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  • 1.
    Aare, Sudhakar
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Ochala, Julien
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Norman, Holly S
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Radell, Peter
    Eriksson, Lars I
    Göransson, Hanna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Chen, Yi-Wen
    Hoffman, Eric P
    Larsson, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Mechanisms underlying the sparing of masticatory versus limb muscle function in an experimental critical illness model2011Inngår i: Physiological Genomics, ISSN 1094-8341, E-ISSN 1531-2267, Vol. 43, nr 24, s. 1334-1350Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Acute quadriplegic myopathy (AQM) is a common debilitating acquired disorder in critically ill intensive care unit (ICU) patients which is characterized by tetraplegia/generalized weakness of limb and trunk muscles. Masticatory muscles, on the other hand, are typically spared or less affected, yet the mechanisms underlying this striking muscle-specific difference remain unknown. This study aims to evaluate physiological parameters and the gene expression profiles of masticatory and limb muscles exposed to factors suggested to trigger AQM, such as mechanical ventilation, immobilization, neuromuscular blocking agents (NMBA), corticosteroids (CS) and sepsis for five days by using a unique porcine model mimicking the ICU conditions. Single muscle fiber cross-sectional area and force-generating capacity, i.e., maximum force normalized to fiber cross-sectional area (specific force), revealed maintained masseter single muscle fiber cross-sectional area and specific-force after five days exposure to all triggering factors. This is in sharp contrast to observations in limb and trunk muscles, showing a dramatic decline in specific force in response to five days exposure to the triggering factors. Significant differences in gene expression were observed between craniofacial and limb muscles, indicating a highly complex and muscle specific response involving transcription and growth factors, heat shock proteins, matrix metalloproteinase inhibitor, oxidative stress responsive elements and sarcomeric proteins underlying the relative sparing of cranial versus spinal nerve innervated muscles during exposure to the ICU intervention.

  • 2.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Emami Khoonsari, Payam
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk kemi.
    Shevchenko, Ganna
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Gordh, Torsten
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Ericson, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Kultima, Kim
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk kemi.
    Increased CSF Levels of Apolipoproteins and Complement Factors in Trigeminal Neuralgia Patients-In Depth Proteomic Analysis Using Mass Spectrometry2020Inngår i: Journal of Pain, ISSN 1526-5900, E-ISSN 1528-8447, Vol. 21, nr 9-10, s. 1075-1084Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The main cause of trigeminal neuralgia (TN) is compression of a blood vessel at the root entry zone of the trigeminal nerve. However, a neurovascular conflict does not seem to be the only etiology and other mechanisms are implicated in the development of the disease. We hypothesized that TN patients may have distinct protein expression in the CSF. In this study, lumbar CSF from TN patients (n = 17), scheduled to undergo microvascular decompression, and from controls (n = 20) was analyzed and compared with in depth mass spectrometry TMTbased quantitative proteomics. We identified 2552 unique proteins, of which 46 were significantly altered (26 increased, and 20 decreased, q-value < .05) in TN patients compared with controls. An over-representation analysis showed proteins involved in high-density lipoprotein, such as Apolipoprotein A4, Apolipoprotein M, and Apolipoprotein A1, and the extracellular region, including proteins involved in the complement cascade to be over-represented. We conclude that TN patients have distinct protein expression in the CSF compared to controls. The pathophysiological background of the protein alterations found in this study warrants further investigation in future studies. Perspective: In this article, cerebrospinal fluid from patients with trigeminal neuralgia was analyzed using in depth shotgun proteomics, revealing 46 differentially expressed proteins compared to controls. Among these, apolipoproteins and proteins involved in the complement system were elevated and signif-icantly over-represented, implying an inflammatory component in the pathophysiology of the disease.

  • 3.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Lannsjö, Marianne
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Rehabiliteringsmedicin. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Gävleborg.
    Howells, Tim
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Raininko, Raili
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Wikström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Enblad, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Extended anatomical grading in diffuse axonal injury using MRI: Hemorrhagic lesions in the substantia nigra and mesencephalic tegmentum indicate poor long-term outcome2017Inngår i: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 5, nr 34, s. 341-352Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Clinical outcome after traumatic diffuse axonal injury (DAI) is difficult to predict. In this study, three magnetic resonance imaging (MRI) sequences were used to quantify the anatomical distribution of lesions, to grade DAI according to the Adams grading system, and to evaluate the value of lesion localization in combination with clinical prognostic factors to improve outcome prediction. Thirty patients (mean 31.2 years ±14.3 standard deviation) with severe DAI (Glasgow Motor Score [GMS] <6) examined with MRI within 1 week post-injury were included. Diffusion-weighted (DW), T2*-weighted gradient echo and susceptibility-weighted (SWI) sequences were used. Extended Glasgow outcome score was assessed after 6 months. Number of DW lesions in the thalamus, basal ganglia, and internal capsule and number of SWI lesions in the mesencephalon correlated significantly with outcome in univariate analysis. Age, GMS at admission, GMS at discharge, and low proportion of good monitoring time with cerebral perfusion pressure <60 mm Hg correlated significantly with outcome in univariate analysis. Multivariate analysis revealed an independent relation with poor outcome for age (p = 0.005) and lesions in the mesencephalic region corresponding to substantia nigra and tegmentum on SWI (p  = 0.008). We conclude that higher age and lesions in substantia nigra and mesencephalic tegmentum indicate poor long-term outcome in DAI. We propose an extended MRI classification system based on four stages (stage I—hemispheric lesions, stage II—corpus callosum lesions, stage III—brainstem lesions, and stage IV—substantia nigra or mesencephalic tegmentum lesions); all are subdivided by age (≥/<30 years).

    Fulltekst (pdf)
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  • 4.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Lewén, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Howells, Tim
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Raininko, Raili
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Wikström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Enblad, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Intracranial pressure elevations in diffuse axonal injury: association with nonhemorrhagic MR lesions in central mesencephalic structures2019Inngår i: Journal of Neurosurgery, ISSN 0022-3085, E-ISSN 1933-0693, Vol. 131, nr 2, s. 604-611Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: Increased intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI) with diffuse axonal injury (DAI) is not well defined. This study investigated the occurrence of increased ICP and whether clinical factors and lesion localization on MRI were associated with increased ICP in patients with DAI.

    Methods: Fifty-two patients with severe TBI (median age 24 years, range 9–61 years), who had undergone ICP monitoring and had DAI on MRI, as determined using T2*-weighted gradient echo, susceptibility-weighted imaging, and diffusion-weighted imaging (DWI) sequences, were enrolled. The proportion of good monitoring time (GMT) with ICP > 20 mm Hg during the first 120 hours postinjury was calculated and associations with clinical and MRI-related factors were evaluated using linear regression.

    Results: All patients had episodes of ICP > 20 mm Hg. The mean proportion of GMT with ICP > 20 mm Hg was 5%, and 27% of the patients (14/52) spent more than 5% of GMT with ICP > 20 mm Hg. The Glasgow Coma Scale motor score at admission (p = 0.04) and lesions on DWI sequences in the substantia nigra and mesencephalic tegmentum (SN-T, p = 0.001) were associated with the proportion of GMT with ICP > 20 mm Hg. In multivariable linear regression, lesions on DWI sequences in SN-T (8% of GMT with ICP > 20 mm Hg, 95% CI 3%–13%, p = 0.004) and young age (−0.2% of GMT with ICP > 20 mm Hg, 95% CI −0.07% to −0.3%, p = 0.002) were associated with increased ICP.

    Conclusions: Increased ICP occurs in approximately one-third of patients with severe TBI who have DAI. Age and lesions on DWI sequences in the central mesencephalon (i.e., SN-T) are associated with elevated ICP. These findings suggest that MR lesion localization may aid prediction of increased ICP in patients with DAI.

    Abbreviations: ADC = apparent diffusion coefficient; CPP = cerebral perfusion pressure; DAI = diffuse axonal injury; DWI = diffusion-weighted imaging; EVD = external ventricular drain; GCS = Glasgow Coma Scale; GMT = good monitoring time; GOSE = Glasgow Outcome Scale–Extended; ICC = intraclass correlation coefficient; ICP = intracranial pressure; MAP = mean arterial blood pressure; NICU = neurointensive care unit; SN-T = substantia nigra and mesencephalic tegmentum; SWI = susceptibility-weighted imaging; TBI = traumatic brain injury; T2*GRE = T2*-weighted gradient echo.

