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  • 1.
    Bogatikov, Evgenii
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Towards Better Understanding of Etiological Mechanisms at the Neuromuscular Junction2019Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    The neuromuscular junction (NMJ) serves as a model for understanding the mechanisms that determine communication between neurons and their target cells. Disorders of the NMJ can be either autoimmune or genetic (hereditary). The autoimmune disorder myasthenia gravis (MG) is caused by antibodies against the presynaptic nerve terminal or the postsynaptic muscle membrane, which make up the NMJ. The most common antibodies are directed against the acetylcholine receptor (AChR) or muscle specific tyrosine kinase (MuSK). An alternative to expand on preclinical in-vivo methods for studying mechanisms underlying diseases of neuromuscular transmission is to apply physiologic in-vitro models that would allow tissue-tissue as well as cell-cell interactions. A system that would allow cell-cell interactions in a biological fashion is the micro-electrode array (MEA) chip that allows co-culturing of motor neurons and muscle cells.

    The primary hypothesis is that the suggested MEA can be used in creating a reliable model for healthy and diseased NMJ, allowing for manipulations and treatment assays. The secondary hypothesis is that small non-coding RNA, so called microRNAs (miRNA) have a specific role in neuromuscular transmission and in MG.

    Study I demonstrated a method of long-term muscle cell culture on the MEA chips, which allows us to trace the development of muscle cells through the observation of their electrical activity at subcellular resolution. The maturation of skeletal muscle tissue was accompanied by a gradual increase in the amplitude and frequency of extracellular individual electrical spikes. The mature muscle tissue demonstrated the steady electrical activity with synchronized spike propagation in different directions across the chip.

    Study II showed a specific upregulated profile of miRNAs in the muscles of MuSK antibody seropositive MG mice. Transfection of these miRNAs, miR-1933 and miR-1930, promoted downregulation of several proteins and further confirmation with qPCR revealed a specific blocking of IMPA1 and MRPL27, which are involved in intracellular signal transduction and mitochondrial biogenesis in skeletal muscles.

    Study III revealed no correlation between the morphology of skeletal muscle cells and their electrical activity at an early developmental stage. However, the application of recombinant rat agrin increased the number of AChRs clusters in the culture of skeletal muscle and promoted a higher degree of spontaneous activity.

    List of papers
    1. Long-Term High-Density Extracellular Recordings Enable Studies of Muscle Cell Physiology
    Open this publication in new window or tab >>Long-Term High-Density Extracellular Recordings Enable Studies of Muscle Cell Physiology
    2018 (English)In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 9, article id 1424Article in journal (Refereed) Published
    Abstract [en]

    Skeletal (voluntary) muscle is the most abundant tissue in the body, thus making it an important biomedical research subject. Studies of neuromuscular transmission, including disorders of ion channels or receptors in autoimmune or genetic neuromuscular disorders, require high-spatial-resolution measurement techniques and an ability to acquire repeated recordings over time in order to track pharmacological interventions. Preclinical techniques for studying diseases of neuromuscular transmission can be enhanced by physiologic ex vivo models of tissue-tissue and cell-cell interactions. Here, we present a method, which allows tracking the development of primary skeletal muscle cells from myoblasts into mature contracting myotubes over more than 2 months. In contrast to most previous studies, the myotubes did not detach from the surface but instead formed functional networks between the myotubes, whose electrical signals were observed over the entire culturing period. Primary cultures of mouse myoblasts differentiated into contracting myotubes on a chip that contained an array of 26,400 platinum electrodes at a density of 3,265 electrodes per mm(2). Our ability to track extracellular action potentials at subcellular resolution enabled study of skeletal muscle development and kinetics, modes of spiking and spatio-temporal relationships between muscles. The developed system in turn enables creation of a novel electrophysiological platform for establishing ex vivo disease models.

