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Purpose: We investigated whether a critical rise of intracranial pressure (ICP) leading to a loss of cerebral perfusion pressure (CPP) could serve as a surrogate marker of brain death (BD)., Materials and Methods: We retrospectively analyzed ICP and CPP of patients in whom BD was diagnosed (n = 32, 16-79 years). Intracranial pressure and CPP were recorded using parenchymal (n = 27) and ventricular probes (n = 5). Data were analyzed from admission until BD was diagnosed., Results: Intracranial pressure was severely elevated (mean ± SD, 95.5 ± 9.8 mm Hg) in all patients when BD was diagnosed. In 28 patients, CPP was negative at the time of diagnosis (-8.2 ± 6.5 mm Hg). In 4 patients (12.5%), CPP was reduced but not negative. In these patients, minimal CPP was 4 to 18 mm Hg. In 1 patient, loss of CPP occurred 4 hours before apnea completed the BD syndrome., Conclusions: Brain death was universally preceded by a severe reduction of CPP, supporting loss of cerebral perfusion as a critical step in BD development. Our data show that a negative CPP is neither sufficient nor a prerequisite to diagnose BD. In BD cases with positive CPP, we speculate that arterial blood pressure dropped below a critical closing pressure, thereby causing cessation of cerebral blood flow., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The objective of our study was to examine the relation of the intracranial pressure (ICP), cerebral perfusion pressure (CPP), regional cerebral blood flow (rCBF), and vasomotion in the acute phase in rats after having induced subarachnoid haemorrhage (SAH). The experiments were carried out on a total of 21 Wistar rats by means of neuroleptanalgesia and controlled mechanical ventilation. In 16 animals SAH was induced according to the method described by Solomon et al. with a fractionated application of 0.5 ml autologous blood into the cisterna magna. In a control group 0.5 ml of physiological saline solution was injected under identical conditions. The parameters were registered continuously before, during and at least 3 hours after the bolus application. The rCBF and vasomotion were recorded by laser-doppler fluxmetry. The ICP and the systemic arterial blood pressure were registered simultaneously. In the course of the experiment blood gas analyses were carried out regularly for documentary reasons of normoventilation. Our results show that the Cushing-response-after having induced SAH-led to a deterioration of the cerebral perfusion. In the control group however an increase in ICP and rCBF was recorded. The frequency and amplitude of the oscillations of Doppler signals, described as vasomotion, were significantly reduced in the SAH group as compared to the control group (p = 0.0004) during the course of the experiment. After having induced SAH an impairment of the cerebral autoregulation becomes apparent which seems to manifest itself on the level of microvascular structures as a suppressed behaviour pattern of vasomotion. Although basal vessels may constrict distal parenchymal vessels tend to dilate after SAH. The dilation-described as a reduction of vasomotion-could also be measured in clinical situations by means of laserdoppler fluxmetry.

The influence of arterial blood pressure (ABP) on the intracranial pulse pressure relationship (PPR) was studied in 17 patients in 29 recordings, with a total period of registration of 71.5 hours. The relationship between ICP and ABP was analysed by sampling the data every 15 seconds during spontaneous fluctuations of both these variables, and the analysis was performed on the basis of a mathematical model which includes pulsatory components. MABP and ABP amplitude had an opposite effect on the slope of PPR. Flattening of the PPR slope was caused by a MABP increase or an ABP amplitude decrease. The slope became steeper with decreasing MABP or increasing ABP amplitude. In accordance with the theoretical assumptions the quotient MABP/ABP-AMP was found to be suitable to express these opposite effects on PPR. Qualitatively, the same pattern of reaction was found in all patients. Rapid changes in PPR occurring during monitoring can be explained by a change in MABP/ABP-AMP relationship, regardless whether ABP changes influence intracranial elastance or not. The breakpoint of the PPR was recorded only on two occasions and could be explained in one by the influence of ABP. Monitoring of PPR as a measure of intracranial elastance and correlation of PPR with the patient's condition it not permitted unless at least the influence of ABP is analysed in each individual case.

The authors analyse the relationship between the muscle activity during paroxysms of decerebration and the intracranial pressure. These relationships differ, and depend upon the presence or absence of mesencephalic herniation and patency of the perimesencephalic cisterns, as well as on whether the decerebration posturing has been spontaneous or induced by external stimulus. It is suggested that the magnitude of ICP reaction during decerebration is connected with the possibility of compensating the increased intracranial volume and with the strain imposed upon the brain stem at the mesencephalic level. Close correlations between the vegetative variables occuring during spontaneous DR paroxysms suggest a common excitatory neuronal mechanism. In cases when decerebration is provoked by external stimuli the response becomes more complex and not uniform.

Decerebrate rigidity, intracranial pressure and vegetative signs were studied in 25 patients. Advanced statistical techniques were used to analyse the interrelationships between muscle activity (IEMG), blood pressure (ABP), intracranial pressure (ICP), pulse rate (HR), respiratory rate (RR), and central venous pressure (CVP) occurring during paroxysms of decerebration. The pattern of reaction is influenced by compression or stress imposed on the brain stem at the tentorial incisure and is related to the degree of cisternal obstruction. Significant differences in reaction were disclosed between provoked and spontaneous decerebration posturing.

Background and purpose: Here, we studied the safety of apnea testing (AT) for the determination of brain death with regard to intracranial pressure (ICP), cerebral perfusion and arterial blood gas parameters. We hypothesized that ICP only increases when cerebral perfusion pressure (CPP) remains positive during AT. Methods: A total of 34 patients who fulfilled brain death criteria were identified by chart review (2009–2017). We analysed ICP, CPP and mean arterial pressure (MAP) prior to AT, during AT and after AT, as well as arterial pH, paCO2, paO2 and arterial O2 saturation at the start and end of AT. Results: Intracranial pressure was 87.9 ± 17.7 mmHg (mean ± SD) prior to AT, 89.9 ± 17.2 mmHg during AT and 86.4 ± 15.2 mmHg after AT (P = 0.9). CPP was −6.9 ± 12.8 mmHg prior to AT, −7.1 ± 13.7 mmHg during AT and −8.6 ± 13.0 mmHg after AT (P = 0.98), respectively. MAP was 82.9 ± 14.6 mmHg prior to AT, 84.7 ± 13.9 mmHg during AT and 79.7 ± 9.6 mmHg after AT (P = 0.57), respectively. A total of 10 patients had positive CPP (8.6 ± 4.3 mmHg), but ICP did not increase during AT. Arterial pH decreased from 7.43 ± 0.06 to 7.22 ± 0.06 (P < 0.05), paCO2 increased from 38.6 ± 4.2 to 69.6 ± 8.0 mmHg (P < 0.05), paO2 decreased from 416.3 ± 113.4 to 289.2 ± 146.5 mmHg (P < 0.05), and O2 saturation was stable at 99.8 ± 0.4% and 98.2 ± 3.2% (P = 0.39). Conclusions: Apnea testing had no detrimental effect on ICP, CPP, MAP or oxygenation, regardless of the presence of an initially positive CPP. The lack of further ICP elevations is presumably explained by critical closing pressures above individual CPP levels during AT. [ABSTRACT FROM AUTHOR]