| 1. |
- Toth, Arnold, et al.
(författare)
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Microbleeds may expand acutely after traumatic brain injury
- 2016
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Ingår i: Neuroscience Letters. - : Elsevier. - 0304-3940 .- 1872-7972. ; 617, s. 207-212
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Tidskriftsartikel (refereegranskat)abstract
- Background and purpose: Susceptibility weighted imaging (SWI) is a very sensitive tool for the detection of microbleeds in traumatic brain injury (TBI). The number and extent of such traumatic microbleeds (TMBs) have been shown to correlate with the severity of the injury and the clinical outcome. However, the acute dynamics of TMBs have not been revealed so far. Since TBI is known to constitute dynamic pathological processes, we hypothesized that TMBs are not constant in their appearance, but may progress acutely after injury.Materials and methods: We present here five closed moderate/severe (Glasgow coma scale≤13) TBI patients who underwent SWI very early (average=23.4 h), and once again a week (average=185.8 h) after the injury. The TMBs were mapped at both time points by a conventional radiological approach and their numbers and volumes were measured with manual tracing tools by two observers. TMB counts and extents were compared between time points.Results: TMBs were detected in four patients, three of them displaying an apparent TMB change. In these patients, TMB confluence and apparent growth were detected in the corpus callosum, coronal radiation or subcortical white matter, while unchanged TMBs were also present. These changes caused a decrease in the TMB count associated with an increase in the overall TMB volume over time.Conclusion: We have found a compelling evidence that diffuse axonal injury-related microbleed development is not limited strictly to the moment of injury: the TMBs might expand in the acute phase of TBI. The timing of SWI acquisition may be relevant for optimizing the prognostic utility of this imaging biomarker.
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| 2. |
- Farkas, Orsolya, et al.
(författare)
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Effects of pituitary adenylate cyclase activating polypeptide in a rat model of traumatic brain injury
- 2004
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Ingår i: Regulatory Peptides. - : Elsevier. - 0167-0115 .- 1873-1686. ; 123:1-3, s. 69-75
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Tidskriftsartikel (refereegranskat)abstract
- Pituitary adenylate cyclase activating polypeptide (PACAP) is a widely distributed neuropeptide that has numerous different actions. Recent studies have shown that PACAP exerts neuroprotective effects not only in vitro but also in vivo, in animal models of global and focal cerebral ischemia, Parkinson's disease and axonal injuries. Traumatic brain injury has an increasing mortality and morbidity and it evokes diffuse axonal injury which further contributes to its damaging effects. The aim of the present study was to examine the possible neuroprotective effect of PACAP in a rat model of diffuse axonal injury induced by impact acceleration. Axonal damage was assessed by immunohistochemistry using an antiserum against beta-amyloid precursor protein, a marker of altered axoplasmic transport considered as key feature in axonal injury. In these experiments, we have established the dose response curves for PACAP administration in traumatic axonal injury, demonstrating that a single post-injury intracerebroventricular injection of 100 microg PACAP significantly reduced the density of damaged, beta-amyloid precursor protein-immunoreactive axons in the corticospinal tract.
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| 3. |
- Kövesdi, Erzsébet, et al.
(författare)
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Posttraumatic administration of pituitary adenylate cyclase activating polypeptide in central fluid percussion injury in rats
- 2008
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Ingår i: Neurotoxicity research. - : Springer. - 1029-8428 .- 1476-3524. ; 13:2, s. 71-78
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Tidskriftsartikel (refereegranskat)abstract
- Several in vitro and in vivo experiments have demonstrated the neuroprotective effects of pituitary adenylate cyclase activating polypeptide (PACAP) in focal cerebral ischemia, Parkinson's disease and traumatic brain injury (TBI). The aim of the present study was to analyze the effect of PACAP administration on diffuse axonal injury (DAI), an important contributor to morbidity and mortality associated with TBI, in a central fluid percussion (CFP) model of TBI. Rats were subjected to moderate (2 Atm) CFP injury. Thirty min after injury, 100 mu g PACAP was administered intracerebroventricularly. DAI was assessed by immunohistochemical detection of beta-amyloid precursor protein, indicating impaired axoplasmic transport, and RMO-14 antibody, representing foci of cytoskeletal alterations (neurofilament compaction), both considered classical markers of axonal damage. Analysis of damaged, immunoreactive axonal profiles revealed significant axonal protection in the PACAP-treated versus vehicle-treated animals in the corticospinal tract, as far as traumatically induced disturbance of axoplasmic transport and cytoskeletal alteration were considered. Similarly to our former observations in an impact acceleration model of diffuse TBI, the present study demonstrated that PACAP also inhibits DAI in the CFP injury model. The finding indicates that PACAP and derivates can be considered potential candidates for further experimental studies, or purportedly for clinical trials in the therapy of TBI.
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| 4. |
- Tamas, Andrea, et al.