    Place, publisher, year, edition, pages
    FRONTIERS MEDIA SA, 2018
    Keywords
    muscle, spikes, spike analysis, physiology, microelectrode array (MEA) chip, skeletal
    National Category
    Physiology
    Identifiers
    urn:nbn:se:uu:diva-367028 (URN)10.3389/fphys.2018.01424 (DOI)000446852800001 ()30356837 (PubMedID)
    Funder
    Swedish Research Council, VR-523-2014-2048Swedish Research Council, VR-2016-2184Göran Gustafsson Foundation for Research in Natural Sciences and Medicine
    Available from: 2018-11-28 Created: 2018-11-28 Last updated: 2019-10-23Bibliographically approved
    2. miR-1933-3p is upregulated in skeletal muscles of MuSK+ EAMG mice and affects Impa1 and Mrpl27
    Open this publication in new window or tab >>miR-1933-3p is upregulated in skeletal muscles of MuSK+ EAMG mice and affects Impa1 and Mrpl27
    2020 (English)In: Neuroscience research, ISSN 0168-0102, E-ISSN 1872-8111, Vol. 151, p. 46-52Article in journal (Refereed) Published
    Abstract [en]

    MuSK antibody seropositive (MuSK+) Myasthenia Gravis (MG) typically affects skeletal muscles of the bulbar area, including the omohyoid muscle, causing focal fatigue, weakness and atrophy. The profile of circulating extracellular microRNA (miRNA) is changed in MuSK + MG, but the intracellular miRNA profile in skeletal muscles of MuSK + MG and MuSK + experimental autoimmune MG (EAMG) remains unknown. This study elucidated the intracellular miRNA profile in the omohyoid muscle of mice with MuSK + EAMG. The levels of eleven mouse miRNAs were elevated and two mouse miRNAs were reduced in muscles of MuSK + EAMG mice. Transient expression of miR-1933-3p and miR-1930-5p in mouse muscle (C2C12) cells revealed several downregulated genes, out of which five had predicted binding sites for miR-1933-3p. The mRNA expression of mitochondrial ribosomal protein L27 (Mrpl27) and Inositol monophosphatase I (Impa1) was reduced in miR-1933-3p transfected C2C12 cells compared to control cells (p = 0.032 versus p = 0.020). Further, transient expression of miR-1933-3p reduced Impa1 protein accumulation in C2C12 cells. These findings provide novel insights of dysregulated miRNAs and their intracellular pathways in muscle tissue afflicted with MuSK + EAMG, providing a possible link to mitochondrial dysfunction and muscle atrophy observed in MuSK + MG.

    Keywords
    EAMG, Experimental autoimmune myasthenia gravis, MuSK antibody, miR-1933-3p, microRNA
    National Category
    Cell Biology
    Identifiers
    urn:nbn:se:uu:diva-395566 (URN)10.1016/j.neures.2019.02.003 (DOI)000510847800005 ()30763589 (PubMedID)
    Funder
    Swedish Research Council, VR-523-2014-2048
    Available from: 2019-10-21 Created: 2019-10-21 Last updated: 2020-03-25Bibliographically approved
    3. Evaluation of muscle action potential parameters in relation to morphology of skeletal muscle cell culture on high-density microelectrode array chips
    Open this publication in new window or tab >>Evaluation of muscle action potential parameters in relation to morphology of skeletal muscle cell culture on high-density microelectrode array chips
    (English)Manuscript (preprint) (Other academic)
    National Category
    Neurosciences
    Identifiers
    urn:nbn:se:uu:diva-395669 (URN)
    Available from: 2019-10-22 Created: 2019-10-22 Last updated: 2019-10-23
  • 2.
    Bogatikov, Evgenii
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Lindblad, Ida
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Punga, Tanel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    miR-1933-3p is upregulated in skeletal muscles of MuSK+ EAMG mice and affects Impa1 and Mrpl272020In: Neuroscience research, ISSN 0168-0102, E-ISSN 1872-8111, Vol. 151, p. 46-52Article in journal (Refereed)
    Abstract [en]

    MuSK antibody seropositive (MuSK+) Myasthenia Gravis (MG) typically affects skeletal muscles of the bulbar area, including the omohyoid muscle, causing focal fatigue, weakness and atrophy. The profile of circulating extracellular microRNA (miRNA) is changed in MuSK + MG, but the intracellular miRNA profile in skeletal muscles of MuSK + MG and MuSK + experimental autoimmune MG (EAMG) remains unknown. This study elucidated the intracellular miRNA profile in the omohyoid muscle of mice with MuSK + EAMG. The levels of eleven mouse miRNAs were elevated and two mouse miRNAs were reduced in muscles of MuSK + EAMG mice. Transient expression of miR-1933-3p and miR-1930-5p in mouse muscle (C2C12) cells revealed several downregulated genes, out of which five had predicted binding sites for miR-1933-3p. The mRNA expression of mitochondrial ribosomal protein L27 (Mrpl27) and Inositol monophosphatase I (Impa1) was reduced in miR-1933-3p transfected C2C12 cells compared to control cells (p = 0.032 versus p = 0.020). Further, transient expression of miR-1933-3p reduced Impa1 protein accumulation in C2C12 cells. These findings provide novel insights of dysregulated miRNAs and their intracellular pathways in muscle tissue afflicted with MuSK + EAMG, providing a possible link to mitochondrial dysfunction and muscle atrophy observed in MuSK + MG.

