Johann Sellner

Paracelsus Medical University Salzburg, Salzburg, Salzburg, Austria

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Publications (88)340.3 Total impact

  • Andrea Harrer, Georg Pilz, Peter Wipfler, Katrin Oppermann, Johann Sellner, Wolfgang Hitzl, Elisabeth Haschke-Becher, Shahrzad Afazel, Theo Rispens, Desiree van der Kleij, Eugen Trinka, Jörg Kraus
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    ABSTRACT: Strongly decreased leukocyte counts and a reduced CD4/CD8 T cell ratio in the cerebrospinal fluid (CSF) of natalizumab (NZB)-treated multiple sclerosis (MS) patients may have implications on central nervous (CNS) immune surveillance. With regard to NZB-associated progressive multifocal leukoencephalopathy we aimed at delineating a relationship between free NZB, cell-bound NZB, adhesion molecule (AM) expression, and the treatment-associated shift in the CSF T cell ratio. Peripheral blood (PB) and CSF T cells from fifteen NZB-treated MS patients, and CSF T cells from ten patients with non-inflammatory neurological diseases and five newly diagnosed MS patients were studied. Intercellular adhesion molecule-1 (ICAM-1), leukocyte function antigen-1 (LFA-1), very late activation antigen-4 (VLA-4), NZB saturation levels, and T cell ratios were analyzed by flow cytometry. NZB concentrations were measured by ELISA. Lower NZB saturation levels (P <.02) and a higher surface expression of ICAM-1 and LFA-1 (P <.001) were observed on CSF CD8 T cells. CSF T cell ratios (0.3-2.1) and NZB concentrations (0.01-0.42 µg/ml) showed a pronounced interindividual variance. A correlation between free NZB, cell-bound NZB, or AM expression levels and the CSF T cell ratio was not found. Extremely low NZB concentrations and a normalized CSF T cell ratio were observed in one case. The differential NZB saturation and AM expression of CSF CD8 T cells may contribute to their relative enrichment in the CSF. The reduced CSF T cell ratio appeared sensitive to steady-state NZB levels as normalization occurred quickly. Latter may be important concerning a fast reconstitution of CNS immune surveillance. This article is protected by copyright. All rights reserved. © 2015 British Society for Immunology.
    Clinical & Experimental Immunology 01/2015; · 3.28 Impact Factor
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    ABSTRACT: To assess the general interest in and motivation for cross-border mobility among residents and junior neurologists from member states of the European Union and neighboring countries.
    Neurology 09/2014; 83(13):e-128-e131. · 8.30 Impact Factor
  • Antonella Macerollo, Johann Sellner
    Neurology 07/2014; 83(3):e45-7. · 8.30 Impact Factor
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    European Journal of Neurology 07/2014; 21(7):941-5. · 3.85 Impact Factor
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    ABSTRACT: Around the world, there are marked differences in neurology training, including training duration and degree of specialization. In the United States, adult neurology residency is composed of 1 year of internal medicine training (preliminary year) and 3 years of neurology-specific training. Child neurology, which is not the focus of this article, is 2 years of pediatrics and 3 years of neurology training. The route to adult neurology residency training in the United States is standardized and is similar to most other US specialties. Whereas US medical graduates often receive stepwise guidance from their medical school regarding application for residency training, international graduates often enter this complex process with little or no such assistance. Despite this discrepancy, about 10%-15% of residency positions in the United States are filled by international medical graduates.(1,2) In adult neurology specifically, 35% of matched positions were filled by international graduates in 2013, 75% of whom were not US citizens.(1) In an effort to provide a preliminary understanding of the application process and related terminology (table 1) and thereby encourage international residency applicants, we describe the steps necessary to apply for neurology residency in the United States.
