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  • 1.
    Bäckryd, Emmanuel
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Pain and Rehabilitation Center.
    Edström, Sofia
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Gerdle, Björn
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Pain and Rehabilitation Center.
    Ghafouri, Bijar
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Pain and Rehabilitation Center.
    Do fragments and glycosylated isoforms of alpha-1-antitrypsin in CSF mirror spinal pathophysiological mechanisms in chronic peripheral neuropathic pain? An exploratory, discovery phase study2018In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 18, article id 116Article in journal (Refereed)
    Abstract [en]

    Background: Post-translational modifications (PTMs) generate a tremendous protein diversity from the similar to 20,000 protein-coding genes of the human genome. In chronic pain conditions, exposure to pathological processes in the central nervous system could lead to disease-specific PTMs detectable in the cerebrospinal fluid (CSF). In a previous hypothesis-generating study, we reported that seven out of 260 CSF proteins highly discriminated between neuropathic pain patients and healthy controls: one isoform of angiotensinogen (AG), two isoforms of alpha-1-antitrypsin (AT), three isoforms of haptoglobin (HG), and one isoform of pigment epithelium-derived factor (PEDF). The present study had three aims: (1) To examine the multivariate inter-correlations between all identified isoforms of these seven proteins; (2) Based on the results of the first aim, to characterize PTMs in a subset of interesting proteins; (3) To regress clinical pain data using the 260 proteins as predictors, thereby testing the hypothesis that the above-mentioned seven discriminating proteins and/or the characterized isoforms/fragments of aim (2) would be among the proteins having the highest predictive power for clinical pain data. Methods: CSF samples from 11 neuropathic pain patients and 11 healthy controls were used for biochemical analysis of protein isoforms. PTM characterization was performed using enzymatic reaction assay and mass spectrometry. Multivariate data analysis (principal component analysis and orthogonal partial least square regression) was applied on the quantified protein isoforms. Results: We identified 5 isoforms of AG, 18 isoforms of AT, 5 isoforms of HG, and 5 isoforms of PEDF. Fragments and glycosylated isoforms of AT were studied in depth. When regressing the pain intensity data of patients, three isoforms of AT, two isoforms of PEDF, and one isoform of angiotensinogen "reappeared" as major results, i.e., they were major findings both when comparing patients with healthy controls and when regressing pain intensity in patients. Conclusions: Altered levels of fragments and/or glycosylated isoforms of alpha-1-antitrypsin might mirror pathophysiological processes in the spinal cord of neuropathic pain patients. In particular, we suggest that a putative disease-specific combination of the levels of two different N-truncated fragments of alpha-1-antitrypsin might be interesting for future CSF and/or plasma biomarker investigations in chronic neuropathic pain.

  • 2.
    Habig, Kathrin
    et al.
    Justus Liebig University, Germany.
    Schaenzer, Anne
    Justus Liebig University, Germany.
    Schirner, Wolfgang
    Justus Liebig University, Germany.
    Lautenschlaeger, Gothje
    Justus Liebig University, Germany.
    Dassinger, Benjamin
    Justus Liebig University, Germany.
    Olausson, Håkan
    Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Birklein, Frank
    Johannes Gutenberg University of Mainz, Germany.
    Gizewski, Elke R.
    Medical University of Innsbruck, Austria.
    Kraemer, Heidrun H.
    Justus Liebig University, Germany.
    Low threshold unmyelinated mechanoafferents can modulate pain2017In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 17, article id 184Article in journal (Refereed)
    Abstract [en]

