| 1. |
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| 2. |
- Büki, Andras, 1966-, et al.
(författare)
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Initial Clinical Experience with a Combined Pulsed Holmium-Neodymium-YAG Laser in Minimally Invasive Neurosurgery*
- 1999
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Ingår i: Minimally Invasive Neurosurgery. - : Thieme Medical Publishers. - 0946-7211 .- 1439-2291. ; 42:1, s. 35-40
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Tidskriftsartikel (refereegranskat)abstract
- Various biophysical features of the laser beam have already been utilized in clinical neurosurgery. However, the application of this therapeutic modality has by no means been overexploited. The history of laser application in neurosurgery has shown that there is no universal laser system capable of performing all surgical tasks in a suitable manner. The best results in traditional neurosurgery were achieved with instruments combining various wavelengths, such as the CO2 and neodymium-YAG lasers. A pulsed holmium-YAG and neodymium-YAG (Ho:YAG and Nd:YAG) combined laser have been recently developed to meet the special requirements of minimally invasive neurosurgery. The system consists of a compact double-crystal single-head solid-state laser system generating 2 different wavelengths (Ho:YAG 2.08 microns and Nd:YAG 1.05 microns), selected for their capabilities of efficient coagulation and ablation. The two wavelengths are coupled into a common flexible optical fiber, which allows endoscopic application. The wavelengths can act simultaneously or separately without any interchange of the instruments. The system was employed first for experimental and subsequently for clinical purposes, primarily for endoscopic operations. In this work the initial clinical experience is reported. The excellent haemostatic properties of the Nd:YAG laser and the ablative properties of the Ho:YAG laser were confirmed. It was concluded that simultaneous application of the two laser modalities within one flexible fiber offers new perspectives in tissue handling in endoscopic neurosurgery and as in open microsurgery.
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| 3. |
- Büki, Andras, 1966-, et al.
(författare)
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Moderate Posttraumatic Hypothermia Decreases Early Calpain-Mediated Proteolysis and Concomitant Cytoskeletal Compromise in Traumatic Axonal Injury
- 1999
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Ingår i: Experimental Neurology. - : Academic Press. - 0014-4886 .- 1090-2430. ; 159:1, s. 319-328
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Tidskriftsartikel (refereegranskat)abstract
- Traumatic brain injury (TBI) in animals and man generates widespread axonal injury characterized by focal axolemmal permeability changes, induction of calpain-mediated proteolysis, and neurofilament side-arm modification associated with neurofilament compaction (NFC) evolving to axonal disconnection. Recent observations have suggested that moderate hypothermia is neuroprotective in several models of TBI. Nevertheless, the pathway by which hypothermia prevents traumatic axonal injury (TAI) is still a matter of debate. The present study was conducted to evaluate the effects of moderate, early posttraumatic hypothermia on calpain-mediated spectrin proteolysis (CMSP), implicated in the pathogenesis of TAI. Using moderate (32 degrees C) hypothermia of 90 min duration without rewarming, the density of CMSP immunoreactive/damaged axons was quantified via LM analysis in vulnerable brain stem fiber tracts of hypothermic and normothermic rats subjected to impact acceleration TBI (90 min postinjury survival). To assess the influence of posthypothermic rewarming, a second group of animals was subjected to 90 min of hypothermia followed by 90 min of rewarming to normothermic levels when CMSP was analyzed to detect if any purported CMSP prevention persisted (180 min postinjury survival). Additionally, to determine if this protection translated into comparable cytoskeletal protection in the same foci showing decreased CMSP, antibodies targeting altered/compacted NF subunits were also employed. Moderate hypothermia applied in the acute postinjury period drastically reduced the number of damaged axons displaying CMSP at both time points and significantly reduced NFC immunoreactivity at 180 min postinjury. These results suggest that the neuroprotective effects of hypothermia in TBI are associated with the inhibition of axonal/cytoskeletal damage.
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| 4. |
- Büki, Andras, 1966-, et al.
