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Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.
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PMID:Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema. 797 25

We have been focusing on potential metabolic derangement associated with severe head injury and a clinical trail directed toward treating brain tissue acidosis is currently underway. More specifically, we based this study on the hypothesis that following brain trauma brain tissue acidosis develops which may contribute to the prolongation of coma and neurologic deficit. Tromethamine (THAM), a safe and low toxicity agent which buffers in major part by causing a hypocapnic alkalosis, was selected for trial. Patients admitted with GCS < 8 were randomized into one of three arms: control: THAM plus hyperventilation; hyperventilation alone. Each regimen was maintained for 5 days post injury. Our analysis of 3 and 6 months Glasgow outcome score showed that prophylactic hyperventilation retards recovery, and the use of THAM overcomes the apparent deleterious effects of hyperventilation. One explanation is that the reduced ICP instability observed in THAM treated patients may account for this improvement. Is THAM effective in buffering traumatized brain tissue? What factors account for improvement in ICP stability? We addressed these questions in experimental studies utilizing MR spectroscopy to measure brain lactate production and tissue pH in fluid percussed anaesthetized cats. The protocol was designed to match our clinical trial, and brain injured animals were randomized into control, THAM, and hyperventilated groups. We observed that brain lactate production increased with trauma and remained above control at 8 hrs post injury. Lactate production in THAM treated animals was not elevated. Highest lactate production was associated with injured animals treated with sustained hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Traumatic brain tissue acidosis: experimental and clinical studies. 842 51

Continuous measurements of mean arterial pressure (MAP), ICP, and jugular venous oxygen saturation (SjO2) were performed in 11 patients with severe head injury (GCS 3-7) to assess the dependence of SjO2 from the cerebral perfusion pressure (CPP), trying to establish an indirect measure of cerebrovascular autoregulation. Changes in CPP resulting from spontaneous fluctuations in MAP or ICP induced highly significant alterations in SjO2 in the range of 0.14-0.56% SjO2 mmHg-1 CPP in all patients and all periods after trauma. The analysis of the distribution of the SjO2:CPP-ratios showed the highest frequency of values in the range of 0.0-0.25% SjO2 mmHg-1 CPP in 9 of the 11 patients. Within the first 2 days after trauma, a more pronounced dependency of SjO2 from changes in CPP was found, but this was not statistically significant. No predictable relationship of the SjO2:CPP-ratio to the level of ICP could be demonstrated in the patients. Because changes in SjO2 induced by alterations in CPP were found in all patients and throughout the acute phase of severe head injury, these changes more probably reflect physiological alterations in CBF with varying perfusion pressure rather than impaired autoregulation after head trauma. Although assessment of cerebral autoregulation by estimation of the SjO2:CPP-ratio offers new possibilities for monitoring of these patients, the high frequency of erroneous readings or irregular fluctuations of the SjO2-signal from the fibreoptic catheter limits the usefulness of the SjO2-dependency from CPP for practical use in the intensive care unit.
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PMID:Correlation of jugular venous oxygen saturation to spontaneous fluctuations of cerebral perfusion pressure in patients with severe head injury. 858 22

The authors have investigated the relationships between the amplitude of the ICP pulse wave, the mean values of ICP and CPP, and the outcome of 56 head injured ventilated patients. The ICP was monitored continuously using a Camino transducer (35 patients) or subdural catheter (21 patients). The mean Glasgow Coma Score was 6 (range 3-13; 5 patients had a GCS > 8 after resuscitation). Patients were grouped according to their Glasgow Outcome Score assessed at 12 months after injury. The amplitude of ICP pulse waveform was assessed using the fundamental harmonic of the pulse waveform (AMP) to avoid distortion caused by different frequency responses of the pressure transducers used in the study. Statistical analysis revealed that in patients with fatal outcome the ICP pulse amplitude increased when the mean ICP increased to 25 mmHg and then began to decrease. The upper breakpoint of the AMP-ICP relationship was not present in patients with good/moderate outcome. The moving correlation coefficient between the fundamental harmonic of ICP pulse wave and the mean ICP (RAP: R-symbol of correlation between A-amplitude and P-pressure) was introduced to describe the time-dependent changes in correlation between amplitude and mean ICP. The RAP was significantly lower in patients who died or remained in the vegetative state. In 7 patients who died from uncontrollable intracranial hypertension RAP was oscillating or decreased to 0 or negative values well before brain-stem herniation. The combination of an ICP above 20 mmHg for a period longer than 6 hours with low correlation between the amplitude and pressure (RAP < 0.5) was described as an predictive index of an unfavourable outcome.
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PMID:Significance of intracranial pressure waveform analysis after head injury. 880 Mar 28