  • 5.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Shevchenko, Ganna
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Mi, Jia
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Musunuri, Sravani
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Bergquist, Jonas
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Proteomic Differences Between Focal And Diffuse Traumatic Brain Injury In Human Brain Tissue2018Inngår i: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 35, nr 16, s. A238-A239Artikkel i tidsskrift (Annet vitenskapelig)
  • 6.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Shevchenko, Ganna
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Mi, Jia
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Musunuri, Sravani
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Bergquist, Jonas
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Analytisk kemi.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
    Proteomic differences between focal and diffuse traumatic brain injury in human brain tissue2018Inngår i: Scientific Reports, E-ISSN 2045-2322, Vol. 8, artikkel-id 6807Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The early molecular response to severe traumatic brain injury (TBI) was evaluated using biopsies of structurally normal-appearing cortex, obtained at location for intracranial pressure (ICP) monitoring, from 16 severe TBI patients. Mass spectrometry (MS; label free and stable isotope dimethyl labeling) quantitation proteomics showed a strikingly different molecular pattern in TBI in comparison to cortical biopsies from 11 idiopathic normal pressure hydrocephalus patients. Diffuse TBI showed increased expression of peptides related to neurodegeneration (Tau and Fascin, p < 0.05), reduced expression related to antioxidant defense (Glutathione S-transferase Mu 3, Peroxiredoxin-6, Thioredoxin-dependent peroxide reductase; p < 0.05) and increased expression of potential biomarkers (e.g. Neurogranin, Fatty acid-binding protein, heart p < 0.05) compared to focal TBI. Proteomics of human brain biopsies displayed considerable molecular heterogeneity among the different TBI subtypes with consequences for the pathophysiology and development of targeted treatments for TBI.

    Fulltekst (pdf)
    fulltext
  • 7.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Tenovuo, Olli
    Univ Turku, Turku Brain Injury Ctr, Turku, Finland; Turku Univ Hosp, Turku, Finland.
    Peul, Wilco
    Leiden Univ, HAGA, Neurosurg Ctr Holland, HMC, The Hague, Netherlands; Leiden Univ, LUMC, Neurosurg Ctr Holland, HMC, The Hague, Netherlands; Leiden Univ, HAGA, Neurosurg Ctr Holland, HMC, Leiden, Netherlands; Leiden Univ, LUMC, Neurosurg Ctr Holland, HMC, Leiden, Netherlands.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi. Lund Univ, Skåne Univ Hosp, Dept Clin Sci Lund, Neurosurg, Lund, Sweden.
    "Omics" in traumatic brain injury: novel approaches to a complex disease2021Inngår i: Acta Neurochirurgica, ISSN 0001-6268, E-ISSN 0942-0940, Vol. 163, nr 9, s. 2581-2594Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Background

    To date, there is neither any pharmacological treatment with efficacy in traumatic brain injury (TBI) nor any method to halt the disease progress. This is due to an incomplete understanding of the vast complexity of the biological cascades and failure to appreciate the diversity of secondary injury mechanisms in TBI. In recent years, techniques for high-throughput characterization and quantification of biological molecules that include genomics, proteomics, and metabolomics have evolved and referred to as omics.

    Methods

    In this narrative review, we highlight how omics technology can be applied to potentiate diagnostics and prognostication as well as to advance our understanding of injury mechanisms in TBI.

    Results

    The omics platforms provide possibilities to study function, dynamics, and alterations of molecular pathways of normal and TBI disease states. Through advanced bioinformatics, large datasets of molecular information from small biological samples can be analyzed in detail and provide valuable knowledge of pathophysiological mechanisms, to include in prognostic modeling when connected to clinically relevant data. In such a complex disease as TBI, omics enables broad categories of studies from gene compositions associated with susceptibility to secondary injury or poor outcome, to potential alterations in metabolites following TBI.

    Conclusion

    The field of omics in TBI research is rapidly evolving. The recent data and novel methods reviewed herein may form the basis for improved precision medicine approaches, development of pharmacological approaches, and individualization of therapeutic efforts by implementing mathematical “big data” predictive modeling in the near future.

    Fulltekst (pdf)
    FULLTEXT01
  • 8.
    Abu Hamdeh, Sami
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Virhammar, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Sehlin, Dag
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Alafuzoff, Irina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk och experimentell patologi.
    Cesarini, Kristina G
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Marklund, Niklas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Enblad: Neurokirurgi.
    Brain tissue Aβ42 levels are linked to shunt response in idiopathic normal pressure hydrocephalus2019Inngår i: Journal of Neurosurgery, ISSN 0022-3085, E-ISSN 1933-0693, Vol. 130, nr 1, s. 121-129Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective The authors conducted a study to test if the cortical brain tissue levels of soluble amyloid beta (Aβ) reflect the propensity of cortical Aβ aggregate formation and may be an additional factor predicting surgical outcome following idiopathic normal pressure hydrocephalus (iNPH) treatment.

    Methods Highly selective ELISAs (enzyme-linked immunosorbent assays) were used to quantify soluble Aβ40, Aβ42, and neurotoxic Aβ oligomers/protofibrils, associated with Aβ aggregation, in cortical biopsy samples obtained in patients with iNPH (n = 20), sampled during ventriculoperitoneal (VP) shunt surgery. Patients underwent pre- and postoperative (3-month) clinical assessment with a modified iNPH scale. The preoperative CSF biomarkers and the levels of soluble and insoluble Aβ species in cortical biopsy samples were analyzed for their association with a favorable outcome following the VP shunt procedure, defined as a ≥ 5-point increase in the iNPH scale.

    Rrsults The brain tissue levels of Aβ42 were negatively correlated with CSF Aβ42 (Spearman's r = -0.53, p < 0.05). The Aβ40, Aβ42, and Aβ oligomer/protofibril levels in cortical biopsy samples were higher in patients with insoluble cortical Aβ aggregates (p < 0.05). The preoperative CSF Aβ42 levels were similar in patients responding (n = 11) and not responding (n = 9) to VP shunt treatment at 3 months postsurgery. In contrast, the presence of cortical Aβ aggregates and high brain tissue Aβ42 levels were associated with a poor outcome following VP shunt treatment (p < 0.05).

    Conclusions Brain tissue measurements of soluble Aβ species are feasible. Since high Aβ42 levels in cortical biopsy samples obtained in patients with iNPH indicated a poor surgical outcome, tissue levels of Aβ species may be associated with the clinical response to shunt treatment.