    Neurology 04/2014; 82(14):e112-5. · 8.30 Impact Factor
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    ABSTRACT: Background and purposeThe neurological outcome of acute encephalitis can be devastating and early prognosis remains difficult. Biomarkers that quantify the extent of early brain injury are needed to improve the prognostic accuracy and aid patient management. Our objective was to assess whether cerebrospinal fluid (CSF) protein biomarkers of neuroaxonal and glial cell injury are elevated in distinct forms of acute encephalitis and predictive of poor outcome.Methods This was a prospective study of patients presenting with acute encephalitis to three teaching hospitals in London, UK. Levels of neurofilament heavy chain (NfH, SMI35) and S100B were quantified in CSF using enzyme-linked immunosorbent assay. The outcome was assessed by the Glasgow Outcome Scale (GOS).ResultsFifty-six patients with acute encephalitis were recruited and classified into the following diagnostic categories: infectious (n = 20), inflammatory (n = 14) and unknown etiology (n = 22). Pathological levels of NfH and S100B were observed in 24/56 (43%) and 54/56 (96%), respectively. Patients with infectious encephalitis had significantly higher NfH levels compared with the other two groups (P < 0.05). A poor outcome (GOS < 5) was associated with significantly higher CSF NfH levels within samples taken 2 weeks after symptom onset.Conclusions This study suggests that longitudinal CSF NfH levels are of superior prognostic value compared with CSF S100B levels. Prolonged release of NfH, a marker of neuroaxonal damage, was associated with poor outcome. Potentially there is a window of opportunity for future neuroprotective treatment strategies in encephalitis.
    European Journal of Neurology 03/2014; · 3.85 Impact Factor
  • Martin Rakusa, Walter Struhal, Johann Sellner
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    ABSTRACT: "The secret of happiness is freedom. The secret of freedom is courage."(1)-Thucydides (Ancient Greek historian and author, 460-404 bc).
    Neurology 02/2014; 82(6):536-9. · 8.30 Impact Factor
  • Johann Sellner, Israel Steiner
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    ABSTRACT: The clinical spectrum of viral hepatitis ranges from asymptomatic and inapparent to fulminant and fatal acute infection. Both acute and chronic liver dysfunction can lead to hepatic encephalopathy. Further neurological manifestations of hepatic viruses include various disorders of the central and peripheral nervous system (CNS and PNS, respectively). These can develop either as an isolated complication or in the setting of other extrahepatic manifestations. Alternatively, neurological signs and symptoms precede hepatitis, develop in the post-acute phase, or occur with anicteric hepatitis. This chapter summarizes the current knowledge of neurological manifestations of hepatic viruses and also covers conditions related to neurotoxicity caused by different antiviral drugs.
    Handbook of Clinical Neurology 01/2014; 123C:647-661.
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    ABSTRACT: Abstract There is controversy whether determination of antibodies against myelin, myelin oligodendrocyte glycoprotein, and myelin basic protein in serum from patients with a first episode suggestive of multiple sclerosis is of prognostic value. We evaluated whether detection of anti-myelin antibodies in serum indicate a worse course with earlier time to a second relapse and increased progression of disability. We conducted a prospective study at the Department of Neurology, Inselspital Bern, Switzerland from 2004-2008 in patients presenting with a clinically isolated syndrome (CIS) and a follow-up of at least four months. Anti-myelin antibodies were assessed by Western blot. Results were correlated with clinical course and sex. Among 93 consecutive patients with a CIS, 74 (80%) were positive for either one or both anti-myelin antibodies. A relapse occurred in 49 (53%) and the median EDSS was 2 (range 1-3.5) after a mean observation period of 20 months. Presence of anti-myelin antibodies at CIS neither increased the risk for a second relapse nor for progression of disability. Stratification for gender did not reveal differences for any of the clinical surrogates. The sole determination of anti-myelin antibodies in serum is of limited prognostic value for the identification of patients with different short-term course.
    The International journal of neuroscience 11/2013; · 1.53 Impact Factor
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    ABSTRACT: The objective of this article, written by executives of the European Association of Young Neurologists and Trainees (EAYNT), is to illustrate the status quo of neurology training in Europe and give an outlook on ongoing efforts and prospects for junior neurologists. The European Union is an economic and political union that currently encompasses 27 member states with more than 500 million inhabitants (or 7.3% of the world population) (interested readers are referred to http://en.wikipedia.org/wiki/European_Union). Countries of the European Union act as a single market with free movement of citizens, goods, services, and finances. As a consequence, a diploma and postgraduate training obtained in one EU country will be automatically recognized by all other EU member states. At the Lisbon European Council in March 2000, the Heads of State or Government signed a treaty that expresses their ambition of making Europe "the most competitive and dynamic knowledge-based economy in the world, capable of sustainable economic growth with more and better jobs and greater social cohesion" (www.en.wikipedia.org/wiki/Lisbon_Strategy). More than 1.6 million physicians in all the different medical specialties are represented by the European Union of Medical Specialists (UEMS). The UEMS was founded in 1958 and the objectives include the study, promotion, and harmonization of the highest level of training of medical specialists, medical practice, and health care within the European Union. The European Board of Neurology (UEMS-EBN; www.uems-neuroboard.org) is in charge of the implementation of the UEMS policy regarding neurology.
