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  • 1.
    Berntsson, Shala G.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Gauffin, Helena
    Univ Linköping, Med Fac, Dept Clin & Expt Med, Neurol, Linköping, Sweden.
    Melberg, Atle
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Holtz, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology. Univ Linköping, Med Fac, Dept Clin & Expt Med, Neurol, Linköping, Sweden.
    Inherited Ataxia and Intrathecal Baclofen for the Treatment of Spasticity and Painful Spasms2019In: Stereotactic and Functional Neurosurgery, ISSN 1011-6125, E-ISSN 1423-0372, Vol. 97, no 1, p. 18-23Article in journal (Refereed)
    Abstract [en]

    Background: Intrathecal baclofen (ITB) treatment is considered a powerful tool in the management of severe spasticity in neurological conditions such as multiple sclerosis, cerebral palsy, and traumatic spinal cord and brain injury.

    Objectives: The objective of this study was to assess the effectiveness of the ITB in patients with inherited ataxia suffering from severe painful spasms and/or spasticity.

    Method: A total of 5 patients with spinocerebellar ataxia 3 or 7 or Friedreich's ataxia were included in this observational multicenter study. The patients were interviewed and completed outcome measures assessing pain (The Brief Pain Inventory), fatigue (Fatigue Severity Scale), and life satisfaction (LiSAT-9) before and 1 year after the treatment. Spasticity (Modified Ashworth Scale) and spasm frequency (SPFS) were measured objectively for each patient.

    Results: The mean treatment time was 1.9 years. Evaluation of established standard forms revealed symptomatic relief from spasticity, spasms, pain, and fatigue in addition to improved body posture, sleep, and life satisfaction after ITB treatment.

    Conclusions: We report the potential beneficial effects of ITB treatment in patients with inherited ataxia who also suffer from spasticity/spasms. ITB treatment indication in neurological disorders allows for extension to the treatment of spasticity/spasms in patients with hereditary ataxia.