  • 9.
    Adamczuk, Katarzyna
    et al.
    Katholieke Univ Leuven, Lab Cognit Neurol, B-3000 Louvain, Belgium.;Katholieke Univ Leuven, Leuven Inst Neurosci & Dis, Alzheimer Res Ctr, B-3000 Louvain, Belgium..
    Schaeverbeke, Jolien
    Katholieke Univ Leuven, Lab Cognit Neurol, B-3000 Louvain, Belgium.;Katholieke Univ Leuven, Leuven Inst Neurosci & Dis, Alzheimer Res Ctr, B-3000 Louvain, Belgium..
    Vanderstichele, Hugo M. J.
    ADx NeuroSci, B-9052 Ghent, Belgium..
    Lilja, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi. GE Healthcare, S-75125 Uppsala, Sweden..
    Nelissen, Natalie
    Katholieke Univ Leuven, Lab Cognit Neurol, B-3000 Louvain, Belgium.;Univ Oxford, Dept Psychiat, Oxford OX3 7JX, England..
    Van Laere, Koen
    Katholieke Univ Leuven, Leuven Inst Neurosci & Dis, Alzheimer Res Ctr, B-3000 Louvain, Belgium.;Katholieke Univ Leuven, Nucl Med & Mol Imaging Dept, B-3000 Louvain, Belgium.;Katholieke Univ Leuven Hosp, B-3000 Louvain, Belgium..
    Dupont, Patrick
    Katholieke Univ Leuven, Lab Cognit Neurol, B-3000 Louvain, Belgium.;Katholieke Univ Leuven, Leuven Inst Neurosci & Dis, Alzheimer Res Ctr, B-3000 Louvain, Belgium..
    Hilven, Kelly
    Katholieke Univ Leuven, Lab Neuroimmunol, B-3000 Louvain, Belgium..
    Poesen, Koen
    Katholieke Univ Leuven, Lab Mol Neurobiomarker Res, B-3000 Louvain, Belgium.;UZ Leuven, Lab Med, B-3000 Louvain, Belgium..
    Vandenberghe, Rik
    Katholieke Univ Leuven, Lab Cognit Neurol, B-3000 Louvain, Belgium.;Katholieke Univ Leuven, Leuven Inst Neurosci & Dis, Alzheimer Res Ctr, B-3000 Louvain, Belgium.;Univ Hosp Leuven, Dept Neurol, B-3000 Louvain, Belgium..
    Diagnostic value of cerebrospinal fluid A beta ratios in preclinical Alzheimer's disease2015Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 7, artikkel-id 75Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: In this study of preclinical Alzheimer's disease (AD) we assessed the added diagnostic value of using cerebrospinal fluid (CSF) A beta ratios rather than A beta 42 in isolation for detecting individuals who are positive on amyloid positron emission tomography (PET). Methods: Thirty-eight community-recruited cognitively intact older adults (mean age 73, range 65-80 years) underwent F-18-flutemetamol PET and CSF measurement of A beta 1-42, A beta 1-40, A beta 1-38, and total tau (ttau). F-18-flutemetamol retention was quantified using standardized uptake value ratios in a composite cortical region (SUVRcomp) with reference to cerebellar grey matter. Based on a prior autopsy validation study, the SUVRcomp cut-off was 1.57. Sensitivities, specificities and cut-offs were defined based on receiver operating characteristic analysis with CSF analytes as variables of interest and F-18-flutemetamol positivity as the classifier. We also determined sensitivities and CSF cut-off values at fixed specificities of 90 % and 95 %. Results: Seven out of 38 subjects (18 %) were positive on amyloid PET. A beta 42/ttau, A beta 42/A beta 40, A beta 42/A beta 38, and A beta 42 had the highest accuracy to identify amyloid-positive subjects (area under the curve (AUC) >= 0.908). A beta 40 and A beta 38 had significantly lower discriminative power (AUC = 0.571). When specificity was fixed at 90 % and 95 %, A beta 42/ttau had the highest sensitivity among the different CSF markers (85.71 % and 71.43 %, respectively). Sensitivity of A beta 42 alone was significantly lower under these conditions (57.14 % and 42.86 %, respectively). Conclusion: For the CSF-based definition of preclinical AD, if a high specificity is required, our data support the use of A beta 42/ttau rather than using A beta 42 in isolation.

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  • 10.
    Addo, Rebecka N.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap. Stockholm Univ, Dept Psychol, Gosta Ekman Lab, Frescati Hagvag 9A, S-10691 Stockholm, Sweden..
    Wiens, Stefan
    Stockholm Univ, Dept Psychol, Gosta Ekman Lab, Frescati Hagvag 9A, S-10691 Stockholm, Sweden..
    Nord, Marie
    Stockholm Univ, Dept Psychol, Gosta Ekman Lab, Frescati Hagvag 9A, S-10691 Stockholm, Sweden..
    Larsson, Maria
    Stockholm Univ, Dept Psychol, Gosta Ekman Lab, Frescati Hagvag 9A, S-10691 Stockholm, Sweden..
    Olfactory Functions in Adults With Autism Spectrum Disorders2017Inngår i: Perception, ISSN 0301-0066, E-ISSN 1468-4233, Vol. 46, nr 3-4, s. 530-537Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Autism spectrum disorders (ASD) are often characterized by atypical sensory behavior (hyperor hyporeactivity) although evidence is scarce regarding olfactory abilities in ASD; 16 adults with high-functioning ASD (mean age: 38.2, SD: 9.7) and 14 healthy control subjects (mean age: 42.0 years, SD: 12.5) were assessed in odor threshold, free and cued odor identification, and perceived pleasantness, intensity, and edibility of everyday odors. Although results showed no differences between groups, the Bayes Factors (close to 1) suggested that the evidence for no group differences on the threshold and identification tests was inconclusive. In contrast, there was some evidence for no group differences on perceived edibility (BF01 = 2.69) and perceived intensity (BF01 = 2.80). These results do not provide conclusive evidence for or against differences between ASD and healthy controls on olfactory abilities. However, they suggest that there are no apparent group differences in subjective ratings of odors.

    Fulltekst (pdf)
    fulltext
  • 11.
    Affatato, Oreste
    et al.
    Uppsala universitet, WoMHeR (Centre for Women’s Mental Health during the Reproductive Lifespan). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Dahlén, Amelia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Rukh, Gull
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Schiöth, Helgi B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Mwinyi, Jessica
    Uppsala universitet, WoMHeR (Centre for Women’s Mental Health during the Reproductive Lifespan). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Assessing volumetric brain differences in migraine and depression patients: a UK Biobank study2023Inngår i: BMC Neurology, E-ISSN 1471-2377, Vol. 23, nr 1, artikkel-id 284Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Migraine and depression are two of the most common and debilitating conditions. From a clinical perspective, they are mostly prevalent in women and manifest a partial overlapping symptomatology. Despite the high level of comorbidity, previous studies hardly investigated possible common patterns in brain volumetric differences compared to healthy subjects. Therefore, the current study investigates and compares the volumetric difference patterns in sub-cortical regions between participants with migraine or depression in comparison to healthy controls.

    Methods: The study included data from 43 930 participants of the large UK Biobank cohort. Using official ICD10 diagnosis, we selected 712 participants with migraine, 1 853 with depression and 23 942 healthy controls. We estimated mean volumetric difference between the groups for the different sub-cortical brain regions using generalized linear regression models, conditioning the model within the levels of BMI, age, sex, ethnical background, diastolic blood pressure, current tobacco smoking, alcohol intake frequency, Assessment Centre, Indices of Multiple Deprivation, comorbidities and total brain volume.

    Results: We detected larger overall volume of the caudate (mean difference: 66, 95% CI [-3, 135]) and of the thalamus (mean difference: 103 mm(3), 95% CI [-2, 208]) in migraineurs than healthy controls. We also observed that individuals with depression appear to have also larger overall (mean difference: 47 mm(3), 95% CI [-7, 100]) and gray matter (mean difference: 49 mm(3), 95% CI [2, 95]) putamen volumes than healthy controls, as well as larger amygdala volume (mean difference: 17 mm(3), 95% CI [-7, 40]).

    Conclusion: Migraineurs manifested larger overall volumes at the level of the nucleus caudate and of the thalamus, which might imply abnormal pain modulation and increased migraine susceptibility. Larger amygdala and putamen volumes in participants with depression than controls might be due to increased neuronal activity in these regions.

    Fulltekst (pdf)
    FULLTEXT01
  • 12.
    Affatato, Oreste
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi.
    Moulin, Thiago
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi.
    Pisanu, Claudia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi. Univ Cagliari, Dept Biomed Sci, Cagliari, Italy..
    Babasieva, Victoria S.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi. IM Sechenov First Moscow State Med Univ, Inst Pharm, Dept Pharmacol, Moscow, Russia..
    Russo, Marco
    Azienda USL IRCCS Reggio Emilia, Neuromotor & Rehabil Dept, Neurol Unit, Reggio Emilia, Italy..
    Aydinlar, Elif I.
    Acibadem Univ, Dept Neurol, Sch Med, Istanbul, Turkey..
    Torelli, Paola
    Univ Parma, Dept Med & Surg, Headache Ctr, Parma, Italy..
    Chubarev, Vladimir N.
    IM Sechenov First Moscow State Med Univ, Inst Pharm, Dept Pharmacol, Moscow, Russia..
    Tarasov, Vadim V.
    IM Sechenov First Moscow State Med Univ, Inst Pharm, Dept Pharmacol, Moscow, Russia.;IM Sechenov First Moscow State Med Univ, Inst Translat Med & Biothechnol, Moscow, Russia..
    Schiöth, Helgi B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi. IM Sechenov First Moscow State Med Univ, Inst Translat Med & Biothechnol, Moscow, Russia..
    Mwinyi, Jessica
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Schiöth: Funktionell farmakologi.
    High efficacy of onabotulinumtoxinA treatment in patients with comorbid migraine and depression: a meta-analysis2021Inngår i: Journal of Translational Medicine, ISSN 1479-5876, E-ISSN 1479-5876, Vol. 19, nr 1, artikkel-id 133Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Background: Migraine and depression are highly prevalent and partly overlapping disorders that cause strong limitations in daily life. Patients tend to respond poorly to the therapies available for these diseases. OnabotulinumtoxinA has been proven to be an effective treatment for both migraine and depression. While many studies have addressed the effect of onabotulinumtoxinA in migraine or depression separately, a growing body of evidence suggests beneficial effects also for patients comorbid with migraine and depression. The current meta-analysis systematically investigates to what extent onabotulinumtoxinA is efficient in migraineurs with depression.