(författare)
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Occlusive hydrocephalus complicating tuberous sclerosis : report of two cases
- 1996
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Ingår i: European Journal of Neurology. - Oxford : Blackwell Publishing. - 1351-5101 .- 1468-1331. ; 3:3, s. 255-259
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Tidskriftsartikel (refereegranskat)abstract
- Two patients-6 and 14 years old-with tuberous sclerosis are presented. Both developed a subependymal giant cell astrocytoma from nodules located near to the foramen of Monro. They caused obstruction of the cerebrospinal fluid pathways. Signs of raised intracranial pressure were detected in both patients, and one of them had also developed infantile spasm-Blitz-Nick-Salaam seizures. Cutaneous stigmata being characteristic for this entity were observed in both cases, but their mental development was unaffected. Diagnosis was based on computed tomography. Angiography did not reveal pathological vessels. The tumours were completely excised through transcallosal exposure in both cases. The patients have been symptom-free during the follow-up time of 1 and 2 years. Although the incidence of malignant transformation of tuberous sclerosis is less than 15% the disease generally has a poor prognosis which can be ascribed to sudden increase of intracranial pressure caused by obstruction of cerebrospinal fluid pathways by paraventricular tumours. However, regular follow-up of paraventricular nodules and maintenance of patency of cerebrospinal fluid pathways by microsurgical methods in patients suffering from mild cerebral disorders offers a better chance of survival.
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| 5. |
- Büki, Andras, 1966-, et al.
(författare)
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Peptidergic innervation of human cerebral blood vessels and saccular aneurysms
- 1999
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Ingår i: Acta Neuropathologica. - : Springer. - 0001-6322 .- 1432-0533. ; 98:4, s. 383-388
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Tidskriftsartikel (refereegranskat)abstract
- Peptidergic innervation of the human cerebral vasculature has not yet been described in detail and its role in the maintenance of cerebral autoregulation still needs to be established. Similarly, few data exist on the innervation of vascular malformations. The aim of this study was to clarify the peptidergic innervation patterns of human cerebral arteries of various sizes, and, for the first time, that of saccular aneurysms. Light microscopic study of whole-mount preparations of human cerebral arteries and aneurysm sacs resected either during tumor removal or after neck-clipping were carried out by means of silver-intensified light microscopic immunocytochemistry visualizing neuropeptide-Y, calcitonin gene-related peptide and substance P immunoreactivity. Systematic morphological investigations confirmed the presence of longitudinal fiber bundles on the adventitia and a network-like deeper peptidergic system at the adventitia-media border, while in smaller pial and intraparenchymal vessels, only sparse longitudinal immunopositive axons could be detected. The innervation pattern was totally absent in the wall of saccular aneurysms with the complete disappearance of peptidergic nerve fibers in some areas. To the best of our knowledge neither the disappearance of this network on small pial and intraparenchymal vessels, nor the absence of an innervation pattern in saccular aneurysms have been described before. Nonhomogeneous peptidergic innervation of the human cerebral vascular tree might be one of the factors responsible for the distinct autoregulatory properties of the capacitance and resistance vessels. Malfunction of this vasoregulatory system might lead to the impairment of autoregulation during pathological conditions such as subarachnoid hemorrhage.
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| 6. |
- Büki, Andras, 1966-, et al.