  • 2.
    Bridel, Claire
    et al.
    Vrije Univ Amsterdam Med Ctr, Neurochem Lab, Dept Clin Chem, Neurosci Campus Amsterdam, NL-1081 HV Amsterdam, Netherlands.
    van Wieringen, Wessel N.
    Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, Amsterdam, Netherlands;Vrije Univ Amsterdam, Dept Math, Amsterdam, Netherlands.
    Zetterberg, Henrik
    Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden;Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden;UCL Inst Neurol, Dept Mol Neurosci, Queen Sq, London, England;UCL, Dementia Res Inst, London, England.
    Tijms, Betty M.
    Vrije Univ Amsterdam Med Ctr, Dept Neurol, Neurosci Campus Amsterdam, Amsterdam, Netherlands;Vrije Univ Amsterdam Med Ctr, Alzheimer Ctr, Neurosci Campus Amsterdam, Amsterdam, Netherlands.
    Teunissen, Charlotte E.
    Vrije Univ Amsterdam Med Ctr, Neurochem Lab, Dept Clin Chem, Neurosci Campus Amsterdam, NL-1081 HV Amsterdam, Netherlands.
    Alvarez-Cermeno, Jose C.
    Ramon y Cajal Univ Hosp, Multiple Sclerosis Unit, Madrid, Spain.
    Andreasson, Ulf
    Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden.
    Axelsson, Markus
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Backstrom, David C.
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
    Bartos, Ales
    Charles Univ Prague, Dept Neurol, Fac Med 3, Prague, Czech Republic;Gen Univ Hosp, Prague, Czech Republic;Natl Inst Mental Hlth, Klecany, Czech Republic.
    Bjerke, Maria
    Univ Antwerp, Dept Biomed Sci, Reference Ctr Biol Markers Dementia BIODEM, Inst Born Bunge, Antwerp, Belgium.
    Blennow, Kaj
    Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden;Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Boxer, Adam
    Univ Calif San Francisco, Dept Neurol, Memory & Aging Ctr, San Francisco, CA USA.
    Brundin, Lou
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, Stockholm, Sweden;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden.
    Burman, Joachim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Christensen, Tove
    Aarhus Univ, Dept Biomed, Aarhus, Denmark;Rigshosp, Dept Neurol, Copenhagen Univ Hosp, Copenhagen, Denmark.
    Fialova, Lenka
    Gen Univ Hosp, Prague, Czech Republic;First Fac Med, Inst Med Biochem, Prague, Czech Republic;Charles Univ Prague, Diagnost Lab, Prague, Czech Republic.
    Forsgren, Lars
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
    Frederiksen, Jette L.
    Rigshosp, Dept Neurol, Copenhagen Univ Hosp, Copenhagen, Denmark.
    Gisslen, Magnus
    Univ Gothenburg, Sahlgrenska Acad, Dept Infect Dis, Gothenburg, Sweden.
    Gray, Elizabeth
    Univ Oxford, Nuffield Dept Clin Neurosci, Oxford, England.
    Gunnarsson, Martin
    Orebro Univ Hosp, Dept Neurol, Fac Med & Hlth, Orebro, Sweden.
    Hall, Sara
    Lund Univ, Clin Memory Res Unit, Dept Clin Sci, Fac Med, Lund, Sweden;Lund Univ, Wallenberg Ctr Mol Med, Lund, Sweden.
    Hansson, Oskar
    Lund Univ, Clin Memory Res Unit, Dept Clin Sci, Fac Med, Lund, Sweden;Lund Univ, Wallenberg Ctr Mol Med, Lund, Sweden.
    Herbert, Megan K.
    Univ Gothenburg, Sahlgrenska Acad, Dept Internal Med & Clin Nutr, Inst Med, Gothenburg, Sweden;Sahlgrens Univ Hosp, Dept Endocrinol, Gothenburg, Sweden.
    Jakobsson, Joel
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Jessen-Krut, Jan
    Univ Gothenburg, Sahlgrenska Acad, Dept Infect Dis, Gothenburg, Sweden.
    Janelidze, Shorena
    Lund Univ, Clin Memory Res Unit, Dept Clin Sci, Fac Med, Lund, Sweden;Lund Univ, Wallenberg Ctr Mol Med, Lund, Sweden.
    Johannsson, Gudmundur
    Univ Gothenburg, Sahlgrenska Acad, Dept Internal Med & Clin Nutr, Inst Med, Gothenburg, Sweden;Sahlgrens Univ Hosp, Dept Endocrinol, Gothenburg, Sweden.
    Jonsson, Michael
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Kappos, Ludwig
    Univ Hosp, Dept Med, Basel, Switzerland;Univ Basel, Basel, Switzerland.
    Khademi, Mohsen
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, Stockholm, Sweden;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden.
    Khalil, Michael
    Med Univ Graz, Dept Neurol, Graz, Austria.
    Kuhle, Jens
    Univ Hosp, Dept Med, Basel, Switzerland;Univ Basel, Basel, Switzerland.
    Landen, Mikael
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Leinonen, Ville
    Univ Eastern Finland, Inst Clin Med, Neurosurg, Kuopio, Finland;Kuopio Univ Hosp, Dept Neurosurg, Kuopio, Finland.
    Logroscino, Giancarlo
    Univ Bari, Unit Neurodegenerat Dis, Dept Clin Res Neurol, Bari, Italy.
    Lu, Ching-Hua
    Blizard, North East London & Essex MND Care Ctr, Neurosci & Trauma Ctr, London, England;China Med Univ Hosp, Dept Neurol, Taichung, Taiwan.
    Lycke, Jan
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Magdalinou, Nadia K.
