BACKGROUND: Cardiac arrest (CA) is a sudden event that is often characterized by hypoxic-ischemic brain injury (HIBI), leading to significant mortality and long-term disability. Brain tissue oxygenation (PbtO2) is an invasive tool for monitoring brain oxygen tension, but it is not routinely used in patients with CA because of the invasiveness and the absence of high-quality data on its effect on outcome. We conducted a systematic review of experimental and clinical evidence to understand the role of PbtO2 in monitoring brain oxygenation in HIBI after CA and the effect of targeted PbtO2 therapy on outcomes.
METHODS: The search was conducted using four search engines (PubMed, Scopus, Embase, and Cochrane), using the Boolean operator to combine mesh terms such as PbtO2, CA, and HIBI.
RESULTS: Among 1,077 records, 22 studies were included (16 experimental studies and six clinical studies). In experimental studies, PbtO2 was mainly adopted to assess the impact of gas exchanges, drugs, or systemic maneuvers on brain oxygenation. In human studies, PbtO2 was rarely used to monitor the brain oxygen tension in patients with CA and HIBI. PbtO2 values had no clear association with patients\' outcomes, but in the experimental studies, brain tissue hypoxia was associated with increased inflammation and neuronal damage.
CONCLUSIONS: Further studies are needed to validate the effect and the threshold of PbtO2 associated with outcome in patients with CA, as well as to understand the physiological mechanisms influencing PbtO2 induced by gas exchanges, drug administration, and changes in body positioning after CA.

Multimodal monitoring of brain activity, physiology, and neurochemistry is an important approach to gain insight into brain function, modulation, and pathology. With recent progress in micro- and nanotechnology, micro-nano-implants have become important catalysts in advancing brain research. However, to date, only a limited number of brain parameters have been measured simultaneously in awake animals in spite of significant recent progress in sensor technology. Here we have provided a cost and time effective approach to designing a headstage to conduct a multimodality brain monitoring in freely moving animals. To demonstrate this method, we have designed a user-configurable headstage for our micromachined multimodal neural probe. The headstage can reliably record direct-current electrocorticography (DC-ECoG), brain oxygen tension (PbrO2), cortical temperature, and regional cerebral blood flow (rCBF) simultaneously without significant signal crosstalk or movement artifacts for 72 h. Even in a noisy environment, it can record low-level neural signals with high quality. Moreover, it can easily interface with signal conditioning circuits that have high power consumption and are difficult to miniaturize. To the best of our knowledge, this is the first time where multiple physiological, biochemical, and electrophysiological cerebral variables have been simultaneously recorded from freely moving rats. We anticipate that the developed system will aid in gaining further insight into not only normal cerebral functioning but also pathophysiology of conditions such as epilepsy, stroke, and traumatic brain injury.

We report on the change in brain oxygen tension (PbtO2) over the first 24 h of monitoring in a series of 25 patients with severe traumatic brain injury (TBI) and relate this to outcome. The trend in PbtO2 for the whole group was to increase with time (mean PbtO2 17.4 [1.75] vs 24.7 [1.60] mmHg, first- vs last-hour data, respectively; p = 0.002). However, a significant increase in PbtO2 occurred in only 17 patients (68 %), all surviving to intensive care unit discharge (p = 0.006). Similarly, a consistent increase in PbtO2 with time occurred in only 13 patients, the correlation coefficient for PbtO2 versus time being ≥0.5 for all survivors. There were eight survivors and four non-survivors, with low correlation coefficients (<0.5). Significantly more patients with a correlation coefficient ≥0.5 for PbtO2 versus time survived in intensive care (p = 0.039). The cumulative length of time that PbtO2 was <20 mmHg was not significantly different among these three groups. In conclusion, although for the cohort as a whole PbtO2 increased over the first 24 h, the individual trends of PbtO2 were related to outcome. There was a significant association between improving PbtO2 and survival, despite these patients having cumulative durations of hypoxia similar to those of non-survivors.

OBJECTIVE: Intraventricular nicardipine (IVTN) is a treatment option for severe vasospasm in patients with subarachnoid hemorrhage (SAH). However, its acute effects on cerebral hemodynamics have not been studied in detail.
METHODS: Between June 2008 and December 2010, IVTN was administered (mainly 4mg every 8h) to 11 SAH patients (54 doses) with multimodality monitoring for refractory vasospasm. Retrospective analyses on physiological parameters were made from baseline and up to 6h after IVTN injection. Statistical analysis was performed with a mixed-effects model.
RESULTS: Mean intracranial pressure (ICP) increased slightly, reaching its peak at 20min after IVTN injection (2.5±0.9mmHg (mean±standard error), P<0.01), and decreased gradually thereafter over the next hour. Mean cerebral perfusion pressure transiently decreased 20-30min after injection (3.7±1.8mmHg, P<0.05). Mean arterial pressure, partial pressure of brain oxygen tension (PbtO2), cerebral blood flow (CBF), autoregulation indices did not change significantly. Lactate/pyruvate ratio and glucose remained stable. One patient underwent transcranial Doppler ultrasonography monitoring while on IVTN, which showed a transient increase in mean flow velocity with concomitant decrease in Pulsatility index, suggesting vasodilation in the distal resistance vessels.
CONCLUSIONS: The vasodilatory effect of IVTN transiently increased ICP, but did not significantly affect PbtO2, CBF or oxidative glucose metabolism in the immediate phase after injection.

Near-infrared spectroscopy (NIRS) has gained acceptance for cerebral monitoring, especially during cardiac surgery, though there are few data showing its validity. We therefore aimed to correlate invasive brain tissue oxygen measurements (PtiO2) with the corresponding NIRS-values (regional oxygen saturation, rSO2). We also studied whether NIRS was able to detect ischemic events, defined as a PtiO2-value of <15 mmHg. Eleven patients were studied with invasive brain tissue oxygen monitoring and continuous-wave NIRS. PtiO2-correlation with corresponding NIRS-values was calculated. We found no correlation between PtiO2- and NIRS-readings. Measurement of rSO2 was no better than flipping a coin in the detection of cerebral ischemia when a commonly agreed ischemic PtiO2 cut-off value of <15 mmHg was chosen. Continuous-wave-NIRS was unable to reliably detect ischemic cerebral episodes, defined as a PtiO2 value <15 mmHg. Displayed NIRS-values did not correlate with invasively measured PtiO2-values. CW-NIRS should not be used for the detection of cerebral ischemia.