically indicated, revealed that 162/180 patients developed focal damage during the first two weeks. During 4.5 years of cumulative recording, 6777 SDs occurred in 161/180 patients and 238 electrographic seizures in 14/180. Ten patients died early; 90/170 developed delayed infarction ipsilateral to the electrodes. Primary objective was to show that a 60-min cutoff for the peak total SD-induced depression duration of a recording day during delayed neuromonitoring (PTDDDdelayed) predicts delayed infarction with sensitivity >0.60 and specificity >0.80. Primary analysis was significant regarding sensitivity [ = 0.756 (95% confidence interval: 0.654–0.840), P = 0.0014] but specificity was 0.588 (0.472–0.696), i.e. lower than 0.80 (P < 0.0001). Nevertheless, the area under the receiver operating characteristic curve of PTDDDdelayed was 0.758 (0.685–0.831, P < 0.0001) for delayed infarction and 0.878 (0.814–0.941, P < 0.0001) for DCI (delayed neurological deficit and/or ipsilateral infarction). In secondary analysis, a new cutoff value of 180min indicated delayed ipsilateral infarction with a targeted sensitivity of 0.622 and specificity of 0.825, and the prespecified 60-min cutoff indicated DCI with a sensitivity of 0.740 and specificity of 0.815. The results suggest that PTDDDdelayed not only indicates impending infarction but also transitory neurological deficits.
| Original language | English |
|---|---|
| Pages (from-to) | 64-64 |
| Journal | Journal of Cerebral Blood Flow and Metabolism |
| Volume | 42 |
| Issue number | 1_SUPPL |
| DOIs | |
| Publication status | Published - 29 May 2022 |