@article{MingMyallHernandezetal.2021,
  author    = {Ming, Damien K. and Myall, Ashleigh C. and Hernandez, Bernard and Weiße, Andrea Y. and Peach, Robert L. and Barahona, Mauricio and Rawson, Timothy M. and Holmes, Alison H.},
  title     = {Informing antimicrobial management in the context of COVID-19: understanding the longitudinal dynamics of C-reactive protein and procalcitonin},
  series = {BMC Infectious Diseases},
  volume    = {21},
  journal   = {BMC Infectious Diseases},
  doi       = {10.1186/s12879-021-06621-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-370797},
  year      = {2021},
  abstract  = {Background To characterise the longitudinal dynamics of C-reactive protein (CRP) and Procalcitonin (PCT) in a cohort of hospitalised patients with COVID-19 and support antimicrobial decision-making. Methods Longitudinal CRP and PCT concentrations and trajectories of 237 hospitalised patients with COVID-19 were modelled. The dataset comprised of 2,021 data points for CRP and 284 points for PCT. Pairwise comparisons were performed between: (i) those with or without significant bacterial growth from cultures, and (ii) those who survived or died in hospital. Results CRP concentrations were higher over time in COVID-19 patients with positive microbiology (day 9: 236 vs 123 mg/L, p < 0.0001) and in those who died (day 8: 226 vs 152 mg/L, p < 0.0001) but only after day 7 of COVID-related symptom onset. Failure for CRP to reduce in the first week of hospital admission was associated with significantly higher odds of death. PCT concentrations were higher in patients with COVID-19 and positive microbiology or in those who died, although these differences were not statistically significant. Conclusions Both the absolute CRP concentration and the trajectory during the first week of hospital admission are important factors predicting microbiology culture positivity and outcome in patients hospitalised with COVID-19. Further work is needed to describe the role of PCT for co-infection. Understanding relationships of these biomarkers can support development of risk models and inform optimal antimicrobial strategies.},
  language  = {en}
}
@article{LuijtenLeonhardvanderEijketal.2021,
  author    = {Luijten, Linda W G and Leonhard, Sonja E and van der Eijk, Annemiek A and Doets, Alex Y and Appeltshauser, Luise and Arends, Samuel and Attarian, Shahram and Benedetti, Luana and Briani, Chiara and Casasnovas, Carlos and Castellani, Francesca and Dardiotis, Efthimios and Echaniz-Laguna, Andoni and Garssen, Marcel P J and Harbo, Thomas and Huizinga, Ruth and Humm, Andrea M and Jellema, Korn{\´e} and van der Kooi, Anneke J and Kuitwaard, Krista and Kuntzer, Thierry and Kusunoki, Susumu and Lascano, Agustina M and Martinez-Hernandez, Eugenia and Rinaldi, Simon and Samijn, Johnny P A and Scheidegger, Olivier and Tsouni, Pinelopi and Vicino, Alex and Visser, Leo H and Walgaard, Christa and Wang, Yuzhong and Wirtz, Paul W and Ripellino, Paolo and Jacobs, Bart C},
  title     = {Guillain-Barr{\´e} syndrome after SARS-CoV-2 infection in an international prospective cohort study},
  series = {Brain},
  volume    = {144},
  journal   = {Brain},
  organization    = {The IGOS consortium},
  doi       = {10.1093/brain/awab279},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-371609},
  pages     = {3392-3404},
  year      = {2021},
  abstract  = {In the wake of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, an increasing number of patients with neurological disorders, including Guillain-Barr{\´e} syndrome (GBS), have been reported following this infection. It remains unclear, however, if these cases are coincidental or not, as most publications were case reports or small regional retrospective cohort studies. The International GBS Outcome Study is an ongoing prospective observational cohort study enrolling patients with GBS within 2 weeks from onset of weakness. Data from patients included in this study, between 30 January 2020 and 30 May 2020, were used to investigate clinical and laboratory signs of a preceding or concurrent SARS-CoV-2 infection and to describe the associated clinical phenotype and disease course. Patients were classified