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1.	Czigler, Andras, et al. (författare) Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury : Protective effects of the Mitochondria-Targeted Antioxidative Peptide SS-31 2019 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 36:23, s. 3309-3315 Tidskriftsartikel (refereegranskat)abstract Traumatic brain injury (TBI) induces cerebrovascular oxidative stress, which is associated with neurovascular uncoupling, autoregulatory dysfunction, and persisting cognitive decline in both pre-clinical models and patients. However, single mild TBI (mTBI), the most frequent form of brain trauma, increases cerebral generation of reactive oxygen species (ROS) only transiently. We hypothesized that comorbid conditions might exacerbate long-term ROS generation in cerebral arteries after mTBI. Because hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive and spontaneously hypertensive rats (SHR) and assessed changes in cytoplasmic and mitochondrial superoxide (O2-) production by confocal microscopy in isolated middle cerebral arteries (MCA) 2 weeks after mTBI using dihydroethidine (DHE) and the mitochondria-targeted redox-sensitive fluorescent indicator dye MitoSox. We found that mTBI induced a significant increase in long-term cytoplasmic and mitochondrial O2- production in MCAs of SHRs and increased expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit Nox4, which were reversed to the normal level by treating the animals with the cell-permeable, mitochondria-targeted antioxidant peptide SS-31 (5.7 mg kg-1 day-1, i.p.). Persistent mTBI-induced oxidative stress in MCAs of SHRs was significantly decreased by inhibiting vascular NADPH oxidase (apocyinin). We propose that hypertension- and mTBI-induced cerebrovascular oxidative stress likely lead to persistent dysregulation of cerebral blood flow (CBF) and cognitive dysfunction, which might be reversed by SS-31 treatment.
2.	Czigler, Andras, et al. (författare) Prostaglandin E2, a postulated mediator of neurovascular coupling, at low concentrations dilates whereas at higher concentrations constricts human cerebral parenchymal arterioles 2020 Ingår i: Prostaglandins & other lipid mediators. - : Elsevier. - 1098-8823 .- 2212-196X. ; 146 Tidskriftsartikel (refereegranskat)abstract There is considerable controversy regarding the vasoactive action of prostaglandin E2 (PGE2). On the one hand, indirect evidence implicates that astrocytic release of PGE2 contributes to neurovascular coupling responses mediating functional hyperemia in the brain. On the other hand, overproduction of PGE2 was also reported to contribute to cerebral vasospasm associated with subarachnoid hemorrhage. The present study was conducted to resolve this controversy by determining the direct vasoactive effects of PGE2 in resistance-sized human cerebral parenchymal arterioles. To achieve this goal PGE2-induced isotonic vasomotor responses were assessed in parenchymal arterioles isolated from fronto-temporo-parietal cortical tissues surgically removed from patients and expression of PGE2 receptors were examined. In functionally intact parenchymal arterioles lower concentrations of PGE2 (from 10-8 to 10-6 mol/l) caused significant, endothelium-independent vasorelaxation, which was inhibited by the EP4 receptor blocker BGC201531. In contrast, higher concentrations of PGE2 evoked significant EP1-dependent vasoconstriction, which could not be reversed by the EP4 receptor agonist CAY10598. We also confirmed previous observations that PGE2 primarily evokes constriction in intracerebral arterioles isolated from R. norvegicus. Importantly, vascular mRNA and protein expression of vasodilator EP4 receptors was significantly higher than that of vasoconstrictor EP1 receptors in human cerebral arterioles. PGE2 at low concentrations dilates whereas at higher concentrations constricts human cerebral parenchymal arterioles. This bimodal vasomotor response is consistent with both the proposed vasodilator role of PGE2 during functional hyperemia and its putative role in cerebral vasospasm associated with subarachnoid hemorrhage in human patients.
3.	Czigner, Andrea, et al. (författare) Dynamics and regional distribution of c-fos protein expression in rat brain after a closed head injury 2004 Ingår i: International Journal of Molecular Medicine. - : Spandidos Publications. - 1107-3756 .- 1791-244X. ; 14:2, s. 247-252 Tidskriftsartikel (refereegranskat)abstract The objective of this study was to define the time- and brain-area-related distribution of c-fos expression in the brain during the first 24 h following a closed head injury in rats. In the control groups (n = 32), only a few c-fos positive nuclei were observed in the brain and the c-fos staining did not change during the next 24 h. In the closed head injury group c-fos-positive cells were rare in the brain regions during the first 30 min. During the next 2 h, the number of c-fos-positive cells increased rapidly in the basal ganglions, the ventricular ependyma cells the corticospinal tract, the area postrema, the cerebral neocortex, and the corpus callosum. The increase was highest in the corpus callosum (317 +/- 44.5 mm(-2)), in the thalamic reticular nucleus (474.8 +/- 49.2 mm(-2)), in the dentate hilus (1090 +/- 187 mm(-2)) and in the cerebral neocortex (992 +/- 93 mm(-2)). Thereafter, the elevated c-fos expression gradually decreased and at 6 h post-closed head injury no significant differences were observed between the controls and the trauma group. We conclude that a closed head injury induces a large, transient increase of c-fos expression in the brain. Since the observed time course and regional differences in c-fos expression are in good agreement with the cognitive and memory deficits observed after human TBI it can be utilized in further investigations, especially to test the effects of various forms of pharmacological or cellular therapy.
4.	Magyar-Sumegi, Zsofia Dina, et al. (författare) Acute neuroendocrine changes after traumatic brain injury 2024 Ingår i: Brain & spine. - : Elsevier. - 2772-5294. ; 4 Forskningsöversikt (refereegranskat)abstract INTRODUCTION: Post-traumatic hypopituitarism (PTHP) is a significant, but often neglected consequence of traumatic brain injury (TBI).RESEARCH QUESTION: We aimed to provide a comprehensive overview of epidemiology, pathophysiology, clinical features and diagnostic approaches of PTHP.MATERIALS AND METHODS: MEDLINE, EMBASE, Cochrane Library and Web of Science were searched. 45 articles of human studies evaluating acute endocrine changes following mild, moderate and severe TBI were selected.RESULTS: Severity of TBI seems to be the most important risk factor of PTHP. Adrenal insufficiency (AI) was present in 10% of TBI patients (prevalence can be as high as 50% after severe TBI), and hypocortisolemia is a predictor of mortality and long-term hypopituitarism. Suppression of the thyroid axis in 2-33% of TBI patients may be an independent predictor of adverse neurological outcome, as well. 9-36% of patients with severe TBI exhibit decreased function of the somatotrophic axis with a divergent effect on the central nervous system. Arginine-Vasopressin (AVP) deficiency is present in 15-51% of patients, associated with increased mortality and unfavorable outcome. Due to shear and injury of the stalk hyperprolactinemia is relatively common (2-50%), but it bears little clinical significance. Sex hormone levels remain within normal values.DISCUSSION AND CONCLUSION: PTHP occurs frequently after TBI, affecting various axis and determining patients' outcome. However, evidence is scarce regarding exact epidemiology, diagnosis, and effective clinical application of hormone substitution. Future studies are needed to identify patients at-risk, determine the optimal timing for endocrine testing, and refine diagnostic and treatment approaches to improve outcome.
