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Background: Polymethylmethacrylate (PMMA) assisted ventral discectomy has been criticized for high rates of graft migration and pseudarthrosis when compared with various other fusion procedures for the treatment of cervical degenerative disc disease (DDD), therefore rendering it not the preferred choice of treatment today. Recently however spine surgery has been developing towards preservation rather than restriction of motion, indicating that fusion might not be necessary for clinical success. This study presents a long term comparison of clinical and radiological data from patients with pseudarthrosis and solid arthrodesis after PMMA assisted ventral discectomy was performed., Methods: From 1986 to 2004 416 patients underwent ventral discectomy and PMMA interposition for DDD. The clinical and radiological outcome was assessed for 50 of 127 eligible patients after a mean of 8.1 years. Based on postoperative radiographs the patients were dichotomized in those with a pseudarthrosis (group A) and those with solid arthrodesis (group B)., Results: Pseudarthrosis with movement of more than 2 of the operated segment was noted in 17 cases (group A). In 33 cases no movement of the vertebral segment could be detected (group B). The analysis of the clinical data assessed through the neck disability index (NDI), the visual analogue scale (VAS) of neck and arm pain and Odom's criteria did not show any significant differences between the groups.Patients from group B showed a trend to higher adjacent segment degeneration (ASD) than group A (p = 0.06). This correlated with the age of the patients., Conclusions: PMMA assisted discectomy shows a high rate of pseudarthrosis. But the clinical long-term success does not seem to be negatively affected by this.

Experimental data suggest that lumbar torsion contributes to lumbar disc degenerative changes, such as instability, spondylolisthesis and spinal canal stenosis. However, some basic mechanical characteristics of the lumbar spine under torsional loading have not yet been reported in detail. For example, the function of the facet joints under combined mechanical loads such as torsion with superimposed flexion or extension postures is an area of interest about which little biomechanical data have been reported. In this study, the kinematic response to axial torsion with superimposed axial compression (200 N), compression-flexion (3 and 6 Nm) and compression-extension (3 and 6 Nm) was investigated in 10 cadaveric lumbar functional spinal units. Range of motion (ROM), and helical axes of motion (HAM), were analyzed. There was no difference in ROM between no preload, pure compressive and flexion-compression preload conditions. The ROM was significantly reduced by both extension-compression preload conditions (11% reduction for 3 Nm and 19% reduction for 6 Nm of extension) compared to the pure compressive preload. For no preload, the average HAM position in the transverse plane of the intervertebral disc was near the posteriormost part of the disc and located laterally on the side contralateral to the applied torsional moment. In the transverse plane, the HAM position showed a discrete trend towards the posterior part of the specimens during extension. Kinematic data were visualized using computer animation techniques and CT-based reconstructions of the respective specimens. This information may be used for identifying and characterizing physiologic and pathologic motion and for specifying conservative and surgical treatment concepts and, thus, may find application to identifying indications for spinal fusion or in evaluating the effect of future semi-flexible instrumentation.

Background: The timing and extent of surgery continue to be a matter of discussion in current craniosynostosis management., Patients and Methods: We retrospectively reviewed the first 159 children seen from 1996 to 2000 of a total of 243 patients presenting with suspected craniosynostosis. We did not establish a surgical indication in 74 children (47%), either because their malformations were of different origin without associated craniosynostosis (11/7%) or they presented with only mild clinical manifestations of sutural synostosis (63/40%). In 85 cases (53%), we established a surgical indication. Parents did not follow our recommendation in two cases (1%). In 83 cases, we performed diagnosis-related remodeling at the age of 4-12 months. Demographic data, clinical follow-up findings, and regular photo documentation were analyzed., Results: After a mean follow-up of 3 years and 8 months, the results were satisfactory in 68 cases (82%). Of 15 cases (18%) with only limited improvement, two children were submitted to a second intervention. Another two children had to be reoperated on immediately for insufficient hemostasis. In the largest subgroup of children (47) with sagittal synostosis, there was no difference in outcome between surgery performed before and after 6 months of age., Discussion: Surgical indication and assessment of results are based on subjective criteria which limit the comparison with the literature. Our results correspond to those of similar published series. Most of the unfavorable results could be attributed either to inadequate adaptation of the surgical technique to the individual form of the malformation or to a significant secondary loss of correction in multi-sutural synostosis., Conclusions: The overall results of surgery within the first year of life were satisfactory in 82%. Standard procedures need to be adapted carefully to the individual form of craniosynostosis to avoid unfavorable results. We therefore propose a new surgical technique based on a statistically averaged modular system of skull models to replace freehand remodeling.

Object: The majority of patients with poor-grade subarachnoid hemorrhage (SAH), that is, World Federation of Neurosurgical Societies (WFNS) Grades IV and V, have high morbidity and mortality rates. The objective of this study was to investigate cerebral metabolism in patients with low- compared with high-grade SAH by using bedside microdialysis and to evaluate whether microdialysis parameters are of prognostic value for outcome in SAH., Methods: A prospective investigation was conducted in 149 patients with SAH (mean age 50.9 +/- 12.9 years); these patients were studied for 162 +/- 84 hours (mean +/- standard deviation). Lesions were classified as low-grade SAH (WFNS Grades I-III, 89 patients) and high-grade SAH (WFNS Grade IV or V, 60 patients). After approval by the local ethics committee and consent from the patient or next of kin, a microdialysis catheter was inserted into the vascular territory of the aneurysm after clip placement. The microdialysates were analyzed hourly for extracellular glucose, lactate, lactate/pyruvate (L/P) ratio, glutamate, and glycerol. The 6- and 12-month outcomes according to the Glasgow Outcome Scale and functional disability according to the modified Rankin Scale were assessed. In patients with high-grade SAH, cerebral metabolism was severely deranged compared with those who suffered low-grade SAH, with high levels (p < 0.05) of lactate, a high L/P ratio, high levels of glycerol, and, although not significant, of glutamate. Univariate analysis revealed a relationship among hyperglycemia on admission, Fisher grade, and 12-month outcome (p < 0.005). In a multivariate regression analysis performed in 131 patients, the authors identified four independent predictors of poor outcome at 12 months, in the following order of significance: WFNS grade, patient age, L/P ratio, and glutamate (p < 0.03)., Conclusions: Microdialysis parameters reflected the severity of SAH. The L/P ratio was the best metabolic independent prognostic marker of 12-month outcome. A better understanding of the causes of deranged cerebral metabolism may allow the discovery of therapeutic options to improve the prognosis, especially in patients with high-grade SAH, in the future.