according to the SARS-CoV-2 case definitions of the European Centre for Disease Prevention and Control and laboratory recommendations of the World Health Organization. Forty-nine patients with GBS were included, of whom eight (16\%) had a confirmed and three (6\%) a probable SARS-CoV-2 infection. Nine of these 11 patients had no serological evidence of other recent preceding infections associated with GBS, whereas two had serological evidence of a recent Campylobacter jejuni infection. Patients with a confirmed or probable SARS-CoV-2 infection frequently had a sensorimotor variant 8/11 (73\%) and facial palsy 7/11 (64\%). The eight patients who underwent electrophysiological examination all had a demyelinating subtype, which was more prevalent than the other patients included in the same time window [14/30 (47\%), P = 0.012] as well as historical region and age-matched control subjects included in the International GBS Outcome Study before the pandemic [23/44 (52\%), P = 0.016]. The median time from the onset of infection to neurological symptoms was 16 days (interquartile range 12-22). Patients with SARS-CoV-2 infection shared uniform neurological features, similar to those previously described in other post-viral GBS patients. The frequency (22\%) of a preceding SARS-CoV-2 infection in our study population was higher than estimates of the contemporaneous background prevalence of SARS-CoV-2, which may be a result of recruitment bias during the pandemic, but could also indicate that GBS may rarely follow a recent SARS-CoV-2 infection. Consistent with previous studies, we found no increase in patient recruitment during the pandemic for our ongoing International GBS Outcome Study compared to previous years, making a strong relationship of GBS with SARS-CoV-2 unlikely. A case-control study is required to determine if there is a causative link or not.},
  language  = {en}
}
@article{MerkiesvanSchaikLegeretal.2019,
  author    = {Merkies, Ingemar S.J. and van Schaik, Ivo N. and L{\´e}ger, Jean-Marc and Bril, Vera and van Geloven, Nan and Hartung, Hans-Peter and Lewis, Richard A. and Sobue, Gen and Lawo, John-Philip and Durn, Billie L. and Cornblath, David R. and De Bleecker, Jan L. and Sommer, Claudia and Robberecht, Wim and Saarela, Mika and Kamienowski, Jerzy and Stelmasiak, Zbigniew and Tackenberg, Bj{\"o}rn and Mielke, Orell},
  title     = {Efficacy and safety of IVIG in CIDP: Combined data of the PRIMA and PATH studies},
  series = {Journal of the Peripheral Nervous System},
  volume    = {24},
  journal   = {Journal of the Peripheral Nervous System},
  organization    = {PRIMA Trial Investigators and the PATH Study Group},
  doi       = {10.1111/jns.12302},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-224013},
  pages     = {48-55},
  year      = {2019},
  abstract  = {Intravenous immunoglobulin (IVIG) is a potential therapy for chronic inflammatory demyelinating polyneuropathy (CIDP). To investigate the efficacy and safety of the IVIG IgPro10 (Privigen) for treatment of CIDP, results from Privigen Impact on Mobility and Autonomy (PRIMA), a prospective, open-label, single-arm study of IVIG in immunoglobulin (Ig)-na{\"i}ve or IVIG pre-treated subjects (NCT01184846, n = 28) and Polyneuropathy And Treatment with Hizentra (PATH), a double-blind, randomized study including an open-label, single-arm IVIG phase in IVIG pre-treated subjects (NCT01545076, IVIG restabilization phase n = 207) were analyzed separately and together (n = 235). Efficacy assessments included change in adjusted inflammatory neuropathy cause and treatment (INCAT) score, grip strength and Medical Research Council (MRC) sum score. Adverse drug reactions (ADRs) and ADRs/infusion were recorded. Adjusted INCAT response rate was 60.7\% in all PRIMA subjects at Week 25 (76.9\% in IVIG pre-treated subjects) and 72.9\% in PATH. In the pooled cohort (n = 235), INCAT response rate was 71.5\%; median time to INCAT improvement was 4.3 weeks. No clear demographic differences were noticed between early (responding before Week 7, n = 148) and late responders (n = 21). In the pooled cohort, median change from baseline to last observation was -1.0 (interquartile range -2.0; 0.0) point for INCAT score; +8.0 (0.0; 20.0) kPa for maximum grip strength; +3.0 (1.0; 7.0) points for MRC sum score. In the pooled cohort, 271 ADRs were reported in 105 subjects (44.7\%), a rate of 0.144 ADRs per infusion. This analysis confirms the efficacy and safety of IgPro10, a recently FDA-approved IVIG for CIDP, in a population of mainly pre-treated subjects with CIDP [Correction added on 14 March 2019 after first online publication: the INCAT response rate has been corrected.].},