5.	Mondello, Stefania, et al. (författare) Circulating brain injury exosomal proteins following Moderate-to-Severe traumatic brain injury : temporal profile, outcome prediction and therapy implications 2020 Ingår i: Cells. - : MDPI. - 2073-4409. ; 9:4 Tidskriftsartikel (refereegranskat)abstract Brain injury exosomal proteins are promising blood biomarker candidates in traumatic brain injury (TBI). A better understanding of their role in the diagnosis, characterization, and management of TBI is essential for upcoming clinical implementation. In the current investigation, we aimed to explore longitudinal trajectories of brain injury exosomal proteins in blood of patients with moderate-to-severe TBI, and to evaluate the relation with the free-circulating counterpart and patient imaging and clinical parameters. Exosomal levels of glial (glial fibrillary acidic protein (GFAP)) and neuronal/axonal (ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), neurofilament light chain (NFL), and total-tau (t-tau)) proteins were measured in serum of 21 patients for up 5 days after injury using single molecule array (Simoa) technology. Group-based trajectory analysis was used to generate distinct temporal exosomal biomarker profiles. We found altered profiles of serum brain injury exosomal proteins following injury. The dynamics and levels of exosomal and related free-circulating markers, although correlated, showed differences. Patients with diffuse injury displayed higher acute exosomal NFL and GFAP concentrations in serum than those with focal lesions. Exosomal UCH-L1 profile characterized by acutely elevated values and a secondary steep rise was associated with early mortality (n = 2) with a sensitivity and specificity of 100%. Serum brain injury exosomal proteins yielded important diagnostic and prognostic information and represent a novel means to unveil underlying pathophysiology in patients with moderate-to-severe TBI. Our findings support their utility as potential tools to improve patient phenotyping in clinical practice and therapeutic trials.
6.	Szarka, Nikolett, et al. (författare) Effect of Growth Hormone on Neuropsychological Outcomes and Quality of Life of Patients with Traumatic Brain Injury : A Systematic Review 2021 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 38:11, s. 1467-1483 Forskningsöversikt (refereegranskat)abstract One of the most devastating chronic consequences of traumatic brain injury (TBI) is cognitive impairment. One of the possible underlying causes is growth hormone deficiency (GHD) caused by TBI-induced hypopituitarism. Currently, TBI patients are not routinely screened for pituitary function, and there are no standard therapies when GHD is diagnosed. Further, the possible positive effects of GH replacement on cognitive function and quality of life after TBI are not well established. We aimed to assess the current knowledge regarding the effect of GH therapy on cognitive function and quality of life after TBI. We performed a literature search in PubMed, Embase, and Central(R) databases from inception to October 2019. We extracted data on each term of severity (mild-moderate-severe) of TBI with and without GHD, time since injury, parameters of growth hormone treatment (dosing, length), and cognitive outcomes in terms of verbal and non-verbal memory, and executive, emotional, and motor functions, and performed a meta-analysis on the results of a digit span test assessing working memory. We identified 12 studies (containing two randomized controlled trials) with 264 mild-to-moderate-to-severe TBI patients (Glasgow Coma Score [GCS] varied between 6 and 15) with (n = 255) or without (n = 9) GHD who received GH therapy. GH was administered subcutaneously in gradually increasing doses, monitoring serum insulin-like growth factor-I (IGF-I) level. After TBI, regardless of GCS, 6-12 months of GH therapy, started in the chronic phase post-TBI, induced a moderate improvement in processing speed and memory capacities, decreased the severity of depression, and led to a marked improvement in quality of life. Limitations include the relatively low number of patients involved and the divergent neuropsychological tests used. These results indicate the need for further multi-centric controlled studies to substantiate the use of GH replacement therapy as a potential tool to alleviate TBI-related cognitive impairment and improve quality of life.
7.	Szarka, Nikolett, et al. (författare) Single mild traumatic brain injury induces persistent disruption of the blood-brain barrier, neuroinflammation and ognitive decline in hypertensive rats 2019 Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 20:13, s. 3223-3223 Tidskriftsartikel (refereegranskat)abstract Traumatic brain injury (TBI) induces blood-brain barrier (BBB) disruption, which contributes to secondary injury of brain tissue and development of chronic cognitive decline. However, single mild (m)TBI, the most frequent form of brain trauma disrupts the BBB only transiently. We hypothesized, that co-morbid conditions exacerbate persistent BBB disruption after mTBI leading to long term cognitive dysfunction. Since hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive Wistar and spontaneously hypertensive rats (SHR) and we assessed BBB permeability, extravasation of blood-borne substances, neuroinflammation and cognitive function two weeks after trauma. We found that mTBI induced a significant BBB disruption two weeks after trauma in SHRs but not in normotensive Wistar rats, which was associated with a significant accumulation of fibrin and increased neuronal expression of inflammatory cytokines TNFα, IL-1β and IL-6 in the cortex and hippocampus. SHRs showed impaired learning and memory two weeks after mild TBI, whereas cognitive function of normotensive Wistar rats remained intact. Future studies should establish the mechanisms through which hypertension and mild TBI interact to promote persistent BBB disruption, neuroinflammation and cognitive decline to provide neuroprotection and improve cognitive function in patients with mTBI.
8.	Tényi, Dalma, et al. (författare) Concussive convulsions : A YouTube video analysis 2016 Ingår i: Epilepsia. - : John Wiley & Sons. - 0013-9580 .- 1528-1167. ; 57:8, s. 1310-1316 Tidskriftsartikel (refereegranskat)abstract Objective: To analyze seizure-like motor phenomena immediately occurring after concussion (concussive convulsions).Methods: Twenty-five videos of concussive convulsions were obtained from YouTube as a result of numerous sports-related search terms. The videos were analyzed by four independent observers, documenting observations of the casualty, the head injury, motor symptoms of the concussive convulsions, the postictal period, and the outcome.Results: Immediate responses included the fencing response, bear hug position, and bilateral leg extension. Fencing response was the most common. The side of the hit (p = 0.039) and the head turning (p = 0.0002) was ipsilateral to the extended arm. There was a tendency that if the blow had only a vertical component, the bear hug position appeared more frequently (p = 0.12). The motor symptom that appeared with latency of 6 ± 3 s was clonus, sometimes superimposed with tonic motor phenomena. Clonus was focal, focally evolving bilateral or bilateral, with a duration of 27 ± 19 s (5-72 s). Where lateralization of clonus could be determined, the side of clonus and the side of hit were contralateral (p = 0.039).Significance: Concussive convulsions consist of two phases. The short-latency first phase encompasses motor phenomena resembling neonatal reflexes and may be of brainstem origin. The long-latency second phase consists of clonus. We hypothesize that the motor symptoms of the long-latency phase are attributed to cortical structures; however, they are probably not epileptic in origin but rather a result of a transient cortical neuronal disturbance induced by mechanical forces.
9.	Toth, Luca, et al. (författare) Age-related decline in circulating IGF-1 associates with impaired neurovascular coupling responses in older adults 2022 Ingår i: GeroScience. - : Springer. - 2509-2715 .- 2509-2723. ; 44:6, s. 2771-2783 Tidskriftsartikel (refereegranskat)abstract Impairment of moment-to-moment adjustment of cerebral blood flow (CBF) to the increased oxygen and energy requirements of active brain regions via neurovascular coupling (NVC) contributes to the genesis of age-related cognitive impairment. Aging is associated with marked deficiency in the vasoprotective hormone insulin-like growth factor-1 (IGF-1). Preclinical studies on animal models of aging suggest that circulating IGF-1 deficiency is causally linked to impairment of NVC responses. The present study was designed to test the hypotheses that decreases in circulating IGF-1 levels in older adults also predict the magnitude of age-related decline of NVC responses. In a single-center cross-sectional study, we enrolled healthy young (n = 31, 11 female, 20 male, mean age: 28.4 + / - 4.2 years) and aged volunteers (n = 32, 18 female, 14 male, mean age: 67.9 + / - 4.1 years). Serum IGF-1 level, basal CBF (phase contrast magnetic resonance imaging (MRI)), and NVC responses during the trail making task (with transcranial Doppler sonography) were assessed. We found that circulating IGF-1 levels were significantly decreased with age and associated with decreased basal CBF. Age-related decline in IGF-1 levels predicted the magnitude of age-related decline in NVC responses. In conclusion, our study provides additional evidence in support of the concept that age-related circulating IGF-1 deficiency contributes to neurovascular aging, impairing CBF and functional hyperemia in older adults.