  • 3.
    Bogatikov, Evgenii
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Evaluation of motor unit potential parameters in relation to morphology of skeletal muscles culture on MEA chipsManuscript (preprint) (Other academic)
  • 4. Bogatikov, Evgenii
    et al.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Evaluation of muscle action potential parameters in relation to morphology of skeletal muscle cell culture on high-density microelectrode array chipsManuscript (preprint) (Other academic)
  • 5.
    Elf, Kristin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Ronne-Engström, Elisabeth
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Semnic, Robert
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Rostami-Berglund, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Sundblom, Jimmy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Zetterling, Maria
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Continuous EEG monitoring after brain tumor surgery2019In: Acta Neurochirurgica, ISSN 0001-6268, E-ISSN 0942-0940, Vol. 161, no 9, p. 1835-1843Article in journal (Refereed)
    Abstract [en]

    Background

    Prolonged seizures generate cerebral hypoxia and increased intracranial pressure, resulting in an increased risk of neurological deterioration, increased long-term morbidity, and shorter survival. Seizures should be recognized early and treated promptly.

    The aim of the study was to investigate the occurrence of postoperative seizures in patients undergoing craniotomy for primary brain tumors and to determine if non-convulsive seizures could explain some of the postoperative neurological deterioration that may occur after surgery.

    Methods

    A single-center prospective study of 100 patients with suspected glioma. Participants were studied with EEG and video recording for at least 24 h after surgery.

    Results

    Seven patients (7%) displayed seizure activity on EEG recording within 24 h after surgery and another two patients (2%) developed late seizures. One of the patients with early seizures also developed late seizures. In five patients (5%), there were non-convulsive seizures. Four of these patients had a combination of clinically overt and non-convulsive seizures and in one patient, all seizures were non-convulsive. The non-convulsive seizures accounted for the majority of total seizure time in those patients. Non-convulsive seizures could not explain six cases of unexpected postoperative neurological deterioration. Postoperative ischemic lesions were more common in patients with early postoperative seizures.

    Conclusions

    Early seizures, including non-convulsive, occurred in 7% of our patients. Within this group, non-convulsive seizure activity had longer durations than clinically overt seizures, but only 1% of patients had exclusively non-convulsive seizures. Seizures were not associated with unexpected neurological deterioration.

  • 6.
    Pazarlis, Konstantinos A.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Schizas, Nikos
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Sandén, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Försth, Peter
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Study protocol for a randomised controlled trial with clinical, neurophysiological, laboratory and radiological outcome for surgical versus non-surgical treatment for lumbar spinal stenosis: the Uppsala Spinal Stenosis Trial (UppSten)2019In: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 9, article id e030578Article in journal (Refereed)
    Abstract [en]

    Introduction: Symptomatic lumbar spinal stenosis is the most common indication for spinal surgery. However, more than one-third of the patients undergoing surgery for lumbar stenosis report dissatisfaction with the results. On the other hand, conservative treatment has shown positive results in some cases. This trial will compare the outcomes of surgical versus non-surgical treatment for lumbar stenosis. The study includes a multidimensional follow-up, aiming to study the association between outcome and other studied parameters, mainly electromyography and nerve conduction. Moreover, it may contribute to a better understanding of the pathophysiology of lumbar stenosis and to the development of future pharmacological treatments.