A 7-year-old boy diagnosed with Williams-Beuren syndrome was admitted for spontaneous right hemispheric intracerebral hemorrhage. Cerebral angiography did not reveal any source of bleeding. After a short period of clinical improvement under conservative treatment, the boy deteriorated rapidly. CT showed the beginning of a complete infarction of both hemispheres. Operative evacuation of the bleeding and bilateral osteoclastic decompression had no perceptible influence on the clinical course. To the present day, the boy has remained in a vegetative state. Reports in the literature suggest that Williams syndrome with cerebral infarction is associated with a markedly poorer prognosis when there is additional intracerebral bleeding., (Copyright 2003 S. Karger AG, Basel)

Three-dimensional (3D) rotational radiography, initially developed to visualize intracranial aneurysms, is applied to the cervical spine after conventional myelography. We call this process 3D rotational myelography. 3D reconstruction and then postprocessing allows imaging in multiple planes. Spinal or nerve root sheath alterations caused by bony or soft tissue can be visualized and differentiated by using this technique.

Objective: To analyze the time course and changes of cerebral microdialysis parameters after aneurysmal subarachnoid hemorrhage (SAH) in respect to the clinical course (asymptomatic, delayed, and acute ischemic neurologic deficits) to evaluate the method of bedside microdialysis in these patients., Design: Prospective, controlled study during a 3-yr period., Setting: Neurosurgical intensive care unit at a primary level university hospital, supervised and staffed by members of both the department of neurosurgery and the department of anesthesiology and intensive care medicine., Patients: Ninety-seven patients (51 females/21 males; 52 +/- 13 yrs; World Federation of Neurological Surgeons Scale grades 0-5) after aneurysmatic SAH., Measurements and Main Results: A microdialysis catheter (CMA 100) was inserted into the region most likely to be affected by vasospasm directly after aneurysm clipping, connected to a pump, and perfused with Ringer solution (0.3 microL/min). The dialysates were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate ratio, glutamate, and glycerol (CMA 600). Patients were classified according to clinical presentation as being asymptomatic or having acute (AIND) or delayed (DIND) ischemic neurologic deficits. DIND patients (n = 18) had significantly higher lactate and glutamate concentrations on days 1-8 post-SAH and a higher lactate-pyruvate ratio on days 3-8 post-SAH compared with asymptomatic patients (n = 57; p <.025). Glucose and glycerol levels did not differ in asymptomatic and DIND patients. AIND patients (n = 22) had the worst metabolic pattern: the extracellular glucose concentration was low, whereas the lactate, lactate-pyruvate ratio, glutamate, and glycerol levels were significantly elevated compared with asymptomatic and DIND patients. In 83% of the DIND patients, the changes in metabolites indicative of cerebral ischemia preceded the onset of symptomatic vasospasm. All DIND patients clinically improved in their Glasgow Coma Scale scores with induced hypertension, intentional hypervolemia, and/or hemodilution therapy (p =.01)., Conclusion: Cerebral bedside microdialysis is a safe and promising technique for monitoring (impending) regional cerebral ischemia. The dialysate changes can indicate early the onset of delayed neurologic deterioration and are in good accordance with the clinical course of SAH patients. In the future, this technique may be used to monitor the efficacy of the intensive care therapy of these patients.

Decompressive craniectomy is often the final option in the management of posttraumatic intracranial hypertension. Aim of this study was to investigate the effect of secondary decompression on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and neurological outcome. 62 patients decompressed after severe head injury were included in the retrospective study. Decompression was performed when ICP could not be controlled by non-surgical treatment. Mean age was 36.6 yrs, 77.4% were male. Initial Glasgow Coma Score (GCS) was 6. Outcome was determined 6 months after trauma according to the Glasgow Outcome Scale (GOS) and the functional Barthel-Index (BI). In the last hour before decompression ICP was 40.5 +/- 1.6 mmHg and CPP was 65.3 +/- 2.1 mmHg (being maintained, if necesary, by catecholamines). ICP was significantly reduced to 9.8 +/- 1.3 mmHg by surgery and CPP improved to 78.2 +/- 2.3 mmHg. 12 hrs following decompression mean ICP rose to 21.6 +/- 1.7 mmHg again (CPP: 73.6 +/- 1.7 mmHg), but in the following period ICP could be kept below 25 mmHg in the majority of patients. 6 months after trauma 22.5% of the patients had died (except one all these patients were aged more than 50 yrs). 48.4% of patients survived with an unfavourable outcome (GOS 2 + 3), while 29.1% had a favourable outcome (GOS 4 + 5). Decompressive craniectomy is highly effective to treat otherwise uncontrollable intracranial hypertension and improves CPP. A satisfactory outcome, however, is only achieved under strict consideration of negative predictors (e.g. age).