    Background: Human, hairy skin contains a subgroup of C-fibers, the C-low threshold mechanoreceptive afferents ((C-LTMR) C-tactile or C-touch (CT) fibers) that are linked with the signaling of affective aspects of human touch. Recent studies suggest an involvement of these afferents in the modulation of pain in healthy volunteers. Small fiber neuropathy (SFN) is associated with a damage of C-fibers. Therefore, an impairment of C-LTMRs can be assumed. We aimed to elaborate a possible role of CT-afferents in pain modulation by investigating healthy volunteers and SFN-patients. Methods: Experiment I: 20 SFN-patients (12 women, median age 52.0 years) and 20 healthy controls (14 women, median age 43.0 years) participated in this prospective fMRI and psychophysical study. Heat-pain (HP), CT-targeted touch (slow brushing) and HP combined with CT-targeted touch were applied in randomized order to the left shank in a block design. The participants rated pain intensity on a visual analogue scale. Experiment II: We investigated a possible impact of pain intensity on CT induced pain modulation (10 healthy participants). The intensity of HP stimulation was chosen to induce pain intensity 50/100 (NRS). HP stimulation was applied with and without CT-targeted touch. Results: Experiment I: CT-stimulation was sufficient to reduce heat pain in healthy participants (p = 0.016), but not in SFN-patients. HP induced pain intensity was significantly higher (32,2 vs 52,6) in SFN-patients. During HP, bold responses in pain associated areas were observed in both groups. Additional CT-stimulation elicited no significant difference of bold responses compared to HP. Experiment II: In healthy volunteers, we reproduced a significant reduction of HP intensity by CT-stimulation (p = 0.038). Conclusions: CT input seems to be sufficient to modulate pain, independent of intensity of the pain stimulus. As a prerequisite, the CT fibers have to be intact as in healthy volunteers. If CT fibers are impaired -as in SFN-, CT-targeted touch does not modulate pain intensity. The location of CT-induced pain modulation might be attributed to the level of the dorsal horn since the cortical activation pattern of heat pain with and without CT-targeted touch did not differ in healthy subjects and in SFN-patients.

  • 3.
    Hertze, Joakim
    et al.
    Lund University, Malmö, Sweden; Skåne University Hospital, Lund and Malmö, Sweden.
    Nägga, Katarina
    Lund University, Malmö, Sweden; Skåne University Hospital, Lund and Malmö, Sweden.
    Minthon, Lennart
    Lund University, Malmö, Sweden; Skåne University Hospital, Lund and Malmö, Sweden.
    Hansson, Oskar
    Lund University, Malmö, Sweden; Skåne University Hospital, Lund and Malmö, Sweden.
    Changes in cerebrospinal fluid and blood plasma levels of IGF-II and its binding proteins in Alzheimer's disease: an observational study2014In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 14, article id 64Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The Insulin-like Growth Factor (IGF)-related system is implicated in neuroregeneration and cell repair, as well as regulating lifespan. IGF-II, one component of this system, has also been found to affect memory functions in a rat model. In this study we explored changes in the IGF-related system in patients with Alzheimer's disease (AD), including changes in IGF-II levels.

    METHODS: We measured blood plasma and cerebrospinal fluid (CSF) levels of IGF-I, IGF-II, IGFBP-2 and IGFBP-3 in 72 healthy controls and 92 patients with AD.

    RESULTS: We found significantly lower blood plasma levels of IGF-II and IGFBP-3 in patients with AD, compared with controls. The levels of IGF-II and IGFBP-2 were significantly elevated in the CSF from patients with AD. We also found correlations between established CSF biomarkers for AD (tau and P-tau) and components of the IGF system.

    CONCLUSIONS: CSF and blood plasma levels of IGF-II and some of its binding proteins are changed in patients with AD. Further investigation into this area may unravel important clues to the nature of this disease.

  • 4.
    Muhl, Linnea
    et al.
    Linköping University.
    Kulin, Jenny
    Linköping University.
    Dagonnier, Marie
    Florey Institute Neurosci and Mental Heatlh, Australia; University of Melbourne, Australia.
    Churilov, Leonid
    Florey Institute Neurosci and Mental Heatlh, Australia; University of Melbourne, Australia.
    Dewey, Helen
    Florey Institute Neurosci and Mental Heatlh, Australia; University of Melbourne, Australia; Austin Heatlh, Australia.
    Linden, Thomas
    Gothenburg University, Sweden.
    Bernhardt, Julie
    Florey Institute Neurosci and Mental Heatlh, Australia; University of Melbourne, Australia.
    Mobilization after thrombolysis (rtPA) within 24 hours of acute stroke: what factors influence inclusion of patients in A Very Early Rehabilitation Trial (AVERT)?2014In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 14, no 163Article in journal (Refereed)
    Abstract [en]

    Background: A key treatment for acute ischaemic stroke is thrombolysis (rtPA). However, treatment is not devoid of side effects and patients are carefully selected. AVERT (A Very Early Rehabilitation Trial), a large, ongoing international phase III trial, tests whether starting out of bed activity within 24 hours of stroke onset improves outcome. Patients treated with rtPA can be recruited if the physician allows (447 included to date). This study aimed to identify factors that might influence the inclusion of rtPA treated patients in AVERT.

    Methods: Data from all patients thrombolysed at Austin Health, Australia, between September 2007 and December 2011 were retrospectively extracted from medical records. Factors of interest included: demographic and stroke characteristics, 24 hour clinical response to rtPA treatment, cerebral imaging and process factors (day and time of admission).

    Results: 211 patients received rtPA at Austin Health and 50 (24%) were recruited to AVERT (AVERT). Of the 161 patients not recruited, 105 (65%) were eligible, and could potentially have been included (pot-AVERT). There were no significant differences in demographics, Oxfordshire classification or stroke severity (NIHSS) on admission between groups. Size and localization of stroke on imaging and symptomatic intracerebral heamorrhage rate did not differ. Patients included in AVERT showed less change in NIHSS 24 hours post rtPA (median change = 1, IQR (-1,4)) than those in the pot-AVERT group (median change = 3, IQR (0,6)) by the median difference of 2 points (95% CI: 0.3; p = 0.03). A higher proportion of rtPA treated AVERT patients were admitted on weekdays (p = 0.04).

    Linnea MujhlConclusion: Excluding a possible clinical instability, no significant clinical differences were identified between thrombolysed patients included in AVERT and those who were not. Over 500 AVERT patients will be treated with rtPA at trial end. These results suggest we may be able to generalize findings to other rtPA treated patients beyond the trial population.

  • 5.
    Ruborg, Rebecca
    et al.
    Örebro University, Sweden.
    Gunnarsson, Karin
    Örebro University, Sweden.
    Ström, Jakob O.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Chemistry. Örebro University, Sweden; Neuro and Rehabmed Kliniken, Sweden.
    Predictors of post-stroke body temperature elevation2017In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 17, article id 218Article in journal (Refereed)
    Abstract [en]

    Background: Growing evidence indicates that elevated body temperature after stroke is associated with unfavorable outcome. The aim of the current study was to investigate which factors predict temperature elevation within 48 h of stroke onset. Specifically, we hypothesized that temperature elevation would be associated with stroke symptom severity and that hemorrhagic stroke would cause a more pronounced temperature increase compared to ischemic stroke. Methods: The medical records of 400 stroke patients were retrospectively reviewed. Multiple linear regression analysis was used to determine which factors were associated with elevated body temperature. Results: Several factors were significantly associated with peak body temperature (the highest recorded body temperature) within 48 h of stroke onset: stroke severity measured by the National Institutes of Health Stroke Scale (NIHSS) (regression coefficient; (RC) 0.022), female gender (RC 0.157), tympanic/non-rectal temperature reading (RC -0.265), swallowing difficulties (RC 0.335), intubation (RC 0.470), antipyretic treatment (RC 0.563), and C-reactive protein amp;gt; 50 or signs of infection at admission (RC 0.298). Contrary to our expectations, patients with intracerebral hemorrhage did not have higher peak body temperatures than patients with ischemic stroke. Conclusions: In conclusion, temperature elevation within the first 48 h of stroke onset is common, can be partially predicted using information at admission and is strongly associated with stroke severity. The strong association with stroke severity may, at least partly, explain the previously described association between post-stroke temperature elevation and unfavorable outcome.

  • 6.
    Tinghög, Petter
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Björkenstam, Charlotte
    Karolinska Institutet, Stockholm, Sweden.
    Carstensen, John
    Linköping University, Department of Medical and Health Sciences, Division of Health and Society. Linköping University, Faculty of Health Sciences.
    Jansson, Catarina
    Karolinska Institutet, Stockholm, Sweden.
    Glaser, Anna
    Karolinska Institutet, Stockholm, Sweden.
    Hillert, Jan
    Karolinska Institutet, Stockholm, Sweden.
    Alexanderson, Kristina
    Karolinska Institutet, Stockholm, Sweden.
    Co-morbidities increase the risk of disability pension among MS patients: a population-based nationwide cohort study2014In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 14, no 117Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Multiple sclerosis (MS) is a chronic and often disabling disease. In 2005, 62% of the MS patients in Sweden aged 16-65 years were on disability pension. The objective of this study is to investigate whether the presence of common co-morbidities increase MS patients' risk for disability pension.

    METHODS:

    This population-based cohort study included 4 519 MS patients and 4 972 174 non-MS patients who in 2005 were aged 17-64 years, lived in Sweden, and were not on disability pension. Patients with MS were identified in the nationwide in- and outpatient registers, while four different registers were used to construct three sets of measures of musculoskeletal, mental, and cardiovascular disorders. Time-dependent proportional hazard models with a five-year follow up were performed, adjusting for socio-demographic factors.

    RESULTS:

    All studied disorders were elevated among MS patients, regardless of type of measure used. MS patients with mental disorders had a higher risk for disability pension than MS patients with no such co-morbidities. Moreover, mental disorders had a synergistic influence on MS patients' risk for disability pension. These findings were also confirmed when conducting sensitivity analyses. Musculoskeletal disorders appeared to increase MS patients' risk for disability pension. The results with regard to musculoskeletal disorders' synergistic influence on disability pension were however inconclusive. Cardiovascular co-morbidity had no significant influence on MS-patients' risk for disability pension.

    CONCLUSIONS:

    Co-morbidities, especially mental disorders, significantly contribute to MS patients' risk of disability pension, a finding of relevance for MS management and treatment.

  • 7.
    Wästfelt, Maja
    et al.
    Örebro Univ, Sweden.
    Cao, Yang
    Orebro Univ, Sweden; Karolinska Inst, Sweden.
    Ström, Jakob
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Chemistry. Orebro Univ, Sweden.
    Predictors of post-stroke fever and infections: a systematic review and meta-analysis2018In: BMC Neurology, ISSN 1471-2377, E-ISSN 1471-2377, Vol. 18, article id 49Article in journal (Refereed)
    Abstract [en]

    Background: fever after stroke is common, and often caused by infections. In the current study, we aimed to test the hypothesis that pneumonia, urinary tract infection and all-cause fever (thought to include at least some proportion of endogenous fever) have different predicting factors, since they differ regarding etiology. Methods: PubMed was searched systematically for articles describing predictors for post-stroke pneumonia, urinary tract infection and all-cause fever. A total of 5294 articles were manually assessed; first by title, then by abstract and finally by full text. Data was extracted from each study, and for variables reported in 3 or more articles, a meta-analysis was performed using a random effects model. Results: Fifty-nine articles met the inclusion criteria. It was found that post stroke pneumonia is predicted by age OR 1.07 (1.04-1.11), male sex OR 1.42 (1.17-1.74), National Institutes of Health Stroke Scale (NIHSS) OR 1.07 (1.05-1.09), dysphagia OR 3.53 (2.69-4.64), nasogastric tube OR 5.29 (3.01-9.32), diabetes OR 1.15 (1.08-1.23), mechanical ventilation OR 4.65 (2.50-8.65), smoking OR 1.16 (1.08-1.26), Chronic Obstructive Pulmonary Disease (COPD) OR 4.48 (1.82-11.00) and atrial fibrillation OR 1.37 (1.22-1.55). An opposite relation to sex may exist for UTI, which seems to be more common in women. Conclusions: The lack of studies simultaneously studying a wide range of predictors for UTI or all-cause fever calls for future research in this area. The importance of new research would be to improve our understanding of fever complications to facilitate greater vigilance, monitoring, prevention, diagnosis and treatment.

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