(författare)
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Postinjury cyclosporin a administration limits axonal damage and disconnection in traumatic brain injury
- 1999
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 16:6, s. 511-521
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Tidskriftsartikel (refereegranskat)abstract
- Recent observations concerning presumed calcium-induced mitochondrial damage and focal intraaxonal proteolysis in the pathogenesis of traumatic axonal injury (TAI) have opened new perspectives for therapeutic intervention. Studies from our laboratory demonstrated that cyclosporin A (CsA), a potent inhibitor of Ca2+-induced mitochondrial damage, administered 30 min prior to traumatic brain injury preserved mitochondrial integrity in those axonal foci destined to undergo delayed disconnection. We attributed this neuroprotection to the inhibition by CsA of mitochondrial permeability transition (MPT). Additional experiments proved that CsA pretreatment also significantly reduced calcium-induced, calpain-mediated spectrin proteolysis (CMSP) and neurofilament compaction (NFC), pivotal events in the pathogenesis of axonal failure and disconnection. Given these provocative findings the goal of the current study was to evaluate the potential of CsA to inhibit calcium-induced axonal damage in a more clinically relevant postinjury treatment paradigm. To this end, cyclosporin A was administered intrathecally to Sprague Dawley rats 30 min following impact acceleration traumatic brain injury. The first group of animals were sacrificed 120 min postinjury and the density of CMSP and NFC immunoreactive damaged axonal segments of CsA-treated and vehicle-treated injured animals were quantitatively analyzed. A second group of CsA- versus vehicle-treated rats was sacrificed at 24 h postinjury to compare the density of damaged axons displaying beta amyloid precursor protein (APP) immunoreactivity, a signature protein of axonal perturbation and disconnection. Postinjury CsA administration resulted in a significant decrease (>60%) in CMSP/NFC immunoreactivity in corticospinal tracts and medial longitudinal fasciculi. A similar decrease was detected in the density of APP immunoreactive damaged axons, indicating an attenuation of axonal disconnection at 24 h postinjury in CsA-treated animals. These results once again suggest that the maintenance of the functional integrity of the mitochondria can prevent TAI, presumably via the preservation of the local energy homeostasis of the axon. Moreover and perhaps more importantly, these studies also demonstrate the efficacy of CsA administration when given in the early posttraumatic period. Collectively, our findings suggest that a therapeutic window exists for the use of drugs targeting mitochondria and energy regulation in traumatic brain injury.
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| 7. |
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| 8. |
- Büki, Andras, 1966-, et al.
(författare)
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The role of calpail-mediated spectrin proteolysis in traumatically induced axonal injury
- 1999
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Ingår i: Journal of Neuropathology and Experimental Neurology. - : American Association of Neuropathologists. - 0022-3069 .- 1554-6578. ; 58:4, s. 365-375
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Tidskriftsartikel (refereegranskat)abstract
- In animals and man, traumatic brain injury (TBI) results in axonal injury (AI) that contributes to morbidity and mortality. Such injured axons show progressive change leading to axonal disconnection. Although several theories implicate calcium in the pathogenesis of AI, experimental studies have failed to confirm its pivotal role. To explore the contribution of Ca2+-induced proteolysis to axonal injury, this study was undertaken in an animal model of TBI employing antibodies targeting both calpain-mediated spectrin proteolysis (CMSP) and focal neurofilament compaction (NFC), a marker of intra-axonal cytoskeletal perturbation, at 15-120 minutes (min) postinjury. Light microscopy (LM) revealed that TBI consistently evoked focal, intra-axonal CMSP that was spatially and temporally correlated with NFC. These changes were seen at 15 min postinjury with significantly increasing number of axons demonstrating CMSP immunoreactivity over time postinjury. Electron microscopy (EM) demonstrated that at 15 min postinjury CMSP was confined primarily to the subaxolemmal network. With increasing survival (30-120 min) CMSP filled the axoplasm proper. These findings provide the first direct evidence for focal CMSP in the pathogenesis of generalized/diffuse AI. Importantly, they also reveal an initial subaxolemmal involvement prior to induction of a more widespread axoplasmic change indicating a spatial-temporal compartmentalization of the calcium-induced proteolytic process that may be amenable to rapid therapeutic intervention.
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| 9. |
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| 10. |
- Okonkwo, David O., et al.
(författare)
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Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury
- 1999
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Ingår i: NeuroReport. - : Lippincott Williams & Wilkins. - 0959-4965 .- 1473-558X. ; 10:2, s. 353-358
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Tidskriftsartikel (refereegranskat)abstract
- In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.
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| 11. |
- Povlishock, John T., et al.