    Methods: A systematic literature search was performed based on PubMed, Scopus and Web of Science from the earliest date till October 30th, 2020. Mean, standard deviation (SD) and sample size have been used to evaluate improvement in depressive symptoms and migraine using random- effects empirical Bayes model.

    Results: Our search retrieved 259 studies, eight of which met the inclusion criteria. OnabotulinumtoxinA injections administered to patients with both chronic migraine and major depressive disorder led to mean reduction of - 8.94 points (CI [ - 10.04,- 7.84], p < 0.01) in the BDI scale, of - 5.90 points (CI [ - 9.92,- 1.88], p < 0.01) in the BDI-II scale and of - 6.19 points (CI [ - 9.52,- 2.86], p < 0.01) in the PHQ-9 scale, when evaluating depressive symptoms. In the case of the migraine-related symptoms, we found mean reductions of - 4.10 (CI [ - 7.31,- 0.89], p = 0.01) points in the HIT6 scale, - 32.05 (CI [ - 55.96,- 8.14], p = 0.01) in the MIDAS scale, - 1.7 (CI [ - 3.27,- 0.13], p = 0.03) points in the VAS scale and of - 6.27 (CI [ - 8.48,- 4.07], p < 0.01) migraine episodes per month. Comorbid patients showed slightly better improvements in BDI, HIT6 scores and migraine frequency compared to monomorbid patients. The latter group manifested better results in MIDAS and VAS scores.

    Conclusion: Treatment with onabotulinumtoxinA leads to a significant reduction of disease severity of both chronic migraine and major depressive disorder in patients comorbid with both diseases. Comparative analyses suggest an equivalent strong effect in monomorbid and comorbid patients, with beneficial effects specifically seen for certain migraine features.

    Fulltekst (pdf)
    FULLTEXT01
  • 13.
    Affatato, Oreste
    et al.
    Uppsala universitet, WoMHeR (Centre for Women’s Mental Health during the Reproductive Lifespan). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Rukh, Gull
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Schiöth, Helgi B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Mwinyi, Jessica
    Uppsala universitet, WoMHeR (Centre for Women’s Mental Health during the Reproductive Lifespan). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Funktionell farmakologi och neurovetenskap.
    Volumetric Differences in Cerebellum and Brainstem in Patients with Migraine: A UK Biobank Study2023Inngår i: Biomedicines, E-ISSN 2227-9059, Vol. 11, nr 9, artikkel-id 2528Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The cerebellum and the brainstem are two brain structures involved in pain processing and modulation that have also been associated with migraine pathophysiology. The aim of this study was to investigate possible associations between the morphology of the cerebellum and brainstem and migraine, focusing on gray matter differences in these brain areas.

    Methods: The analyses were based on data from 712 individuals with migraine and 45,681 healthy controls from the UK Biobank study. Generalized linear models were used to estimate the mean gray matter volumetric differences in the brainstem and the cerebellum. The models were adjusted for important biological covariates such as BMI, age, sex, total brain volume, diastolic blood pressure, alcohol intake frequency, current tobacco smoking, assessment center, material deprivation, ethnic background, and a wide variety of health conditions. Secondary analyses investigated volumetric correlation between cerebellar sub-regions.

    Results: We found larger gray matter volumes in the cerebellar sub-regions V (mean difference: 72 mm3, 95% CI [13, 132]), crus I (mean difference: 259 mm3, 95% CI [9, 510]), VIIIa (mean difference: 120 mm3, 95% CI [0.9, 238]), and X (mean difference: 14 mm3, 95% CI [1, 27]).

    Conclusions: Individuals with migraine show larger gray matter volumes in several cerebellar sub-regions than controls. These findings support the hypothesis that the cerebellum plays a role in the pathophysiology of migraine.

    Fulltekst (pdf)
    FULLTEXT01
  • 14. Aghanavesi, S
    et al.
    Bergquist, F
    Nyholm, Dag
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Landtblom: Neurologi.
    Senek, Marina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Memedi, M
    Motion Sensor-Based Assessment of Parkinson's Disease Motor Symptoms During Leg Agility Tests: Results From Levodopa Challenge2020Inngår i: IEEE journal of biomedical and health informatics, ISSN 2168-2194, E-ISSN 2168-2208, Vol. 24, nr 1, s. 111-119Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Parkinson's disease (PD) is a degenerative, progressive disorder of the central nervous system that mainly affects motor control. The aim of this study was to develop data-driven methods and test their clinimetric properties to detect and quantify PD motor states using motion sensor data from leg agility tests. Nineteen PD patients were recruited in a levodopa single dose challenge study. PD patients performed leg agility tasks while wearing motion sensors on their lower extremities. Clinical evaluation of video recordings was performed by three movement disorder specialists who used four items from the motor section of the unified PD rating scale (UPDRS), the treatment response scale (TRS) and a dyskinesia score. Using the sensor data, spatiotemporal features were calculated and relevant features were selected by feature selection. Machine learning methods like support vector machines (SVM), decision trees, and linear regression, using ten-fold cross validation were trained to predict motor states of the patients. SVM showed the best convergence validity with correlation coefficients of 0.81 to TRS, 0.83 to UPDRS #31 (body bradykinesia and hypokinesia), 0.78 to SUMUPDRS (the sum of the UPDRS items: #26-leg agility, #27-arising from chair, and #29-gait), and 0.67 to dyskinesia. Additionally, the SVM-based scores had similar test-retest reliability in relation to clinical ratings. The SVM-based scores were less responsive to treatment effects than the clinical scores, particularly with regards to dyskinesia. In conclusion, the results from this study indicate that using motion sensors during leg agility tests may lead to valid and reliable objective measures of PD motor symptoms.

  • 15.
    Aghanavesi, Somayeh
    et al.
    Dalarna Univ, Falun, Sweden.
    Memedi, Mevludin
    Örebro Univ, Örebro, Sweden.
    Dougherty, Mark
    Dalarna Univ, Falun, Sweden.
    Nyholm, Dag
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurologi.
    Westin, Jerker
    Dalarna Univ, Falun, Sweden.
    Verification of a Method for Measuring Parkinson's Disease Related Temporal Irregularity in Spiral Drawings2017Inngår i: Sensors, E-ISSN 1424-8220, Vol. 17, nr 10, artikkel-id 2431Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    -value = 0.02). Test-retest reliability of TIS was good with Intra-class Correlation Coefficient of 0.81. When assessing changes in relation to treatment, TIS contained some information to capture changes from Off to On and wearing off effects. However, the correlations between TIS and clinical scores (UPDRS and Dyskinesia) were weak. TIS was able to differentiate spiral drawings drawn by patients in an advanced stage from those drawn by healthy subjects, and TIS had good test-retest reliability. TIS was somewhat responsive to single-dose levodopa treatment. Since TIS is an upper limb high-frequency-based measure, it cannot be detected during clinical assessment.

