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Biomedical subjects

A Unterberg

Publications and source records attributed to A Unterberg.

At least 37 records · Page 2Linked to original sources
PubMed1999

The European Brain Injury Consortium survey of head injuries.

To provide a picture of contemporary practice, a survey was carried out of severely and moderately head injured patients admitted to 67 'neuro' centres in 12 European countries. 1,005 adult head injuries were recruited over a three month period. Sixty items of information on demography, clinical features, investigations, management and early complications were captured on a simple, two-page questionnaire and, information on outcome at six months on a third page. The median age of the subjects was 38 years, 74% were male and 51% injured in road traffic accidents; 57% of patients were transferred to the 'neuro' centre from another hospital. Assessment of clinical responsiveness was limited by the use of sedation and intubation and information from four early time points (pre-hospital, arrival at the Accident and Emergency department, post-resuscitation, and arrival at the 'neuro' unit) was combined to stratify the subjects as severe (58%), moderate (17%) or intermediate (19%). In 48% of patients classified the CT scan showed features of a 'mass lesion' and in 40% showed a subarachnoid haemorrhage. Fifty-five centres provided the data on outcome for 94% of the cases recruited in these centres six months after injury. 31% died, 3% were vegetative, 16% severely disabled, 20% moderately disabled and 31% had made a good recovery. Comparison of the data from different parts of Europe showed differences in the frequency of secondary transfer, cause of injury, occurrence of major extracranial injury, CT scan findings, intracranial operation, clinical severity of injury and utilisation of the components of intensive care and the occurrence of a favourable outcome, although the latter difference was not statistically significant when variations in the initial severity of injury were taken into account. The findings in the present survey are compared with newly analysed information for three previous large series: the International Data Bank involving the UK, the Netherlands and the USA, the North American Traumatic Coma Data Bank, and data from four centres in the UK. The comparisons showed substantial similarities and also differences that may reflect variations in policy for admission of the head injury to 'neuro' units, and evolution in methods of assessment, investigation and management. The effects of these differences on outcome requires further, rigorous prospective study.

Adolescent↗
PubMed1997

EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium.

Guidelines for the management of severe head injury in adults as evolved by the European Brain Injury Consortium are presented and discussed. The importance of preventing and treating secondary insults is emphasized and the principles on which treatment is based are reviewed. Guidelines presented are of a pragmatic nature, based on consensus and expert opinion, covering the treatment from accident site to intensive care unit. Specific aspects pertaining to the conduct of clinical trials in head injury are highlighted. The adopted approach is further discussed in relation to other approaches to the development of guidelines, such as evidence based analysis.

Adult↗
PubMed1996

Vasomotor and permeability effects of bradykinin in the cerebral microcirculation.

All components of an intracerebral kallikrein-kinin system have been described. Thus, bradykinin (BK) acting from the parenchymal site as well as from the blood site may influence cerebral microcirculation. BK is a potent dilator of extra- and intraparenchymal cerebral arteries when acting from the perivascular site. The vasomotor effect of BK is mediated by B2 receptors which appear to be located at the abluminal membrane of the endothelial cell. The effect of BK is mediated by NO. prostanoids, free radicals, H2O2 or leukotrienes depending on the animal species and on the location of the artery. Selective opening of the blood-brain barrier for small tracers (Na(+)-fluorescein; MW, 376) has been found in cats during cortical superfusion or intraarterial application of BK. This leakage is mediated by B2 receptors located at the luminal and abluminal membrane of the endothelial cells. Formation of brain edema has been found after ventriculo-cisternal perfusion or interstitial infusion of BK. This can be explained by increase of vascular permeability and cerebral blood flow due to arterial dilation thus enhancing driving forces for the extravasation. An increase of the BK concentration in the interstitial space of the brain up to concentrations which induce extravasation, dilatation and oedema formation has been found under several pathological conditions. Thus, BK may be involved in oedema formation after cold lesion, concussive brain injury, traumatic spinal cord and ischemic brain injury. The mediator role of BK in brain edema is further supported by therapeutic results. Brain swelling due to cold lesion or ischemia could be diminished by treatment with kallikrein-inhibitors. Similarly, dilatation of cerebral arterioles after concussive brain injury was reduced by blockade of B2 receptors. Thus, all criteria favour BK as one mediator of vasogenic oedema.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Continuous monitoring of jugular bulb oxygen saturation in comatose patients--therapeutic implications.