A recently developed monitoring technology makes an on-line assessment of intracranial compliance (ICC) possible. Aims of our research: 1. Course and values of ICC (critical threshold: < 0.5 ml/mmHg) in episodes of pathological intracranial pressure (ICP) (> 20 mmHg) and reduced cerebral oxygenation (brain tissue PO2 (PtiO2) < 10 mmHg). 2. Mean ICC in different ages. 3. Relationship between ICC and outcome. 4. Evaluation of ICC as routine monitoring parameter by calculation of s.c. time-of-good-data-quality (TGDQ). Computer data assessment of 7 patients with severe closed head-injury was performed providing 830 hours of data. TGDQ resulted from the formula: TGDQ (%) = artifact free time (min) x 100 (%)/total monitoring time (min). Outcome was assessed 6 months posttrauma (Glasgow Outcome Score (GOS). 1. Analysis revealed 43 episodes of pathologically elevated ICP and 39 of critical ICC. In 17 cases overlapping periods were found. In 9 of these ICC preceded ICP. Reduced cerebral oxygenation was neither related with high ICP nor low ICC. 2. ICC was found to be age-related. At a cut-off-point of 20 mmHg in ICP, ICC in children (< or = 16 years) was 0.9, in adults (17-60 years) 0.7 and in elderly (> 60 years) 0.6 ml/mmHg. 3. Adverse outcome was indicated best by high ICP (up to 45% of monitoring time) followed by low ICC (up to 41% of monitoring time). 4. TGDQ in ICC was 72% compared to 95% in ICP and 98% in PtiO2. In predicting adverse outcome, ICP was equal to ICC. The different ICC in each age class points to the need of age-adjusted thresholds. Further refinements of ICC technology are needed to improve ICC data quality and therefore become a useful tool in neuromonitoring.

The temporal profile of nitric oxide metabolite concentrations i.e. nitrite and nitrate (NOx) was investigated in brain parenchyma of patients following aneurysmal subarachnoid hemorrhage (SAH). In a subset of ten patients (7F/3M, age: 47 +/- 14 yrs) included in a prospective clinical trial on neurochemical intensive-care monitoring, microdialysis (MD) probes (CMA70, Sweden) were implanted at time of aneurysm surgery. Samples from patients clipped electively (n = 3) were considered "normal" in regard to SAH patients (n = 7). MD was performed for 162 +/- 63 hrs. NOx was measured off-line using a highly sensitive, fluorometric assay (2-3-diaminonaphtalene, DAN). NOx concentrations determined from electively operated patients averaged 36.7 +/- 9.6 microM (n = 59, pooled data). Regardless of the development of delayed ischemic neurological deficits (DIND), SAH patients showed a specific temporal profile of NOx consisting of an initial peak followed by an exponential decay. In detail, NOx decreased from initial values of 46.2 +/- 34.8 microM to 23.5 +/- 9.0 microM on day 6-7 after SAH (p < 0.05). Following SAH extracellular concentrations of NO metabolites decrease over time. This is in agreement with hypothetical NO scavenging by products of hemolysis. However, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.

We evaluated bedside cerebral on-line microdialysis for early detection of cerebral hypoxia in patients with traumatic brain injury. 24 severely head injured patients (Glasgow Coma Score < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring using the LICOX (GMS mbH, Germany) microcatheter device. The catheter was placed into the non-lesioned frontal white matter within 32.2 (7-48) hrs post injury. The microdialysis catheter (CMA 100, Sweden) was placed close to the PtiO2 probe via a 2- or 3-way skull screw, connected to a pump and perfused with Ringer solution (0.3 microliter/min). The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate-ratio and glutamate (CMA 600, Sweden). We identified 252 episodes of impending hypoxia (PtiO2 < 15 mm Hg; 11,810 minutes) and 38 episodes of cerebral hypoxia (PtiO2 < 10 mm Hg; 1996 minutes). Before cerebral hypoxia, glucose decreased significantly. Glutamate was unchanged when no hypoxia or impending hypoxia occurred but increased 3-4 fold before a hypoxic episode appeared. We conclude that early metabolic detection of cerebral hypoxia before a critical decrease in brain tissue PtiO2 is seen and possibly allows earlier changes in treatment (e.g. reduction of hyperventilation therapy).

In a prospective clinical investigation on neurochemical intensive care monitoring, the authors' aim was to elucidate the temporal profile of nitric oxide metabolite concentrations-that is, nitrite and nitrate (NO(x))--and compounds related to energy-metabolism in the cerebral interstitium of patients after aneurysmal subarachnoid hemorrhage (SAH). During aneurysm surgery, microdialysis probes were implanted in cerebral white matter of the vascular territory most likely affected by vasospasm. Temporal profiles of NO(x) were analyzed in a subset of 10 patients (7 female, 3 male, mean age = 47 +/- 14 years). Microdialysis was performed for 152 +/- 63 hours. Extracellular metabolites (glucose, lactate, pyruvate, glutamate) were recovered from the extracellular fluid of the cerebral parenchyma. NO(x) was measured using a fluorometric assay. After early surgery, SAH patients revealed characteristic decreases of NO(x) from initial values of 46.2 +/- 34.8 micromol/L to 23.5 +/- 9.0 micromol/L on day 7 after SAH (P < 0.05). Decreases in NO(x) were seen regardless of development of delayed ischemia (DIND). Overall NO(x) correlated intraindividually with glucose, lactate, and glutamate (r = 0.58, P < 0.05; r = 0.32, P < 0.05; r = 0.28, P < 0.05; respectively). After SAH, cerebral extracellular concentrations of NO metabolites decrease over time and are associated with concomitant alterations in energy-or damage-related compounds. This could be related to reduced NO availability, potentially leading to an imbalance of vasodilatory and vasoconstrictive factors. On the basis of the current findings, however, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.

Ibn Sina (often known by his last name in Latin, Avicenna; 980-1037 A.D.) was the most famous physician and philosopher of his time. His Canon of Medicine, one of the most famous books in the history of medicine, surveyed the entire medical knowledge available from ancient and Muslim sources and provided his own contributions. In this article the authors present a unique picture of the neurosurgical technique of Ibn Sina and briefly summarize his life and work.

Neuronal fibres of the hippocampal formation of normal and chronic epileptic rats were investigated by fluorescent tracing methods using the pilocarpine model of limbic epilepsy. Two months after onset of spontaneous limbic seizures, hippocampal slices were prepared and maintained in vitro for 10 h. Small crystals of fluorescent dye [fluorescein (fluoro-emerald) and tetramethylrhodamine (fluoro-ruby)] were applied to different hippocampal regions. The main findings were: (i) in control rats there was no supragranular labelling when the mossy fibre tract was stained in stratum radiatum of area CA3. However, in epileptic rats a fibre network in the inner molecular layer of the dentate gyrus was retrogradely labelled; (ii) a retrograde innervation of area CA3 by CA1 pyramidal cells was disclosed by labelling remote CA1 neurons after dye injection into the stratum radiatum of area CA3 in chronic epileptic rats; (iii) labelling of CA1 neurons apart from the injection site within area CA1 was observed in epileptic rats but not in control animals; and (iv), a subicular-hippocampal projection was present in pilocarpine-treated rats when the tracer was injected just below the stratum pyramidale of area CA1. The findings show that fibre rearrangement in distinct regions of the epileptic hippocampal formation can occur as an aftermath of pilocarpine-induced status epilepticus.

