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Neurosurgical therapy aims to minimise the secondary brain damage after a severe head injury. This includes the evacuation of an intracranial space occupying bleeding, the reduction of intracranial volumes, in hematocephalus an external ventricular drainage, and the conservative therapy in order to influence an increased intracranial pressure (ICP) and a decreased p(ti)0. When conservative treatment fails to act a decompressive craniectomy might be successful in lowering ICP. From September 1997 until July 2004 we operated on 737 patients with severe head injuries. 103 patients (14%) were treated by means of a decompressive craniectomy.

The prognosis after decompression depends on the clinical signs and symptoms on admission, the patients age and the existence of major extracranial injuries. Our guidelines for an indication for decompressive craniectomy after failure of conservative interventions and evacuation of space occupying hematomas include a patients age below 50 years without multiple trauma, a patients age below 30 years in the presence of major extracranial injuries, a severe brain swelling on CT scan, the exclusion of a primary brainstem lesion or injury and the intervention before irreversible brainstem damage and secondarily while monitoring ICP and p(ti)0 in an interval up to 48 hours after the accident before irreversible brainstem damage or generalised brain damage has occurred.

Cerebrolysin is used as a neurotrophic agent for the treatment of ischemic stroke and Alzheimer’s Disease. Exploratory studies in patients with post-acute traumatic brain injury have shown that this treatment might help improve recovery. Aim of this study was to investigate whether addition of Cerebrolysin to the initial treatment regimen of moderate and severe head injury patients would improve their outcome.

At 6 months, 67% of the patients (Cerebrolysin group) attained good outcome (GOS 3–5). The study group was compared with the historical cohort of patients from the hospital trauma data bank, with age, sex and admitting GCS matching. More patients tended to a good outcome in the Cerebrolysin group (P = 0.065). No significant side-effect requiring cessation of Cerebrolysin was noted.

It can be concluded that the use of Cerebrolysin as part of the initial management of moderate and severe head injury is safe and well tolerated. The results suggest that Cerebrolysin is beneficial in regard to the outcome in these patients, especially in elderly patients.

Neurological change is more likely to occur when jugular venous oxygen saturation (SjvO) is less than 50%. However, the value indicating cellular damage has not been clearly defined. We determined the critical SjvO value below which intracerebral extracellular metabolic abnormalities occurred in 25 patients with severe head injury.

All patients received standard treatment with normoventilation and maintenance of intracranial pressure < 20 mmHg. SjvO was measured from the dominant jugular bulb using a calibrated fibreoptic catheter. Intracerebral metabolic monitoring was performed by collecting perfusate from a microdialysis probe placed in the frontal lobe anterior to the intracranial catheter. Excitotoxin (glutamate) and other extracellular metabolites (lactate, glucose and glycerol) were measured frequently using enzymatic and colorimetric methods.

We observed biphasic relationships between SjvO and all intracerebral metabolites. Analysis of variance showed that there were rapid increases in glutamate, glycerol and lactate when SjvO dropped below 40, 43 and 45% respectively. Extracellular glucose decreased when SjvO dropped below 42%.

Our findings suggested that the ischemic threshold for SjvO in patients with severe head injury is 45%, below which secondary brain damage occurred.

The specificity of jugular bulb saturation (SjO) and arteriovenous oxygen difference (AVDO) to detect global cerebral ischemia remains controversial. An absolute increase in the arteriovenous difference of carbon dioxide tension (AVDpCO) and, more specifically, the estimated respiratory quotient (eRQ = AVDpCO/AVDO) may indicate anaerobic CO production. We compared these variables with SjO to predict global cerebral ischemia.

We selected 36 patients from a cohort of 69 consecutive patients suffering from severe traumatic brain injury. All patients had jugular bulb sampling within 6 hours after injury. Brain death at 48 hours was used as a surrogate index of irreversible ischemia to build a receiver operating characteristics (ROC) curve analysis.

The mean (± standard deviation) eRQ in the 13 patients who died early (3.7 ± 3.2 mmHg/ml/dl) was higher than the survivors (1.78 ± 0.45 mmHg/ml/dl, = 0.03). There was no differences in SjO between groups. The area under the ROC curves for eRQ, but not that of AVDpCO, was greater ( = 0.04) than that of SjO.