(författare)
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Effect of PACAP in central and peripheral nerve injuries
- 2012
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Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 13:7, s. 8430-8448
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Forskningsöversikt (refereegranskat)abstract
- Pituitary adenylate cyclase activating polypeptide (PACAP) is a bioactive peptide with diverse effects in the nervous system. In addition to its more classic role as a neuromodulator, PACAP functions as a neurotrophic factor. Several neurotrophic factors have been shown to play an important role in the endogenous response following both cerebral ischemia and traumatic brain injury and to be effective when given exogenously. A number of studies have shown the neuroprotective effect of PACAP in different models of ischemia, neurodegenerative diseases and retinal degeneration. The aim of this review is to summarize the findings on the neuroprotective potential of PACAP in models of different traumatic nerve injuries. Expression of endogenous PACAP and its specific PAC1 receptor is elevated in different parts of the central and peripheral nervous system after traumatic injuries. Some experiments demonstrate the protective effect of exogenous PACAP treatment in different traumatic brain injury models, in facial nerve and optic nerve trauma. The upregulation of endogenous PACAP and its receptors and the protective effect of exogenous PACAP after different central and peripheral nerve injuries show the important function of PACAP in neuronal regeneration indicating that PACAP may also be a promising therapeutic agent in injuries of the nervous system.
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| 5. |
- Tamás, Andrea, et al.
(författare)
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Postinjury administration of pituitary adenylate cyclase activating polypeptide (PACAP) attenuates traumatically induced axonal injury in rats
- 2006
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 23:5, s. 686-695
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Tidskriftsartikel (refereegranskat)abstract
- Pituitary adenylate cyclase activating polypeptide (PACAP) has several different actions in the nervous system. Numerous studies have shown its neuroprotective effects both in vitro and in vivo. Previously, it has been demonstrated that PACAP reduces brain damage in rat models of global and focal cerebral ischemia. Based on the protective effects of PACAP in cerebral ischemia and the presence of common pathogenic mechanisms in cerebral ischemia and traumatic brain injury (TBI), the aim of the present study was to investigate the possible protective effect of PACAP administered 30 min or 1 h postinjury in a rat model of diffuse axonal injury. Adult Wistar male rats were subjected to impact acceleration, and PACAP was administered intracerebroventricularly 30 min (n = 4), and 1 h after the injury (n = 5). Control animals received the same volume of vehicle at both time-points (n = 5). Two hours after the injury, brains were processed for immunohistochemical localization of damaged axonal profiles displaying either beta-amyloid precursor protein (beta-APP) or RMO-14 immunoreactivity, both considered markers of specific features of traumatic axonal injury. Our results show that treatment with PACAP (100 microg) 30 min or 1 h after the induction of TBI resulted in a significant reduction of the density of beta-APP-immunopositive axon profiles in the corticospinal tract (CSpT). There was no significant difference between the density of beta-APP-immunopositive axons in the medial longitudinal fascicle (MLF). PACAP treatment did not result in significantly different number of RMO-14-immunopositive axonal profiles in either brain areas 2 hours post-injury compared to normal animals. While the results of this study highlighted the complexity of the pathogenesis and manifestation of diffuse axonal injury, they also indicate that PACAP should be considered a potential therapeutic agent in TBI.
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| 6. |
- Toth, Arnold, et al.
(författare)
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Both hemorrhagic and non-hemorrhagic traumatic MRI lesions are associated with the microstructural damage of the normal appearing white matter
- 2018
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Ingår i: Behavioural Brain Research. - : Elsevier. - 0166-4328 .- 1872-7549. ; 340, s. 106-116
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Tidskriftsartikel (refereegranskat)abstract
- Traumatic microbleeds (TMBs) and non-hemorrhagic lesions (NHLs) on MRI are regarded as surrogate markers of diffuse axonal injury. However, the actual relation between lesional and diffuse pathology remained unclear, since lesions were related to clinical parameters, largely influenced by extracranial factors. The aim of this study is to directly compare TMBs, NHLs and their regional features with the co-existing diffuse injury of the normal appearing white matter (NAWM) as measured by diffusion tensor imaging (DTI). Thirty-eight adults with a closed traumatic brain injury (12 mild, 4 moderate and 22 severe) who underwent susceptibility weighted imaging (SWI), Tl-, T2 weighted and FLAIR MRI and routine CT were included in the study. TMB (on SWI) and NHL (on T1-, T2 weighted and FLAIR images) features and Rotterdam scores were evaluated. DTI metrics such as fractional anisotropy (FA) and mean diffusivity (MD) were measured over different NAWM regions. Clinical parameters including age; Glasgow Coma Scale; Rotterdam score; TMB and NHL features were correlated to regional NAWM diffusivity using multiple regression. Overall NHL presence and basal ganglia area TMB load were significantly, negatively correlated with the subcortical NAWM FA values (partial r = -0.37 and -0.36; p = 0.006 and 0.025, respectively). The presence of any NHL, or TMBs located in the basal ganglia area indicates diffuse NAWM damage even after adjusting for clinical and CT parameters. To estimate DAI, a conventional lesional MRI pathology evaluation might at least in part substitute the use of quantitative DTI, which is yet not widely feasible in a clinical setting. (C) 2017 Elsevier B.V. All rights reserved.
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| 7. |
- Auer, Tibor, et al.