In a patient with progressive ophthalmological problems, including uncontrolled intraocular pressure related to a cavernous sinus dural arteriovenous fistula, urgent intervention may be necessary to prevent permanent visual loss. We report a case in which inadequate transarterial embolisation and lack of access for transvenous catheterisation, including a direct approach through the superior ophthalmic vein, preceded percutaneous puncture of the superior ophthalmic vein deep within the orbit, permitting venous occlusion without complications. This case demonstrates that deep orbital puncture of the vein is feasible for occlusion of a cavernous sinus dural arteriovenous fistula.

Objectives: To study the occurrence of secondary insults and the influence of extracranial injuries on cerebral oxygenation and outcome in patients with closed severe head injury (Glasgow Coma Scale score < or =8)., Design: Two-year prospective, clinical study., Setting: Two intensive care units in a level III trauma center., Patients: We studied 119 patients. Eighty patients had severe head injury and were divided into two categories: "isolated" severe head injury patients (n = 36, Injury Severity Score <30), and severe head injury patients with associated extracranial injuries (n = 44, Injury Severity Score >29). Thirty-nine patients with extracranial injuries and no head injury served as the control group., Interventions: After patients were admitted to the intensive care unit, we began continuous multimodal cerebral monitoring of intracranial pressure, mean arterial blood pressure, cerebral perfusion pressure, end-tidal Co2, brain tissue Po2 (Licox), jugular bulb oxyhemoglobin saturation in severe head injury patients, and mean arterial blood pressure in the control group. Targets of management included intracranial pressure <20 mm Hg, cerebral perfusion pressure >60 mm Hg, Paco2 > 30 mm Hg, control of cerebral oxygenation, and delayed surgery for non-life-threatening extracranial lesions., Measurements and Main Results: Data were analyzed for critical thresholds. The occurrence of secondary insults (intracranial pressure >20 mm Hg, mean arterial blood pressure <70 mm Hg, cerebral perfusion pressure <60 mm Hg, end-tidal Co2 <30 torr, brain tissue Po2 <10 torr, jugular bulb oxyhemoglobin saturation <50%) was comparable in patients with isolated severe head injury and those with severe head injury with associated extracranial lesions (Abbreviated Injury Scale score < or =5). The duration of intracranial hypertension and arterial hypotension significantly correlated with an unfavorable outcome, independent of the Injury Severity Score. In patients with severe head injury, 1-yr outcome was 29% dead or vegetative, 17% severely disabled, and 54% moderate or good outcome. This was similar to patients with severe head injury and extracranial injuries (31% dead or vegetative, 14% severely disabled, and 56% moderate or good outcome) and was independent of the Injury Severity Score. Patients with no head injury had less secondary insults (mean arterial blood pressure <70 mm Hg, p <.01) and a better outcome compared with both severe head injury groups (p <.044)., Conclusions: In patients with severe head injury who have targeted management including intracranial pressure- and cerebral perfusion pressure-guided therapy and delayed surgery for extracranial lesions, the occurrence of secondary insults in the intensive care unit and long-term neurological outcome were comparable and independent of the presence of extracranial lesions (Abbreviated Injury Severity level < or =5). A severe head injury is still a major contributor predicting an unfavorable outcome in multiply injured patients.

Object: Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH., Methods: In 60 patients a microdialysis catheter was inserted into the brain parenchyma that is most likely to be affected by vasospasm directly after aneurysm clipping. Hourly analyses of glucose, pyruvate, lactate, and glutamate levels were performed using a bedside device. Blood-flow velocities were obtained using serial TCD measurements. Cerebral angiography was routinely performed on Day 7 after aneurysm clipping or earlier in cases of clinical deterioration (30 patients). In all patients the results of microdialysis monitoring, TCD ultrasonography, and angiography were correlated. The mean duration of monitoring was 7.3+/-2.5 days. In patients with acute ischemic neurological deficits (18 patients) immediate microdialysis-recorded alterations were observed if the probe was placed close to the malperfused region. In 13 of 15 patients with symptomatic vasospasm (delayed ischemic neurological deficit [DIND]), the microdialysis-recorded values revealed secondary deterioration. In terms of confirming DIND, microdialysis had the highest specificity (0.89, 95% confidence interval [CI] 0.78-1) compared with TCD ultrasonography (0.63, 95% CI 0.46-0.8) and angiography (0.53, 95% CI 0.35-0.7). For microdialysis, the positive likelihood ratio was 7.8, whereas this was significantly lower for TCD ultrasonography (1.7) and angiography (2.1)., Conclusions: Although angiography also demonstrates vessel narrowing in asymptomatic patients, online microdialysis reveals characteristic metabolic changes that occur during vasospasm. Thus, online microdialysis may be used to confirm the diagnosis of vasospasm.

The presence of an abscess in a pituitary tumor is a very rare finding. The authors report the case of a 69-year-old man with a pituitary adenoma confirmed by neuroimaging results, in whom a high fever, meningismus, and left-sided ophthalmoplegia developed 4 days after tooth extraction. The results of serial cranial magnetic resonance imaging were highly indicative of an abscess formation within the pituitary adenoma. During surgery the tumor was approached transsphenoidally and removed. Histological examination confirmed the presence of an abscess formation within the pituitary adenoma. It is most likely that the tooth extraction caused a bacteremia, which led to an inflammation with abscess formation within the pituitary adenoma. The authors conclude that invasive dental procedures should be avoided before planned resection of a pituitary adenoma.