    Methods and analysis: UppSten is a single-centre randomised controlled trial in which 150 patients with symptomatic lumbar spinal stenosis will be randomised into one of two treatment arms. The patients in the surgical arm will undergo laminectomy; the patients in the non-surgical arm will be given a structured physical training programme. The primary outcome of the study will be the Oswestry Disability Index. Secondary outcomes will include motor amplitude and degree of denervation activity obtained by means of nerve conduction studies and electromyography. Patient-reported outcome measures will be also used as secondary outcomes. Blood sample analysis and the investigation of potential inflammation markers are the additional secondary outcome parameters. Laboratory evaluation will include blood sample collection before the treatment initiation and after 6 months. Flavum ligament biopsies will be performed in the surgical group. Finally, tertiary outcomes will include neurophysiological measures, the objective walking ability and radiological evaluation.

    Ethics and dissemination: The study is approved by the Local Ethics Committee (Dnr 2017-506), the Hospital's Clinical Trials Committee (2018-0001) and the National Biobank Council and Uppsala Biobank (BbA-827-2018-025). 

  • 7.
    Rostedt Punga, Anna
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology. Uppsala Univ Hosp, Uppsala, Sweden.
    Jabre, Joe F.
    Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
    Amandusson, Åsa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology. Uppsala Univ Hosp, Uppsala, Sweden.
    Facing the challenges of electrodiagnostic studies in the very elderly (>80 years) population2019In: Clinical Neurophysiology, ISSN 1388-2457, E-ISSN 1872-8952, Vol. 130, no 7, p. 1091-1097Article in journal (Refereed)
    Abstract [en]

    Objective: Studies on electrodiagnostic (EDX) methods usually exclude the very elderly. This also holds true for studies of normal EDX values. We analyzed the outcome and diagnostic value of EDX and collected reference data in a large cohort of patients >= 80 years of age. Methods: Referral information, ICD-10 diagnoses and EDX data were retrieved from all patients >= 80 years of age referred for EDX studies at our department in 1995-2015. Normative data, including reference ranges, were obtained using the extrapolated norms (e-norms) method. Results: 1966 unique patients (2335 examinations) were included. Only 11% were considered to have normal findings. 66% had pathological EDX findings in accordance with the indication for referral. Carpal tunnel syndrome was by far the most common diagnosis. Normative data retrieved using e-norms were similar to those of reference values from healthy subjects regarding EMG multiMUP data, but typically provided a wider normality window when applied to nerve conduction parameters. Conclusions: EDX studies are valuable in the diagnostic work-up of very elderly patients. Using the e-norms method may be a useful alternative when obtaining reference values in this age group. Significance: Our findings provide additional insights to the challenges of evaluating very elderly patients with neuromuscular disease and underline the importance of including this growing part of the patient population in EDX research.

  • 8.
    Sabre, Liis
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Evoli, Amelia
    Catholic Univ, Dept Neurol, Rome, Italy.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Cognitive dysfunction in mice with passively induced MuSK antibody seropositive myasthenia gravis2019In: Journal of the Neurological Sciences, ISSN 0022-510X, E-ISSN 1878-5883, Vol. 399, p. 15-21Article in journal (Refereed)
    Abstract [en]

    Recent reports on cognitive dysfunction, in addition to skeletal muscle fatigue, in muscle-specific tyrosine kinase antibody seropositive (MuSK+) myasthenia gravis (MG) patients led us to study cognition in mice with MuSK+passive transfer MG (PTMG). Twelve 7-week-old female wild-type C57BL/6J mice were passively immunized with IgG from MuSK+ MG patients and 12 control mice received intraperitoneal saline injections. Mice were evaluated with clinical, neurophysiological and behavioral tests (Barnes maze (BM) and novel object recognition (NOR)), and the muscles were immunostained to evaluate the neuromuscular junction in the end of the study. Two-thirds of the immunized mice developed clinically distinct MuSK + PTMG. MuSK + PTMG mice spent less time exploring the novel object in the NOR test (MuSK+ mice 36.4% +/- 14.0 vs controls 52.4% +/- 13.0, p = .02), unrelated to the muscle weakness and regardless of rodents' innate preference of novelty. In the BM test, control mice were more eager to use the direct strategy than the MuSK+ mice (MuSK+ 17.3% vs controls 29.5%, p = .02). Our findings shed new light on cognition dysfunction in human MuSK + MG patients and indicate that recognition memory in the perirhinal cortex could be affected in MuSK + MG.