    Fulltekst (pdf)
    fulltext
  • 16.
    Aghanavesi, Somayeh
    et al.
    Dalarna Univ, Dept Comp Engn, Falun, Sweden..
    Westin, Jerker
    Dalarna Univ, Dept Comp Engn, Falun, Sweden..
    Bergquist, Filip
    Univ Gothenburg, Dept Pharmacol, Inst Neurosci & Physiol, Gothenburg, Sweden..
    Nyholm, Dag
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Landtblom: Neurologi.
    Askmark, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Landtblom: Neurologi.
    Aquilonius, Sten-Magnus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Landtblom: Neurologi.
    Constantinescu, Radu
    Univ Gothenburg, Dept Clin Neurosci, Gothenburg, Sweden..
    Medvedev, Alexander
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Reglerteknik. Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Avdelningen för systemteknik.
    Spira, Jack
    Sensidose AB, Sollentuna, Sweden..
    Ohlsson, Fredrik
    Chalmers Univ, Gothenburg, Sweden..
    Thomas, Ilias
    Dalarna Univ, Dept Stat, Falun, Sweden..
    Ericsson, Anders
    Irisity AB, Gothenburg, Sweden..
    Buvarp, Dongni Johansson
    Univ Gothenburg, Dept Clin Neurosci & Rehabil, Gothenburg, Sweden..
    Memedi, Mevludin
    Orebro Univ, Informat, Orebro, Sweden..
    A multiple motion sensors index for motor state quantification in Parkinson's disease2020Inngår i: Computer Methods and Programs in Biomedicine, ISSN 0169-2607, E-ISSN 1872-7565, Vol. 189, artikkel-id 105309Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aim: To construct a Treatment Response Index from Multiple Sensors (TRIMS) for quantification of motor state in patients with Parkinson's disease (PD) during a single levodopa dose. Another aim was to compare TRIMS to sensor indexes derived from individual motor tasks.

    Method: Nineteen PD patients performed three motor tests including leg agility, pronation-supination movement of hands, and walking in a clinic while wearing inertial measurement unit sensors on their wrists and ankles. They performed the tests repeatedly before and after taking 150% of their individual oral levodopa-carbidopa equivalent morning dose.Three neurologists blinded to treatment status, viewed patients' videos and rated their motor symptoms, dyskinesia, overall motor state based on selected items of Unified PD Rating Scale (UPDRS) part III, Dyskinesia scale, and Treatment Response Scale (TRS). To build TRIMS, out of initially 178 extracted features from upper- and lower-limbs data, 39 features were selected by stepwise regression method and were used as input to support vector machines to be mapped to mean reference TRS scores using 10-fold cross-validation method. Test-retest reliability, responsiveness to medication, and correlation to TRS as well as other UPDRS items were evaluated for TRIMS.

    Results: The correlation of TRIMS with TRS was 0.93. TRIMS had good test-retest reliability (ICC = 0.83). Responsiveness of the TRIMS to medication was good compared to TRS indicating its power in capturing the treatment effects. TRIMS was highly correlated to dyskinesia (R = 0.85), bradykinesia (R = 0.84) and gait (R = 0.79) UPDRS items. Correlation of sensor index from the upper-limb to TRS was 0.89.

    Conclusion: Using the fusion of upper- and lower-limbs sensor data to construct TRIMS provided accurate PD motor states estimation and responsive to treatment. In addition, quantification of upper-limb sensor data during walking test provided strong results.

  • 17. Agosti, Edoardo
    et al.
    Saraceno, Giorgio
    Rampinelli, Vittorio
    Raffetti, Elena
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Geovetenskapliga sektionen, Institutionen för geovetenskaper, Luft-, vatten- och landskapslära. Department of Global Public Health Sciences, Karolinska Institute, Stockholm, Sweden.
    Veiceschi, Pierlorenzo
    Buffoli, Barbara
    Rezzani, Rita
    Giorgianni, Andrea
    Hirtler, Lena
    Alexander, Alex Yohan
    Deganello, Alberto
    Piazza, Cesare
    Nicolai, Piero
    Castelnuovo, Paolo
    Locatelli, Davide
    Peris-Celda, Maria
    Fontanella, Marco Maria
    Doglietto, Francesco
    Quantitative Anatomic Comparison of Endoscopic Transnasal and Microsurgical Transcranial Approaches to the Anterior Cranial Fossa2022Inngår i: Operative Neurosurgery, ISSN 2332-4252, E-ISSN 2332-4260, Vol. 23, nr 4, s. e256-e266Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: 

    Several microsurgical transcranial approaches (MTAs) and endoscopic transnasal approaches (EEAs) to the anterior cranial fossa (ACF) have been described.

    OBJECTIVE: 

    To provide a preclinical, quantitative, anatomic, comparative analysis of surgical approaches to the ACF.

    METHODS: 

    Five alcohol-fixed specimens underwent high-resolution computed tomography. The following approaches were performed on each specimen: EEAs (transcribriform, transtuberculum, and transplanum), anterior MTAs (transfrontal sinus interhemispheric, frontobasal interhemispheric, and subfrontal with unilateral and bilateral frontal craniotomy), and anterolateral MTAs (supraorbital, minipterional, pterional, and frontotemporal orbitozygomatic approach). An optic neuronavigation system and dedicated software (ApproachViewer, part of GTx-Eyes II—UHN) were used to quantify the working volume of each approach and extrapolate the exposure of different ACF regions. Mixed linear models with random intercepts were used for statistical analyses.

    RESULTS: 

    EEAs offer a large and direct route to the midline region of ACF, whose most anterior structures (ie, crista galli, cribriform plate, and ethmoidal roof) are also well exposed by anterior MTAs, whereas deeper ones (ie, planum sphenoidale and tuberculum sellae) are also well exposed by anterolateral MTAs. The orbital roof region is exposed by both anterolateral and lateral MTAs. The posterolateral region (ie, sphenoid wing and optic canal) is well exposed by anterolateral MTAs.

    CONCLUSION: 

    Anterior and anterolateral MTAs play a pivotal role in the exposure of most anterior and posterolateral ACF regions, respectively, whereas midline regions are well exposed by EEAs. Furthermore, certain anterolateral approaches may be most useful when involvement of the optic canal and nerves involvement are suspected.

  • 18.
    Agosti, F.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Funktionell farmakologi. Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol IMBICE, Electrophysiol Lab, La Plata, Buenos Aires, Argentina.;CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina..
    Cordisco Gonzalez, S.
    Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol IMBICE, Electrophysiol Lab, La Plata, Buenos Aires, Argentina.;CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina..
    Martinez Damonte, V.
    Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol IMBICE, Electrophysiol Lab, La Plata, Buenos Aires, Argentina.;CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina..
    Tolosa, M. J.
    Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol IMBICE, Electrophysiol Lab, La Plata, Buenos Aires, Argentina.;CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina..
    Di Siervi, N.
    Univ Buenos Aires, CONICET, ININFA, Inst Invest Farmacol, Buenos Aires, DF, Argentina..
    Schiöth, Helgi B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Funktionell farmakologi.
    Davio, C.
    Univ Buenos Aires, CONICET, ININFA, Inst Invest Farmacol, Buenos Aires, DF, Argentina..
    Perello, M.
    CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina.;Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol, IMBICE,Neurophysiol Lab, La Plata, Buenos Aires, Argentina..
    Raingo, J.
    Univ La Plata, CONICET, Multidisciplinary Inst Cell Biol IMBICE, Electrophysiol Lab, La Plata, Buenos Aires, Argentina.;CIC, Comis Invest Prov Buenos Aires, La Plata, Buenos Aires, Argentina..
    Melanocortin 4 Receptor Constitutive Activity Inhibits L-Type Voltage-Gated Calcium Channels In Neurons2017Inngår i: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 346, s. 102-112Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The melanocortin 4 receptor (MC4R) is a G protein-coupled receptor (GPCR) that is expressed in several brain nuclei playing a crucial role in the regulation of energy balance controlling the homeostasis of the organism. It displays both agonist-evoked and constitutive activity, and moreover, it can couple to different G proteins. Most of the research on MC4R has been focused on agonist-induced activity, while the molecular and cellular basis of MC4R constitutive activity remains scarcely studied. We have previously shown that neuronal N-type voltage-gated calcium channels (Ca(V)2.2) are inhibited by MC4R agonist-dependent activation, while the Ca-V subtypes that carry L- and P/Q-type current are not. Here, we tested the hypothesis that MC4R constitutive activity can affect Ca-V, with focus on the channel subtypes that can control transcriptional activity coupled to depolarization (L-type, Ca(V)1.2/1.3) and neurotransmitter release (N- and P/Q-type, Ca(V)2.2 and Ca(V)2.1). We found that MC4R constitutive activity inhibits specifically Ca(V)1.2/1.3 and Ca(V)2.1 subtypes of Ca-V. We also explored the signaling pathways mediating this inhibition, and thus propose that agonist-dependent and basal MC4R activation modes signal differentially through G(s) and G(i/o) pathways to impact on different Ca-V subtypes. In addition, we found that chronic incubation with MC4R endogenous inverse agonist, agouti and agouti-related peptide (AgRP), occludes Ca-V inhibition in a cell line and in amygdaloid complex cultured neurons as well. Thus, we define new mechanisms of control of the main mediators of depolarization-induced calcium entry into neurons by a GPCR that displays constitutive activity.