10.	Toth, Luca, et al. (författare) The Effect of Mild Traumatic Brain Injury on Cerebral Microbleeds in Aging 2021 Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media S.A.. - 1663-4365. ; 13 Tidskriftsartikel (refereegranskat)abstract A traumatic brain injury (TBI) induces the formation of cerebral microbleeds (CMBs), which are associated with cognitive impairments, psychiatric disorders, and gait dysfunctions in patients. Elderly people frequently suffer TBIs, especially mild brain trauma (mTBI). Interestingly, aging is also an independent risk factor for the development of CMBs. However, how TBI and aging may interact to promote the development of CMBs is not well established. In order to test the hypothesis that an mTBI exacerbates the development of CMBs in the elderly, we compared the number and cerebral distribution of CMBs and assessed them by analysing susceptibility weighted (SW) MRI in young (25 +/- 10 years old, n = 18) and elder (72 +/- 7 years old, n = 17) patients after an mTBI and in age-matched healthy subjects (young: 25 +/- 6 years old, n = 20; aged: 68 +/- 5 years old, n = 23). We found significantly more CMBs in elder patients after an mTBI compared with young patients; however, we did not observe a significant difference in the number of cerebral microhemorrhages between aged and aged patients with mTBI. The majority of CMBs were found supratentorially (lobar and basal ganglion). The lobar distribution of supratentorial CMBs showed that aging enhances the formation of parietal and occipital CMBs after mTBIs. This suggests that aging and mTBIs do not synergize in the induction of the development of CMBs, and that the different distribution of mTBI-induced CMBs in aged patients may lead to specific age-related clinical characteristics of mTBIs.
11.	Toth, Luca, et al. (författare) Traumatic brain injury-induced cerebral microbleeds in the elderly 2021 Ingår i: GeroScience. - : Springer. - 2509-2715 .- 2509-2723. ; 43:1, s. 125-136 Forskningsöversikt (refereegranskat)abstract Traumatic brain injury (TBI) was shown to lead to the development of cerebral microbleeds (CMBs), which are associated with long term cognitive decline and gait disturbances in patients. The elderly is one of the most vulnerable parts of the population to suffer TBI. Importantly, ageing is known to exacerbate microvascular fragility and to promote the formation of CMBs. In this overview, the effect of ageing is discussed on the development and characteristics of TBI-related CMBs, with special emphasis on CMBs associated with mild TBI. Four cases of TBI-related CMBs are described to illustrate the concept that ageing exacerbates the deleterious microvascular effects of TBI and that similar brain trauma may induce more CMBs in old patients than in young ones. Recommendations are made for future prospective studies to establish the mechanistic effects of ageing on the formation of CMBs after TBI, and to determine long-term consequences of CMBs on clinically relevant outcome measures including cognitive performance, gait and balance function.
12.	Auer, Tibor, et al. (författare) 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 Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 60:11-12, s. 480-488 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.
13.	Bazarian, Jeffrey J., et al. (författare) Serum GFAP and UCH-L1 for prediction of absence of intracranial injuries on head CT (ALERT-TBI) : a multicentre observational study 2018 Ingår i: Lancet Neurology. - : Lancet Publishing Group. - 1474-4422 .- 1474-4465. ; 17:9, s. 782-789 Tidskriftsartikel (refereegranskat)abstract Background: More than 50 million people worldwide sustain a traumatic brain injury (TBI) annually. Detection of intracranial injuries relies on head CT, which is overused and resource intensive. Blood-based brain biomarkers hold the potential to predict absence of intracranial injury and thus reduce unnecessary head CT scanning. We sought to validate a test combining ubiquitin C-terminal hydrolase-L1 (UCH-L1) and glial fibrillary acidic protein (GFAP), at predetermined cutoff values, to predict traumatic intracranial injuries on head CT scan acutely after TBI.Methods: This prospective, multicentre observational trial included adults (≥18 years) presenting to participating emergency departments with suspected, non-penetrating TBI and a Glasgow Coma Scale score of 9-15. Patients were eligible if they had undergone head CT as part of standard emergency care and blood collection within 12 h of injury. UCH-L1 and GFAP were measured in serum and analysed using prespecified cutoff values of 327 pg/mL and 22 pg/mL, respectively. UCH-L1 and GFAP assay results were combined into a single test result that was compared with head CT results. The primary study outcomes were the sensitivity and the negative predictive value (NPV) of the test result for the detection of traumatic intracranial injury on head CT.Findings: Between Dec 6, 2012, and March 20, 2014, 1977 patients were recruited, of whom 1959 had analysable data. 125 (6%) patients had CT-detected intracranial injuries and eight (<1%) had neurosurgically manageable injuries. 1288 (66%) patients had a positive UCH-L1 and GFAP test result and 671 (34%) had a negative test result. For detection of intracranial injury, the test had a sensitivity of 0·976 (95% CI 0·931-0·995) and an NPV of 0·996 (0·987-0·999). In three (<1%) of 1959 patients, the CT scan was positive when the test was negative.Interpretation: These results show the high sensitivity and NPV of the UCH-L1 and GFAP test. This supports its potential clinical role for ruling out the need for a CT scan among patients with TBI presenting at emergency departments in whom a head CT is felt to be clinically indicated. Future studies to determine the value added by this biomarker test to head CT clinical decision rules could be warranted.Funding: Banyan Biomarkers and US Army Medical Research and Materiel Command.
14.	Beneš, Vladimír, et al. (författare) Response to the future of the EANS neurosurgeons of Europe, unite! 2015 Ingår i: Acta Neurochirurgica. - : Springer. - 0001-6268 .- 0942-0940. ; 157:11, s. 1829-1830 Tidskriftsartikel (refereegranskat)
15.	Berta, Balázs, et al. (författare) A case of destructive cervical spondylarthropathy related to chronic dialysis : [A case of destructive cervical spondylarthropathy related to chronic dialysis] 2021 Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 74:5-6, s. 211-215 Tidskriftsartikel (refereegranskat)abstract A case of a 61-year-old male patient suffered chronic renal failure and dialysed for 23 years with destructive cervical spondylarthropathy is presented. The patient presented with sudden onset of cervical pain radiating into his shoulders without neurological deficits. CT and MRI of the cervical and thoracic spine revealed severe destructive changes and compressive fractures of C6 and C7 vertebrae which caused the narrowing of the nerve root canals at these levels. A 360-degree fixation was performed to treat the unstable fracture and the patient's pain (C6 and C7 corpectomy, autolog bone graft replacement of the two vertebral bodies, anterior plate fixation and posterior instrumentation with screws and rods). Postoperatively the patient had no significant pain, no neurological deficit and he was able to manage independent life himself. During the immediate follow-up CT of the neck showed the satisfactory position of the bone graft and the metal implantations. The 6 months follow-up CT revealed the anterior migration of the two screws from the Th1 vertebral body and 2 mm ventral elevation of the caudal end of the plate from the anterior surface of the Th1 vertebral body. The 1-year follow-up could not be performed because the patient died due to cardio-pulmonary insufficiency. This is the second Hungarian report of a chronic dialysis related severe spondylarthropathy which may cause pathologic fractures of the vertebral bodies. The typical radiological and histological findings are discussed. This disease affect patients' quality of life and the conservative treatment alone seems to be ineffective in most cases. Based on the literature and personal experiences, the authors suggest 360-degree fixation of the spine to provide sufficient stability for the vertebrae of "bad bone quality", and early mobilisation of the patient can be achieved.
16.	Bogner, Péter, et al. (författare) Stroke-ellátást támogató teleradiológiai hálózat a Nyugat- és Dél-Dunántúlon : [Teleradiology-based stroke network in Western and Southern Transdanubia in Hungary] 2021 Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 162:17, s. 668-675 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.
