Search

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.

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 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.

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 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.

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.

Objective of this study was the characterization of traumatic brain injury induced by a "Controlled Cortical Impact" with magnetic resonance imaging techniques. The impact was applied to the intact dura of the left hemisphere in Sprague-Dawley rats. The pneumatic impactor was accelerated to a velocity of 7 m/s contusing the left temporo-parietal hemisphere to a depth of 2 mm. Posttraumatic hemispheric swelling and water content were determined gravimetrically, Evans Blue extravasation photometrically, and volume of ischemia by TTC-staining and planimetry. Magnetic resonance imaging was performed by a Bruker biospec 24/40, 90 min, 24 and 72 h post trauma using a T2w RARE sequence, a T1w sequence, before and after application of contrast agent, and a set of diffusion weighted images for calculation of ADC-maps. Data analysis was performed using a cluster algorithm enabling to interpret corresponding image pairs simultaneously. T2w imaging indicates the maximum edema about 24 h post trauma. Blood-brain barrier damage, detected by T1w imaging, is more predominant in the early posttraumatic phase. The cluster algorithm detects different edema components: from the necrotic core to the perifocal vasogenic rim. MRI in combination with the cluster algorithm will hopefully be a valuable tool in testing neuroprotective agents.

This study investigates the influence on tromethamine (THAM) on ischemic volume induced by permanent middle cerebral artery occlusion (MCAO) in rats. 14 male Sprague Dawley rats underwent left sided permanent MCAO by electro coagulation. Animals were treated either by 3-M THAM given intravenously in a single dosage of 0.6 mmol/kg body weight (THAM group: n = 7) 10 min following MCAO and again 1, 2, 3, 4 and 5 hours later or by NaCl 0.9% (placebo group: n = 7) in the same mode. Mean arterial blood pressure (MABP) was monitored for 30 min post MCAO and arterial blood gases were taken 10 min after the first injection. The extent of ischemia volume was assessed by planimetry of coronal sections stained with triphenyl-tetrazolium chloride (TTC) and with hematoxilin/eosin (HE). Tests for significance were accomplished by ANOVA on ranks. A difference of p < 0.05 was considered significant. The THAM group showed an insignificant decrease in MABP 1 min after injection (THAM: 75 +/- 11 mmHg, placebo: 86 +/- 10 mmHg). Arterial pH was significantly different (THAM: 7.46 +/- 0.04; placebo: 7.32 +/- 0.03). In TTC staining, the ischemia volume--given in absolute values and percentage of the total left volume--was significantly reduced in the THAM group (THAM: 43.9 +/- 8.3 mm3/7.0 +/- 1.3%; placebo: 95.2 +/- 13.8 mm3/14.2 +/- 2.0%). In HE staining, the reduction of ischemia, volume did not reach statistical significance (THAM: 49.1 +/- 9.9 mm3/9.6 +/- 1.8%; placebo: 66.3 +/- 14.5 mm3/13.1 +/- 2.8%). Based on these results, a moderate neuroprotective effect of THAM in experimental cerebral infarction could be demonstrated.

We studied 32 consecutive patients with known or suspected cerebrovascular abnormalities studied with spiral CT following a intravenous bolus injection of iodinated contrast medium with a power injector. Flow was 3 or 4 ml/s. In an attempt to define the appropriate delay time and scan duration a cranial angio-CT without table increment was performed on 10 patients. Enhancement was measured by manually placed regions of interest within the left middle cerebral artery and the inferior sagittal sinus. All patients except one had intraarterial angiography (DSA) for comparison. In 6 patients with an arteriovenous malformation (AVM) follow-up was possible after one and/or two embolisation procedures. These patients had plain and contrast-enhanced spiral CT. The diagnosis was aneurysm in 9 (8 berry aneurysms, one giant fusiform aneurysm), AVM in 13 (all supratentorial) and traumatic arteriovenous fistula in one. In 9 patients there were no detectable pathological vascular findings. After 3D reconstruction the size (between 5 and 28 mm), location and the relationship to the parent vessel of the aneurysms, the extent of the AVMs and the distribution of the embolisation material could be demonstrated clearly. The main feeding vessel(s), nidus and draining veins were reliably shown. The decreased extent of the AVMs after embolisation was clearly demonstrated. There was no difference in diagnosis when DSA and 3D-CT were compared by two independent radiologists. We consider arterial spiral CT with 3D reconstruction to have the potential of offering important diagnostic information for the treatment of intracranial AVMs and aneurysms.

Despite the availability of excellent neuroradiological examination techniques, a decision to operate is usually still reached largely on the basis of a diagnosis of radical and/or medullary cervical compression syndrome made by clinical neurological examination. Computer tomography has allowed a decisive improvement in the diagnosis of these processes, since the position of parts of discs that have prolapsed or sequestrated dorsally or dorsolaterally relative to the spinal cord and the nerve roots can be visualized directly. Since core spin tomography does not yield information that is any more helpful in the diagnosis, despite the considerably higher level of technical sophistication and higher costs, we are of the opinion that there is no call to apply this procedure routinely for the diagnosis of medial and lateral cervical disc rupture. Since the neurological symptoms do not always allow localization of the radicular or medullary damage to the segment or segments affected, it is sometimes necessary to perform myelography with water-soluble contrast media for this purpose. The microsurgical procedures available are restricted foraminotomy for the relief of cervical nerve root compression and ventral diskectomy for the relief of spinal cord compression.