  • 9.
    Sanders, Donald B.
    et al.
    Duke Univ, Med Ctr, Box 3403, Durham, NC 27710 USA.
    Arimura, Kimiyoshi
    Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Neurol & Geriatr, Kagoshima, Japan.
    Cui, LiYing
    Chinese Acad Med Sci, Peking Union Med Coll Hosp, Beijing, Peoples R China.
    Ertas, Mustafa
    Istanbul Fac Med, Istanbul, Turkey.
    Farrugia, Maria Elena
    Inst Neurol Sci, Glasgow, Lanark, Scotland.
    Gilchrist, James
    Southern Illinois Univ, Sch Med, Springfield, IL USA.
    Kouyoumdjian, Joao Aris
    Fac Med Sao Jose Rio Preto FAMERP, Sao Paulo, Brazil.
    Padua, Luca
    Univ Cattolica Sacro Cuore, Fdn Policlin Univ Agostino Gemelli IRCCS, Dept Geriatr Neurosci & Orthopaed, Rome, Italy.
    Pitt, Matthew
    Great Ormond St Hosp Sick Children, Dept Clin Neurophysiol, London, England.
    Stålberg, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Guidelines for single fiber EMG2019In: Clinical Neurophysiology, ISSN 1388-2457, E-ISSN 1872-8952, Vol. 130, no 8, p. 1417-1439Article in journal (Refereed)
    Abstract [en]

    This document is the consensus of international experts on the current status of Single Fiber EMG (SFEMG)and the measurement of neuromuscular jitter with concentric needle electrodes (CNE - CN-jitter). The panel of authors was chosen based on their particular interests and previous publications within a specific area of SFEMG or CN-jitter. Each member of the panel was asked to submit a section on their particular area of interest and these submissions were circulated among the panel members for edits and comments. This process continued until a consensus was reached. Donald Sanders and Erik Stalberg then edited the final document.

  • 10.
    Stålberg, Erik
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    van Dijk, Hans
    Univ Ulm, Dept Orthodont, Ulm, Germany;Maastricht Univ, Acad Ctr Epileptol, Dept Neurol, Med Ctr,Kempenhaeghe, Heeze, Netherlands.
    Falck, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Kimura, Jun
    Univ Iowa Hlth Care, Dept Neurol, Iowa City, IA USA.
    Neuwirth, Christoph
    Cantonal Hosp St Gallen, Neuromuscular Dis Unit ALS Clin, St Gallen, Switzerland.
    Pitt, Matthew
    Great Ormond St Hosp Sick Children, Dept Clin Neurophysiol, London, England.
    Podnar, Simon
    Univ Med Ctr Ljubljana, Div Neurol, Ljubljana, Slovenia.
    Rubin, Devon, I
    Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA.
    Rutkove, Seward
    Harvard Med Sch, Boston, MA 02115 USA.
    Sanders, Donald B.
    Duke Univ, Dept Neurol, Sch Med, Durham, NC 27706 USA.
    Sonoo, Masahiro
    Teikyo Univ, Dept Neurol, Sch Med, Tokyo, Japan.
    Tankisi, Hatice
    Aarhus Univ Hosp, Dept Neurophysiol, Aarhus, Denmark.
    Zwarts, Machiel
    Maastricht Univ, Acad Ctr Epileptol, Dept Neurol, Med Ctr,Kempenhaeghe, Heeze, Netherlands.
    Standards for quantification of EMG and neurography2019In: Clinical Neurophysiology, ISSN 1388-2457, E-ISSN 1872-8952, Vol. 130, no 9, p. 1688-1729Article, review/survey (Refereed)
    Abstract [en]

    This document is an update and extension of ICCN Standards published in 1999. It is the consensus of experts on the current status of EMG and Neurography methods. A panel of authors from different countries with different approach to routines in neurophysiological methods was chosen based on their particular interest and previous publications. Each member of the panel submitted a section on their particular area of interest and these submissions were circulated among the panel members for edits and comments. This process continued until a consensus was reached. The document covers EMG topics such as conventional EMG, Macro EMG, applications of surface EMG and electrical impedance myography. Single Fiber EMG is not included, since it is the topic in a separate IFCN document. A neurography section covers topics such as motor and sensory neurography, F wave recordings, H-reflex, short segment recordings, CMAP scan and motor unit number methods. Other sections cover repetitive nerve stimulation and Pediatric electrodiagnostic testing. Each method includes a description of methodologies, pitfalls, and the use of reference values. Clinical applications accompany some of these sections.