17.	Brophy, Gretchen M., et al. (författare) Biokinetic analysis of ubiquitin C-terminal hydrolase-L1 (UCH-L1) in severe traumatic brain injury patient biofluids 2011 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 28:6, s. 861-870 Tidskriftsartikel (refereegranskat)abstract Ubiquitin C-terminal hydrolase-L1 (UCH-L1) is a neuron-specific enzyme that has been identified as a potential biomarker of traumatic brain injury (TBI). The study objectives were to determine UCH-L1 exposure and kinetic metrics, determine correlations between biofluids, and assess outcome correlations in severe TBI patients. Data were analyzed from a prospective, multicenter study of severe TBI (Glasgow Coma Scale [GCS] score ≤ 8). Cerebrospinal fluid (CSF) and serum data from samples taken every 6 h after injury were analyzed by enzyme-linked immunosorbent assay (ELISA). UCH-L1 CSF and serum data from 59 patients were used to determine biofluid correlations. Serum samples from 86 patients and CSF from 59 patients were used to determine outcome correlations. Exposure and kinetic metrics were evaluated acutely and up to 7 days post-injury and compared to mortality at 3 months. There were significant correlations between UCH-L1 CSF and serum median concentrations (r(s)=0.59, p<0.001), AUC (r(s)=0.3, p=0.027), Tmax (r(s)=0.68, p<0.001), and MRT (r(s)=0.65, p<0.001). Outcome analysis showed significant increases in median serum AUC (2016 versus 265 ng/mL*min, p=0.006), and Cmax (2 versus 0.4 ng/mL, p=0.003), and a shorter Tmax (8 versus 19 h, p=0.04) in those who died versus those who survived, respectively. In the first 24 h after injury, there was a statistically significant acute increase in CSF and serum median Cmax((0-24h)) in those who died. This study shows a significant correlation between UCH-L1 CSF and serum median concentrations and biokinetics in severe TBI patients, and relationships with clinical outcome were detected.
18.	Büki, Andras, 1966-, et al. (författare) A koponyasérülés által kiváltott axonkárosodás és kezelésének lehetóségei : [Therapeutic possibilities in axonal injury caused by head trauma] 2002 Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 143:10, s. 499-503 Forskningsöversikt (refereegranskat)abstract Traumatic brain injury is putting an extreme burden on societies all over the world. While surgical and neuro-intensive treatment is traditionally aimed at space occupying or focal lesions, traumatic brain injury is frequently associated with diffuse axonal injury, which significantly contributes to its morbidity and mortality. Current taught appreciates that diffuse axonal injury is a progressive event gradually evolving from focal alterations in axolemmal permeability and the underlying axonal ultrastructure to axonal disconnection, a process amenable of therapeutic interventions. This review is primarily focusing on the clinical/neuroradiological manifestation and our contemporary knowledge of the pathobiology of traumatically evoked (diffuse-) axonal injury with particular emphasize on recent- to date, primarily experimental-therapeutic approaches that in the future might offer potential aid to the head injured.
19.	Büki, Andras, 1966-, et al. (författare) Agyi erek és vascularis malformatio peptiderg innervatiojának vizsgálata immunhisztokémiai módszerekkel 1994 Ingår i: Agyérbetegségek. - : Magyar Stroke Tarsasag. ; :1, s. 16-16 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
20.	Büki, Andras, 1966-, et al. (författare) Baleseti agysérültek ellátásának irányelvei -2017 : [GUIDELINES FOR THE TREATMENT OF TRAUMATICBRAIN INJURY – 2017] 2017 Ingår i: Ideggyógyászati szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 70:7-8, s. 223-245 Forskningsöversikt (refereegranskat)abstract Traumatic brain injury (TBI) is recognized to be the main cause of death and disability in the first four decades representing a major socio-economical problem worldwide. Recent communications revealed a particularly worrying image about the quality of care for TBI in Hungary. For any improvement a systematic approach characterized by utilization of scientific evidence based guidelines forming the basis for close monitoring of the actual care are considered a prerequisite. In Hungary the first evidence based guidelines in the field of TBI have been issued by the National Society for Anesthesiology and Intensive Care more than two decades ago followed by joint guidelines of the Hungarian Neurosurgical Society and the Hungarian College of Neurosurgeons. These publications were primarily based on the work of the European Brain Injury Consortium as well as guidelines issued by the Brain Trauma Foundation. Recent renewal of the latter and a need to refresh the outdated national guidelines was met by a call from regulatory authorities to issue the updated version of the Hungarian TBI-guidelines. The present review is aimed to briefly summarize the most fundamental elements of the national head injury guidelines that would hopefully be officially issued in a far more detailed format soon.
21.	Büki, Andras, 1966-, et al. (författare) BIOMARKERS OF TRAUMATIC BRAIN- AND SPINAL CORD INJURY 2022 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 39:15-16, s. A7-A7 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Biomarkers of traumatic brain injury have long been investigated, yet their application in real life clinical practice is less than widespread.Research efforts under the umbrella of InTBIR and specifically CENTER TBI provided novel results based on a bulk of data collected.The symposium aims to provide an update on contemporary knowledge on purported clinical application of core biomarkers while also sharing novel data on emerging markers and novel technologies and approaches that may further improve our diagnostic and prognostic capabilities in the treatment of traumatic brain injury.The session will provide a critical review and update on biomarkers of spinal cord injury.
22.	Büki, Andras, 1966-, et al. (författare) Clinical and model research of neurotrauma 2009 Ingår i: Methods in Molecular Biology. - Totowa, NJ : Humana Press. - 1064-3745 .- 1940-6029. ; 566, s. 41-55 Tidskriftsartikel (refereegranskat)abstract Modeling traumatic brain injury represents a major challenge for neuroscientists - to represent extremely complex pathobiological processes kept under close surveillance in the most complex organ of a laboratory animal. To ensure that such models also reflect those alterations evoked by and/or associated with traumatic brain injury (TBI) in man, well-defined, graded, simple injury paradigms should be used with clear endpoints that also enable us to assess the relevance of our findings to human observations. It is of particular importance that our endpoints should harbor clinical significance, and to this end, biological markers ultimately associated with the pathological processes operant in TBI are considered the best candidate. This chapter provides protocols for relevant experimental models of TBI and clinical materials for neuroproteomic analysis.
23.	Büki, Andras, 1966-, et al. (författare) Cytochrome c release and caspase activation in traumatic axonal injury 2000 Ingår i: Journal of Neuroscience. - : Society for Neuroscience. - 0270-6474 .- 1529-2401. ; 20:8, s. 2825-2834 Tidskriftsartikel (refereegranskat)abstract Axonal injury is a feature of traumatic brain injury (TBI) contributing to both morbidity and mortality. The traumatic axon injury (TAI) results from focal perturbations of the axolemma, allowing for calcium influx triggering local intraaxonal cytoskeletal and mitochondrial damage. This mitochondrial damage has been posited to cause local bioenergetic failure, leading to axonal failure and disconnection; however, this mitochondrial damage may also lead to the release of cytochrome c (cyto-c), which then activates caspases with significant adverse intraaxonal consequences. In the current communication, we examine this possibility. Rats were subjected to TBI, perfused with aldehydes at 15-360 min after injury, and processed for light microscopic (LM) and electron microscopic (EM) single-labeling immunohistochemistry to detect extramitochondrially localized cytochrome c (cyto-c) and the signature protein of caspase-3 activation (120 kDa breakdown product of alpha-spectrin) in TAI. Combinations of double-labeling fluorescent immunohistochemistry (D-FIHC) were also used to demonstrate colocalization of calpain activation with cyto-c release and caspase-3-induction. In foci of TAI qualitative-quantitative LM demonstrated a parallel, significant increase in cyto-c release and caspase-3 activation over time after injury. EM analysis demonstrated that cyto-c and caspase-3 immunoreactivity were associated with mitochondrial swelling-disruption in sites of TAI. Furthermore, D-IFHC revealed a colocalization of calpain activation, cyto-c release, and caspase-3 induction in these foci, which also revealed progressive TAI. The results demonstrate that cyto-c and caspase-3 participate in the terminal processes of TAI. This suggests that those factors that play a role in the apoptosis in the neuronal soma are also major contributors to the demise of the axonal appendage.