  • 19. Agosti, Francina
    et al.
    Lopez Soto, Eduardo J.
    Cabral, Agustina
    Castrogiovanni, Daniel
    Schiöth, Helgi B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Funktionell farmakologi.
    Perello, Mario
    Raingo, Jesica
    Melanocortin 4 receptor activation inhibits presynaptic N-type calcium channels in amygdaloid complex neurons2014Inngår i: European Journal of Neuroscience, ISSN 0953-816X, E-ISSN 1460-9568, Vol. 40, nr 5, s. 2755-2765Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The melanocortin 4 receptor (MC4R) is a G protein-coupled receptor involved in food intake and energy expenditure regulation. MC4R activation modifies neuronal activity but the molecular mechanisms by which this regulation occurs remain unclear. Here, we tested the hypothesis that MC4R activation regulates the activity of voltage-gated calcium channels and, as a consequence, synaptic activity. We also tested whether the proposed effect occurs in the amygdala, a brain area known to mediate the anorexigenic actions of MC4R signaling. Using the patch-clamp technique, we found that the activation of MC4R with its agonist melanotan II specifically inhibited 34.5 +/- 1.5% of N-type calcium currents in transiently transfected HEK293 cells. This inhibition was concentration-dependent, voltage-independent and occluded by the G(s) pathway inhibitor cholera toxin. Moreover, we found that melanotan II specifically inhibited 25.9 +/- 2.0% of native N-type calcium currents and 55.4 +/- 14.4% of evoked inhibitory postsynaptic currents in mouse cultured amygdala neurons. Invivo, we found that the MC4R agonist RO27-3225 increased the marker of cellular activity c-Fos in several components of the amygdala, whereas the N-type channel blocker conotoxin GVIA increased c-Fos expression exclusively in the central subdivision of the amygdala. Thus, MC4R specifically inhibited the presynaptic N-type channel subtype, and this inhibition may be important for the effects of melanocortin in the central subdivision of the amygdala.

  • 20.
    Agoston, Denes V.
    et al.
    Uniformed Serv Univ Hlth Sci, Dept Anat, Bethesda, MD 20814 USA.;Karolinska Inst, Dept Neurosci, Stockholm, Sweden..
    Sköld, Mattias K.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi. Karolinska Inst, Dept Neurosci, Stockholm, Sweden..
    Editorial: When Physics Meets Biology; Biomechanics and Biology of traumatic Brain injury2016Inngår i: Frontiers in Neurology, E-ISSN 1664-2295, Vol. 7, artikkel-id 91Artikkel i tidsskrift (Annet vitenskapelig)
  • 21. Ahl, Matilda
    et al.
    Avdic, Una
    Strandberg, Maria Compagno
    Chugh, Deepti
    Andersson, Emelie
    Hållmarker, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Department of Internal Medicine, Mora Hospital, Mora, Sweden.
    James, Stefan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Deierborg, Tomas
    Ekdahl, Christine T
    Physical Activity Reduces Epilepsy Incidence: a Retrospective Cohort Study in Swedish Cross-Country Skiers and an Experimental Study in Seizure-Prone Synapsin II Knockout Mice2019Inngår i: Sports medicine - open, ISSN 2199-1170, Vol. 5, nr 1, artikkel-id 52Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Epilepsy patients commonly exercise less than the general population. Animal studies indicate beneficial effects of physical activity in established epilepsy, while its effect on the development is currently less known.

    METHODS: Here, we investigated the incidence of epilepsy during 20 years in a cohort of participants from the long-distance Swedish cross-country ski race Vasaloppet (n = 197,685) and compared it to the incidence of non-participating-matched controls included in the Swedish population register (n = 197,684). Individuals diagnosed with diseases such as stroke and epilepsy before entering the race were excluded from both groups. Experimentally, we also determined how physical activity could affect the development of epilepsy in epilepsy-prone synapsin II knockout mice (SynIIKO), with and without free access to a running wheel.

    RESULTS: We identified up to 40-50% lower incidence of epilepsy in the Vasaloppet participants of all ages before retirement. A lower incidence of epilepsy in Vasaloppet participants was seen regardless of gender, education and occupation level compared to controls. The participants included both elite and recreational skiers, and in a previous survey, they have reported a higher exercise rate than the general Swedish population. Sub-analyses revealed a significantly lower incidence of epilepsy in participants with a faster compared to slower finishing time. Dividing participants according to specified epilepsy diagnoses revealed 40-50% decrease in focal and unspecified epilepsy, respectively, but no differences in generalized epilepsy. Voluntary exercise in seizure-prone SynIIKO mice for 1 month before predicted epilepsy development decreased seizure manifestation from > 70 to 40%. Brain tissue analyses following 1 month of exercise showed increased hippocampal neurogenesis (DCX-positive cells), while microglial (Iba1) and astrocytic activation (GFAP), neuronal Map2, brain-derived neurotrophic factor and its receptor tyrosine receptor kinase B intensity were unaltered. Continued exercise for additionally 2 months after predicted seizure onset in SynIIKO mice resulted in a 5-fold reduction in seizure manifestation (from 90 to 20%), while 2 months of exercise initiated at the time of predicted seizure development gave no seizure relief, suggesting exercise-induced anti-epileptogenic rather than anti-convulsive effect.

    CONCLUSION: The clinical study and the experimental findings in mice indicate that physical activity may prevent or delay the development of epilepsy.

    Fulltekst (pdf)
    fulltext
  • 22. Ahl, Matilda
    et al.
    Taylor, Marie K.
    Avdic, Una
    Lundin, Anna
    Andersson, My
    Amandusson, Åsa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk neurofysiologi.
    Kumlien, Eva
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurologi.
    Compagno Strandberg, Maria
    Ekdahl, Christine T.
    Immune response in blood before and after epileptic and psychogenic non-epileptic seizures2023Inngår i: Heliyon, E-ISSN 2405-8440, Vol. 9, nr 3, artikkel-id e13938Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Inflammatory processes may provoke epileptic seizures and seizures may promote an immune reaction. Hence, the systemic immune reaction is a tempting diagnostic and prognostic marker in epilepsy. We explored the immune response before and after epileptic and psychogenic non-epileptic seizures (PNES). Serum samples collected from patients with videoEEG-verified temporal or frontal lobe epilepsy (TLE or FLE) or TLE + PNES showed increased interleukin-6 (IL-6) levels in between seizures (interictally), compared to controls. Patients with PNES had no increase in IL-6. The IL-6 levels increased transiently even further within hours after a seizure (postictally) in TLE but not in FLE patients. The postictal to interictal ratio of additionally five immune factors were also increased in TLE patients only. We conclude that immune factors have the potential to be future biomarkers for epileptic seizures and that the heterogeneity among different epileptic and non-epileptic seizures may be disclosed in peripheral blood sampling independent of co-morbidities.

    Fulltekst (pdf)
    fulltext
  • 23.
    Ahlström, Isabell
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Fysioterapi.
    Hellström, Karin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Fysioterapi.
    Emtner, Margareta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Sjukgymnastik. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Lungmedicin och allergologi.
    Anens, Elisabeth
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Fysioterapi.
    Reliability of the Swedish version of the Exercise Self-Efficacy Scale (S-ESES): a test-retest study in adults with neurological disease2015Inngår i: Physiotherapy Theory and Practice, ISSN 0959-3985, E-ISSN 1532-5040, Vol. 31, nr 3, s. 194-199Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To examine the test-retest reliability of the Swedish translated version of the Exercise Self-Efficacy Scale (S-ESES) in people with neurological disease and to examine internal consistency.

    Design: Test-retest study.

    Subjects: A total of 30 adults with neurological diseases including: Parkinson's disease; Multiple Sclerosis; Cervical Dystonia; and Charcot Marie Tooth disease.

    Method: The S-ESES was sent twice by surface mail. Completion interval mean was 16 days apart. Weighted kappa, intraclass correlation coefficient 2,1 [ICC (2,1)], standard error of measurement (SEM), also expressed as a percentage value (SEM%), and Cronbach's alpha were calculated.