Object: The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury., Methods: Thirty-five severely head injured patients (with Glasgow Coma Scale scores < or = 8) were studied. Patients underwent continuous brain tissue PO2 (PtiO2) monitoring. The PtiO2 catheter was placed into the unaffected frontal white matter within 32.2 hours postinjury (range 7-48 hours). The microdialysis catheter was placed close to the PtiO2 probe via a 2- or 3-way skull screw that was connected to a pump and perfused with Ringer's solution at 0.3 microl/minute. The microdialysis samples were collected hourly and analyzed at the bedside for glucose, lactate, lactate-pyruvate ratio, and glutamate. Data were analyzed for identification of episodes of impending (PtiO2 10-15 mm, Hg > 5-minute duration) and present cerebral hypoxia (PtiO2 10 mm Hg, > 5-minute duration). In 62% of the patients hypoxic episodes occurred and were most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, extracellular glutamate concentrations were increased (p = 0.006) whereas energy metabolites remained stable. During cerebral hypoxia, the extracellular glutamate (p < 0.001) and lactate (p = 0.001) concentrations were significantly higher than during normal oxygenation, whereas the lactate-pyruvate ratio was only slightly increased (p = 0.088, not significant)., Conclusions: The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.

Objective: We investigated the usefulness of a microscope-based navigational system (Multi Koordinaten Manipulator; Zeiss, Oberkochen, Germany) for removal of the posterior wall of the internal auditory canal (IAC) via the retrosigmoid route., Methods: A cadaveric study was performed to assess the navigational localization error for the retrosigmoid approach to the IAC. Computed tomographic findings for 47 acoustic neuroma cases were divided into three groups, on the basis of the relationship between the labyrinth and the sigmoid-fundus line (medial, on the line, or lateral). Furthermore, the shortest distances between the most medial labyrinthine extension and the resection line were measured. In 20 acoustic neuroma operations, the different features and the practicality of the microscope-based navigational system for opening of the IAC were evaluated., Results: The mean anatomic localization errors were 0.67 +/- 0.2 mm (95th percentile, 1.32 mm) for navigation to the IAC and 0.71 +/- 0.37 mm (95th percentile, 1.68 mm) for navigation to the posterior semicircular canal. The average distances between the most medial labyrinthine extension and the resection line were 3.65, 3.36, and 2.0 mm for the lateral, on-the-line, and medial groups, respectively. Direct contouring of structures at risk does not take into account the localization error, nor does it provide reliable navigational information. A novel indirect contouring concept that takes into account the localization error (the safety corridor method) was therefore introduced., Conclusion: The value of navigational assistance for opening of the IAC is promising but still limited. Further development is required before the clinical effects of this navigational approach can be evaluated.

Summary: A 59-year-old man with neurofibromatosis type 1 (NF1) presented with bruits and neck pain due to a space occupying lesion in the right neck tissue. Digital subtraction angiography (DSA) showed an arteriovenous fistula (AVF) of the right extracranial vertebral artery (VA) with a giant venous pouch and an intracranial berry aneurysm of the right middle cerebral artery (MCA). First, the MCA aneurysm was surgically clipped, then the patient was treated by embolisation with coils. The coils were placed transarterially from the left VA resulting in a partial thrombosis of the venous pouch. Complete closure was achieved secondarily by retrograde transvenous catheterization. Etiology and treatment modalities are discussed.

Purpose: Neuronal network reorganization might be involved in epileptogenesis in human and rat limbic epilepsy. Apart from aberrant mossy fiber sprouting, a more widespread fiber rearrangement in the hippocampal formation might occur. Therefore, we studied sprouting in area CA1 because this region is most affected in human temporal lobe epilepsy., Methods: In slices from hippocampi of patients operated on for temporal lobe epilepsy (n = 134), from pilocarpine-treated rats (n = 74), and from control rats (n = 15), viable neurons were labeled with fluorescent dextran amines., Results: In human hippocampi as well as in pilocarpine-treated rats, the degree of nerve cell loss varied. In 67 of 134 slices from human specimens with distinct Ammon's horn sclerosis and in 23 of 74 slices from pilocarpine-treated rats, a severe shrunken area CA1 presented with a similar picture: few damaged neurons were labeled, and aberrant fiber connections were not visible. This was in contrast to human resected hippocampi and hippocampi from pilocarpine-treated rats with no or moderate loss of neurons. In these cases, pyramidal cells remote from the injection site were labeled (human tissue, n = 59 of 134; pilocarpine-treated rats, n = 39 of 74). In human resected hippocampi without obvious pathology and in control animals, no pyramidal neurons were labeled apart from the injection site., Conclusions: Axon collaterals of CA1 pyramidal cells are increased in human temporal lobe epilepsy and in pilocarpine-treated rats. Adjacent CA1 pyramidal cells project via aberrant collaterals to the stratum pyramidale and the stratum radiatum of area CA1. This network reorganization can contribute to hyperexcitability via increased backward excitation.

Overwhelming inflammatory immune response can result in systemic inflammation and septic shock. To prevent excessive and deleterious action of proinflammatory cytokines after they have produced their initial beneficial effects, the immune system can release several anti-inflammatory mediators, including interleukin-10, interleukin-1 receptor antagonist, and soluble tumor necrosis factor receptors, thus initiating a compensatory anti-inflammatory response syndrome. However, in vivo the delicate balance between pro- and anti-inflammatory responses is additionally controlled by the central nervous system. Therefore, proinflammatory cytokines stimulate the hypothalamic-pituitary-adrenal axis and enhance sympathetic nerve system activity. The mediators of these neuroimmune pathways can again suppress immune cell functions to control systemic inflammation. The question is, however, what happens if the immunoinhibitory CNS pathways are activated without systemic inflammation? This can result from production of cytokines in the brain following infection, injury, or ischemia or in response to various stressors (e.g., life events, depression, anxiety) or directly from brainstem irritation. The answer is that this may generate a brain-mediated immunodepression. Many animal and clinical studies have demonstrated a stress and brain cytokine mediated decrease in the cellular immune response at the lymphocyte level. More recently, the importance of monocytes in systemic immunocapacity has been shown. Monocytic inactivation with decreased capability of antigen presentation and depressed secretion of proinflammatory cytokines increases the risk of infectious complications. Interestingly, cytokines in the brain and other stressors can also generate systemic immunodepression at the monocyte level. In this scenario the catecholamine-induced release of the potent anti-inflammatory cytokine interleukin-10 is a newly discovered mechanism of the brain-mediated monocyte deactivation in addition to the "well known" immunosuppressive action of glucocorticoids. Furthermore, other neuropeptides such as alpha-melanocyte-stimulating hormone and beta-endorphin which can be released in stressful situations have also inhibitory effects on immune cells. Thus mediators of the CNS are implicated in the regulation of immune functions and may play a role in both conditioning the host's response to endogenous or exogenous stimuli and generating a "brain-mediated" immunodepression.

