Artificial disc versus spinal fusion in the treatment of cervical spine degenerations in tetraplegics: a comparison of clinical results.

STUDY DESIGN: Comparative prospective study. OBJECTIVES: To determine functionality of the cervical spine when using ProDisc C in comparison with the conventional method of treatment (decompression and fusion) in paraplegics. SETTING: Spinal Cord Injury Centre in Germany. METHODS: Two homogeneous groups were studied. The patients were treated with ventral decompression and either had a fusion with an iliac bone graft and plate (group 1) or had received a disc replacement (group 2). Pre- and postoperatively, the subjective scores of SF 36 and Neck Disability Score were determined. Also, objective data of the Spinal Cord Independence Measure (SCIM) III and mobility of the cervical spine, using the neutral-0-method, were evaluated. Prosthesis implementation and union or fusion were monitored by X-rays. Complications and alterations of the neurology were recorded according to the American Spinal Injury Association Score. RESULTS: Neurological remissions of the radicular syndrome that caused the operation were observed. In one case, the dislocation of the prosthesis necessitated an alternative treatment. Mobility of the cervical spine after 6 months was higher in group 2. Both groups showed signs of improvement in the Neck Disability Score and in SF 36. None of the two groups had changes in their SCIM score. One case in group 2 showed ventral blocking; all cases of group 1 fused successfully. CONCLUSION: Usage of prostheses results in improved total mobility of the cervical spine in comparison with the outcomes of a fusion. This study also confirmed these results in tetraplegics.

Leukocyte-endothelium-interaction in pial vessels following global, cerebral ischaemia.

BACKGROUND: Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. METHODS: Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. FINDINGS: Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p < 0.001) and a smaller increase of the venular diameters (p < 0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. INTERPRETATION: In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia.

Influence of platelet-activating factor on cerebral microcirculation in rats: part 2. Local application.

BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) is involved in the development of secondary brain damage after ischemic and traumatic brain injury. On the basis of data from studies in peripheral organs, we hypothesized that PAF-mediated effects after cerebral injury could be secondary to alterations in cerebral microcirculation. METHODS: Changes in cerebral microcirculation focusing on leukocyte-endothelium interactions were quantified with the use of a closed cranial window model in Sprague-Dawley rats (n=33) by means of intravital fluorescence microscopy. The brain surface was superfused with PAF in concentrations from 10(-3) (n=3) to 10(-12) mol/L (n=6) for 20 minutes (5 mL/h). RESULTS: PAF 10(-4) mol/L (n=4) increased the number of rolling and adherent leukocytes in venules from 9.7+/-0.4 to 19.7+/-2.3 cells/100 mm. min (P=NS versus control) and from 2.2+/-0.5 to 4.3+/-0.7 cells/100 mm. min (P<0.05 versus control), respectively. Lower concentrations did not elicit leukocyte-endothelium interactions. Vessel diameters remained unchanged except for a transient increase of arteriolar diameters during superfusion with PAF 10(-4) and 10(-6) mol/L (n=6). Although only a limited area of the brain surface was exposed to PAF, the mediator induced a significant dose-dependent transitory arterial hypotension and caused irreversible circulatory shock at the high concentration (PAF 10(-3) mol/L). Arterial hypotension after administration of PAF 10(-3) mol/L could be attenuated by the intravenous pretreatment with the PAF antagonist WEB 2170BS. CONCLUSIONS: PAF, when locally released after brain injury, can penetrate the blood-brain barrier and induce systemic effects, including arterial hypotension. Its role as a mediator in the development of secondary brain damage seems, at least in the initial phase, not to be associated with disturbances of cerebral microcirculation or activation of leukocytes.

The effect of hypertonic fluid resuscitation on brain edema in rabbits subjected to brain injury and hemorrhagic shock.

Small-volume resuscitation with 7.2% NaCl/10% dextran 60 (HHS) restores cardiovascular stability faster than all other therapeutic modalities currently known. This study was undertaken to elucidate the effects of HHS on the brain, specifically on the formation of posttraumatic brain edema. HHS was administered to anesthetized albino rabbits with or without a focal cryogenic brain lesion and hemorrhagic shock. Specific gravity of small tissue samples was determined 4 h after injury and values were topographically assembled to form a color-coded map of both hemispheres, allowing for a high resolution mapping of brain edema. Cerebral blood flow on the side of the lesion, as assessed by the H2 clearance method, increased transiently after injury but remained unchanged from baseline during shock and after infusion of HHS, indicating intact cerebrovascular autoregulation. The cryogenic lesion without subsequent HHS infusion resulted in significant brain edema formation in grey and white matter of the exposed hemisphere. In injured animals, resuscitation with HHS led to a global reduction of brain water content in both hemispheres. We conclude that small-volume resuscitation with HHS does not worsen posttraumatic brain edema. To the contrary, our results show that it decreases cerebral water content even in regions close to the injury. This makes it worthwhile to investigate the benefits of HHS for the treatment of intracranial hypertension.