    Results: The relative reliability of the test-retest results showed substantial agreement measured using weighted kappa (MD = 0.62) and a very high-reliability ICC (2,1) (0.92). Absolute reliability measured using SEM was 5.3 and SEM% was 20.7. Excellent internal consistency was shown, with an alpha coefficient of 0.91 (test 1) and 0.93 (test 2).

    Conclusion: The S-ESES is recommended for use in research and in clinical work for people with neurological diseases. The low-absolute reliability, however, indicates a limited ability to measure changes on an individual level.

  • 24.
    Ahmad, Abdulbaghi
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Childhood trauma and posttraumatic stress disorder: A developmental and cross-cultural approach1999Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    This thesis aims to identify child-specific cross-cultural protecting and vulnerability factors regarding traumatic experiences and posttraumatic stress reactions. Children between 6-18 years were interviewed from three different socio-cultural backgrounds. In Iraqi Kurdistan, 20 participants in a mass-escape tragedy (MET), 54 orphans and 45 survivors of the genocide operation "Anfal" were interviewed. In Sweden, a sample of 32 Kurdistanian refugee children and a comparable Swedish sample were included. The frequencies of posttraumatic stress disorder (PTSD) were 20%, 43%. 87%, 9,7% and 12.5% respectively.

    The relatively low frequencies of PTSD in the follow-up sample 2 months, 4 months, 14 months and 26 months after the MET suggest the child functioning in a complete, authoritative family, as a protecting factor. The significant of this developmentally based child-specific functioning level within the supportive family system can also explain the fluctuating PTSD-related symptom scores in this sample parallel to the changes in the socio-economic situation in the region. The over time decrease in behavioural problems among fostercare orphans and their low PTSD frequencies as compared with the increase in behavioural problems and the high PTSD frequencies among orphanage samples further support this suggestion. Child trauma scores and captivity duration predicted for PTSD in "Anfal" survivors, irrespective of parents' trauma scores and PTSD or fathers re-union with the family, suggesting child-specific vulnerability more than contagion effect. Despite PTSD, children in Kurdistan performed high functioning levels, probably indicating a child-specific manifestation of hypervigilance. The Kurdistanian refugee sample revealed lower lifetime reexperiencing PTSD symptom scores than the Swedish sample, indicating a healing effect on the former coming to Sweden and a resilience deficit for the later growing up in a highly sheltered society.

    There are more similarities than differences between children from Kurdistan and Sweden in reporting traumatic experiences and exhibiting posttraumatic stress symptoms. Developmentally based child characteristics have a determinant role as protective or vulnerability factors in childhood trauma and PTSD, even if socio-cultural factors also play a role.

  • 25.
    Ahmad, Abdulbaghi
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Childhood trauma and posttraumatic stress disorder: A developmental and cross-cultural approach1999Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    This thesis aims to identify child-specific cross-cultural protecting and vulnerability factors regarding traumatic experiences and posttraumatic stress reactions. Children between 6-18 years were interviewed from three different socio-cultural backgrounds. In Iraqi Kurdistan, 20 participants in a mass-escape tragedy (MET), 54 orphans and 45 survivors of the genocide operation "Anfal" were interviewed. In Sweden, a sample of 32 Kurdistanian refugee children and a comparable Swedish sample were included. The frequencies of posttraumatic stress disorder (PTSD) were 20%, 43%. 87%, 9,7% and 12.5% respectively.

    The relatively low frequencies of PTSD in the follow-up sample 2 months, 4 months, 14 months and 26 months after the MET suggest the child functioning in a complete, authoritative family, as a protecting factor. The significant of this developmentally based child-specific functioning level within the supportive family system can also explain the fluctuating PTSD-related symptom scores in this sample parallel to the changes in the socio-economic situation in the region. The over time decrease in behavioural problems among fostercare orphans and their low PTSD frequencies as compared with the increase in behavioural problems and the high PTSD frequencies among orphanage samples further support this suggestion. Child trauma scores and captivity duration predicted for PTSD in "Anfal" survivors, irrespective of parents' trauma scores and PTSD or fathers re-union with the family, suggesting child-specific vulnerability more than contagion effect. Despite PTSD, children in Kurdistan performed high functioning levels, probably indicating a child-specific manifestation of hypervigilance. The Kurdistanian refugee sample revealed lower lifetime reexperiencing PTSD symptom scores than the Swedish sample, indicating a healing effect on the former coming to Sweden and a resilience deficit for the later growing up in a highly sheltered society.

    There are more similarities than differences between children from Kurdistan and Sweden in reporting traumatic experiences and exhibiting posttraumatic stress symptoms. Developmentally based child characteristics have a determinant role as protective or vulnerability factors in childhood trauma and PTSD, even if socio-cultural factors also play a role.

    Delarbeid
    1. Symptoms of post-traumatic stress disorder among displaced Kurdish children in Iraq; victims of a man-made disaster after the Gulf war.
    Åpne denne publikasjonen i ny fane eller vindu >>Symptoms of post-traumatic stress disorder among displaced Kurdish children in Iraq; victims of a man-made disaster after the Gulf war.
    1992 (engelsk)Inngår i: Nordic Journal Psychiatry, Vol. 46, nr 5, s. 315-319Artikkel i tidsskrift (Fagfellevurdert) Published
    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-26241 (URN)
    Tilgjengelig fra: 2007-02-15 Laget: 2007-02-15 Sist oppdatert: 2020-03-10
    2. The socioemotional development of orphans in orphanages and traditional foster care in Iraqi Kurdistan
    Åpne denne publikasjonen i ny fane eller vindu >>The socioemotional development of orphans in orphanages and traditional foster care in Iraqi Kurdistan
    1996 (engelsk)Inngår i: Child Abuse & Neglect, Vol. 20, s. 1161-Artikkel i tidsskrift (Fagfellevurdert) Published
    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-55922 (URN)
    Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2020-03-10
    3. A 26-month follow-up of posttraumatic stress symptoms in children after the mass-escape tragedy in Iraqi Kurdistan
    Åpne denne publikasjonen i ny fane eller vindu >>A 26-month follow-up of posttraumatic stress symptoms in children after the mass-escape tragedy in Iraqi Kurdistan
    1998 (engelsk)Inngår i: Nord J Psychiatry, Vol. 52, s. 357-Artikkel i tidsskrift (Fagfellevurdert) Published
    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-56716 (URN)
    Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2020-03-10
    4. Reliability and validity of a child-specific cross-cultural instrument for assessing posttraumatic stress disorder
    Åpne denne publikasjonen i ny fane eller vindu >>Reliability and validity of a child-specific cross-cultural instrument for assessing posttraumatic stress disorder
    Vise andre…
    2000 (engelsk)Inngår i: European Child and Adolescent Psychiatry, ISSN 1018-8827, E-ISSN 1435-165X, Vol. 9, nr 4, s. 285-294Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    The Posttraumatic Stress Symptoms in Children (PTSS-C) was developed as a cross-cultural semi-structured interview to diagnose posttraumatic stress disorder (PTSD) and to identify PTSD-non-related posttraumatic stress symptoms in children after various traumatic experiences. The psychometric properties were studied in two different child populations in Iraqi Kurdistan (the survivors of the military operation “Anfal”, and the orphans), in a sample of Kurdistanian refugee children in Sweden, and in a comparison sample of Swedish children. The instrument yielded satisfactory internal consistency, high interrater agreement, and excellent validity on cross-validation with the Child Posttraumatic Stress Disorder Reaction Index (CPTSD-RI) and the Diagnostic Interview for Children and Adolescents (DICA) according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).

    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-56320 (URN)10.1007/s007870070032 (DOI)
    Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2020-03-10bibliografisk kontrollert
    5. Posttraumatic stress disorder in children after the military operation "Anfal" in Iraqi Kurdistan
    Åpne denne publikasjonen i ny fane eller vindu >>Posttraumatic stress disorder in children after the military operation "Anfal" in Iraqi Kurdistan
    2000 (engelsk)Inngår i: European Child and Adolescent Psychiatry, ISSN 1018-8827, E-ISSN 1435-165X, Vol. 9, nr 4, s. 235-243Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

     Five years after the military operation “Anfal” in Iraqi Kurdistan, 45 families were randomly selected among the survivors in two displacement camps. The Posttraumatic Stress Symptoms for Children (PTSS-C) and the Harvard Trauma Questionnaire (HTQ) were administered to the oldest child and the caregiver in each family, respectively. Posttraumatic stress disorder (PTSD) was reported in 87% of children and 60% of their caregivers. While childhood PTSD was only significantly predicted by child trauma score and the duration of captivity, it was neither predicted by maternal PTSD nor did it disappear after the reunion with the PTSD-free father. However, the small sample size makes the results hypotheses rather than conclusive.