    UCL Inst Neurol, Reta Lila Weston Inst Neurol Studies, Queen Sq, London, England.
    Malaspina, Andrea
    Blizard, North East London & Essex MND Care Ctr, Neurosci & Trauma Ctr, London, England;Barts, Inst Cell & Mol Med, London, England;Barts, London Sch Med & Dent, London, England;Barts, Barts Hlth NHS Trust, London, England.
    Mattsson, Niklas
    Lund Univ, Clin Memory Res Unit, Dept Clin Sci, Fac Med, Lund, Sweden;Lund Univ, Wallenberg Ctr Mol Med, Lund, Sweden.
    Meeter, Lieke H.
    Erasmus MC, Alzheimer Ctr, Rotterdam, Netherlands;Erasmus MC, Dept Neurol, Rotterdam, Netherlands;Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Amsterdam, Netherlands.
    Mehta, Sanjay R.
    Univ Calif San Diego, Div Infect Dis, La Jolla, CA 92093 USA.
    Modvig, Signe
    Rigshosp, Dept Clin Immunol, Copenhagen Univ Hosp, Copenhagen, Denmark.
    Olsson, Tomas
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, Stockholm, Sweden;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden.
    Paterson, Ross W.
    UCL Inst Neurol, Dementia Res Ctr, Queen Sq, London, England.
    Perez-Santiago, Josue
    Univ Puerto Rico, Puerto Rico OMICS Ctr, Ctr Comprehens Canc, San Juan, PR 00936 USA.
    Piehl, Fredrik
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, Stockholm, Sweden;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden.
    Pijnenburg, Yolande A. L.
    Vrije Univ Amsterdam Med Ctr, Dept Neurol, Neurosci Campus Amsterdam, Amsterdam, Netherlands;Vrije Univ Amsterdam Med Ctr, Alzheimer Ctr, Neurosci Campus Amsterdam, Amsterdam, Netherlands.
    Pyykko, Okko T.
    Univ Eastern Finland, Inst Clin Med, Neurosurg, Kuopio, Finland;Kuopio Univ Hosp, Dept Neurosurg, Kuopio, Finland.
    Ragnarsson, Oskar
    Orebro Univ Hosp, Dept Neurol, Fac Med & Hlth, Orebro, Sweden.
    Rojas, Julio C.
    Univ Calif San Francisco, Dept Neurol, Memory & Aging Ctr, San Francisco, CA USA.
    Christensen, Jeppe Romme
    Aarhus Univ, Dept Biomed, Aarhus, Denmark;Rigshosp, Dept Neurol, Copenhagen Univ Hosp, Copenhagen, Denmark.
    Sandberg, Linda
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
    Scherling, Carole S.
    Belmont Univ, Dept Psychol Sci, Nashville, TN USA;Belmont Univ, Neurosci Program, Nashville, TN USA.
    Schott, Jonathan M.
    UCL Inst Neurol, Dementia Res Ctr, Queen Sq, London, England.
    Sellebjerg, Finn T.
    Rigshosp, Dept Neurol, Copenhagen Univ Hosp, Copenhagen, Denmark.
    Simone, Isabella L.
    Univ Bari, Dept Basic Med Sci Neurosci & Sense Organs, Bari, Italy;San Camillo Forlanini Hosp, Rome, Italy.
    Skillback, Tobias
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Stilund, Morten
    Aarhus Univ, Dept Biomed, Aarhus, Denmark.
    Sundstrom, Peter
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
    Svenningsson, Anders
    Karolinska Inst, Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
    Tortelli, Rosanna
    Univ Bari, Unit Neurodegenerat Dis, Dept Clin Res Neurol, Bari, Italy;Pia Fdn Cardinale G Panico, Lecce, Italy.
    Tortorella, Carla
    Univ Bari, Dept Basic Med Sci Neurosci & Sense Organs, Bari, Italy.
    Trentini, Alessandro
    Univ Ferrara, Dept Biomed & Specialist Surg Sci, Ferrara, Italy.
    Troiano, Maria
    Univ Bari, Dept Basic Med Sci Neurosci & Sense Organs, Bari, Italy.
    Turner, Martin R.
    Univ Oxford, Nuffield Dept Clin Neurosci, Oxford, England.
    van Swieten, John C.
    Erasmus MC, Alzheimer Ctr, Rotterdam, Netherlands;Erasmus MC, Dept Neurol, Rotterdam, Netherlands.
    Vagberg, Mattias
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
    Verbeek, Marcel M.
    Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Neurol, Nijmegen, Netherlands;Radboud Alzheimer Ctr, Dept Lab Med, Nijmegen, Netherlands.
    Villar, Luisa M.
    Ramon y Cajal Univ Hosp, Dept Immunol, Madrid, Spain.
    Visser, Pieter Jelle
    Vrije Univ Amsterdam Med Ctr, Dept Neurol, Neurosci Campus Amsterdam, Amsterdam, Netherlands;Vrije Univ Amsterdam Med Ctr, Alzheimer Ctr, Neurosci Campus Amsterdam, Amsterdam, Netherlands;Maastricht Univ, Dept Psychiat & Neuropsychol, Sch Mental Hlth & Neurosci, Alzheimer Ctr Limburg, Maastricht, Netherlands.
    Wallin, Anders
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Weiss, Andreas
    Evotec AG, Manfred Eigen Campus, Hamburg, Germany.
    Wikkelso, Carsten
    Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Sahlgrenska Acad, Gothenburg, Sweden.
    Wild, Edward J.
    UCL Inst Neurol, Queen Sq, London, England.
    Diagnostic Value of Cerebrospinal Fluid Neurofilament Light Protein in Neurology: A Systematic Review and Meta-analysis2019In: JAMA Neurology, ISSN 2168-6149, E-ISSN 2168-6157, Vol. 76, no 9, p. 1035-1048Article, review/survey (Refereed)
    Abstract [en]