Leukocyte/endothelial interactions and blood-brain barrier permeability in rats during cerebral superfusion with LTB4.

The experimental study analyses the vasomotor response (change of diameter of pial arterioles and venules), and blood-brain barrier function of the pia-arachnoidea at the rat brain surface before, during and after cerebral superfusion with 1.5 or 15.0 nM LTB4 in mock CSF. Leukocyte dynamics were studied by assessment of their centerline velocity, of rolling along ("roller") and attachment to ("sticker") the venular wall of white blood cells intravitally stained by Rhodamin 6G. Superfusion of the brain with LTB4 at both dose levels led to dilation of arterioles to 130% (p < 0.001), while of venules to 117% (p < 0.001) of control. The centerline velocity of leukocytes increased from 0.7 to 0.9 mm/s, however, only after superfusion with LTB4 at the high dose level. LTB4 induced a dose-dependent rolling (p < 0.01) and sticking of leukocytes (p < 0.001). Yet, a delay of about 60 min between cerebral administration of LTB4 and the maximal response of leukocyte rolling and sticking was observed. Whereas the blood-brain barrier was not opened by cerebral superfusion with 1.5 or 15.0 nM LTB4, for i.v. Na(+)-fluorescein, barrier leakage was promptly induced by 30.0 nM. The present findings demonstrate that cerebral administration of LTB4 by superfusion of the exposed brain surface is eliciting a pronounced vasomotor response, whereas the induction of leukocyte/endothelial interactions is less impressive.

[Hypertonic solutions in treatment of intracranial pressure]. / Hypertone Lösungen zur Behandlung des intrakraniellen Drucks.

Administration of hypertonic solutions is the method of choice for acute treatment of intracranial hypertension. Recording of the intracranial pressure during treatment facilitates adjustment of the dosis to the actual ICP-response, avoiding thereby administration of an excessive osmotic load as a basis to prolong therapeutical efficacy. The mechanisms underlying reduction of the intracranial pressure by hypertonic solutions are still controversially discussed. Dehydration of normal probably also of edematous brain parenchyma and constriction of cerebral resistance vessels as an autoregulatory response causing reduction of the intracranial blood volume are the most likely options. Administration of hypertonic/hyperoncotic solutions has regained attention on account of its unmatched therapeutical efficacy to reestablish normal conditions in severe hemorrhagic shock. Administration of, e.g. 7.2% NaCl/10% Dextran 60 in an amount equivalent of only 10% of the shed blood volume is immediately normalizing cardiac output and improving the microcirculation in peripheral organs. These therapeutical properties are relevant in head injury, since inflicted patients quite often are suffering from peripheral trauma and consequently from hemorrhagic shock. No evidence has been obtained in a variety of experimental studies that hypertonic/hyperoncotic solutions have adverse effects on the brain in the presence of a cerebral lesion. To the contrary, the fluid mixture has been found to lower the increased intracranial pressure. Administration of hypertonic/hyperoncotic solutions appears therefore appropriate in acute cerebral insults from head injury and impending circulatory failure from shock in order to inhibit development of secondary brain damage.

[Anesthesiologic efficacy of propanidid as a liposome dispersion. An experimental study with rats]. / Anästhesiologische Wirksamkeit von Propanidid als Liposomendispersion. Eine experimentelle studie mit ratten.

BACKGROUND: Propanidid, an ultra-short-acting i.v. anaesthetic agent, was widely used in the 1960s. Reports of anaphylactoid reactions in patients associated with release of histamine following administration of the drug, however, led to withdrawal of this useful anaesthetic. Since the adverse side effects of the former solution could be attributed to the solvent cremophor, attempts have recently been made to produce a propanidid solution without addition of the solvent. We report on comparative investigations employing a new liposomal solution (B. Braun, Melsungen, FRG) and the conventional cremophor preparation with regard to anaesthetic properties, haemodynamic side effects, and electroencephalographic effects (EEG). METHODS: Sprague-Dawley rats (n = 46) were implanted with venous and arterial lines and epidural EEG electrodes during chloral-hydrate anaesthesia. The following day, arterial blood pressure (ABP), heart rate (HR), and EEG were monitored in awake animals and then after induction of anaesthesia by a bolus of the respective propanidid preparation, followed by an infusion period of 15 min in six different experimental groups. Animals of groups L-60, L-90, L-120, or C-60, C-90, or C-120 groups received 60, 90, or 120 mg.100 g-1.h-1 of the liposomal (L) or cremophor (C) preparation. During anaesthesia, the corneal reflex and nociception to tail-clamping were also tested. At termination of the infusion, blood samples were drawn for determination of plasma propanidid concentrations. RESULTS: Both preparations were similarly effective in induction and maintenance of anaesthesia in a dose-dependent manner; both similarly lowered ABP and HR. The corneal reflex and nociceptive responses to tail clamping were also comparably suppressed. However, whereas the liposomal preparation was well tolerated at higher dose levels, the cremophor preparation caused considerable dose-dependent mortality of 11%, 86%, and 86% in animals in groups C-60, C-90, and C-120, respectively. Both preparations were found to induce a burst-suppression pattern in the EEG associated with clonic seizures, with a lower incidence with the liposomal preparation (22% and 50% in groups L-90 and L-120) as compared to the cremophor preparation (100% and 89% in groups C-90 and C-120). A remarkable variability in propanidid plasma concentrations was found at the end of the infusion period, although no differences were observed between both preparations. Discontinuation of infusion of propanidid resulted in rapid awakening (less than 5 min), irrespective of whether the liposomal or conventional preparation was employed. CONCLUSION: The present findings demonstrate largely identical anaesthetic potencies of a new liposomal solution as compared to the conventional cremophor preparation of propanidid. The liposomal preparation, however, was superior as far as tolerance and incidence of clonic seizures was concerned. The present findings should prompt further studies on the suitability of liposomal propanidid as a short-acting anaesthetic agent in patients.