24.	Büki, Andras, 1966-, et al. (författare) Embryóból és felnőttből származó humán agyi erek peptiderg beidegzése : összehasonlító immunhisztokémiai vizsgálatok humán szövetmintákon [Comparative human immunohistochemical investigations of peptidergic innervation of embryonal and adult cerebral blood vessels] 1997 Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 3-4:50, s. 84-87 Tidskriftsartikel (refereegranskat)abstract Peptidergic fibres innervating human embryonic and adult cerebral blood vessels were screened for calcitonine gene-related peptide, neuropeptide-Y and substance-P immunopositive fibres, the mediaadventitia border displayed a network-like fibre arrange ment. There was no significant difference either in the distribution of the individual peptidergic fibres or in the age-dependent appearance of peptidergic networks. On the basis of these results it seems to be unlikely that the different clinical course of juvenile and adult subarachnoid haemorrhages could be the result of an age specific difference of peptidergic fibre distribution influencing the neurogenic mecha nisms of cerebral autoregulation.]
25.	Büki, Andras, 1966-, et al. (författare) Initial Clinical Experience with a Combined Pulsed Holmium-Neodymium-YAG Laser in Minimally Invasive Neurosurgery* 1999 Ingår i: Minimally Invasive Neurosurgery. - : Thieme Medical Publishers. - 0946-7211 .- 1439-2291. ; 42:1, s. 35-40 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.
26.	Büki, Andras, 1966-, et al. (författare) Minor and repetitive head injury 2014 Ingår i: Advances and Technical Standards in Neurosurgery. - Cham : Springer. - 9783319090658 - 9783319090665 ; , s. 147-192 Bokkapitel (refereegranskat)abstract Traumatic brain injury (TBI) is the leading cause of death and disability in the young, active population and expected to be the third leading cause of death in the whole world until 2020. The disease is frequently referred to as the silent epidemic, and many authors highlight the "unmet medical need" associated with TBI.The term traumatically evoked brain injury covers a heterogeneous group ranging from mild/minor/minimal to severe/non-salvageable damages. Severe TBI has long been recognized to be a major socioeconomical health-care issue as saving young lives and sometimes entirely restituting health with a timely intervention can indeed be extremely cost efficient.Recently it has been recognized that mild or minor TBI should be considered similarly important because of the magnitude of the patient population affected. Other reasons behind this recognition are the association of mild head injury with transient cognitive disturbances as well as long-term sequelae primarily linked to repeat (sport-related) injuries.The incidence of TBI in developed countries can be as high as 2-300/100,000 inhabitants; however, if we consider the injury pyramid, it turns out that severe and moderate TBI represents only 25-30 % of all cases, while the overwhelming majority of TBI cases consists of mild head injury. On top of that, or at the base of the pyramid, are the cases that never show up at the ER - the unreported injuries.Special attention is turned to mild TBI as in recent military conflicts it is recognized as "signature injury."This chapter aims to summarize the most important features of mild and repetitive traumatic brain injury providing definitions, stratifications, and triage options while also focusing on contemporary knowledge gathered by imaging and biomarker research.Mild traumatic brain injury is an enigmatic lesion; the classification, significance, and its consequences are all far less defined and explored than in more severe forms of brain injury.Understanding the pathobiology and pathomechanisms may aid a more targeted approach in triage as well as selection of cases with possible late complications while also identifying the target patient population where preventive measures and therapeutic tools should be applied in an attempt to avoid secondary brain injury and late complications.
27.	Büki, Andras, 1966-, et al. (författare) Moderate Posttraumatic Hypothermia Decreases Early Calpain-Mediated Proteolysis and Concomitant Cytoskeletal Compromise in Traumatic Axonal Injury 1999 Ingår i: Experimental Neurology. - : Academic Press. - 0014-4886 .- 1090-2430. ; 159:1, s. 319-328 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.
28.	Büki, Andras, 1966-, et al. (författare) Novel application of tyramide signal amplification (TSA) : ultrastructural visualization of double-labeled immunofluorescent axonal profiles 2000 Ingår i: Journal of Histochemistry and Cytochemistry. - : Sage Publications. - 0022-1554 .- 1551-5044. ; 48:1, s. 153-161 Tidskriftsartikel (refereegranskat)abstract Fluorescent immunocytochemistry (FICC) allows multiple labeling approaches when enzyme-based techniques are difficult to combine, such as in double-labeling experiments targeting small-caliber axonal segments. Nevertheless, the conversion of FICC to a product visible at the electron microscopic (EM) level requires labor-intensive procedures, thus justifying the development of more user-friendly conversion methods. This study was initiated to simplify the conversion of FICC to EM by employing the unique properties of tyramide signal amplification (TSA), which allowed the simultaneous targeting of a fluorescent tag and biotin label to the same antigenic site. Briefly, one of two antigenic sites typically co-localized in damaged axonal segments was visualized by the application of a fluorescent secondary antibody, with the other tagged via a biotinylated antibody. Next, an ABC kit was used, followed by the simultaneous application of fluorophore-tyramide and biotin-tyramide. After temporary mounting for fluorescent digital photomicroscopy, sections were incubated in ABC and reacted with diaminobenzidine before EM analysis. Double-labeling fluorescent immunocytochemistry with TSA clearly delineated damaged axonal segments. In addition, these same axonal segments yielded high-quality EM images with discrete electron-dense reaction products, thereby providing a simple and reproducible means for following fluorescent analysis with EM.
29.	Büki, Andras, 1966-, et al. (författare) Obituary Ronald L. Hayes 2024 Ingår i: Acta Neurochirurgica. - : Springer. - 0001-6268 .- 0942-0940. ; 166:1 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
30.	Büki, Andras, 1966-, et al. (författare) Occlusive hydrocephalus complicating tuberous sclerosis : report of two cases 1996 Ingår i: European Journal of Neurology. - Oxford : Blackwell Publishing. - 1351-5101 .- 1468-1331. ; 3:3, s. 255-259 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.
31.	Büki, Andras, 1966-, et al. (författare) Peptidergic innervation of human cerebral blood vessels and saccular aneurysms 1999 Ingår i: Acta Neuropathologica. - : Springer. - 0001-6322 .- 1432-0533. ; 98:4, s. 383-388 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.
32.	Büki, Andras, 1966-, et al. (författare) Postinjury cyclosporin a administration limits axonal damage and disconnection in traumatic brain injury 1999 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 16:6, s. 511-521 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.
33.	Büki, Andras, 1966-, et al. (författare) Preinjury administration of the calpain inhibitor MDL-28170 attenuates traumatically induced axonal injury 2003 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 20:3, s. 261-268 Tidskriftsartikel (refereegranskat)abstract Traumatic brain injury (TBI) evokes diffuse (traumatic) axonal injury (TAI), which contributes to morbidity and mortality. Damaged axons display progressive alterations gradually evolving to axonal disconnection. In severe TAI, the tensile forces of injury lead to a focal influx of Ca2+, initiating a series of proteolytic processes wherein the cysteine proteases, calpain and caspase modify the axonal cytoskeleton, causing irreversible damage over time postinjury. Although several studies have demonstrated that the systemic administration of calpain inhibitors reduces the extent of ischemic and traumatic contusional injury a direct beneficial effect on TAI has not been established to date. The current study was initiated to address this issue in an impact acceleration rat-TBI model in order to provide further evidence on the contribution of calpain-mediated proteolytic processes in the pathogenesis of TAI, while further supporting the utility of calpain-inhibitors. A single tail vein bolus injection of 30 mg/kg MDL-28170 was administered to Wistar rats 30 min preinjury. After injury the rats were allowed to survive 120 min when they were perfused with aldehydes. Brains were processed for immunohistochemical localization of damaged axonal profiles displaying either amyloid precursor protein (APP)- or RMO-14-immunoreactivity (IR), both considered markers of specific features of TAI. Digital data acquisition and statistical analysis demonstrated that preinjury administration of MDL-28170 significantly reduced the mean number of damaged RMO-14- as well as APP-IR axonal profiles in the brainstem fiber tracts analyzed. These results further underscore the role of calpain-mediated proteolytic processes in the pathogenesis of DAI and support the potential use of cell permeable calpain-inhibitors as a rational therapeutic approach in TBI.