Summary: Endovascular treatment of high flow arteriovenous fistula following a stab wound injury in a 25 year old man is reported. Previously performed proximal embolisation and surgicalligation failed to occlude the fistula but resulted in changes to the normal vascular anatomy and significant clinical and cosmetic disturbances. A direct puncture of the draining vein was performed and the fistulous connection occluded by placement of detachable coils and deposition of glue. Follow-up showed disappearance of the AVF as well as complete clinical recovery.

Proinflammatory cytokines are produced in the brain after various kinds of insult (ischemia, trauma, infection). In this process interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha are most important. These cytokines are key mediators of inflammation. Furthermore, these cytokines can act as neurotransmitters and develop direct effects on the central nervous system (CNS) including fever, sleep and stimulation of the neuroendocrine as well as sympathetic nervous system. Moreover, IL-1beta and TNF-alpha may also be involved in brain repair and regenerating processes. However, most of the data about the role of cytokines in the brain have been obtained from either in vitro studies or bolus injections into the brain parenchyma or cerebroventricular system. On the other hand, it is known that cytokines are released continuously into the brain after a cerebral insult over a period of 24 to 48 h. In order to further complete the knowledge about the interactions between neural and immune cells to overcome the primary insult and initiate repair and regeneration in the CNS, a new animal model of local inflammation reaction was established using chronic intracerebral infusion of rat recombinant cytokines., (Copyright 1999 Elsevier Science B.V.)

Leukocytosis after cerebral injury is well described and may participate in the generation of cerebral damage. However, the mechanisms of brain-induced leukocytosis are still speculative. Since it is known that proinflammatory cytokines are involved in neuroimmunomodulation and since others and we have demonstrated high cytokine levels in the cerebrospinal fluid following injury, we supposed that brain cytokines may also influence leukocyte counts. In order to evaluate this hypothesis, we established an animal model using continuous intracerebroventricular (i.c.v.), intrahypothalamic (i.h.), or intravenous infusion of the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and IL-1beta. Controls received vehicle solution. With this experimental paradigm we could show that i.c.v. and i.h. infusion of IL-1beta but not TNF-alpha dramatically increased neutrophil counts, whereas lymphocytes dropped. Blocking the hypothalamic-pituitary-adrenal (HPA) axis by hypophysectomy abolished the neutrophilia, whereas the lymphopenia remained unchanged. Furthermore, application of the beta2-adrenoreceptor antagonist propranolol prevented the decrease of lymphocytes and diminished the neutrophilia. All parameters normalized within 48 h after termination of infusion. So, our results demonstrate that brain IL-1beta can modify blood leukocyte counts through stimulation of both the sympathetic nervous system (SNS) and the HPA axis.

Object: Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume., Methods: The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin-stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12+/-1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9+/-1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16+/-2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18+/-1 mm Hg)., Conclusion: Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.

It is well established that systemic inflammation induces a counter-regulatory anti-inflammatory response particularly resulting in deactivation of monocytes/macrophages. However, recently we demonstrated a systemic anti-inflammatory response without preceding signs of systemic inflammation in patients with brain injury/surgery and release of cytokines into the cerebrospinal fluid (CSF). In order to analyze the mechanisms and pathways of systemic immunodepression resulting from sterile cerebral inflammation we established an animal model using continuous intra-cerebroventricular (i.c.v.) or intra-hypothalamic (i.h.) infusion of rat recombinant (rr) tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta for 48 h. Controls received intra-venous (i.v.) cytokine administration. Interestingly, i.c.v. and i.h. infusion of IL-1beta but not TNF-alpha produced distinct signs of central nervous system (CNS) inflammation. Correspondingly, i.c.v. infusion of IL-1beta particularly diminished the TNF-alpha but increased the IL-10 concentration in whole blood cultures after endotoxin stimulation. All parameters normalized within 48 h after termination of the infusion. Blocking the hypothalamic-pituitary-adrenal (HPA) axis by hypophysectomy (HPX) led to complete recovery of the diminished TNF-alpha concentration and temporarily inhibited the IL-10 increase. Blocking the sympathetic nervous system (SNS) transmission by application of the beta2-adrenoreceptor antagonist propranolol not only inhibited the increase but further downregulated the endotoxin induced IL-10 concentration in the media of whole blood cell cultures, whereas the TNF-alpha decrease was only partially prevented. Interestingly, HPX and propranolol also diminished the cell invasion into the CSF. In summary, activation of both the HPA axis and the SNS plays an important role in systemic anti-inflammatory response resulting from cytokines in brain and cerebral inflammation., (Copyright 1999 Elsevier Science B.V.)

The hydrostatic dual-switch valve (DSV) was implanted in 56 patients suffering from hydrocephalus of different causes. Evaluation of the clinical status 3 and 6 months after the operation revealed excellent and good neurological recoveries in the vast majority of cases. Only 7 patients demonstrated an unsatisfactory result according to the grading of Stein and Langfitt. The CT follow-up, evaluated by the reduction of the Evans index, was characterized by only minimal or even no reduction of the ventricular size in more than half of the patients. Only 2 patients of our series developed overdrainage-related problems. 5 cases are presented to illucidate the danger of overdrainage resulting from the implantation of conventional differential-pressure valves, and the possible solution of this problem by hydrostatic devices like the DSV. Our series gives strong evidence, that reestablishing physiological pressure-ranges after shunting is paralleled by a good clinical outcome independent of the ventricular size after shunting.