Comatose patients run a high risk of developing cerebral ischaemia which may considerably influence final outcome. It would therefore be extremely useful if one could monitor cerebral blood flow in these patients. Since there is a close correlation between the arteriovenous difference of oxygen and cerebral blood flow, it was a logical step to place a fiberoptic catheter in the jugular bulb for continuous measurement of cerebrovenous oxygen saturation. We have monitored cerebral oxygenation in 54 patients, comatose because of severe head injury, intracerebral haemorrhage or subarachnoid haemorrhage. Normal jugular venous oxygen saturation (SJVO2) ranges between 60 and 90%. A decline to below 50% is considered indicative of cerebral ischaemia. Spontaneous episodes of desaturation (SJVO2 < 50% for at least 15 min) were frequent during the acute phase of these insults. Many of these desaturation episodes could be attributed to hyperventilation, even though considered moderate. Likewise, insufficient cerebral perfusion pressure and severe vasospasm were found to be important causes of desaturation episodes. In many instances, tailoring of ventilation or induced hypervolaemia and hypertension were capable of reversing these low flow states. The new method of continuous cerebrovenous oximetry is expected to contribute to a better outcome by enabling timely detection and treatment of insufficient cerebral perfusion.

Adolescent↗
PubMed1994

Development of traumatic brain edema in old versus young rats.

Age is an important factor of mortality and morbidity following traumatic brain injury. The causes for the adverse effect of old age remain obscure. The aim of this study was to clarify whether age affects the development of posttraumatic brain edema. In Wistar rats, a cortical freezing lesion was applied to the parietal region in ketamine-xylazine anesthesia. 18 young rats (4-6 months) were compared to 15 old animals (36-40 months). In the early peritraumatic and late posttraumatic period blood pressure was monitored. 24 hours after trauma, the brains were removed and hemispheric swelling, water- und electrolyte-contents were measured. In addition, the brains of 3 animals of each group were histologically evaluated. In the old age group, 3 animals died during the 24 hours observation period (mortality 20%), whereas all young rats survived (p < 0.01). The cortical freezing lesion resulted in a hemispheric swelling of 6.9 +/- 0.5% in young, and 10.4 +/- 0.8% in old animals (p < 0.001). Accordingly, the increase of cerebral water content due to the lesion was significantly more pronounced in the group of old rats, i.e. 2.05% in old versus 1.50% in young animals (p < 0.01). The increase of swelling and edema in the old age group could not be attributed to arterial hypertension. On the contrary, mean arterial blood pressure was significantly lower in old animals. Histological examinations did not reveal significant differences between the two groups. Edema generation following a standardized cryogenic lesion is markedly enhanced in old versus young rats. This might be one factor among others for higher mortality and morbidity following traumatic brain injury in old versus young individuals.

Age Factors↗
PubMed1994

Dynamics of posttraumatic brain swelling following a cryogenic injury in rats.

For evaluation of novel therapeutic regimens against brain edema in experimental models, it is important to know the temporal profile of edema formation. Since development of brain swelling and edema following a cryogenic injury is poorly documented in rats, these parameters have been investigated in this study. 17 Sprague-Dawley rats were used. Three rats (controls) were sham-operated. Their brains were removed 15 min after sham-operation. In all other animals a right parietal cryogenic lesion was applied in ketamine-xylazine anesthesia. Systemic blood pressure was monitored during the perioperative period. Brains were removed in defined intervals following cryogenic injury (0.25, 0.5, 1, 3, 6, 12, 24, and 72 h; n = 3 each). Hemispheres were then separated and weighed for determination of brain swelling, dried and weighed again. Cerebral water content was calculated as the difference of hemispheric wet- and dry-weight. Posttraumatic hemispheric swelling reached its maximum (7.9 +/- 0.4%) as early as 12 h post trauma. During the first hour after injury, brain swelling showed a steep, linear increase to 3.9%, i.e. swelling amounted to 50% of its maximum within one hour. 6 h post trauma swelling was 5.7%. After 12 h brain swelling started to decline. 72 h post cryogenic injury, 6.1% hemispheric swelling were found. Development of brain swelling was paralleled by a linear increase in brain water content of the lesioned hemisphere. The maximum of hemispheric water content was seen 24 h post trauma. In non-lesioned hemispheres only a marginal transient increase in cerebral water content was observed. edema has to be considered when planning therapeutic protocols.

Animals↗
PubMed1994

21-Aminosteroid U-74389F reduces vasogenic brain edema.