34.	Büki, Andras, 1966-, et al. (författare) Sclerosis tuberosához társuló, elzáródásos hydrocephalust okozó III : kamra óriássejtes astrocytoma [Subependymal giant cell astrocytoma associated with tuberous sclerosis as a cause of occlusive hydrocephalus] 1996 Ingår i: Gyermekgyógyászat. - : Magyar Gyermekorvosok Tarsasaga. - 0017-5900. ; 47:4, s. 327-332 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
35.	Büki, Andras, 1966-, et al. (författare) Simultaneous occurrence of unilateral multiplex meningeomas and syringomyelia 1994 Ingår i: Iddegyogyaszati Szemle : Clinical Neuroscience. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 5-6:47, s. 161-163 Tidskriftsartikel (refereegranskat)
36.	Büki, Andras, 1966-, et al. (författare) The role of calpail-mediated spectrin proteolysis in traumatically induced axonal injury 1999 Ingår i: Journal of Neuropathology and Experimental Neurology. - : American Association of Neuropathologists. - 0022-3069 .- 1554-6578. ; 58:4, s. 365-375 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.
37.	Bukovics, Peter, et al. (författare) Changes of PACAP level in cerebrospinal fluid and plasma of patients with severe traumatic brain injury 2014 Ingår i: Peptides. - : Elsevier. - 0196-9781 .- 1873-5169. ; 60, s. 18-22 Tidskriftsartikel (refereegranskat)abstract PACAP has well-known neuroprotective potential including traumatic brain injury (TBI). Its level is up-regulated following various insults of the CNS in animal models. A few studies have documented alterations of PACAP levels in human serum. The time course of post-ictal PACAP levels, for example, show correlation with migraine severity. Very little is known about the course of PACAP levels following CNS injury in humans and the presence of PACAP has not yet been detected in cerebrospinal fluid (CSF) of subjects with severe TBI (sTBI). The aim of the present study was to determine whether PACAP occurs in the CSF and plasma (Pl) of patients that suffered sTBI and to establish a time course of PACAP levels in the CSF and Pl. Thirty eight subjects with sTBI were enrolled with a Glasgow Coma Scale ≤8 on admission. Samples were taken daily, until the time of death or for maximum 10 days. Our results demonstrated that PACAP was detectable in the CSF, with higher concentrations in patients with TBI. PACAP concentrations markedly increased in both Pl and CSF in the majority of patients 24-48h after the injury stayed high thereafter. In cases of surviving patients, Pl and CSF levels displayed parallel patterns, which may imply the damage of the blood-brain barrier. However, in patients, who died within the first week, Pl levels were markedly higher than CSF levels, possibly indicating the prognostic value of high Pl PACAP levels.
38.	Chesnut, Randall, et al. (författare) A management algorithm for adult patients with both brain oxygen and intracranial pressure monitoring : the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC) 2020 Ingår i: Intensive Care Medicine. - : Springer. - 0342-4642 .- 1432-1238. ; 46:5, s. 919-929 Tidskriftsartikel (refereegranskat)abstract Background: Current guidelines for the treatment of adult severe traumatic brain injury (sTBI) consist of high-quality evidence reports, but they are no longer accompanied by management protocols, as these require expert opinion to bridge the gap between published evidence and patient care. We aimed to establish a modern sTBI protocol for adult patients with both intracranial pressure (ICP) and brain oxygen monitors in place.Methods: Our consensus working group consisted of 42 experienced and actively practicing sTBI opinion leaders from six continents. Having previously established a protocol for the treatment of patients with ICP monitoring alone, we addressed patients who have a brain oxygen monitor in addition to an ICP monitor. The management protocols were developed through a Delphi-method-based consensus approach and were finalized at an in-person meeting.Results: We established three distinct treatment protocols, each with three tiers whereby higher tiers involve therapies with higher risk. One protocol addresses the management of ICP elevation when brain oxygenation is normal. A second addresses management of brain hypoxia with normal ICP. The third protocol addresses the situation when both intracranial hypertension and brain hypoxia are present. The panel considered issues pertaining to blood transfusion and ventilator management when designing the different algorithms.Conclusions: These protocols are intended to assist clinicians in the management of patients with both ICP and brain oxygen monitors but they do not reflect either a standard-of-care or a substitute for thoughtful individualized management. These protocols should be used in conjunction with recommendations for basic care, management of critical neuroworsening and weaning treatment recently published in conjunction with the Seattle International Brain Injury Consensus Conference.
39.	Chesnut, Randall M., et al. (författare) Perceived Utility of Intracranial Pressure Monitoring in Traumatic Brain Injury : A Seattle International Brain Injury Consensus Conference Consensus-Based Analysis and Recommendations 2023 Ingår i: Neurosurgery. - : Oxford University Press. - 0148-396X .- 1524-4040. ; 93:2, s. 399-408 Tidskriftsartikel (refereegranskat)abstract BACKGROUND: Intracranial pressure (ICP) monitoring is widely practiced, but the indications are incompletely developed, and guidelines are poorly followed. OBJECTIVE: To study the monitoring practices of an established expert panel (the clinical working group from the Seattle International Brain Injury Consensus Conference effort) to examine the match between monitoring guidelines and their clinical decision-making and offer guidance for clinicians considering monitor insertion.METHODS: We polled the 42 Seattle International Brain Injury Consensus Conference panel members' ICP monitoring decisions for virtual patients, using matrices of presenting signs (Glasgow Coma Scale [GCS] total or GCS motor, pupillary examination, and computed tomography diagnosis). Monitor insertion decisions were yes, no, or unsure (traffic light approach). We analyzed their responses for weighting of the presenting signs in decision-making using univariate regression.RESULTS: Heatmaps constructed from the choices of 41 panel members revealed wider ICP monitor use than predicted by guidelines. Clinical examination (GCS) was by far the most important characteristic and differed from guidelines in being nonlinear. The modified Marshall computed tomography classification was second and pupils third. We constructed a heatmap and listed the main clinical determinants representing 80% ICP monitor insertion consensus for our recommendations.CONCLUSION: Candidacy for ICP monitoring exceeds published indicators for monitor insertion, suggesting the clinical perception that the value of ICP data is greater than simply detecting and monitoring severe intracranial hypertension. Monitor insertion heatmaps are offered as potential guidance for ICP monitor insertion and to stimulate research into what actually drives monitor insertion in unconstrained, real-world conditions.