Secretory meningioma is a rare entity which may be characterised by imaging features unusual for other subtypes of meningioma, such as low attenuation on CT, high (fat-tissue equivalent) signal intensity on T1-weighted MRI, marked surrounding oedema, and irregular contrast enhancement. We report a case of secretory meningioma and review the literature.

The purpose of this prospective study was to determine the potential of MR imaging to depict morphologic alterations of the median nerve correlating with the stage of carpal tunnel syndrome (CTS). Eighteen wrists of normal subjects and 81 wrists of patients with CTS were examined. MR imaging was performed with proton-density- and T2-weighted spin-echo sequences. Staging of CTS was done on the basis of clinical and electrophysiological testing, including evaluation of the number of previous steroid infiltrations in conservative treatment. Median nerve flattening, cross-sectional area, and signal intensity were measured from the distal radius to the end of the carpal tunnel. Delineation and structure of the median nerve were recorded qualitatively by two experienced radiologists in consensus. Three major MR imaging criteria of early CTS were (a) isolated prestenotic and intracarpal swelling of the median nerve (P < .01), (b) the absence of significant flattening, and (c) a generalized increase in signal intensity retrograde to the distal radius (P < .01). The nerve showed sharply delineated contours and a homogeneous signal pattern. Advanced CTS was characterized by retrograde swelling of the median nerve to the distal radius (P < .01) and decreased signal intensity (P < .05). Demarcation of the nerve became poorer, and its signal pattern appeared fasciculated. After steroid infiltration, the median nerve was difficult to delineate, showed an inhomogeneous structure, and swelling was less pronounced than without steroid infiltration (P < .05). MR imaging yields typical morphologic findings that correlate with the duration and severity of median nerve compression. Hence, MR imaging allows staging of median nerve compression in CTS and thus may contribute to therapeutic decision-making.

The mechanism of immunodepression after brain injury is not yet clear. Here we demonstrate rapid systemic release of the immunoinhibitory cytokine interleukin-10, monocytic deactivation and a high incidence of infection in patients with 'sympathetic storm' due to acute accidental or iatrogenic brain trauma. In vitro studies showed that within minutes catecholamines trigger the secretion of interleukin-10 from unstimulated monocytes through a beta-adrenoreceptor-mediated, cAMP/protein kinase A-dependent pathway. We found that in a rat model of acute brain injury, the beta-receptor antagonist propranolol prevented the increase of interleukin-10 plasma levels. Rapid monocytic interleukin-10 release after sympathetic activation may represent a common pathway for immunodepression induced by stress and injury.

The effects of barium on stimulus-induced rises in [K+]o were studied in the dentate gyrus (DG) and area CA1 of human hippocampal slices. Rises in [K+]o elicited by repetitive stimulation of the hilus, stratum moleculare, alveus, or stratum radiatum were dependent on stimulus intensity and frequency. Barium augmented rises in [K+]o in the DG by about 120% but failed to do so in area CA1. In both DG and area CA1 barium had no effects on population spikes whereas stimulus-induced slow field potentials were reduced. Since barium interferes with K+ uptake and redistribution by blocking leak conductances and inwardly-rectifying currents in astrocytes, our findings suggest that glial cells in the sclerotic hippocampal area CA1 may contribute less to K+ regulation.

In a retrospective study the charts of 72 patients who had decompressive surgery for lumbar stenosis between 1987 and 1990 were evaluated. Mean first follow up was 2.5 years (range 1.5 years to 3.5 years). A second follow up was done 8 years after surgery via mail. The mean age was 59.7 years (females 63.7, males 55 years). The average interval between the onset of complaints to surgery was 6 years. Claudicatio intermittens was found in 34.7% of cases. Patients were divided into four groups according to the classification by Arnoldi from 1976. Laminectomy of hemilaminectomy was performed in 73.6% of cases. In 68.1% nucleotomy was performed. In the first follow up outcome of patients was good in 73.6%. Complete recovery was noted in 61.1%. 11% were not satisfied with operative results. Old patients especially benefitted from the operation. In the second follow up after 8 years only 62.1% of the patients mentioned that their results were unchanged, good or better than at the first evaluation. The other 37.9% complained of a poorer result.

Monitoring of comatose patients in the neurosurgical intensive care unit (NICU) is constantly extended by the development of new methods for monitoring of cerebral function, metabolism and oxygenation. To simplify the interpretation of the rising number of parameters, and to avoid data overflow, a multimodal cerebral monitoring (MCM) system has been developed for the acquisition, display, on-line analysis and recording of physiological parameters from multiple bedside data sources. This article describes the technical details and the design of this computerized data acquisition system for variable applications in clinical patient monitoring and research. A Windows (Microsoft Corporation, Redmont, Washington) platform was equipped with an analog/digital converter board. Software for multimodal cerebral monitoring was developed using LabVIEW for Windows (National Instruments, Austin, Texas), a graphical programming system. Two software modules were created: One for the automatic acquisition of data, display of time dependent trend graphs, processing of on-line histograms, special functions for research, and storage of data in compatible format. The other module serves as an off-line monitor to display recorded data in various modalities. The MCM system has been used in 30 comatose patients with severe head injury. Mean time of MCM is 5.3 days (+/- 2.8 days), resulting in a total running time of the system of about 3800 hrs. Hardware and software proved to run stable and safe. The MCM system has become a valuable tool for monitoring of comatose patients. The simultaneous display of trend graphs of various monitoring parameters and the online processing of histograms improved the survey of the patient's condition in the ICU. Recorded data were analysed offline and contribute to a consecutively increasing data bank.