(författare)
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Initiating mechanisms involved in the pathobiology of traumatically induced Axonal Injury and Interventions targeted at blunting their progression
- 1999
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Ingår i: Acta Neurochirurgica Supplementum. - Vienna : Springer. - 0065-1419. ; 73, s. 15-20
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Tidskriftsartikel (refereegranskat)abstract
- To gain better insight into the initiating factors involved in traumatically induced axonal injury cats and rats were subjected to various forms of traumatic brain injury. Following injury at intervals ranging from 10 min. to 3 hours, the animals were sacrificed and prepared in accordance with multiple immunocytochemical strategies capable of detecting focal changes in the axolemma, the subaxolemmal spectrin network, the underlying cytoskeleton as well as any related abnormalities in axoplasmic transport. Through these approaches it was recognized that the most severe forms of injury resulted in focal abnormalities of axonal permeability which were observed together with calpain-mediated spectrin proteolysis in the subaxolemmal network. These events were associated with compaction of the underlying neurofilaments and some microtubular loss which occurred without any direct evidence of overt axoplasmic proteolysis with the exception of the most severely injured fibers. In addition to these severely injured axonal profiles, other injured axons did not manifest overt changes in axolemmal permeability or early calpain-mediated spectrin proteolysis but demonstrated dramatic neurofilament and microtubular misalignment and impaired axoplasmic transport. Lastly, other small caliber axons showed another form of intraaxonal change manifested in the local pooling of organelles in the nodal and paranodal regions, with the suggestion that some of these changes may be reversible. In relation to these axonal responses the efficacy of various therapeutic investigations were assessed. The use of calcium chelators showed a trend for protection in those axons manifesting altered axolemmal permeability. However, the use of early and delayed hypothermia demonstrated dramatic protection resulting in significant reduction in the number of damaged axonal profiles. These studies illustrate the diversity and complexity of those axonal responses evoked by traumatic brain injury, suggesting that multiple forms of therapy may be needed to blunt these multifaceted forms of progression.
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| 12. |
- Vajda, Z., et al.
(författare)
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Transcranial Doppler-determined pulsatility index in the evaluation of endoscopic third ventriculostomy (preliminary data)
- 1999
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Ingår i: Acta Neurochirurgica. - : Springer. - 0001-6268 .- 0942-0940. ; 141:3, s. 247-250
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Endoscopic 3rd ventriculostomy has become the method of choice in the management of occlusive hydrocephalus. The treatment is accompanied by significantly less peri-operative complications than the cerebrospinal fluid shunting procedures previously employed. Close surveillance of patients, however, is necessary to avoid the consequences of raised intracranial pressure that may develop in case of obstruction of the artificial outlet of the 3rd ventricle. The aim of this study was to confirm the value of transcranial Doppler-determined pulsatility index (PI) in the assessment of the patency of endoscopic 3rd ventriculostomy and to elucidate its usefulness in early postoperative recognition of increased intracranial pressure.Methods: In twenty-two patients suffering from occlusive hydrocephalus, transcranial Doppler sonography (TCD) was performed before, immediately after, and five days after endoscopic fenestration of the floor of the 3rd ventricle. PI was defined with fast Fourier transformation. Mean PI values were determined in both middle cerebral arteries (MCA), over five cardiac cycles.Results: In nineteen cases, PI values showed a significant decrease immediately as well as five days after the intervention as compared to the pre-operative values, and flow-sensitive MRI confirmed the patency of the fenestration in all cases. In one patient the operation failed to produce an effective diversion of cerebrospinal fluid as shown by flow-sensitive MRI, and the pulsatility index was unchanged. In two patients, a significant immediate postfenestration drop in PI was followed by a recurrence of PI to pre-operative levels without any clinical deterioration.Conclusions: Preliminary results suggest that the transcranial Doppler-determined pulsatility index is a useful non-invasive tool for the evaluation of the patency of the fenestration in the early follow-up of patients who underwent endoscopic third ventriculostomy.
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