  language  = {en}
}
@article{MirzaVainshteinDiRonzaetal.2019,
  author    = {Mirza, Myriam and Vainshtein, Anna and DiRonza, Alberto and Chandrachud, Uma and Haslett, Luke J. and Palmieri, Michela and Storch, Stephan and Groh, Janos and Dobzinski, Niv and Napolitano, Gennaro and Schmidtke, Carolin and Kerkovich, Danielle M.},
  title     = {The CLN3 gene and protein: What we know},
  series = {Molecular Genetics \& Genomic Medicine},
  volume    = {7},
  journal   = {Molecular Genetics \& Genomic Medicine},
  doi       = {10.1002/mgg3.859},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-224138},
  year      = {2019},
  abstract  = {Background One of the most important steps taken by Beyond Batten Disease Foundation in our quest to cure juvenile Batten (CLN3) disease is to understand the State of the Science. We believe that a strong understanding of where we are in our experimental understanding of the CLN3 gene, its regulation, gene product, protein structure, tissue distribution, biomarker use, and pathological responses to its deficiency, lays the groundwork for determining therapeutic action plans. Objectives To present an unbiased comprehensive reference tool of the experimental understanding of the CLN3 gene and gene product of the same name. Methods BBDF compiled all of the available CLN3 gene and protein data from biological databases, repositories of federally and privately funded projects, patent and trademark offices, science and technology journals, industrial drug and pipeline reports as well as clinical trial reports and with painstaking precision, validated the information together with experts in Batten disease, lysosomal storage disease, lysosome/endosome biology. Results The finished product is an indexed review of the CLN3 gene and protein which is not limited in page size or number of references, references all available primary experiments, and does not draw conclusions for the reader. Conclusions Revisiting the experimental history of a target gene and its product ensures that inaccuracies and contradictions come to light, long-held beliefs and assumptions continue to be challenged, and information that was previously deemed inconsequential gets a second look. Compiling the information into one manuscript with all appropriate primary references provides quick clues to which studies have been completed under which conditions and what information has been reported. This compendium does not seek to replace original articles or subtopic reviews but provides an historical roadmap to completed works.},
  language  = {en}
}
@article{ArlottiPalmisanoMinafraetal.2019,
  author    = {Arlotti, Mattia and Palmisano, Chiara and Minafra, Brigida and Todisco, Massimiliano and Pacchetti, Claudio and Canessa, Andrea and Pozzi, Nicol{\´o} G. and Cilia, Roberto and Prenassi, Marco and Marceglia, Sara and Priori, Alberto and Rampini, Paolo and Barbieri, Sergio and Servello, Domenico and Volkmann, Jens and Pezzoli, Gianni and Isaias, Ioannis U.},
  title     = {Monitoring subthalamic oscillations for 24 hours in a freely moving Parkinson's disease patient},
  series = {Movement Disorders},
  volume    = {34},
  journal   = {Movement Disorders},
  doi       = {10.1002/mds.27657},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-221249},
  pages     = {757-759},
  year      = {2019},
  abstract  = {No abstract available},
  language  = {en}
}
@article{SteigerwaldTimmermannKuehnetal.2018,
  author    = {Steigerwald, Frank and Timmermann, Lars and K{\"u}hn, Andrea and Schnitzler, Alfons and Reich, Martin M. and Kirsch, Anna Dalal and Barbe, Michael Thomas and Visser-Vandewalle, Veerle and H{\"u}bl, Julius and van Riesen, Christoph and Groiss, Stefan Jun and Moldovan, Alexia-Sabine and Lin, Sherry and Carcieri, Stephen and Manola, Ljubomir and Volkmann, Jens},