    Importance  Neurofilament light protein (NfL) is elevated in cerebrospinal fluid (CSF) of a number of neurological conditions compared with healthy controls (HC) and is a candidate biomarker for neuroaxonal damage. The influence of age and sex is largely unknown, and levels across neurological disorders have not been compared systematically to date.

    Objectives  To assess the associations of age, sex, and diagnosis with NfL in CSF (cNfL) and to evaluate its potential in discriminating clinically similar conditions.

    Data Sources  PubMed was searched for studies published between January 1, 2006, and January 1, 2016, reporting cNfL levels (using the search terms neurofilament light and cerebrospinal fluid) in neurological or psychiatric conditions and/or in HC.

    Study Selection  Studies reporting NfL levels measured in lumbar CSF using a commercially available immunoassay, as well as age and sex.

    Data Extraction and Synthesis  Individual-level data were requested from study authors. Generalized linear mixed-effects models were used to estimate the fixed effects of age, sex, and diagnosis on log-transformed NfL levels, with cohort of origin modeled as a random intercept.

    Main Outcome and Measure  The cNfL levels adjusted for age and sex across diagnoses.

    Results  Data were collected for 10 059 individuals (mean [SD] age, 59.7 [18.8] years; 54.1% female). Thirty-five diagnoses were identified, including inflammatory diseases of the central nervous system (n = 2795), dementias and predementia stages (n = 4284), parkinsonian disorders (n = 984), and HC (n = 1332). The cNfL was elevated compared with HC in a majority of neurological conditions studied. Highest levels were observed in cognitively impaired HIV-positive individuals (iHIV), amyotrophic lateral sclerosis, frontotemporal dementia (FTD), and Huntington disease. In 33.3% of diagnoses, including HC, multiple sclerosis, Alzheimer disease (AD), and Parkinson disease (PD), cNfL was higher in men than women. The cNfL increased with age in HC and a majority of neurological conditions, although the association was strongest in HC. The cNfL overlapped in most clinically similar diagnoses except for FTD and iHIV, which segregated from other dementias, and PD, which segregated from atypical parkinsonian syndromes.

    Conclusions and Relevance  These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed. The cNfL has potential to assist the differentiation of FTD from AD and PD from atypical parkinsonian syndromes.

  • 3. Drissi, Natasha Morales
    et al.
    Warntjes, Marcel
    Wessén, Alexander
    Szakacs, Attila
    Darin, Niklas
    Hallböök, Tove
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Gauffin, Helena
    Engström, Maria
    Structural anomaly in the reticular formation in narcolepsy type 1, suggesting lower levels of neuromelanin2019In: NeuroImage: Clinical, ISSN 0353-8842, E-ISSN 2213-1582, Vol. 23, article id 101875Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to investigate structural changes in the brain stem of adolescents with narcolepsy, a disorder characterized by excessive daytime sleepiness, fragmented night-time sleep, and cataplexy. For this purpose, we used quantitative magnetic resonance imaging to obtain R1 and R2 relaxation rates, proton density, and myelin maps in adolescents with narcolepsy (n = 14) and healthy controls (n = 14). We also acquired resting state functional magnetic resonance imaging (fMRI) for brainstem connectivity analysis. We found a significantly lower R2 in the rostral reticular formation near the superior cerebellar peduncle in narcolepsy patients, family wise error corrected p = .010. Narcolepsy patients had a mean R2 value of 1.17 s-1 whereas healthy controls had a mean R2 of 1.31 s-1, which was a large effect size with Cohen d = 4.14. We did not observe any significant differences in R1 relaxation, proton density, or myelin content. The sensitivity of R2 to metal ions in tissue and the transition metal ion chelating property of neuromelanin indicate that the R2 deviant area is one of the neuromelanin containing nuclei of the brain stem. The close proximity and its demonstrated involvement in sleep-maintenance, specifically through orexin projections from the hypothalamus regulating sleep stability, as well as the results from the connectivity analysis, suggest that the observed deviant area could be the locus coeruleus or other neuromelanin containing nuclei in the proximity of the superior cerebellar peduncle. Hypothetically, the R2 differences described in this paper could be due to lower levels of neuromelanin in this area of narcolepsy patients.

  • 4.
    Feresiadou, Amalia
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Nilsson, Kenneth
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Microbiology.
    Ingelsson, Martin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Press, Rayomand
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden..
    Kmezic, Ivan
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden..
    Nygren, Ingela
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
    Svenningsson, Anders
    Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden..
    Niemelä, Valter
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
    Gordh, Torsten
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Cunningham, Janet
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Psychiatry, University Hospital.
    Kultima, Kim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Burman, Joachim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.
    Measurement of sCD27 in the cerebrospinal fluid identifies patients with neuroinflammatory disease2019In: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 332, p. 31-36Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Laboratory tests to assist in the diagnosis and monitoring of neuroinflammatory diseases are scarce. The soluble form of the CD27 molecule (sCD27) is shed in high concentrations by activated T cells and can be detected in the cerebrospinal fluid. The aim of this study was to investigate whether CSF quantitation of sCD27 could discriminate between inflammatory and non-inflammatory neurological diseases.

    METHODS: The concentration of sCD27 was measured using a commercially available ELISA in 803 well-defined subjects from a study cohort comprised of 338 patients with neuroinflammatory disease, 338 with non-inflammatory neurological disease and 127 controls without neurological disease.