The purpose of this study was to compare brain tissue-PO2 (PtiO2) in lesioned vs. non-lesioned brain tissue. PtiO2 was monitored bifrontally with a "Clark"-type microcatheter in patients following severe head injury (n = 6) and subarachnoid hemorrhage (SAH) (n = 1) from day 2 to day 12 posttrauma/post SAH. Mean arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure and end-tidal CO2 were monitored. Data were stored and analyzed by a multimodal cerebral monitoring system. The CT of five patients was classified as "diffuse injury" and of one patients as "evacuated mass lesion". The patient with SAH (Hunt and Hess IV) had a concomitant intracerebral hematoma which was removed. In all cases, one catheter was placed close to the lesion, while the other was situated in an area with no visible pathology. For analysis, bifrontal PtiO2 data were taken from both on-line monitoring and O2 reactivity tests (FiO2 1.0 for 10 min). Two different patterns were identified: periods of concordance (22% of recordings) and periods in which PtiO2 was lower in lesioned cerebral white matter (78%) but always running parallel. In the latter case, O2-reactivity response was markedly reduced on the lesioned side. Our findings demonstrate a decreased PtiO2 and a reduced O2 reactivity in contused or infarcted brain tissue. Future studies have to clarify which PtiO2 is more important to be used as a guide for therapy.

Continuous monitoring of cerebral metabolism would be desirable for early detection of vasospasm in SAH patients. Bedside-microdialysis, a new technique for on-line monitoring of cerebral metabolism, may reflect changes seen in cerebral vasospasm diagnosed by transcranial Doppler sonography (TCD). This report represents the first case of combined TCD monitoring and on-line microdialysis from the brain extracellular fluid in a SAH patient. A 48-year-old woman suffered subarachnoid hemorrhage grade IV according to Hunt and Hess. Angiography revealed an aneurysm of the left carotid artery. The aneurysm was clipped 45 hours after bleeding. The microdialysis catheter was inserted after aneurysm clipping into the white matter of the left temporal lobe. Sampling of microdialysates started immediately, analyzing time for glucose, lactate, pyruvate and glutamate was four minutes. Postoperatively, the patient was doing well and microdialysis and TCD parameters remained within normal range. On the third postoperative day a shift to anaerob metabolism (decrease of glucose, increase of lactate and the lactate-pyruvate ratio up to pathological levels) and an increase in glutamate was observed suggesting insufficient cerebral perfusion. The patient progressively deteriorated clinically. Vasospasm was diagnosed by TCD monitoring 36 hours after onset of ischemic changes monitored by microdialysis. After elevation of mean arterial blood pressure, TCD values and metabolic parameters normalized. Interestingly, the pathological changes in on-line microdialysis preceded the typical increase in blood flow velocity by TCD and the clinical deterioration. Our case suggests, that bedside-microdialysis may be useful for early detection of vasospasm and continuous surveillance of treatment and may be a new guide to treat ischemic neurological deficits following SAH.

This study investigates the effect of hypoxic brain tissue PO2 on outcome, and examines the incidence of possible causes for cerebral hypoxia. We studied 35 patients with severe head injury (GCS < or = 8). Age was 33.2 (+/- 11.3) years. Total time of monitoring of PtiO2, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and endtidal PCO2 (ETCO2) was 119.3 (+/- 65.7) hours. Data were continuously recorded by a computer system. Outcome was assessed at discharge and after 6 months post injury. 56% of the patients with more than 300 minutes of PtiO2 < 10 mm Hg died, 22% had an unfavourable outcome, 22% had a favourable outcome. Cerebral hypoxia was associated with intracranial hypertension (ICP > 20 mm Hg) in 11.5 (+/- 15.1)%. CPP was compromised below 60 mm Hg in 16.8 (+/- 23.4)%. Hypocarbia (ETCO2 < 28 mm Hg) was present in 48.0% of the time of PtiO2 < 10 mm Hg. No obvious cause for cerebral hypoxia was found in 45% of the data. These result underscore the association of cerebral hypoxia with poor neurological outcome and stress the meaning of monitoring of PtiO2 as an independent parameter in patients following TBI.

Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. Brain tissue PO2 varied when measured in lesioned and nonlesioned tissue. In non lesioned tissue both catheters closely correlated (delta Licox/Paratrend: mean PtiO2 < 5 mm Hg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (delta lesioned/non lesioned: mean PtiO2: 10.3 mm Hg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10 mm Hg, independent of the type of microsensor used. During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.

A harmful effect of prolonged hyperventilation on outcome has been shown in comatose patients after severe head injury. The purpose of this study was to assess the acute effect of moderate hyperventilation for treatment of intracranial hypertension (ICP < 20 mmHg) on invasively measured brain tissue-PO2 (PtiO2), PCO2 (PtiCO2) and pH (tipH) in severely head injured patients. 15 severely head injured patients (GCS < or = 8) were prospectively studied. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), endtidal CO2 (ETCO2), PtiO2, PtiCO2 and tipH (Paratrend or Licox microsensors) were continuously recorded using multimodal monitoring. Following a baseline period of 15 minutes, patients were hyperventilated for 10 minutes. Arterial blood gas analysis was done before, during and after hyperventilation. At least three hyperventilation maneuvers were performed per patient. For statistical analysis the Friedman test was used. Hyperventilation (paCO2: 32.4 +/- 0.6 to 27.7 +/- 0.5 mmHg) significantly reduced ICP from 25.3 +/- 1.5 to 14.2 +/- 1.9 mmHg (p < 0.01). As a consequence, CPP increased by 9.6 +/- 3.4 mmHg to 76.8 +/- 3.2 mmHg. Brain tissue PCO2 decreased from 37.5 +/- 1.3 to 34.6 +/- 1.2 while tipH increased from 7.13 to 7.16. In all patients, hyperventilation led to a reduction of brain tissue PO2 (PtiO2/Licox: 24.6 +/- 1.4 to 21.9 +/- 1.7 mmHg, n.s.; PtiO2/Paratrend: 35.8 +/- 4.3 to 31.9 +/- 4.0 mmHg, n.s.). In one case hyperventilation even had to be stopped after 7 min because the drop in brain tissue PO2 below 10 mmHg signalized imminent hypoxia. As well known, hyperventilation improves CPP due to a reduction in ICP. However, this does not ameliorate cerebral oxygenation as demonstrated by the decrease in PtiO2. This underlines that hyperventilation should only be used with caution in the treatment of intracranial hypertension.