40.	Csecsei, P., et al. (författare) Risk analysis of post-procedural intracranial hemorrhage based on STAY ALIVE Acute Stroke Registry 2020 Ingår i: Journal of Stroke & Cerebrovascular Diseases. - New York : Demos Publishing. - 1052-3057 .- 1532-8511. ; 29:7 Tidskriftsartikel (refereegranskat)abstract Background: Intracranial hemorrhages (ICH) are classified as symptomatic or asymptomatic according to the presence of clinical deterioration. Here, we aimed to find predictive factors of symptomatic intracranial bleeding in a registry-based stroke research.Methods: Data of consecutive patients with acute ischemic stroke (AIS) were extracted from the prospective STAY ALIVE stroke registry. Analysis of the total population and treatment sugroups such as endovascular thrombectomy (EVT), intravenous thrombolysis (IVT), or their combination (IVT+EVT) were also done. Outcome measures were ICH, 30- and 90-day clinical outcome based on the modified Rankin Scale (mRS:0-2 as favorable outcome). The hemorrhage was captured by a non-enhanced CT of the skull within 24 h after procedure.Results: A total of 355 patients (mean age: 68 +/- 11; female N=177 (49.9%); EVT n=131 (36.9%); IVT n=157 (44.2%); IVT+EVT n=67 (18.9%) were included in the analysis. The total number of ICH was 47 (13%), symptomatic (sICH) 12 (3.4%) and asymptomatic (aICH) 35 (9.9%) in the whole population. NIHSS >= 15.5 at 24 post stroke hours predicted sICH with a sensitivity of 100% and a specificity of 92% (p<0.001). Furthermore, lower age, good collateral circulation on initial CT angiography and lower NIHSS score measured at 24 h independently associated with a favorable 90-day outcome, whereas baseline NIHSS and ASPECT score were not.Conclusion: Although partial recanalization, ASPECT< 6, and poor collaterals were significantly associated with sICH, the only independent predictor was NIHSS >= 15.5 at 24 post stroke hours. This suggests a careful evaluation of patients with worsening NIHSS despite an adequate therapy.
41.	Cseplo, Peter, et al. (författare) Hemolyzed Blood Elicits a Calcium Antagonist and High CO2 Reversible Constriction via Elevation of [Ca2+]i in Isolated Cerebral Arteries 2017 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 34:2, s. 529-534 Tidskriftsartikel (refereegranskat)abstract During acute subarachnoid hemorrhage, blood is hemolyzed, which is followed by a significant cerebrovascular spasm resulting in a serious clinical condition. Interestingly, however, the direct vasomotor effect of perivascular hemolyzed blood (HB) has not yet been characterized, preventing the assessment of contribution of vasoconstrictor mechanisms deriving from brain tissue and/or blood and development of possible treatments. We hypothesized that perivascular HB reduces the diameter of the cerebral arteries (i.e., basilar artery [BA]; middle cerebral artery [MCA]) by elevating vascular tissue [Ca2+](i) level. Vasomotor responses were measured by videomicroscopy and intracellular Ca2+ by the Fura2-AM ratiometric method. Adding HB to the vessel chamber reduced the diameter significantly (BA: from 264 +/- 7 to 164 +/- 11 mu m; MCA: from 185 +/- 15 to 155 +/- 14 mu m), which was reversed to control level by wash-out of HB. Potassium chloride (KCl), HB, serum, hemolyzed red blood cell (RBC), plasma, and platelet suspension (PLTs) elicited significant constrictions of isolated basilar arteries. There was a significant increase in K+ concentration in hemolyzed HB (7.02 +/- 0.22 mmol/L) compared to Krebs' solution (6.20 +/- 0.01 mmol/L). Before HB, acetylcholine (ACh), sodium-nitroprussid (SNP), nifedipin, and CO2 elicited substantial dilations in cerebral arteries. In contrast, in the presence of HB dilations to ACh, SNP decreased, but not to nifedipine and CO2. After washout of HB, nitric oxide-mediated dilations remained significantly reduced compared to control. HB significantly increased the ratiometric Ca signal, which returned to control level after washout. In conclusion, perivascular hemolyzed blood elicits significant-nifedipine and high CO2 reversible-constrictions of isolated BAs and MCAs, primarily by increasing intracellular Ca2+, findings that can contribute to the refinement of local treatment of subarachnoid hemorrhage.
42.	Csepregi, Gyula, et al. (författare) Sülyos koponya-agy sérültek ellátása Magyarországon, 2002-ben : [Management of patients with severe head injury in Hungary, in 2002] 2007 Ingår i: Orvosi Hetilap. - : Akademiai Kiado Rt.. - 0030-6002 .- 1788-6120. ; 148:17, s. 771-777 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.
43.	Czeiter, Endre, et al. (författare) Blood biomarkers on admission in acute traumatic brain injury : Relations to severity, CT findings and care path in the CENTER-TBI study 2020 Ingår i: EBioMedicine. - : Elsevier. - 2352-3964. ; 56 Tidskriftsartikel (refereegranskat)abstract BACKGROUND: Serum biomarkers may inform and improve care in traumatic brain injury (TBI). We aimed to correlate serum biomarkers with clinical severity, care path and imaging abnormalities in TBI, and explore their incremental value over clinical characteristics in predicting computed tomographic (CT) abnormalities.METHODS: We analyzed six serum biomarkers (S100B, NSE, GFAP, UCH-L1, NFL and t-tau) obtained <24 h post-injury from 2867 patients with any severity of TBI in the Collaborative European NeuroTrauma Effectiveness Research (CENTER-TBI) Core Study, a prospective, multicenter, cohort study. Univariable and multivariable logistic regression analyses were performed. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC) with 95% confidence intervals.FINDINGS: All biomarkers scaled with clinical severity and care path (ER only, ward admission, or ICU), and with presence of CT abnormalities. GFAP achieved the highest discrimination for predicting CT abnormalities (AUC 0•89 [95%CI: 0•87-0•90]), with a 99% likelihood of better discriminating CT-positive patients than clinical characteristics used in contemporary decision rules. In patients with mild TBI, GFAP also showed incremental diagnostic value: discrimination increased from 0•84 [95%CI: 0•83-0•86] to 0•89 [95%CI: 0•87-0•90] when GFAP was included. Results were consistent across strata, and injury severity. Combinations of biomarkers did not improve discrimination compared to GFAP alone.INTERPRETATION: Currently available biomarkers reflect injury severity, and serum GFAP, measured within 24 h after injury, outperforms clinical characteristics in predicting CT abnormalities. Our results support the further development of serum GFAP assays towards implementation in clinical practice, for which robust clinical assay platforms are required.FUNDING: CENTER-TBI study was supported by the European Union 7th Framework program (EC grant 602150).
44.	Czeiter, Endre, et al. (författare) Brain Injury Biomarkers May Improve the Predictive Power of the IMPACT Outcome Calculator 2012 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 29:9, s. 1770-1778 Tidskriftsartikel (refereegranskat)abstract Outcome prediction following severe traumatic brain injury (sTBI) is a widely investigated field of research. A major breakthrough is represented by the IMPACT prognostic calculator based on admission data of more than 8500 patients. A growing body of scientific evidence has shown that clinically meaningful biomarkers, including glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), and alpha II-spectrin breakdown product (SBDP145), could also contribute to outcome prediction. The present study was initiated to assess whether the addition of biomarkers to the IMPACT prognostic calculator could improve its predictive power. Forty-five sTBI patients (GCS score <= 8) from four different sites were investigated. We utilized the core model of the IMPACT calculator (age, GCS motor score, and reaction of pupils), and measured the level of GFAP, UCH-L1, and SBDP145 in serum and cerebrospinal fluid (CSF). The forecast and actual 6-month outcomes were compared by logistic regression analysis. The results of the core model itself, as well as serum values of GFAP and CSF levels of SBDP145, showed a significant correlation with the 6-month mortality using a univariate analysis. In the core model, the Nagelkerke R-2 value was 0.214. With multivariate analysis we were able to increase this predictive power with one additional biomarker (GFAP in CSF) to R-2 = 0.476, while the application of three biomarker levels (GFAP in CSF, GFAP in serum, and SBDP145 in CSF) increased the Nagelkerke R-2 to 0.700. Our preliminary results underline the importance of biomarkers in outcome prediction, and encourage further investigation to expand the predictive power of contemporary outcome calculators and prognostic models in TBI.