    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-56319 (URN)10.1007/s007870070026 (DOI)
    Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2020-03-10bibliografisk kontrollert
  • 26.
    Ahmadpour, Doryaneh
    et al.
    Chalmers Univ Technol, Dept Biol & Biol Engn, Gothenburg, Sweden.;Motala Hosp, Inst Neurol, Dept Med Specialists, Motala, Sweden..
    Kristoffersson, Anna
    Motala Hosp, Inst Neurol, Dept Med Specialists, Motala, Sweden..
    Fredrikson, Mats
    Linkoping Univ, Forum Ostergotland, Linkoping, Sweden..
    Huang-Link, Yumin
    Linkoping Univ Hosp, Dept Neurol, Linkoping, Sweden..
    Eriksson, Anne
    Motala Hosp, Inst Med, Dept Med Specialists, Motala, Sweden..
    Iacobaeus, Ellen
    Karolinska Inst, Dept Clin Neurosci, Div Neurol, Stockholm, Sweden.;Karolinska Univ Hosp, Stockholm, Sweden..
    Landtblom, Anne-Marie
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurologi. Linkoping Univ Hosp, Dept Neurol, Linkoping, Sweden.;Uppsala Univ, Dept Med Sci, Uppsala, Sweden..
    Haghighi, Sara
    Motala Hosp, Inst Neurol, Dept Med Specialists, Motala, Sweden.;Linkoping Univ Hosp, Dept Neurol, Linkoping, Sweden..
    Inventory study of an early pandemic COVID-19 cohort in South-Eastern Sweden, focusing on neurological manifestations2023Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 18, nr 1, artikkel-id e0280376Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BackgroundNeurological manifestations in patients with COVID-19 have been reported previously as outcomes of the infection.The purpose of current study was to investigate the occurrence of neurological signs and symptoms in COVID-19 patients, in the county of ostergotland in southeastern Sweden. MethodsThis is a retrospective, observational cohort study. Data were collected between March 2020 and June 2020. Information was extracted from medical records by a trained research assistant and physician and all data were validated by a senior neurologist. ResultsSeventy-four percent of patients developed at least one neurological symptom during the acute phase of the infection. Headache (43%) was the most common neurological symptom, followed by anosmia and/or ageusia (33%), confusion (28%), hallucinations (17%), dizziness (16%), sleep disorders in terms of insomnia and OSAS (Obstructive Sleep Apnea) (9%), myopathy and neuropathy (8%) and numbness and tingling (5%). Patients treated in the ICU had a higher male presentation (73%). Several risk factors in terms of co-morbidities, were identified. Hypertension (54.5%), depression and anxiety (51%), sleep disorders in terms of insomnia and OSAS (30%), cardiovascular morbidity (28%), autoimmune diseases (25%), chronic lung diseases (24%) and diabetes mellitus type 2 (23%) founded as possible risk factors. ConclusionNeurological symptoms were found in the vast majority (74%) of the patients. Accordingly, attention to neurological, mental and sleep disturbances is warranted with involvement of neurological expertise, in order to avoid further complications and long-term neurological effect of COVID-19. Furthermore, risk factors for more severe COVID-19, in terms of possible co-morbidities that identified in this study should get appropriate attention to optimizing treatment strategies in COVID-19 patients.

    Fulltekst (pdf)
    FULLTEXT01
  • 27.
    Ahmed, Niaz
    et al.
    Department of Neurology, Karolinska University Hospital, and Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Audebert, Heinrich
    Turc, Guillaume
    Cordonnier, Charlotte
    Christensen, Hanne
    Sacco, Simona
    Sandset, Else Charlotte
    Ntaios, George
    Charidimou, Andreas
    Toni, Danilo
    Pristipino, Christian
    Köhrmann, Martin
    Kuramatsu, Joji B
    Thomalla, Götz
    Mikulik, Robert
    Ford, Gary A
    Martí-Fàbregas, Joan
    Fischer, Urs
    Thoren, Magnus
    Lundström, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Landtblom: Neurologi. Akademiska sjukhuset, Uppsala, Sweden.
    Rinkel, Gabriel Je
    van der Worp, H Bart
    Matusevicius, Marius
    Tsivgoulis, Georgios
    Milionis, Haralampos
    Rubiera, Marta
    Hart, Robert
    Moreira, Tiago
    Lantz, Maria
    Sjöstrand, Christina
    Andersen, Grethe
    Schellinger, Peter
    Kostulas, Konstantinos
    Sunnerhagen, Katharina Stibrant
    Keselman, Boris
    Korompoki, Eleni
    Purrucker, Jan
    Khatri, Pooja
    Whiteley, William
    Berge, Eivind
    Mazya, Michael
    Dippel, Diederik Wj
    Mustanoja, Satu
    Rasmussen, Mads
    Söderqvist, Åsa Kuntze
    Escudero-Martínez, Irene
    Steiner, Thorsten
    Consensus statements and recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 11-13 November 2018.2019Inngår i: European Stroke Journal, ISSN 2396-9873, E-ISSN 2396-9881, Vol. 4, nr 4, s. 307-317Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The purpose of the European Stroke Organisation-Karolinska Stroke Update Conference is to provide updates on recent stroke therapy research and to give an opportunity for the participants to discuss how these results may be implemented into clinical routine. The meeting started 22 years ago as Karolinska Stroke Update, but since 2014 it is a joint conference with European Stroke Organisation. Importantly, it provides a platform for discussion on the European Stroke Organisation guidelines process and on recommendations to the European Stroke Organisation guidelines committee on specific topics. By this, it adds a direct influence from stroke professionals otherwise not involved in committees and work groups on the guideline procedure. The discussions at the conference may also inspire new guidelines when motivated. The topics raised at the meeting are selected by the scientific programme committee mainly based on recent important scientific publications. This year's European Stroke Organisation-Karolinska Stroke Update Meeting was held in Stockholm on 11-13 November 2018. There were 11 scientific sessions discussed in the meeting including two short sessions. Each session except the short sessions produced a consensus statement (Full version with background, issues, conclusions and references are published as web-material and at www.eso-karolinska.org and http://eso-stroke.org) and recommendations which were prepared by a writing committee consisting of session chair(s), scientific secretary and speakers. These statements were presented to the 250 participants of the meeting. In the open meeting, general participants commented on the consensus statement and recommendations and the final document were adjusted based on the discussion from the general participants Recommendations (grade of evidence) were graded according to the 1998 Karolinska Stroke Update meeting with regard to the strength of evidence. Grade A Evidence: Strong support from randomised controlled trials and statistical reviews (at least one randomised controlled trial plus one statistical review). Grade B Evidence: Support from randomised controlled trials and statistical reviews (one randomised controlled trial or one statistical review). Grade C Evidence: No reasonable support from randomised controlled trials, recommendations based on small randomised and/or non-randomised controlled trials evidence.

  • 28.
    Ahmed, Niaz
    et al.
    Department of Neurology, Karolinska University Hospital, Sweden; Department of Clinical Neuroscience, Karolinska Institutet, Sweden.
    Steiner, Thorsten
    Department of Neurology, Klinikum Frankfurt Höchst, Germany; Department of Neurology Heidelberg University Hospital, Germany.
    Caso, Valeria
    Stroke Unit, University of Perugia, Italy.
    Wahlgren, Nils
    Department of Clinical Neuroscience, Karolinska Institutet, Sweden.
    Recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 13–15 November 20162017Inngår i: European Stroke Journal, ISSN 2396-9873, E-ISSN 2396-9881, Vol. 2, nr 2, s. 95-102Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    About the meeting: The purpose of the European Stroke Organisation (ESO)-Karolinska Stroke Update Conference is to provide updates on recent stroke therapy research and to give an opportunity for the participants to discuss how these results may be implemented into clinical routine. