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The physiology underlying the intracranial pressure (ICP) curve morphology is not fully understood. Recent research has suggested that the morphology could be dependent on arterial cerebral inflow and the physiological and pathophysiological properties of the intracranial cavity. If understood, the ICP curve could provide information about the patient's cerebrovascular state important in individualizing treatment in neuro intensive care patients. A mathematical model based on known physiological properties of the intracranial compartment was created. Clinical measurements from ten neuro intensive care patients in whom intracranial arterial blood inflow, venous blood outflow and cerebrospinal fluid flow over the foramen magnum had been measured with phase contrast MRI, concomitant with ICP measurements were used to validate the model. In nine patients the mathematical model was able to create an ICP curve mimicking the measured by using arterial intracranial inflow and adjusting physiological parameters of the model. The venous outflow and cerebrospinal fluid (CSF) flow over the foramen magnum predicted by the model were within physiologically reasonable limits and in most cases followed the MRI measured values in close adjunct. The presented model could produce an ICP curve in close resemblance of the in vivo measured curves. This strengthens the hypothesis that the ICP curve is shaped by the arterial intracranial inflow and the physiological properties of the intracranial cavity.

Background: Continuous monitoring of intracranial pressure (ICP) was introduced in the 1950s. For correct ICP recordings, the zero-reference point for the external pressure gauge must be placed next to a head anatomical structure. We evaluated different anatomical points as zero reference for the ICP device at different head positions and their relation to brain centre (BC), foramen of Monro (Monro), and brain surface., Methods: Patients referred for neuroimaging due to e.g. headache all having normal 3D MRI scans were selected. Monro, BC, Orbit(O), external auditory meatus (EAM), and orbito-meatal (OM) line were identified and projected to mid-sagittal, or axial images. Each scan was evaluated like lying supine, 45° head elevations, upright, and 45° lateral position. Distances from skin to brain surface, BC, and Monro were measured. All values are presented as mean ± SD and/or range in millimetre. For conversion to mmHg, millimetre was multiplied by 0.074., Results: Twenty MRI scans were examined. A zero reference at EAM or glabella was ideal at BC when head was strict supine or in the lateral position. At 45° head elevation, an overestimation of the BC-ICP by 4.8 ± 0.8 and in upright 5.6 ± 0.5 mmHg was found, and 45° lateral underestimated ICP-BC by 6.3 ± 1.0 mmHg. Monro was situated 45 ± 5 mm rostral to the mid-OM line and 24 (18-31) mm inferior and 13 (8-17) mm in front of BC. A zero-reference point aligned with the highest point of the head underestimated BC-ICP and Monro-ICP. If the ICP reading was added 5.9 or 6.3 mmHg, respectively, a deviation from BC-ICP was ≤ 1.8 mmHg and Monro-ICP was ≤ 0.9 mmHg in all head positions., Conclusions: EAM and glabella are defined anatomical structures representing BC when strict supine or lateral but with 12 mmHg variation with different head positions used in clinical practice. The OM line follows Monro at head elevation, but not when the head is turned. When the highest external point on the head is used, ICP values at brain surface as well as Monro and BC are underestimated. This underestimation is fairly constant and, when corrected for, provides the most exact ICP reading.

Current methods to measure cerebral blood flow (CBF) in the neuro critical care setting cannot monitor the CBF continuously. In contrast, continuous measurement of intracranial pressure (ICP) is readily accomplished, and there is a component of ICP that correlates with arterial inflow of blood into the cranial cavity. This property may have utility in using continuous ICP curve analysis to continuously estimate CBF. We examined the data from 13 patients, monitored with an intraventricular ICP device determining the pulsatile amplitude ICP amp as well as the area under the ICP curve (AUC ICP ). Using an elastance measurement, the ICP curve was converted to craniospinal volume (AUC ΔV ). The patients were examined with Phase Contrast Magnetic Resonance Imaging (MRI), measuring flow in the carotid and vertebral arteries. This made it possible to calculate CBF for one cardiac cycle (ccCBF MRtot ) and divide it into the pulsatile (ccCBF MRpuls ) and non-pulsatile (ccCBF MRconst ) flow. ICP derived data and MRI measurements were compared. Linear regression was used to establish wellness of fit and ANOVA was used to calculate the P value. No correlation was found between ICP amp and the ccICP MRpuls (P = 0.067). In contrast there was a correlation between the AUC ICP and ccCBF MRpuls (R 2  = 0.440 P = 0.013). The AUC ΔV correlated more appropriately with the ccCBF MRpuls . (R 2  = 0.688 P < 0.001). Our findings suggests that the pulsatile part of the intracranial pressure curve, especially when transformed into a volume curve, correlates to the pulsatile part of the CBF.

Background: The intracranial pressure (ICP) curve with its different peaks has been extensively studied, but the exact physiological mechanisms behind its morphology are still not fully understood. Both intracranial volume change (ΔICV) and transmission of the arterial blood pressure have been proposed to shape the ICP curve. This study tested the hypothesis that the ICP curve correlates to intracranial volume changes., Methods: Cine phase contrast magnetic resonance imaging (MRI) examinations were performed in neuro-intensive care patients with simultaneous ICP monitoring. The MRI was set to examine cerebral arterial inflow and venous cerebral outflow as well as flow of cerebrospinal fluid over the foramen magnum. The difference in total flow into and out from the cranial cavity (Flow tot ) over time provides the ΔICV. The ICP curve was compared to the Flow tot and the ΔICV. Correlations were calculated through linear and logarithmic regression. Student's t test was used to test the null hypothesis between paired samples., Results: Excluding the initial ICP wave, P1, the mean R 2 for the correlation between the ΔICV and the ICP was 0.75 for the exponential expression, which had a higher correlation than the linear (p = 0.005). The first ICP peaks correlated to the initial peaks of Flow tot with a mean R 2  = 0.88., Conclusion: The first part, or the P1, of the ICP curve seems to be created by the first rapid net inflow seen in Flow tot while the rest of the ICP curve seem to correlate to the ΔICV.