    Neurology 10/2013; 81(18):1626-9. · 8.30 Impact Factor
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    ABSTRACT: To report about a possible association between fingolimod treatment and tumefactive demyelinating lesions (TDL) as seen in a patient developing repeated TDL on continued fingolimod therapy. We performed serial clinical and radiologic assessments and immunophenotyping of blood and CSF immune cells. We also present a literature review about recent similar cases. Clinical course and radiologic findings were consistent with diagnosis of TDL. Immune cell phenotyping showed pronounced shifts in the immune cell composition related to fingolimod treatment. In addition, we observed a subset of highly differentiated effector cells (CD45R0negCCR7neg) within the CD8+ T-cell population, which was about 2-fold enriched in the CSF compared to the peripheral blood. Our observations add further evidence for the development of atypical demyelinating lesions in some patients receiving fingolimod. These might be related to a treatment-associated shift in the immunopathology of specifically susceptible individuals.
    Neurology 10/2013; · 8.30 Impact Factor
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    ABSTRACT: More and more patients with multiple sclerosis (MS) switch from natalizumab to fingolimod because of the risk of progressive multifocal leukoencephalopathy. The duration of the treatment holiday is still under debate referring to a possible recurrence of disease activity. The aim of this study was to evaluate the prognostic value of natalizumab saturation on T cells for the recurrence of clinical and radiological disease activity. Cell surface-bound natalizumab saturation (in%) of CD8+ and CD4+ T cells from five patients with MS was determined before initiation of fingolimod by flow cytometry and related to clinical and MRI outcome during a 6-month follow-up. In two patients with either clinical or radiological disease activity, the natalizumab saturation on CD8+ and CD4+ T cells was <30%. In contrast, the remaining three patients with absence of disease activity had a median natalizumab saturation of 70% (range 59-79%) on CD4+ and 66% (range 52-68%) on CD8+ T cells. The data of this pilot study indicate that clinical and radiological disease activity is closely linked to natalizumab saturation at the time point of switch. The determination of natalizumab saturation may be an essential tool to monitor cessation of natalizumab treatment.
    Acta Neurologica Scandinavica 08/2013; · 2.44 Impact Factor
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    ABSTRACT: An altered expression pattern of adhesion molecules (AM) on the surface of immune cells is a premise for their extravasation into the central nervous system (CNS) and the formation of acute brain lesions in multiple sclerosis (MS). We evaluated the impact of glatiramer acetate (GA) on cell-bound and soluble AM in the peripheral blood of patients with relapsing-remitting MS (RRMS). Fifteen patients treated de-novo with GA were studied on four occasions over a period of 12 months. Surface levels of ICAM-1, ICAM-3, LFA-1 and VLA-4 were assessed in T cells (CD3+CD8+, CD3+CD4+), B cells, natural killer (NK) cells, natural killer T cells (NKT) and monocytes by 5-color flow cytometry. Soluble E-selectin, ICAM-1, ICAM-3, PECAM-1, P-selectin and VCAM-1 were determined with a fluorescent bead-based immunoassay. The pro-migratory pattern in RRMS was verified by comparison with healthy controls and was characterized by an up-regulation of LFA-1 (CD3+CD4+ T cells, B cells), VLA-4 (CD3+CD8+ T cells, NK cells), ICAM-1 (B cells) and ICAM-3 (NK cells). Effects of GA treatment were most pronounced after 6 months and included attenuated levels of LFA-1 (CD3+CD4+) and VLA-4 (CD3+CD4+, CD3+CD8+, NK, NKT, monocytes). Further effects included a lowering of ICAM-1 and ICAM-3 levels in almost all immune cell subsets. Soluble AM levels in RRMS did not differ from healthy controls and remained unaltered after GA treatment. The de-regulated pro-migratory expression profile of cell-bound AM is altered by GA treatment. While this alteration may contribute to the beneficial action of the drug, the prolonged development and unselective changes indicate more secondary immune regulatory phenomena related to these effects.