  title     = {Pulse duration settings in subthalamic stimulation for Parkinson's disease},
  series = {Movement Disorders},
  volume    = {33},
  journal   = {Movement Disorders},
  doi       = {10.1002/mds.27238},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-239402},
  pages     = {165-169},
  year      = {2018},
  abstract  = {Background Stimulation parameters in deep brain stimulation (DBS) of the subthalamic nucleus for Parkinson's disease (PD) are rarely tested in double-blind conditions. Evidence-based recommendations on optimal stimulator settings are needed. Results from the CUSTOM-DBS study are reported, comparing 2 pulse durations. Methods A total of 15 patients were programmed using a pulse width of 30 µs (test) or 60 µs (control). Efficacy and side-effect thresholds and unified PD rating scale (UPDRS) III were measured in meds-off (primary outcome). The therapeutic window was the difference between patients' efficacy and side effect thresholds. Results The therapeutic window was significantly larger at 30 µs than 60 µs (P = ·0009) and the efficacy (UPDRS III score) was noninferior (P = .00008). Interpretation Subthalamic neurostimulation at 30 µs versus 60 µs pulse width is equally effective on PD motor signs, is more energy efficient, and has less likelihood of stimulation-related side effects. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.},
  language  = {en}
}
@article{WilsonAmblerLeeetal.2019,
  author    = {Wilson, Duncan and Ambler, Gareth and Lee, Keon-Joo and Lim, Jae-Sung and Shiozawa, Masayuki and Koga, Masatoshi and Li, Linxin and Lovelock, Caroline and Chabriat, Hugues and Hennerici, Michael and Wong, Yuen Kwun and Mak, Henry Ka Fung and Prats-S{\´a}nchez, Luis and Mart{\´i}nez-Dome{\~n}o, Alejandro and Inamura, Shigeru and Yoshifuji, Kazuhisa and Arsava, Ethem Murat and Horstmann, Solveig and Purrucker, Jan and Lam, Bonnie Yin Ka and Wong, Adrian and Kim, Young Dae and Song, Tae-Jin and Schrooten, Maarten and Lemmens, Robin and Eppinger, Sebastian and Gattringer, Thomas and Uysal, Ender and Tanriverdi, Zeynep and Bornstein, Natan M and Ben Assayag, Einor and Hallevi, Hen and Tanaka, Jun and Hara, Hideo and Coutts, Shelagh B and Hert, Lisa and Polymeris, Alexandros and Seiffge, David J and Lyrer, Philippe and Algra, Ale and Kappelle, Jaap and Salman, Rustam Al-Shahi and J{\"a}ger, Hans R and Lip, Gregory Y H and Mattle, Heinrich P and Panos, Leonidas D and Mas, Jean-Louis and Legrand, Laurence and Karayiannis, Christopher and Phan, Thanh and Gunkel, Sarah and Christ, Nicolas and Abrigo, Jill and Leung, Thomas and Chu, Winnie and Chappell, Francesca and Makin, Stephen and Hayden, Derek and Williams, David J and Kooi, M Eline and van Dam-Nolen, Dianne H K and Barbato, Carmen and Browning, Simone and Wiegertjes, Kim and Tuladhar, Anil M and Maaijwee, Noortje and Guevarra, Christine and Yatawara, Chathuri and Mendyk, Anne-Marie and Delmaire, Christine and K{\"o}hler, Sebastian and van Oostenbrugge, Robert and Zhou, Ying and Xu, Chao and Hilal, Saima and Gyanwali, Bibek and Chen, Christopher and Lou, Min and Staals, Julie and Bordet, R{\´e}gis and Kandiah, Nagaendran and de Leeuw, Frank-Erik and Simister, Robert and van der Lugt, Aad and Kelly, Peter J and Wardlaw, Joanna M and Soo, Yannie and Fluri, Felix and Srikanth, Velandai and Calvet, David and Jung, Simon and Kwa, Vincent I H and Engelter, Stefan T and Peters, Nils and Smith, Eric E and Yakushiji, Yusuke and Necioglu Orken, Dilek and Fazekas, Franz and Thijs, Vincent and Heo, Ji Hoe and Mok, Vincent and Veltkamp, Roland and Ay, Hakan and Imaizumi, Toshio and Gomez-Anson, Beatriz and Lau, Kui Kai and Jouvent, Eric and Rothwell, Peter M and Toyoda, Kazunori and Bae, Hee-Yoon and Marti-Fabregas, Joan and Werring, David J},
  title     = {Cerebral microbleeds and stroke risk after ischaemic stroke or transient ischaemic attack: a pooled analysis of individual patient data from cohort studies},
  series = {The Lancet Neurology},
  volume    = {18},
  journal   = {The Lancet Neurology},