Dihydroergotamine (DHE) is used in our recently introduced therapy of post-traumatic brain oedema and is suggested to reduce ICP through reduction in both cerebral blood volume and brain water content. This study aims at increasing our knowledge of the mechanisms behind the ICP reducing effect of DHE by analysing cerebrovascular effects of a bolus dose of DHE in severely head injured patients (GCS < 8). Mean hemispheric cerebral blood flow (CBF) calculated from the clearance of i.v. 133Xenon, ICP, and cerebral arterio-venous difference in oxygen content (AVDO2), were measured before and after hyperventilation and after a bolus dose of DHE (4 micrograms/kg). The patients were divided into two groups, one with preserved and one with impaired cerebrovascular CO2-reactivity to hyperventilation, the latter being predictive of poor outcome. The haemodynamic effects of DHE were compared to those of hyperventilation. Regional CBF and brain volume SPECT measurements were performed in two patients. DHE increased cerebrovascular resistance (CVR) by about 20% and significantly reduced ICP in both groups of patients, resulting in unchanged AVDO2. Hyperventilation with preserved CO2-reactivity caused a similar decrease in ICP as by DHE but with a much larger increase in CVR (by 70%) and a substantial increase in AVDO2. Hyperventilation with impaired CO2-reactivity reduced ICP but otherwise had no significant cerebrovascular effects. The study supports the concept that the ICP reducing effect of DHE results more from constriction of the large veins than from arterial vasoconstriction, also implying a relatively smaller risk of ischaemia with DHE than with hyperventilation.
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PMID:Cerebral haemodynamic effects of dihydroergotamine in patients with severe traumatic brain lesions. 884 93

The number of parameters (i.e., EEG or ICP-intracranial pressure) routinely monitored under clinical situations is limited. The brain function analyzer described in this paper enables simultaneous, continuous on-line monitoring of cerebral blood flow (CBF) and volume (CBV), intramitochondrial NADH redox state, extracellular K+ concentrations, DC potential, electrocorticography and ICP from the cerebral cortex. Brain function of 14 patients with severe head injury (GCS < or = 8), who were hospitalized in the neurosurgical or general intensive care unit was monitored using this analyzer. Leao cortical spreading depression (SD) has been reported in many experimental animals but not in the human cerebral cortex. In one of the patients monitored, spreading depression was observed. This is the first time that spontaneous repetitive cortical SD cycles have been recorded from the cerebral cortex of a patient suffering from severe head injury. Typical SD cycles appeared 4-5 h after the beginning of monitoring this patient. During the first 3-4 cycles the responses of this patient were very similar to the responses to SD recorded in normoxic experimental animals. Electrocorticography was depressed whereas extracellular K+ levels increased. The metabolic response to spreading depression was characterized by oxidation of intramitochondrial NADH concomitant to a large increase in CBF. During brain death, an ischemic depolarization, characterized by decrease in CBF and an irreversible increase in extracellular K+, was recorded.
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PMID:Cortical spreading depression recorded from the human brain using a multiparametric monitoring system. 897 24