(författare)
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SÚLYOS KOPONYA-AGY SÉRÜLÉS VIZSGÁLATADIFFÚZIÓS TENZOR ÉS FUNKCIONÁLISMR-KÉPALKOTÁSSAL ALACSONY TÉRERÔN : [Diffusion tensor and functional MR imaging of severe traumatic craniocerebral injury at low magnetic field]
- 2007
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Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 60:11-12, s. 480-488
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Tidskriftsartikel (refereegranskat)abstract
- Aim of the study: Presentation of diffusion tensor imaging (DTI) performed at low magnetic field (1 Tesla) in the algorithm of work-up of a patient suffering from severe traumatic brain injury (TBI).Method: DTI and functional MRI (fMRI) were applied at 1 Tesla for visualization of neural pathways and examination of sensory functions of a patient with severe TBI. DTI-measurement was also performed on a healthy patient for comparison.Results: DTI acquired at low magnetic field yielded appropriate visualization of neural pathways. DTI confirmed the results of the clinical and fMRI examinations in the patient suffering from severe TBI.Conclusion: An optimized DTI can be useful in the examination of patients with TBI, moreover, it may also help in the establishment of diagnoses of other central nervous system diseases affecting neuronal pathways. The presented results suggest that DTI of appropriate quality can be performed at low magnetic field.
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| 8. |
- Bogner, Péter, et al.
(författare)
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Stroke-ellátást támogató teleradiológiai hálózat a Nyugat- és Dél-Dunántúlon : [Teleradiology-based stroke network in Western and Southern Transdanubia in Hungary]
- 2021
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Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 162:17, s. 668-675
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Tidskriftsartikel (refereegranskat)abstract
- Összefoglaló. Bevezetés: A stroke kezelésének lehetőségei az utóbbi években jelentősen megváltoztak: a thrombolysis után bevezetésre került a mechanikus thrombectomia, és a terápiás időablak is jelentősen kitágult az utóbbi évek nagy multicentrikus tanulmányai alapján. Ezek a lehetőségek új igényeket fogalmaztak meg a képalkotó diagnosztikával szemben: az ischaemia okozta morfológiai elváltozások mellett az artériás és a kollaterális rendszer állapotát, valamint bizonyos esetekben az agy szöveti perfúzióját is szükséges meghatározni. Ezeket a komplex kiértékelési feladatokat ma már mesterségesintelligencia-algoritmusok támogathatják, melyek a kiértékelést pár perc alatt elvégezve segítenek a terápiás döntés kialakításában. Célkitűzés: A Dél- és a Nyugat-dunántúli régióban hat intézmény részvételével egy dedikált stroke teleradiológiai hálózat kialakítása. Módszer: A stroke-CT-kiértékelő szoftver és a képkommunikáció integrációja, a vizsgálati protokollok technikai paramétereinek egységesítése, a kiértékelési eredmények teleradiológiai megjelenítése valósult meg a hálózat kialakítása során. Eredmények: A hálózat egységesítette nemcsak a stroke-CT-protokollok beállításait, de beutalási és értékelési szempontjait is. A stroke-CT-kiértékelések és a mechanikus thrombectomiák száma is emelkedett az elmúlt egy évben. Következtetés: A dedikált teleradiológiai stroke-hálózat segítségével optimalizálni kívánjuk a régió stroke-ellátását: egyrészt lehetőleg ne maradjanak ellátatlanul a thrombectomiából valószínűleg profitáló betegek, másrészt ne terheljük az ellátórendszert olyan esetekkel, melyekről a teljes dokumentáció ismeretében derül ki, hogy nem javasolt a beavatkozás.
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| 9. |
- 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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| 10. |
- Csepregi, Gyula, et al.
(författare)
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Sülyos koponya-agy sérültek ellátása Magyarországon, 2002-ben : [Management of patients with severe head injury in Hungary, in 2002]
- 2007
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Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 148:17, s. 771-777
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Tidskriftsartikel (refereegranskat)abstract
- In Hungary, epidemiological and clinical data regarding brain injury were rather scarce. The Hungarian Society for Neurotrauma aimed to make a nation-wide study about the number and the mortality of patients with severe head trauma, the organization of management, the diagnostics and monitoring in use, and finally about the clinical practice of management. A national survey was carried out with questionnaires asking about data of 2001, and a prospective, three-month-long data collection based on case studies was also executed in 2002. The Hungarian National Ambulance and Emergency Service centralized information gathering on rescue, and transportation. To collect data of hospital care, a network of regional coordinators and hospital communicators was developed. The responders covered 76% of the hospital neurotrauma care in the country. The number of brain trauma patients was close to 14,000 per year: 71.3% mild, 19.4% moderate, and 9.4% severe trauma. According to prospective study the mortality of those patients who were admitted as severe head injury patients was 55% and the mortality of those who got into severe condition later was 35% during the acute care. These data showed much worse outcome than those published in Western European countries and North America. In the background the authors found communication disorder between prehospital and hospital care, extreme long time spent until the patients got to the first CT-exam and to the definitive care. The implementation of Hungarian and international head trauma guidelines did not spread widely.
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