The eRQ, more than AVDpCO, appears to be a potentially more informative index of global cerebral ischemia than SjO.

This study investigated the changes in extracellular chemistry during reversible human cerebral ischaemia. Delayed analysis was performed on samples taken from a subgroup of patients during aneurysm surgery previously reported [12]. Frozen microdialysis samples from 14 patients who had all undergone temporary clipping of the ipsilateral internal carotid artery (ICA) were analysed for another 15 amino acids with HPLC and for glycerol with CMA-600. Changes were characterised according to whether cerebral tissue oxygen pressure (PO) decreases were brief or prolonged.

Brief ICA clipping (maximum duration of 16 minutes) in 11 patients was not associated with changes in amino acids or glycerol. Cerebral ischaemia, defined by a PO decrease below 1.1 kPa for at least 30 minutes during ICA occlusion, occurred in 3 patients. None of whom developed an infarct in the monitored region. This prolonged reversible ischaemia was associated with transient delayed increases in -amino butyric acid (GABA) as well as glutamate and glycerol, each by two-to-three folds. This study demonstrates detectable transient increases in human extracellular glutamate, GABA and glycerol during identified periods of reversible cerebral ischaemia, maximal 30–60 minutes after onset of ischaemia, but not in other amino acids detected by HPLC.

We evaluated the effect of intracranial hypertension on cerebral metabolism in patients with high grade aneurysmal subarachnoid hemorrhage (SAH) using bedside cerebral microdialysis (MD). Thirty-six patients with SAH were studied and classified into two groups (intracranial pressure, ICP > 20 mmHg, = 25) and (ICP < 20 mmHg, = 11). ICP was monitored hourly using an intraventricular drainage ( = 36). The MD catheter was placed after aneurysm clipping into the vascular territory of interest and was perfused with Ringer’s solution (0.3 µl/min). The MD samples were collected hourly for measurements of glucose, lactate, and glutamate (CMA 600, Sweden). Lactate/pyruvate ratio was also calculated. To calculate group specific differences, the 24 hours median values of the first 7 days after SAH were compared. Differences were considered statistically significant at < 0.05.

Patient groups were comparable for age, severity of SAH, Fisher’s grade and duration of MD sampling. In patients with ICP > 20 mmHg from day 1 to 7 after SAH, extracellular concentrations of glucose were significantly lower, while the lactate/pyruvate ratio was higher compared to SAH patients with normal ICP values. The differences between groups in glutamate levels was only significant on day 1 after SAH due to high inter-individual differences. We concluded that intracranial hypertension in associated with an anaerobic cerebral metabolism indicated cerebral ischemia in high grade SAH patients.

Previous studies have demonstrated that a brief period of ischemia protect against subsequent severe ischemic insults to the brain, i.e. preconditioning. We evaluated the effects of ischemic preconditioning, produced by 2 min proximal temporary artery occlusion, on brain tissue gases and acidity during clipping of cerebral aneurysm.

Twelve patients with aneurysmal subarachnoid hemorrhage were recruited. All patients received standard anesthetics. After craniotomy, a calibrated multiparameter catheter was inserted to measure oxygen (PtO) tension, carbon dioxide (PtCO) tension and pH (pHt) in tissue at risk of ischemia during temporary artery occlusion. In patients assigned to the preconditioning group, proximal artery was occluded initially for 2 min and was allowed to reperfuse for 30 min. All patients underwent cerebral artery occlusion for clipping of aneurysm. The rate of change in PtO, PtCO and pHt after artery occlusion were compared between groups using unpaired test.

Baseline brain tissue gases and pHt were similar between groups. Following artery occlusion, the decline in PtO and pHt were significantly slower in the preconditioning group compared with the routine care group.

These results suggested that ischemic preconditioning attenuates tissue hypoxia during subsequent artery occlusion. Brief occlusion of the proximal artery may be a simple maneuver for brain protection during complex cerebrovascular surgery.