Background: The study focuses on three questions related to the clinical usefulness of microdialysis in severe brain trauma: (1) How frequently is disturbed cerebral energy metabolism observed in various types of lesions? (2) How often does the biochemical pattern indicate cerebral ischaemia and mitochondrial dysfunction? (3) How do these patterns relate to mortality?, Method: The study includes 213 consecutive patients with severe brain trauma (342 intracerebral microdialysis catheters). The patients were classified into four groups according to the type of lesion: extradural haematoma (EDH), acute subdural haematoma (SDH), cerebral haemorrhagic contusion (CHC) and no mass lesion (NML). Altogether about 150,000 biochemical analyses were performed during the initial 96 h after trauma., Results: Compromised aerobic metabolism occurred during 38 % of the study period. The biochemical pattern indicating mitochondrial dysfunction was more common than that of ischaemia. In EDH and NML aerobic metabolism was generally close to normal. In SDH or CHC it was often severely compromised. Mortality was increased in SDH with impaired aerobic metabolism, while CHC did not exhibit a similar relation., Conclusions: Compromised energy metabolism is most frequent in patients with SDH and CHC (32 % and 49 % of the study period, respectively). The biochemical pattern of mitochondrial dysfunction is more common than that of ischaemia (32 % and 6 % of the study period, respectively). A correlation between mortality and biochemical data is obtained provided the microdialysis catheter is placed in an area where energy metabolism reflects tissue outcome in a large part of the brain.

Background: Arterial vasospasm after subarachnoid hemorrhage may cause cerebral ischemia. Treatment with hemodilution, reducing blood viscosity, and hypervolemia, increasing cardiac performance and distending the vasospastic artery, are clinically established methods to improve blood flow through the vasospastic arterial bed., Method: Eight patients with transcranial Doppler verified vasospasm after subarachnoid hemorrhage were investigated with global (two-dimensional (133)Xenon) and regional (three-dimensional (99 m)Tc-HMPAO) cerebral blood flow (CBF) measurements, before and after 1/iso- and 2/hypervolemic hemodilution. Hematocrit was reduced to 0.28 from 0.36. Hypervolemia was achieved by increasing blood volume by 1100 ml., Findings: Isovolemic hemodilution increased global cerebral blood flow from 52.25+/-10.12 to 58.56+/-11.73 ml * 100 g(-1) * min(-1) (p<0.05), but after hypervolemic hemodilution CBF returned to 51.38+/-11.34 ml * 100 g(-1) * min(-1). Global cerebral delivery rate of oxygen (CDRO(2)) decreased from 7.94+/-1.92 to 6.98+/-1.66 ml * 100 g(-1) * min(-1) (p<0.001) during isovolemic hemodilution and remained reduced, 6.77+/-1.60 ml * 100 g(-1) * min(-1) (p<0.001), after the hypervolemic hemodilution. As a test of the hemodilution effect on regional CDRO(2) an ischemic threshold was defined as the maximal amount of oxygen transported by a CBF of 10 ml * 100 g(-1) * min(-1) at a Hb 140 g/l which corresponds to a CDRO(2) of 1.83 ml * 100 g(-1) * min(-1). The brain volume with a CDRO(2) exceeding the ichemic threshold was 1300+/-236 ml before intervention. After isovolemic hemodilution the non-ischemic brain volume was reduced to 1206+/-341 (p<0,003). After hypervolemic hemodilution the non-ischemic brain volume remained reduced at 1228+/-347 ml (p<0.05)., Interpretation: The present study of controlled isovolemic hemodilution demonstrated increased global CBF, but there was a pronounced reduction in oxygen delivery capacity. Both CBF and CDRO(2) remained decreased during further hypervolemic hemodilution. We conclude that hemodilution to hematocrit 0.28 is not beneficial for patients with cerebral vasospasm after SAH.

Noninvasive methods for detecting cerebral artery vasospasm, still a serious complication following aneurysmal subarachnoid haemorrhage, are of vital interest. Up-to-date transcranial Doppler ultrasound (TCD) has proved to be sensitive in detecting vasospasm in the middle cerebral artery, but has less accuracy for other cerebral arteries. Transcranial cerebral oximetry (TCCO) is a new non-invasive technique which may increase the reliability for detecting cerebral ischaemia. The purpose of the present study was to evaluate a putative correlation between TCCO and TCD. We examined the two hemispheres in 14 patients with the aim of evaluating a proposed correlation between TCD and TCCO. Analysis of all absolute values (maximum TCD mFV and minimum TCCO saturation, respectively) in all series indicate a correlation between TCCO and TCD, p < 0.01, r = -0.62. All patients with TCD mean flow velocity > 120 cm/s also presented TCCO saturation < 60%. Conversely, all patients with normal TCCO saturation (> or = 63%) presented normal or moderately increased TCD velocities. In clinical neurosurgical practice it is of great interest if a true correlation between TCD and TCCO exists. The present results support the assumption that TCCO may enhance the reliability for detecting cerebral ischaemia after aneurysmal subarachnoid haemorrhage.