    RESULTS: The median value of cerebrospinal fluid sCD27 was 64 pg/mL (IQR 0-200) in controls, 58 pg/mL (IQR 0-130) in patients with non-inflammatory disease and 740 pg/mL (IQR 230-1800) in patients with inflammatory disease. The likelihood ratio of having an inflammatory disease was 10 (sensitivity 74% and specificity 93%) if the sCD27 concentration was >250 pg/mL. In patients with a known inflammatory condition, the likelihood ratio of having an infection was 10 (sensitivity 40% and specificity 96%) if the sCD27 concentration was >2500 pg/mL.

    CONCLUSIONS: The likelihood of having an inflammatory neurological condition is increased with elevated concentrations of sCD27 in cerebrospinal fluid. Rapid tests of sCD27 should be developed to assist clinicians in diagnosis of neuroinflammatory disease.

  • 5.
    Johansson, Dongni
    et al.
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden.
    Thomas, Ilias
    Dalarna Univ, Dept Microdata Anal, Falun, Sweden.
    Ericsson, Anders
    RISE Acreo, Gothenburg, Sweden;Karolinska Inst, Dept Clin Neurosci, Neurol, Stockholm, Sweden.
    Johansson, Anders
    Medvedev, Alexander
    Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Automatic control. Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Division of Systems and Control.
    Memedi, Mevludin
    Orebro Univ, Sch Business, Informat, Orebro, Sweden.
    Nyholm, Dag
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Ohlsson, Fredrik
    RISE Acreo, Gothenburg, Sweden.
    Senek, Marina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Spira, Jack
    Sensidose AB, Sollentuna, Sweden.
    Westin, Jerker
    Dalarna Univ, Dept Microdata Anal, Falun, Sweden.
    Bergquist, Filip
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Pharmacol, Gothenburg, Sweden.
    Evaluation of a sensor algorithm for motor state rating in Parkinson's disease2019In: Parkinsonism & Related Disorders, ISSN 1353-8020, E-ISSN 1873-5126, Vol. 64, p. 112-117Article in journal (Refereed)
    Abstract [en]

    Introduction: A treatment response objective index (TRIS) was previously developed based on sensor data from pronation-supination tests. This study aimed to examine the performance of TRIS for medication effects in a new population sample with Parkinson's disease (PD) and its usefulness for constructing individual dose-response models.

    Methods: Twenty-five patients with PD performed a series of tasks throughout a levodopa challenge while wearing sensors. TRIS was used to determine motor changes in pronation-supination tests following a single levodopa dose, and was compared to clinical ratings including the Treatment Response Scale (TRS) and six sub-items of the UPDRS part III.

    Results: As expected, correlations between TRIS and clinical ratings were lower in the new population than in the initial study. TRIS was still significantly correlated to TRS (r(s) = 0.23, P < 0.001) with a root mean square error (RMSE) of 1.33. For the patients (n = 17) with a good levodopa response and clear motor fluctuations, a stronger correlation was found (r(s) = 0.38, RMSE = 1.29, P < 0.001). The mean TRIS increased significantly when patients went from the practically defined off to their best on state (P = 0.024). Individual dose-response models could be fitted for more participants when TRIS was used for modelling than when TRS ratings were used.

    Conclusion: The objective sensor index shows promise for constructing individual dose-response models, but further evaluations and retraining of the TRIS algorithm are desirable to improve its performance and to ensure its clinical effectiveness.

  • 6.
    Kockum, Karin
    et al.
    Umea Univ, Dept Pharmacol & Clin Neurosci Neurol Ostersund, SE-90187 Umea, Sweden.
    Virhammar, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Riklund, Katrine
    Umea Univ, Dept Radiat Sci Diagnost Radiol, SE-90187 Umea, Sweden.
    Soderstrom, Lars
    Ostersund Hosp, Unit Res Educ & Dev, SE-83131 Ostersund, Sweden.
    Larsson, Elna-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Laurell, Katarina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology. Umea Univ, Dept Pharmacol & Clin Neurosci Neurol Ostersund, SE-90187 Umea, Sweden.
    Standardized image evaluation in patients with idiopathic normal pressure hydrocephalus: consistency and reproducibility2019In: Neuroradiology, ISSN 0028-3940, E-ISSN 1432-1920, Vol. 61, no 12, p. 1397-1406Article in journal (Refereed)
    Abstract [en]

    Purpose

    Assess the agreement for two investigators between computed tomography (CT) and magnetic resonance imaging (MRI) for seven imaging features included in the iNPH Radscale, a radiological screening tool.