    Clinical & Experimental Immunology 04/2013; · 3.28 Impact Factor
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    ABSTRACT: BACKGROUND AND PURPOSE: The main objective of the European Association of Young Neurologists and Trainees (EAYNT), an independent Brussels-based association of junior neurologists, is to represent and promote the interests of European junior neurologists. METHODS AND RESULTS: A wide variety of projects and activities are ongoing, carried out by members of the organization in close collaboration with major European and National Neurology bodies. Most recently, we surveyed European junior neurologists about their views on the European Board of Neurology Examination, the status of e-learning in postgraduate neurology training and migration patterns of young neurologists. CONCLUSIONS: The aim of this paper is to outline the current and future activities of the EAYNT. We run a series of lectures ('EAYNT special sessions') at the major European conferences and disseminate information to young neurologists at the EAYNT booth. We provide information about travel grants, fellowships as well as sharing personal experiences of working abroad. EAYNT members have the opportunity to sit on the scientific subcommittees of the European Federation of Neurological Societies (EFNS) and European Neurological Society (ENS), to chair poster sessions and review abstracts. Furthermore, we continue to provide a forum for young neurologists from all over Europe to network and socialize by means of get-together events and hospital visits.
    European Journal of Neurology 04/2013; 20(4):e54-e58. · 3.85 Impact Factor
  • Article: Commentary.
    Johann Sellner
    Journal of neurosciences in rural practice. 04/2013; 4(2):179-80.
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    ABSTRACT: BACKGROUND: The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood--brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis. RESULTS: Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice. CONCLUSIONS: These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.
    BMC Neuroscience 02/2013; 14(1):19. · 2.85 Impact Factor
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    ABSTRACT: Objective: To report about a possible association between fingolimod treatment and tumefactive demyelinating lesions (TDL) as seen in a patient developing repeated TDL on continued fingolimod therapy. Methods: We performed serial clinical and radiologic assessments and immunophenotyping of blood and CSF immune cells. We also present a literature review about recent similar cases. Results: Clinical course and radiologic findings were consistent with diagnosis of TDL. Immune cell phenotyping showed pronounced shifts in the immune cell composition related to fingolimod treat-ment. In addition, we observed a subset of highly differentiated effector cells (CD45R0negCCR7neg) within the CD81 T-cell population, which was about 2-fold enriched in the CSF compared to the peripheral blood. Conclusion: Our observations add further evidence for the development of atypical demyelinating lesions in some patients receiving fingolimod. These might be related to a treatment-associated shift in the immunopathology of specifically susceptible individuals. Neurology ® 2013;81:1–5 GLOSSARY AQP4 5 aquaporin 4; Gd 5 gadolinium; JCV 5 JC virus; MS 5 multiple sclerosis; NK 5 natural killer; OCB 5 oligoclonal bands; PLEX 5 plasma exchange; PML 5 progressive multifocal leukoencephalopathy; TDL 5 tumefactive demyelinating lesions; TEM 5 effector memory T cells. Treatment options in multiple sclerosis (MS) have become more versatile with the introduction of natalizumab and oral fingolimod during recent years. Both drugs are in broad clinical use and are effective in reducing clinical and radiologic disease activity. 1,2 However, despite or maybe even because of the increased effectiveness, we have to be alert to rare and potentially unknown adverse effects caused by these new drugs. A rare but serious complication of natalizumab therapy is progressive multifocal leukoencephalop-athy (PML), which has not been described for fingolimod so far, with the exception of one patient previously treated with natalizumab. The risk of PML is more than 10-fold increased in a subgroup of patients with the triad of having received natalizumab for more than 2 years, a positive JC virus (JCV) serology, and a history of prior immunosuppressive therapy. In these patients, a switch to fingolimod appears reasonable. However, there is increasing evidence about patients with severe relapses or tumefactive MS lesions during fingolimod treatment. Notably, tumefactive demyelin-ating lesions (TDL) are very rare in MS and occur in the early stage, if at all. 3 Development of a TDL in the later disease course might therefore indicate a shift in the immunopathomechanism triggered by the fingolimod-induced redistribution of immune cells in susceptible individuals. We report a natalizumab-to-fingolimod-switched patient with repeated occurrence of TDL during fingolimod treatment. Case report. The first symptoms occurred in 2001 when a 15-year-old girl experienced hypesthesia of the right cheek. Diagnosis of MS was established in 2003 with the development of a second relapse causing hypesthesia of the right arm. Diagnosis was supported by the detection of typical MS lesions on brain MRI and oligoclonal
