Background and Purpose-In patients with subarachnoid hemorrhage, the assessment of cerebral autoregulation aids in prognosis as well as detection of vasospasm. Mx is a validated index of cerebral autoregulation based on measures of cerebral perfusion pressure and mean flow velocity on transcranial Doppler but is impractical for longer-term monitoring. Near-infrared spectroscopy is noninvasive and suitable for continuous monitoring of cerebral tissue oxygenation using the Tissue Oxygenation Index. In this study, we compared near-infrared spectroscopy-based indices of cerebral autoregulation (TOx) with Mx in patients with subarachnoid hemorrhage. Methods-Arterial blood pressure, intracranial pressure, mean flow velocity, and Tissue Oxygenation Index were recorded.Mx and TOx were calculated as moving correlation coefficients between 10-second averaged values of cerebral perfusion pressure and mean flow velocity and between cerebral perfusion pressure and Tissue Oxygenation Index. We also calculated TOxA, the moving correlation coefficient between arterial blood pressure and Tissue Oxygenation Index. Results-Fifty-one recording sessions were performed in 27 patients with subarachnoid hemorrhage with a total duration of 62.5 hours. Correlations of Mx and TOx over time varied markedly among individual recordings. However, time-averaging over the entire recording interval in each of the 51 recordings, we found correlations between Mx and TOx and between Mx and TOxA were highly significant. This correlation was even stronger after correction for multiple sampling for each patient, reaching rϭ0.81 for Mx and TOx and rϭ0.72 for Mx and TOxA. Conclusion-Near-infrared spectroscopy can be used to continuously assess cerebral autoregulation in adults after subarachnoid hemorrhage. (Stroke.

Monitoring of cerebrovascular pressure reactivity (PRx) has diagnostic and prognostic value in head-injured patients, but requires invasive monitoring of intracranial pressure (ICP). Near infrared spectroscopy (NIRS) is a noninvasive method that is suitable for continuous detection of cerebral blood volume changes. We compared a NIRS-based index of cerebrovascular reactivity, called total hemoglobin reactivity (THx), against standard measurements of PRx in a prospective observational study. Forty patients with closed-head injury were monitored daily with arterial blood pressure (ABP), ICP, and a NIRS-based total hemoglobin index. PRx and THx were calculated as the moving correlation coefficients using 5-min time windows between 10-sec averaged values of ICP and ABP, and total hemoglobin index and ABP, respectively. A total of 120 recordings were performed between the median first (IQR 0.75-2) and fourth (IQR 2-6) day after head injury, giving a total duration of 1760 hours. PRx and THx demonstrated a significant association across averaged individual recordings (r = 0.49, p < 0.0001), and across patients (r = 0.56, p = 0.0002). Assessment of optimal cerebral perfusion pressure (CPP) and ABP using THx was possible in about 50% of recordings, and showed a significant agreement with the optimal CPP and ABP assessed with PRx. THx may be of diagnostic value to optimize therapy oriented toward restoration and continuity of cerebrovascular reactivity, especially in patients for whom direct ICP monitoring is not feasible.

The pulsatile component of intracranial pressure (ICP) has been shown to be a predictor of outcome in normal pressure hydrocephalus (NPH) and traumatic brain injury (TBI). Experimental studies have demonstrated that the pulse amplitude of ICP (AMP(ICP)) is dependent on the mean ICP (mICP), and on the pulse amplitude of the cerebral arterial blood volume (AMP(CaBV)), according to the exponential craniospinal compliance curve. In this study, we compared the influence of mICP and AMP(CaBV) on AMP(ICP) in patients with NPH (infusion study) and TBI (spontaneous recording). We retrospectively analyzed 25 NPH and 43 TBI patients with continuous monitoring of ICP and cerebral blood flow velocity (CBFV), as assessed with transcranial doppler. AMP(CaBV) was extracted from the CBFV waveform. The influence of mICP and AMP(CaBV) on AMP(ICP) were determined using partial coefficients a, b, and c of the multiple regression model: AMP(ICP) = a * mICP + b * AMP(CaBV) + c. AMP(ICP) was more dependent on mICP in NPH patients than in TBI patients (partial coefficient a = 0.93 versus -0.03; p < 0.001). On the contrary, AMP(ICP) was more dependent on AMP(CaBV) in patients with TBI than in those with NPH (b = 0.86 versus 0.10; p < 0.001). This study shows that AMP(ICP) depends mostly on changes in mean ICP during cerebrospinal fluid (CSF) infusion studies in patients with NPH, and on changes in cerebral arterial blood volume (AMP(CaBV)) in TBI patients. Further clinical studies will reveal whether AMP(ICP) is a better indicator of clinical severity and outcome than mICP in TBI and NPH patients.