    Methods

    The study included 35 patients with idiopathic normal pressure hydrocephalus (iNPH) who were treated surgically from 2011 to 2015 at Uppsala University Hospital with preoperative CT and MRI performed with maximum 3 months between scans. Seven features were assessed: Evans’ index, temporal horn size, callosal angle, periventricular white matter changes, narrow high convexity sulci, focally enlarged sulci, and enlarged Sylvian fissures. All scans were assessed by two investigators who were blinded to each other’s results and to clinical data.

    Results

    The agreement between CT and MRI was almost perfect for Evans’ index, temporal horns, narrow sulci, and Sylvian fissures (kappa and intraclass correlation, 0.84–0.91, p ≤ 0.001). There was substantial to almost perfect agreement for callosal angle and focally enlarged sulci. The concordance between modalities was fair for changes in periventricular white matter.

    Conclusion

    CT and MRI are equally good for assessing radiological signs associated with iNPH except for periventricular white matter changes, as MRI has superior soft tissue contrast. The other imaging features can be evaluated consistently, and assessments are reproducible independent of modality. Therefore, the iNPH Radscale is applicable to both CT and MRI and may become an important tool for standardized evaluation in the workup in patients with suspected iNPH.

  • 7.
    Landtblom, Anne-Marie
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Guala, Dimitri
    Merck AB, Stockholm, Sweden; Stockholm Univ, Dept Biochem & Biophys, Sci Life Lab, Solna, Sweden.
    Martin, Claes
    Karolinska Inst, Danderyd Hosp, Div Internal Med, Neurol Unit, Stockholm, Sweden.
    Olsson-Hau, Stefan
    Skåne Univ Hosp, Dept Neurol, Malmö, Sweden.
    Haghighi, Sara
    Motala Hosp, Dept Neurol, Motala, Sweden.
    Jansson, Lillemor
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology. Acad Hosp, Dept Neurol, Uppsala, Sweden.
    Fredrikson, Sten
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
    RebiQoL: A randomized trial of telemedicine patient support program for health-related quality of life and adherence in people with MS treated with Rebif2019In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 7, article id e0218453Article in journal (Refereed)
    Abstract [en]

    RebiQoL was a phase IV multicenter randomized study to assess the impact of a telemedicine patient support program (MSP) on health-related quality of life (HRQoL) in patients with relapsing-remitting MS (RRMS) being administered with Rebif with the RebiSmart device. The primary endpoint was to assess the impact of MSP compared to patients only receiving technical support for RebiSmart on HRQoL at 12 months, using the psychological part of Multiple Sclerosis Impact Scale (MSIS-29), in patients administered with Rebif. A total of 97 patients diagnosed with RRMS were screened for participation in the study of which 3 patients did not fulfill the eligibility criteria and 1 patient withdrew consent. Of the 93 randomized patients, 46 were randomized to MSP and 47 to Technical support only. The demographic characteristics of the patients were well-balanced in the two arms. There were no statistical differences (linear mixed model) in any of the primary (difference of 0.48, 95% CI: -8.30-9.25, p = 0.91) or secondary outcomes (p>0.05). Although the study was slightly underpowered, there was a trend towards better adherence in the MSP group (OR 3.5, 95% CI 0.85-14.40, p = 0.08) although not statistically significant. No unexpected adverse events occurred. This study did not show a statistically significant effect of the particular form of teleintervention used in this study on HRQoL as compared to pure technical support, for MS patients already receiving Rebif with the RebiSmart device.

    Trial Registration: ClinicalTrials.gov: NCT01791244.

  • 8. Leiss, Lina
    et al.
    Mega, Alessandro
    Olsson Bontell, Thomas
    Nistér, Monica
    Smits, Anja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Corvigno, Sara
    Rahman, Mohummad Aminur
    Enger, Per Øyvind
    Miletic, Hrvoje
    Östman, Arne
    Platelet-derived growth factor receptor α/glial fibrillary acidic protein expressing peritumoral astrocytes associate with shorter median overall survival in glioblastoma patients.2019In: Glia, ISSN 0894-1491, E-ISSN 1098-1136Article in journal (Refereed)
    Abstract [en]

    The microenvironment and architecture of peritumoral tissue have been suggested to affect permissiveness for infiltration of malignant cells. Astrocytes constitute a heterogeneous population of cells and have been linked to proliferation, migration, and drug sensitivity of glioblastoma (GBM) cells. Through double-immunohistochemical staining for platelet-derived growth factor receptor α (PDGFRα) and glial fibrillary acidic protein (GFAP), this study explored the intercase variability among 45 human GBM samples regarding density of GFAP+ peritumoral astrocytes and a subset of GFAP+ peritumoral astrocyte-like cells also expressing PDGFRα. Large intercase variability regarding the total peritumoral astrocyte density and the density of PDGFRα+/GFAP+ peritumoral astrocyte-like cells was detected. DNA fluorescence in situ hybridization analyses for commonly altered genetic tumor markers supported the interpretation that these cells represented a genetically unaffected host cell subset referred to as PDGFRα+/GFAP+ peritumoral astrocytes. The presence of PDGFRα+/GFAP+ peritumoral astrocytes was significantly positively correlated to older patient age and peritumoral astrocyte density, but not to other established prognostic factors. Notably, presence of PDGFRα+/GFAP+ peritumoral astrocytes, but not peritumoral astrocyte density, was associated with significantly shorter patient overall survival. The prognostic association of PDGFRα+/GFAP+ peritumoral astrocytes was confirmed in multivariable analyses. This exploratory study thus demonstrates previously unrecognized intercase variability and prognostic significance of peritumoral abundance of a novel PDGFRα+ subset of GFAP+ astrocytes. Findings suggest clinically relevant roles of the microenvironment of peritumoral GBM tissue and encourage further characterization of the novel astrocyte subset with regard to origin, function, and potential as biomarker and drug target.

  • 9.
    Lundström, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Återinsättning av trombocythämmare RESTART ger oss (nästan) hela svaret2019In: Neurologi i sverige, , p. 2Article in journal (Other (popular science, discussion, etc.))
    Abstract [sv]

    Återinsättning av trombocythämmare efter en spontan intrakraniell blödning ökar inte risken för en ny blödning jämfört med att avstå. Tvärtom. Återinsättning verkar till och med minska risken för framtida blödningar. Det är det oväntade resultatet av RESTART-studien som pre-senterades på den europeiska strokekongressen ESOC i Milano, maj 2019. I denna artikel sammanfattas RESTART av Erik Lundström, överläkare vid Akademiska sjukhuset. Pågåen-de studier (RESTART-Fr och STATICH) kommer sannolikt att kunna ge oss ett definitivt svar på denna viktiga kliniska fråga.

  • 10.
    Matic, Teodora
    et al.
    Univ Ljubljana, Fac Comp & Informat Sci, Ljubljana, Slovenia.
    Aghanavesi, Somayeh
    Dalarna Univ, Sch Technol & Business Studies, Comp Engn, Dalarna, Sweden.
    Memedi, Mevludin
    Orebro Univ, Business Sch, Informat, Orebro, Sweden.
    Nyholm, Dag
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Bergquist, Filip
    Univ Gothenburg, Dept Pharmacol, Gothenburg, Sweden.
    Groznik, Vida
    Univ Ljubljana, Fac Comp & Informat Sci, Ljubljana, Slovenia;Univ Primorska, Fac Math Nat Sci & Informat Technol, Koper, Slovenia.
    Zabkar, Jure
    Univ Ljubljana, Fac Comp & Informat Sci, Ljubljana, Slovenia.
    Sadikov, Aleksander
    Univ Ljubljana, Fac Comp & Informat Sci, Ljubljana, Slovenia.
    Unsupervised Learning from Motion Sensor Data to Assess the Condition of Patients with Parkinson's Disease2019In: ARTIFICIAL INTELLIGENCE IN MEDICINE, AIME 2019 / [ed] Riano, D Wilk, S TenTeije, A, 2019, p. 420-424Conference paper (Refereed)
    Abstract [en]

    Parkinson's disease (PD) is a chronic neurodegenerative disorder that predominantly affects the patient's motor system, resulting in muscle rigidity, bradykinesia, tremor, and postural instability. As the disease slowly progresses, the symptoms worsen, and regular monitoring is required to adjust the treatment accordingly. The objective evaluation of the patient's condition is sometimes rather difficult and automated systems based on various sensors could be helpful to the physicians. The data in this paper come from a clinical study of 19 advanced PD patients with motor fluctuations. The measurements used come from the motion sensors the patients wore during the study. The paper presents an unsupervised learning approach applied on this data with the aim of checking whether sensor data alone can indicate the patient's motor state. The rationale for the unsupervised approach is that there was significant inter-physician disagreement on the patient's condition (target value for supervised machine learning). The input to clustering came from sensor data alone. The resulting clusters were matched against the physicians' estimates showing relatively good agreement.

  • 11. Niemelä, Valter
    et al.
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Nyholm, Dag
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Kneider, Maria
    Sahlrenska akademin, Göteborgs universitet.
    Constantinescu, Radu
    Sahlrenska akademin, Göteborgs universitet.
    Paucar, Martin
    Karolinska institutet.
    Svenningsson, Per
    Karolinska institutet.
    Abujrais, Sandy
    Uppsala University.
    Shevchenko, Ganna
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Bergquist, Jonas
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Sundblom, Jimmy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    CSF Proenkephalin decreases with the progression of Huntington's diseaseManuscript (preprint) (Other academic)
    Abstract [en]

    Identifying molecular changes that contribute to the onset and progression of Huntington's disease (HD) is of importance for the development and evaluation of potential therapies. We conducted an unbiased mass-spectrometry proteomic analysis on the cerebrospinal fluid of 12 manifest HD patients (ManHD), 13 presymptomatic gene expansion carriers (pGEC) and 38 controls. In ManHD compared to pGEC 10 proteins were downregulated, and 43 upregulated. Decreased levels of proenkephalin (PENK) and transthyretin along with upregulated proteins (VASN, STC2, SGCE and C7) were all closely linked to HD symptom severity. The decreased PENK levels were replicated in a separate cohort of 23 ManHD and 23 controls where absolute quantitation was performed. We hypothesize that declining PENK levels reflect the degeneration of medium spiny neurons (MSNs) that produce PENK, and that assays for PENK may serve as a surrogate marker for the state of MSNs in HD.   

  • 12.
    Tolf, Andreas
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Fagius, Jan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Carlson, Kristina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Åkerfeldt, Torbjörn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Granberg, Tobias
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden; Karolinska Univ Hosp, Dept Radiol, Div Neuroradiol, Stockholm, Sweden.
    Larsson, Elna-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Burman, Joachim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Sustained remission in multiple sclerosis after hematopoietic stem cell transplantation2019In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 140, no 5, p. 320-327Article in journal (Refereed)
    Abstract [en]

    Objectives: To determine whether treatment with autologous hematopoietic stem cell transplantation (HSCT) can induce sustained complete remission in patients with multiple sclerosis (MS).

    Material and methods: Case series of patients with relapsing‐remitting MS (n = 10) treated at a single center between 2004 and 2007 and followed up for 10 years. The patients were treated with a BEAM/ATG conditioning regimen (n = 9) or a cyclophosphamide/ATG conditioning regimen (n = 1) followed by infusion of unmanipulated autologous hematopoietic stem cells. The primary endpoint was sustained complete remission. Sustained complete remission was defined as “no evidence of disease activity‐4,” sustained for a period of at least 5 years without any ongoing disease‐modifying treatment. Furthermore, MS was considered as “resolved” if intrathecal IgG production and cerebrospinal fluid neurofilament light levels were normalized as well.

    Results: Five out of 10 patients were in sustained complete remission at the end of the study. In three of them, MS was resolved.

    Conclusions: Our data demonstrate that sustained complete remission after autologous HSCT for MS is possible.

     

  • 13.
    Weber, Johan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Gustafsson, Cecilia
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden;Sahlgrens Univ Hosp, Gothenburg, Sweden.
    Malmgren, Kristina
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, Gothenburg, Sweden;Sahlgrens Univ Hosp, Gothenburg, Sweden.
    Strandberg, Moa
    Lund Univ Hosp, Dept Clin Sci, Dept Neurol, Lund, Sweden.
    Can, Umran
    Lund Univ Hosp, Dept Clin Sci, Dept Neurol, Lund, Sweden.
    Strandberg, Maria Compagno
    Lund Univ Hosp, Dept Clin Sci, Dept Neurol, Lund, Sweden.
    Kumlien, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Evaluation for epilepsy surgery - Why do patients not proceed to operation?2019In: Seizure, ISSN 1059-1311, E-ISSN 1532-2688, Vol. 69, p. 241-244Article in journal (Refereed)
    Abstract [en]

    Purpose: To investigate the reasons for not proceeding to surgery in patients undergoing presurgical evaluation for epilepsy. Methods: A retrospective cohort study of 401 consecutive patients who were evaluated for but did not proceed to surgery for epilepsy between 1990 and 2016 at three Swedish epilepsy surgery centers was performed. Reasons for not proceeding to surgery were categorized as inconclusive investigation, seizure onset within eloquent cortex, evidence of multiple seizure foci, infrequent seizures, risk of postoperative severe cognitive decline, patient or caregiver declining surgery or invasive investigation, severe psychiatric or somatic comorbidity, patient death during evaluation and complications during the evaluation. Chi-square tests were performed to compare ordered categorical variables. Results: During the entire time period the main reasons for rejection were inconclusive investigation (34,4%) and multifocal seizure onset (20,0%). The risk for severe cognitive decline postoperatively was more often a cause for rejection in more recent years. Patients declining invasive EEG or surgery accounted for a minor but not insignificant proportion (14,2%) of rejections. Conclusions: Inconclusive results from the presurgical evaluation and multifocal epilepsy were the main causes for not proceeding to surgery. The proportion of patients opting to abstain from surgery was low compared to other recent studies.

  • 14.
    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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