    Neurology 01/2013; · 8.30 Impact Factor
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    J Sellner, E Trinka
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    ABSTRACT: BACKGROUND AND PURPOSE: Epilepsy is a frequent complication of central nervous system (CNS) infections. Post-infectious epilepsy is commonly refractory to medical treatment and plays a pivotal role for the poor long-term outcome of CNS infections. OBJECTIVES: To provide an overview of clinical characteristics and risk factors of seizures associated with CNS infections. In addition, to summarize the state of the art of anticonvulsive treatment and the pre-surgical evaluation process in refractory cases. METHODS: Comprehensive literature search for articles published between January 1970 and December 2011. RESULTS: The occurrence of seizures during the acute course of meningitis, encephalitis and brain abscess is the main risk factor for the development of post-infectious epilepsy. There is a shortage of trials evaluating the efficacy of prophylactic and symptomatic treatment during the course of acute infection. Moreover, there are no randomized-controlled trials studying anticonvulsive drugs and their combinations for the management of post-infectious epilepsy. In a selected group of patients, however, medically refractory focal epilepsy is potentially curable by surgery. CONCLUSIONS: Further studies are required to improve the pathogenetic understanding of post-infectious epilepsy in order to develop preventive measures as well as to evaluate additional medical and surgical treatment strategies for the patients currently not considered for surgery.
    European Journal of Neurology 09/2012; · 3.85 Impact Factor
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    ABSTRACT: Polymerase chain reaction (PCR) as a means to amplify nucleic acids has become an essential element in diagnosis of infections. It has evolved into a simple and rapid, easy- to- use approach. At present there are no published guidelines for the usage of PCR technology for the diagnosis of infections of the nervous system. We reviewed the advantages and pitfalls of PCR in order to guide neurologists and infectious diseases experts in its application for the diagnosis of infections of the nervous system. Medical reference systems were searched, and original papers, meta-analyses, review papers, book chapters and guidelines recommendations were reviewed. The final literature search was performed in May 2012. Recommendations were reached by consensus. The reliability of PCR technology for the diagnosis of neurological infections is currently based on the pathogens. The main contribution of PCR is to the diagnosis of viral infections followed by bacterial CNS infections with the notable exception of tuberculous meningitis. Efficacy for the diagnosis of protozoal infections and helminthic infestations has also been established in many instances. Unfortunately, current molecular PCR technology is far from becoming routine in resource-poor countries where such infections are prevalent. Despite the importance of fungal infections in the context of the immune-compromised host, there is not enough data to recommend the routine use of PCR. PCR technology is currently a reliable method for the diagnosis of viral and bacterial (except tuberculosis) infections, and only for some protozoal infections and helminthic infestations.
    European Journal of Neurology 08/2012; 19(10):1278-91. · 3.85 Impact Factor
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    Neurology 07/2012; 79(4):381-3. · 8.30 Impact Factor

Publication Stats

693 Citations
340.30 Total Impact Points

Institutions

  • 2011–2014
    • Paracelsus Medical University Salzburg
      • Christian Doppler Clinic
      Salzburg, Salzburg, Austria
  • 2013
    • Università degli Studi di Bari Aldo Moro
      Bari, Apulia, Italy
  • 2008–2013
    • Technische Universität München
      • Neurologische Klinik und Poliklinik
      München, Bavaria, Germany
  • 2012
    • Krankenhaus Hietzing mit Neurologischem Zentrum Rosenhügel
      Wiener Neustadt, Lower Austria, Austria
  • 2010–2012
    • King's College London
      • Department of Clinical Neuroscience
      London, ENG, United Kingdom
  • 2009–2011
    • Allgemeines Krankenhaus Linz
      Linz, Upper Austria, Austria
    • Brussels University Association
      Bruxelles, Brussels Capital Region, Belgium
  • 2007–2008
    • Inselspital, Universitätsspital Bern
      • Department of Neurology
      Bern, BE, Switzerland
  • 2005–2006
    • Universität Bern
      • Institut für Infektionskrankheiten
      Bern, BE, Switzerland
  • 2004
    • Universität Heidelberg
      • Neurological Clinic
      Heidelberg, Baden-Wuerttemberg, Germany