45.	Czeiter, Endre, et al. (författare) Calpain inhibition reduces axolemmal leakage in traumatic axonal injury 2009 Ingår i: Molecules. - : MDPI. - 1431-5157 .- 1420-3049. ; 14:12, s. 5115-5123 Tidskriftsartikel (refereegranskat)abstract Calcium-induced, calpain-mediated proteolysis (CMSP) has recently been implicated to the pathogenesis of diffuse (traumatic) axonal injury (TAI). Some studies suggested that subaxolemmal CMSP may contribute to axolemmal permeability (AP) alterations observed in TAI. Seeking direct evidence for this premise we investigated whether subaxolemmal CMSP may contribute to axolemmal permeability alterations (APA) and pre-injury calpain-inhibition could reduce AP in a rat model of TAI. Horseradish peroxidase (HRP, a tracer that accumulates in axons with APA) was administered one hour prior to injury into the lateral ventricle; 30 min preinjury a single tail vein bolus injection of 30 mg/kg MDL-28170 (a calpain inhibitor) or its vehicle was applied in Wistar rats exposed to impact acceleration brain injury. Histological detection of traumatically injured axonal segments accumulating HRP and statistical analysis revealed that pre-injury administration of the calpain inhibitor MDL-28170 significantly reduced the average length of HRP-labeled axonal segments. The axono-protective effect of pre-injury calpain inhibition recently demonstrated with classical immunohistochemical markers of TAI was further corroborated in this experiment; significant reduction of the length of labeled axons in the drug-treated rats implicate CMSP in the progression of altered AP in TAI.
46.	Czeiter, Endre, et al. (författare) Traumatic axonal injury in the spinal cord evoked by traumatic brain injury 2008 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 25:3, s. 205-213 Tidskriftsartikel (refereegranskat)abstract Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated. Detection of such axonal injury in the spinal cord would further the complexity of TBI while also challenging some functional neurobehavioral endpoints frequently used to assess recovery in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI of varying severities. Rats were transcardially fixed with aldehydes at 2, 6, and 24 h post-injury (n = 36); each group included on sham-injured rodent. Semi-serial vibratome sections were reacted with antibodies targeting TAI via alteration in cytoskeletal integrity or impaired axonal transport. Consistent with previous observations in this model, the CCJ contained numerous injured axons. Immunoreactive, damaged axonal profiles were also detected as caudal, as the ThL spinal cord displayed morphological characteristics entirely consistent with those described in the brainstem and the CCJ. Quantitative analyses demonstrated that the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively with the distance from the brainstem. These observations show that TBI can evoke TAI in regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken baby syndrome as well as during the analysis of data in functional recovery in various models of TBI.
47.	DeWitt, Douglas S., et al. (författare) Pre-clinical testing of therapies for traumatic brain injury 2018 Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 35:23, s. 2737-2754 Tidskriftsartikel (refereegranskat)abstract Despite the large number of promising neuroprotective agents identified in experimental traumatic brain injury (TBI) studies, none has yet shown meaningful improvements in long-term outcome in clinical trials. To develop recommendations and guidelines for pre-clinical testing of pharmacological or biological therapies for TBI, the Moody Project for Translational Traumatic Brain Injury Research hosted a symposium attended by investigators with extensive experience in pre-clinical TBI testing. The symposium participants discussed issues related to pre-clinical TBI testing including experimental models, therapy and outcome selection, study design, data analysis, and dissemination. Consensus recommendations included the creation of a manual of standard operating procedures with sufficiently detailed descriptions of modeling and outcome measurement procedures to permit replication. The importance of the selection of clinically relevant outcome variables, especially related to behavior testing, was noted. Considering the heterogeneous nature of human TBI, evidence of therapeutic efficacy in multiple, diverse (e.g., diffuse vs. focused) rodent models and a species with a gyrencephalic brain prior to clinical testing was encouraged. Basing drug doses, times, and routes of administration on pharmacokinetic and pharmacodynamic data in the test species was recommended. Symposium participants agreed that the publication of negative results would reduce costly and unnecessary duplication of unsuccessful experiments. Although some of the recommendations are more relevant to multi-center, multi-investigator collaborations, most are applicable to pre-clinical therapy testing in general. The goal of these consensus guidelines is to increase the likelihood that therapies that improve outcomes in pre-clinical studies will also improve outcomes in TBI patients.
48.	Faludi, Béla, et al. (författare) Combination of severe facialand cervical vascular malformation with obstructive sleep apnea syndrome : Diagnostic and therapeutic approaches 2017 Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 70:1-2, s. 7-13 Forskningsöversikt (refereegranskat)abstract The combination of obstructive sleep apnea syndrome and vascular malformation within the head and neck region is a rare condition, and interestingly, only a few cases have recently been published. Propagation of the vascular mass to the larynx and pharynx can cause breathing and swallowing difficulties. Due to these sypmtoms, examination and initiation of appropriate therapy for such patients are indeed challenging. We reviewed the literature available and present our case of a 64 year old woman emphasizing the complaints of sleep apnea syndrome and vascular malformation of the face and neck region. Polygraphic examination detected severe obstructive sleep apnea syndrome. The MR examination of the neck revealed extensive vascular mass narrowing the pharyngo-laryngeal region, thereby causing temporal bone destruction on the right side with intracranial propagation. ENT examination demonstrated significant narrowing of the pharyngeal lumen and the laryngeal aditus caused by multiple hemangiomas. CPAP titration showed the minimalization of the apnea-hypopnea index on the effective pressure level. Regular CPAP usage resulted in diminishing a majority of the patient's complaints. Our examination clearly demonstrates, obstructive sleep apnea syndrome coupled with significantly obstructing vascular malformation in the head and neck region can be effectively treated safely with a CPAP device, if surgical therapy is not possible. We summarized our findings and the data available in the literature to set up recommendations for the appropriate examination and therapy (including mask fit, etc.) of vascular malformations and hemangiomas causing pharyngolaryngeal obstruction.
49.	Farkas, Orsolya, et al. (författare) Effects of pituitary adenylate cyclase activating polypeptide in a rat model of traumatic brain injury 2004 Ingår i: Regulatory Peptides. - : Elsevier. - 0167-0115 .- 1873-1686. ; 123:1-3, s. 69-75 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.
50.	Hawryluk, Gregory W. J., et al. (författare) A management algorithm for patients with intracranial pressure monitoring : the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC) 2019 Ingår i: Intensive Care Medicine. - : Springer. - 0342-4642 .- 1432-1238. ; 45:12, s. 1783-1794 Tidskriftsartikel (refereegranskat)abstract Background: Management algorithms for adult severe traumatic brain injury (sTBI) were omitted in later editions of the Brain Trauma Foundation's sTBI Management Guidelines, as they were not evidence-based.Methods: We used a Delphi-method-based consensus approach to address management of sTBI patients undergoing intracranial pressure (ICP) monitoring. Forty-two experienced, clinically active sTBI specialists from six continents comprised the panel. Eight surveys iterated queries and comments. An in-person meeting included whole- and small-group discussions and blinded voting. Consensus required 80% agreement. We developed heatmaps based on a traffic-light model where panelists' decision tendencies were the focus of recommendations.Results: We provide comprehensive algorithms for ICP-monitor-based adult sTBI management. Consensus established 18 interventions as fundamental and ten treatments not to be used. We provide a three-tier algorithm for treating elevated ICP. Treatments within a tier are considered empirically equivalent. Higher tiers involve higher risk therapies. Tiers 1, 2, and 3 include 10, 4, and 3 interventions, respectively. We include inter-tier considerations, and recommendations for critical neuroworsening to assist the recognition and treatment of declining patients. Novel elements include guidance for autoregulation-based ICP treatment based on MAP Challenge results, and two heatmaps to guide (1) ICP-monitor removal and (2) consideration of sedation holidays for neurological examination.Conclusions: Our modern and comprehensive sTBI-management protocol is designed to assist clinicians managing sTBI patients monitored with ICP-monitors alone. Consensus-based (class III evidence), it provides management recommendations based on combined expert opinion. It reflects neither a standard-of-care nor a substitute for thoughtful individualized management.

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