  • 11.
    Tankisi, Hatice
    et al.
    Aarhus Univ Hosp, Dept Clin Neurophysiol, Norrebrogade 44, DK-8000 Aarhus C, Denmark;Aarhus Univ, Dept Clin Med, Aarhus, Denmark.
    Burke, David
    Royal Prince Alfred Hosp, Camperdown, NSW, Australia;Univ Sydney, Sydney, NSW, Australia.
    Cui, Liying
    Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Neurol, Beijing, Peoples R China.
    de Carvalho, Mamede
    Univ Lisbon, Fac Med iMM, Lisbon, Portugal;Ctr Hosp Univ Lisboa, Dept Neurosci, Lisbon, Portugal.
    Kuwabara, Satoshi
    Chiba Univ, Grad Sch Med, Dept Neurol, Chiba, Japan.
    Nandedkar, Sanjeev D.
    Natus Neurol, Middleton, WI USA.
    Rutkove, Seward
    Harvard Med Sch, Boston, MA 02115 USA.
    Stålberg, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    van Putten, Michel J. A. M.
    Med Spectrum Twente, Enschede, Netherlands;Univ Twente, Enschede, Netherlands.
    Fuglsang-Frederiksen, Anders
    Aarhus Univ Hosp, Dept Clin Neurophysiol, Norrebrogade 44, DK-8000 Aarhus C, Denmark;Aarhus Univ, Dept Clin Med, Aarhus, Denmark.
    Standards of instrumentation of EMG2020In: Clinical Neurophysiology, ISSN 1388-2457, E-ISSN 1872-8952, Vol. 131, no 1, p. 243-258Article, review/survey (Refereed)
    Abstract [en]

    Standardization of Electromyography (EMG) instrumentation is of particular importance to ensure high quality recordings. This consensus report on "Standards of Instrumentation of EMG" is an update and extension of the earlier IFCN Guidelines published in 1999. First, a panel of experts in different fields from different geographical distributions was invited to submit a section on their particular interest and expertise. Then, the merged document was circulated for comments and edits until a consensus emerged. The first sections in this document cover technical aspects such as instrumentation, EMG hardware and software including amplifiers and filters, digital signal analysis and instrumentation settings. Other sections cover the topics such as temporary storage, trigger and delay line, averaging, electrode types, stimulation techniques for optimal and standardised EMG examinations, and the artefacts electromyographers may face and safety rules they should follow. Finally, storage of data and databases, report generators and external communication are summarized. (C) 2019 The Author(s). Published by Elsevier B.V. on behalf of International Federation of Clinical Neurophysiology.

  • 12.
    Westerberg, Elisabet
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Clinical Neurophysiology.
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Rostedt Punga, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Lifestyle factors and disease-specific differences in subgroups of Swedish Myasthenia Gravis2018In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 138, no 6, p. 557-565Article in journal (Refereed)
    Abstract [en]

    PURPOSE: To evaluate disease-specific differences between Myasthenia Gravis (MG) subgroups and compare patterns of lifestyle between MG patients and population controls.

    METHODS: All MG patients (n=70) in Jönköping County, Sweden, were invited to answer a disease-specific questionnaire, containing questions about disease-specific data, lifestyle, co-morbidity and mental fatigue. The patients were clinically evaluated. Four hundred age- and gender matched population controls were invited to answer the non-disease-specific part of the questionnaire. Disease-specific issues were compared between MG subgroups. Lifestyle related factors and concomitant conditions were compared to the population controls.

    RESULTS: Forty MG patients and 188 population controls participated in the study. In the late onset MG (LOMG; N=18) subgroup, the male predominance was higher than previously reported. In the early onset MG (EOMG; N=17) subgroup, time to diagnosis was longer, fatigue was higher and bulbar weakness was the dominant symptom (65%). Compared to their matched population controls, LOMG patients were more obese (OR 13.7, p=0.015), ate less fish (OR 4.1, p=0.012), tended to smoke more (OR 4.1, p=0.086) and tended to be employed as manual laborers more often (OR 2.82, p=0.083). Mental health problems and sickness benefits were more common among MG patients than in controls and MG patients were less regularly doing focused physical activity.

    CONCLUSIONS: It is important to consider disease-specific differences when tailoring the management of individual MG patients. There is a need for improved knowledge on how to apply primary and secondary prevention measures to lifestyle disorders in MG patients without risk of deterioration.

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