[Therapy of hemorrhagic shock using small volumes of hypertonic-hyperoncotic NaCl-dextran solution--effects on the brain]. / Therapie des hämorrhagischen Schocks mit kleinen Volumina hyperton-hyperonkotischer NaCl-Dextranlösung--Auswirkungen auf das Gehirn.

Infusion of small volumes of hypertonic/hyperoncotic solution (HHL: 7.2% NaCl/10% dextran 60) is highly effective in haemorrhagic shock. Cardiovascular function is restored in a matter of minutes by rapid mobilisation of extravasal fluid. However, little experience has been collected to date on the side effects on the brain by this new form of shock therapy. The present studies on HHL were conducted with particular reference to cerebral blood flow, cerebral oxygen supply, and intracranial pressure. Haemorrhagic shock with a drop in arterial blood pressure to 40 mmHg over a period of 30 min was induced in rabbits under alpha-chloralose anaesthesia by means of bloodletting. Subsequently, the hypertonic/hyperoncotic solution (HHL) was infused into the experimental animals within two minutes. The regional cerebral blood flow (H2-clearance) and the cerebral O2 supply were studied by determining the pO2 of the cerebral cortex in experimental animals without haemorrhagic shock but with infusion of HHL. Finally, separate single tests were conducted to analyse the effect of the infusion of HHL on the intracranial pressure after induction of a focal cold lesion of the brain in combination with the implantation of a rubber balloon in the epidural space as an intracranial space-occupying growth. Infusion of HHL during shock produced rapid normalisation of cardiac output, whereas in normovolaemic animals without shock it produced a temporary increase of this parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment of hemorrhagic hypotension with hypertonic/hyperoncotic solutions: effects on regional cerebral blood flow and brain surface oxygen tension.

Hypertonic/hyperoncotic solutions (e.g. HHS: 7.2% NaCl/10% dextran-60) are highly effective to normalize cardiovascular function in hemorrhagic shock due to rapid mobilization of fluid from the extravascular compartment. Since experiences are limited with regard to potential side effects of this treatment on the central nervous system, the present studies were carried out under particular consideration of the cerebral blood flow and O2 supply. HHS was administered in albino rabbits subjected to alpha-chloralose anesthesia and artificial ventilation with and without hemorrhagic hypovolemia. Hemorrhagic hypovolemia of 30 min duration was induced by withdrawal of approximately one third of the circulating blood volume resulting in a decrease in arterial blood pressure to 40 mm Hg. HHS was studied in addition to normovolemic animals. Cardiac output was rapidly normalized by infusion of HHS in animals with hypovolemia, while it increased intermittently in normovolemic animals. In animals with hemorrhagic shock arterial blood pressure recovered by treatment to approximately 70% of normal, whereas blood pressure remained unchanged after infusion of HHS in normovolemic controls. Cerebral blood flow, which was assessed by H2 clearance at the brain surface, had a range of 43.0-50.3 ml/100 g/min under control conditions. It remained virtually unchanged during hemorrhagic hypovolemia and also after infusion of HHS in normovolemic animals. Treatment of shock by HHS was followed 90 or 120 min later by a moderate increase in regional cerebral blood flow to 61 ml/100 g/min. Local tissue PO2 at the brain surface was obtained by an O2 multiwire electrode in the vicinity of the H2 clearance measurements using a weightless suspension system to avoid compression of the brain surface. Infusion of HHS in normovolemic animals did not affect the O2 supply of the brain. Hemorrhagic hypovolemia which led to a left shift of the cerebral PO2 histogram was followed by gradual normalization after fluid resuscitation. The current findings taken together do not indicate adverse side effects of this efficient method of fluid resuscitation with regard to the cerebral blood and O2 supply. The results make worthwhile further investigations on HHS in the presence of a focal brain lesion causing brain edema to find out whether the HHS are useful also for the treatment of intracranial hypertension.