  organization    = {Microbleeds International Collaborative Network},
  doi       = {10.1016/S1474-4422(19)30197-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-233710},
  pages     = {653-665},
  year      = {2019},
  abstract  = {Background Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. Methods We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. Findings Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19-2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95\% CI 1·20-1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82-3·29) for intracranial haemorrhage and 1·23 (1·08-1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95\% CI 3·08-6·72] for intracranial haemorrhage vs 1·47 [1·19-1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36-9·05] vs 1·43 [1·07-1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69-15·81] vs 1·86 [1·23-2·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95\% CI 48-84] per 1000 patient-years vs 27 intracranial haemorrhages [17-41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46-108] per 1000 patient-years vs 39 intracranial haemorrhages [21-67] per 1000 patient-years). Interpretation In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden.},
  language  = {en}
}
@article{UeceylerUrlaubMayeretal.2019,
  author    = {{\"U}{\c{c}}eyler, Nurcan and Urlaub, Daniela and Mayer, Christine and Uehlein, Sabrina and Held, Melissa and Sommer, Claudia},
  title     = {Tumor necrosis factor-α links heat and inflammation with Fabry pain},
  series = {Molecular Genetics and Metabolism},
  volume    = {127},
  journal   = {Molecular Genetics and Metabolism},
  doi       = {https://doi.org/10.1016/j.ymgme.2019.05.009},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-229190},
  pages     = {200-206},
  year      = {2019},
  abstract  = {Fabry disease (FD) is an X-linked lysosomal storage disorder associated with pain triggered by heat or febrile infections. We modelled this condition by measuring the cytokine expression of peripheral blood mononuclear cells (PBMC) from FD patients in vitro upon stimulation with heat and lipopolysaccharide (LPS). We enrolled 67 FD patients and 37 healthy controls. We isolated PBMC, assessed their gene expression of selected pro- and anti-inflammatory cytokines, incubated them with heat, LPS, globotriaosylceramide (Gb3), and tumor necrosis factor-α (TNF), and measured TNF secretion in the supernatant and intracellular Gb3 accumulation, respectively. We found increased TNF, interleukin (IL-)1β, and toll-like receptor 4 (TLR4) gene expression in FD men (p < .05 to p < .01). TNF and IL-10 were higher, and IL-4 was lower in the subgroup of FD men with pain compared to controls (p < .05 to p < .01). Hereby, TNF was only increased in FD men with pain and classical mutations (p < .05) compared to those without pain. PBMC from FD patients secreted more TNF upon stimulation with LPS (p < .01) than control PBMC. Incubation with Gb3 and an additional α-galactosidase A inhibitor did not further increase TNF secretion, but incubation with TNF greatly increased the Gb3 load in FD PBMC compared to controls (p < .01). Also, LPS incubation and heat challenge (40 °C) increased Gb3 accumulation in PBMC of patients compared to baseline (p < .05 each), while no alterations were observed in control PBMC. Our data show that TNF holds a crucial role in the pathophysiology of FD associated pain, which may open a novel perspective for analgesic treatment in FD pain.},
  language  = {en}
}
@article{GraystonCzannerElhaddetal.2019,
  author    = {Grayston, Rebecca and Czanner, Gabriela and Elhadd, Kareim and Goebel, Andreas and Frank, Bernhard and {\"U}{\c{c}}eyler, Nurcan and Malik, Rayaz A and Alam, Uazman},
  title     = {A systematic review and meta-analysis of the prevalence of small fiber pathology in fibromyalgia: Implications for a new paradigm in fibromyalgia etiopathogenesis},
  series = {Seminars in Arthritis and Rheumatism},
  volume    = {48},
  journal   = {Seminars in Arthritis and Rheumatism},
  doi       = {10.1016/j.semarthrit.2018.08.003},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227566},
  pages     = {933-940},
  year      = {2019},