The authors report on the stability and complications of 73 LICOX brain ti-pO2-microcatheters in 70 patients. Mean monitoring time was 7.5 +/- 4.0 days. Patients prone to cerebral hypoxia (after severe head injury (GCS < 9) or a subarachnoid hemorrhage) had a ti-pO2-microcatheter inserted next to the ICP-probe in the typical frontal position. After the first 15 insertions, instead of the 3-way-screw (needing a 6 mm burrhole), a 1-way-screw (needing a 2.7 mm burrhole) was used for fixation in the bone; by doing so, the procedure can be performed in the ICU and takes only 15 min. Whenever possible a calibration at room air (to determine the sensitivity-drift) and in oxygen free solution (to determine the zero-drift) was performed after removal of the catheters. Ideally the expected pO2 at room air was around 154 mmHg (temperature dependent) and at zero calibration 0 mmHg. Mean sensitivity-drift for 54 catheters was -8.5 +/- 15.4%. Dividing the catheters into groups, depending on the duration of monitoring (1-4, 5-8 and 9-16 days), revealed that the greatest part of the (negative) sensitivity-drift occurred during day 1-4 after insertion. After 1 week of monitoring sometimes a positive drift occurred (being far less than the negative drift during the first 4 days). Compared to the old catheters (-10.3 +/- 17.3%) (on the first half of the patients) the new ones showed a lower sensitivity-drift (-6.8 +/- 13.4%). The zero-drift of 56 catheters was low with mean drift after 7.5 +/- 4.0 days of 1.5 +/- 1.5 mmHg. Here also the highest drift occurred on day 1-4 after insertion. No infection was seen and 2 times (2.7%) a small hematoma, not needing evacuation occurred. As the ti-pO2-catheter (having a smaller diameter) and the ICP-catheter were inserted at the same time, one cannot distinguish which catheter caused the hematoma. A possible explanation for the occurrence of the two hematomas is the insertion of the catheters too close to the midline. The authors conclude that LICOX ti-pO2-monitoring is a safe and reliable method. Further decrease of the complication rate and increase of the catheter-stability may be expected.
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PMID:Brain tissue pO2-monitoring: catheterstability and complications. 919 73

A medline search back to 1975 was undertaken to identify relevant papers published on epidural haematomas. The search was restricted, whenever possible, to adult age and to comatose patients. Forty four relevant reports were identified. Only 4 papers reported results on multivariate analysis. In terms of prognosis, the following parameters were found to be significant: age, time from injury to treatment, immediate coma or lucid interval, presence of pupillary abnormalities, GCS/motor score on admission. CT findings (haematoma volume, degree of midline shift, presence of signs of active haematoma bleeding, associated intradural lesion) and post-operative ICP. To compare different casistics we need more informations about patients's outcome in the referral area of the neurosurgical centers, about the number of direct admissions and about the number of patients showing clinical deterioration.
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PMID:Prognostic factors in severely head injured adult patients with epidural haematoma's. 920 65

A medline search back to 1975 was undertaken to identify relevant papers published on subdural haematomas. The search was restricted, whenever possible, to adult age and comatose patients. Forty relevant reports were identified. Only 3 papers reported results on multivariate analysis. In terms of prognosis, the following parameters were found to be significant: age, time from injury to treatment, presence of pupillary abnormalities, GCS/motor score on admission, immediate coma or lucid interval, CT findings (haematoma volume, degree of midline shift, associated intradural lesion, compression of basal cisterns), post-operative ICP and the type of surgery. Improving the outcome of patients with acute subdural haematoma's is a difficult task. A small subpopulation of patients may have a benign course without surgical haematoma evacuation, but all comatose patients with an acute subdural haematoma should be treated in Centers where neurosurgical facilities and appropriate monitoring are available.
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PMID:Prognostic factors in severely head injured adult patients with acute subdural haematoma's. 920 66

We report on our experience with long-term monitoring of the EEG power spectrum and somatosensory evoked potentials (SSEPs) in 103 patients with severe closed head injury (Glasgow Coma Scale-GCS < or = 8). Patients were monitored for an average of 5 days post injury and monitoring was terminated when they died, regained consciousness or their intracranial physiologic parameters (primarily intracranial pressure-ICP) were stable for 2-3 days. Patients were treated according to a standard protocol that included mechanical ventilation, sedation, and neuromuscular blockade. At 7 of 9 twelve hour time intervals post injury, SSEPs were significantly (p < .05) different between outcome groups using the Glasgow Outcome Score collapsed to 3 categories. The percent slow (delta) activity in the EEG was not significantly different between outcome groups at any time point, post injury. The total power in the EEG power spectrum differed only at the last time epoch post injury (108 hr.). Based on the superior prognostic capabilities of the SSEP, we routinely base critical management decisions on SSEP values. We have not been able to rely on EEG parameters for these same decisions due to the lack of clear distinction between good and poor prognosis groups based on common EEG parameters.
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PMID:Monitoring severe head injury: a comparison of EEG and somatosensory evoked potentials. 953 90


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