21-Aminosteroids have been shown to attenuate neuronal damage and to improve neurological outcome after experimental ischemia. The aim of this study was to determine whether brain edema induced by a cryogenic injury can be influenced by the 21-aminosteroid U-74389F. A cortical freezing lesion was applied to the right parietal region of Sprague-Dawley rats under ketamine-xylazine anesthesia. Systemic blood pressure was monitored in the peritraumatic period. Four different doses of U-74389F (A-D) were studied for their effect on post-traumatic brain swelling and edema. Respective control groups received only the solvent, citric acid buffer. (A) 3 mg/kg b.w.i.p. (total dose) 30 min before, 1 and 12 h; post trauma (p.t.); (B) 9 mg/kg b.w.i.v. 30 min before, 1 and 12 h p.t.; (C) 25 mg/kg b.w.i.v. 30 min before, 1, 6, and 12 h p.t.; (D) 50 mg/kg b.w.i.v. 15 min before, 15 and 30 min as well as 1, 2, 6, and 12 h p.t. 24 h after trauma, brains were removed and hemispheric swelling and water content were determined from the difference between wet and dry weight. Application of the 21-aminosteroid U-74389F moderately reduced post-traumatic brain swelling in all treatment groups: (A) 5%, (B) 9%, (C) 12%, and (D) 14%. In parallel with this, the increase in water content of the traumatized hemisphere was marginally lowered by U-74389F in all groups; in (C) e.g. from 1.9 +/- 0.1% to 1.7 +/- 0.1%, p = 0.07. These two findings taken together indicate that the 21-aminosteroid U-74389F moderately reduces post-traumatic swelling and edema.

Animals↗
PubMed1994

Treatment of traumatic brain edema by multiple doses of mannitol.

Mannitol is frequently used to reduce elevated intracranial pressure often associated with brain edema. In cases of a damaged blood-brain barrier, however, mannitol might aggravate vasogenic cerebral edema, as has recently been stressed. The aim of this study was to investigate whether multiple doses of mannitol administered during development of vasogenic brain edema following a cryogenic cortical injury affect hemispheric swelling and edema. Sprague-Dawley rats were anesthetized with ketamine and xylazine. A cortical freezing lesion was applied to the right parietal region. A first series of eight rats received four doses of 20% mannitol (0.4 g/kg within 10 minutes) thirty minutes, 3, 6 and 9 hours after trauma. Twelve hours after cryogenic injury, the brains were removed for determination of hemispheric swelling and cerebral water content. Eight control rats were infused with saline only. In a second series nine rats received eight doses of 20% mannitol 30 minutes, 3, 6, 9, 12, 15, 18 and 21 hours after trauma. In this series, the brains were removed 24 hours after freezing. Again respective control animals were infused with saline only. Hemispheric swelling was 7.2 +/- 0.5% after four doses of mannitol compared to 7.6 +/- 0.5% in control animals (n.s.). Following eight doses of mannitol hemispheric swelling was 8.9 +/- 0.4% compared to 10.1 +/- 0.4% in control rats (p < 0.05). Accordingly, the water content of traumatized hemispheres was lower following repeated mannitol treatment (80.5 versus 80.8%). Water content in control hemispheres was not affected by mannitol. Taken together, these results indicate that multiple doses of mannitol do not aggravate total hemispheric swelling, nor global water content following induction of vasogenic edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Mediators of vascular and parenchymal mechanisms in secondary brain damage.

Several putative mediators of vasogenic brain edema will be considered with respect to the following criteria: 1) their effect on blood-brain barrier (BBB) permeability, 2) their vasomotor actions which may increase driving forces for transmural bulk flow, 3) their influence on edema formation, 4) their actual tissue concentration in pathological states, and 5) the therapeutic results after specific treatment. Bradykinin (BK) can induce brain edema by increasing BBB permeability to small solutes and enhancing blood pressure in the microcirculation due to arterial dilatation and venous constriction. Its interstitial concentration is enhanced after experimental trauma. Since kallikrein inhibitors reduce brain swelling all criteria favour BK as a mediator of vasogenic edema. Arachidonic acid (AA) opens BBB also for large tracers but exerts only small vasomotor effects. The edema formation is associated with an increase of the AA concentration in the interstitial space. However, convincing therapeutic results on inhibition of AA are still lacking. In addition to the formation of vasogenic edema AA has been found to induce cytotoxic edema. From experiments dealing with the vasomotor effects Ellis et al. (Am J Physiol 255: H397-H400, 1988) concluded an interaction of BK and AA in brain injury. However, our own results do not favour this hypothesis since we found divergent vasomotor and permeability effects of BK and AA. Histamine (HA) opens BBB unspecifically and dilates cerebral vessels, mechanisms by which edema formation can be explained.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMed1993

Monitoring of jugular venous oxygen saturation in comatose patients with subarachnoid haemorrhage and intracerebral haematomas.