  abstract  = {Objectives Fibromyalgia is a condition which exhibits chronic widespread pain with neuropathic pain features and has a major impact on health-related quality of life. The pathophysiology remains unclear, however, there is increasing evidence for involvement of the peripheral nervous system with a high prevalence of small fiber pathology (SFP). The aim of this systematic literature review is to establish the prevalence of SFP in fibromyalgia. Methods An electronic literature search was performed using MEDLINE, EMBASE, PubMed, Web of Science, CINAHL and the Cochrane Library databases. Published full-text, English language articles that provide SFP prevalence data in studies of fibromyalgia of patients over 18years old were included. All articles were screened by two independent reviewers using a priori criteria. Methodological quality and risk of bias were evaluated using the critical appraisal tool by Munn et al. Overall and subgroup pooled prevalence were calculated by random-effects meta-analysis with 95\% CI. Results Database searches found 935 studies; 45 articles were screened of which 8 full text articles satisfied the inclusion criteria, providing data from 222 participants. The meta-analysis demonstrated the pooled prevalence of SFP in fibromyalgia is 49\% (95\% CI: 38-60\%) with a moderate degree of heterogeneity, (I2= 68\%). The prevalence estimate attained by a skin biopsy was 45\% (95\% CI: 32-59\%, I2= 70\%) and for corneal confocal microscopy it was 59\% (95\% CI: 40-78\%, I2= 51\%). Conclusion There is a high prevalence of SFP in fibromyalgia. This study provides compelling evidence of a distinct phenotype involving SFP in fibromyalgia. Identifying SFP will aid in determining its relationship to pain and potentially facilitate the development of future interventions and pharmacotherapy.},
  language  = {en}
}
@article{KirschHassinBaerMatthiesetal.2018,
  author    = {Kirsch, Anna Dalal and Hassin-Baer, Sharon and Matthies, Cordula and Volkmann, Jens and Steigerwald, Frank},
  title     = {Anodic versus cathodic neurostimulation of the subthalamic nucleus: A randomized-controlled study of acute clinical effects},
  series = {Parkinsonism and Related Disorders},
  volume    = {55},
  journal   = {Parkinsonism and Related Disorders},
  doi       = {10.1016/j.parkreldis.2018.05.015},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-325820},
  pages     = {61-67},
  year      = {2018},
  abstract  = {Introduction Stimulation settings of deep brain stimulation (DBS) have evolved empirically within a limited parameter space dictated by first generation devices. There is a need for controlled clinical studies, which evaluate efficacy and safety of established programming practice against novel programming options provided by modern neurostimulation devices. Methods Here, we tested a polarity reversal from conventional monopolar cathodic to anodic stimulation in an acute double-blind, randomized, cross-over study in patients with PD implanted with bilateral STN DBS. The primary outcome measure was the difference between efficacy and side-effect thresholds (current amplitude, mA) in a monopolar review and the severity of motor symptoms (as assessed by MDS-UPDRS III ratings) after 30 min of continuous stimulation in the medication off-state. Results Effect and side effect thresholds were significantly higher with anodic compared to cathodic stimulation (3.36 ± 1.58 mA vs. 1.99 ± 1.37 mA; 6.05 ± 1.52 mA vs. 4.15 ± 1.13 mA; both p < 0.0001). However, using a predefined amplitude of 0.5 mA below the respective adverse effect threshold, blinded MDS-UPDRS-III-ratings were significantly lower with anodic stimulation (anodic: median 17 [min: 12, max: 25]; cathodic: 23 [12, 37]; p < 0.005). Conclusion Effective anodic stimulation requires a higher charge injection into the tissue, but may provide a better reduction of off-period motor symptoms within the individual therapeutic window. Therefore, a programming change to anodic stimulation may be considered in patients suffering from residual off-period motor symptoms of PD despite reaching the adverse effect threshold of cathodic stimulation in the subthalamic nucleus.},
  language  = {en}
}