To prevent secondary cerebral ischemia in comatose patients it would be of great importance to assess cerebral blood flow. Recently monitoring of the jugular venous oxygen saturation (SJVO2) has been shown to continuously evaluate cerebral oxygenation and to estimate cerebral blood flow. While most of these studies have dealt with severely head injured patients, we investigated cerebral oxygenation in 50 comatose patients due to an intracerebral haematoma (n = 14), subarachnoid haemorrhage (n = 12) and severe head injury (n = 24). In these groups of patients, the reaction of SJVO2 to hyperventilation and to lowering of blood pressure was studied. Moderate hyperventilation from 35 to 28 mmHg resulted in a significant decrease of SJVO2 in all groups. A critical SJVO2 between 50 and 55% was found in one half of the patients studied, a pathological SJVO2 below 50% was seen in 23% of the cases. Lowering of arterial blood pressure within the limits of autoregulation resulted in decreases of SJVO2 in patients with intracerebral haematomas only. 55% of these patients showed signs of insufficient cerebral oxygenation. Furthermore the frequency of spontaneous desaturation episodes was studied retrospectively and comparison made between the different groups. These episodes were found more frequently in patients with intracerebral haematomas compared to patients with severe head injury. In conclusion, monitoring of jugular venous oxygen saturation is a valuable tool for detecting and treating insufficient cerebral oxygenation in comatose patients following intracerebral haemorrhage, subarachnoid haemorrhage and severe head injury.

Adolescent↗
PubMed1993

Influence of body position on jugular venous oxygen saturation, intracranial pressure and cerebral perfusion pressure.

Elevation of the head as a common practice to reduce raised intracranial pressure (ICP) has been discussed controversially of late. Some investigators were able to show that besides lowering ICP head elevation may also reduce cerebral perfusion pressure (CPP). For a new evaluation of optimal head position in neurosurgical care it would be of importance to know the influence of body position on cerebral perfusion. We therefore employed continuous jugular venous oximetry, monitoring cerebral oxygenation, to study the effect of 0 degrees, 15 degrees, 30 degrees, and 45 degrees head elevation on ICP, CPP and jugular venous oxygen saturation (SJVO2) in 25 comatose patients with reduced intracranial compliance. As expected, head elevation significantly reduced ICP from 19.8 +/- 1.3 mmHg at 0 degrees to 10.2 +/- 1.2 mmHg at 45 degrees. Already at 30 degrees 92% of the possible effect on ICP was detected. There was no statistically significant change in CPP and SJVO2 associated with varying head position. Individual reactions of CPP to changes in head position, however, were quite unpredictable. The data suggest that an individual approach to head elevation is to be preferred. A moderate head elevation between 15 degrees and 30 degrees significantly reduces ICP and, in general, does not impair cerebral perfusion. Jugular venous oximetry may be used to optimize ICP, CPP and cerebral oxygenation.

Adult↗
PubMed1993

Long-term observations of intracranial pressure after severe head injury. The phenomenon of secondary rise of intracranial pressure.

The long-term course of intracranial pressure (ICP) was studied in 53 patients from a group of 90 patients with severe head injury treated over a 3-year period. In 49 of these, ICP was significantly elevated during the observation period. The maximum in ICP was usually observed 24 to 96 hours posttrauma. A subgroup of patients developed a second rise of ICP. Such a course was observed in 15 (31%) of the 49 patients with intracranial hypertension. In these cases, ICP increased initially to 20 to 30 mm Hg but could be controlled. Thereafter, ICP was decreased again for at least 12 hours. The secondary ICP rise occurred 3 to 10 days after trauma. In six patients, intracranial hypertension became uncontrollable and eventually caused brain death. The outcome of patients with a secondary rise of ICP was worse when compared with that of patients without this complication. A cause of the secondary ICP rise could only be identified in some cases. Delayed traumatic intracerebral hemorrhage, traumatic vasospasm, hypoxia, and hyponatremia were diagnosed in seven cases. In seven other patients, the secondary ICP rise coincided with a pronounced leukocytosis, which was not associated with apparent infections. Because the occurrence and degree of a secondary rise of ICP after severe head injury are important factors affecting outcome, monitoring of ICP after severe head injury should be prolonged.

Adolescent↗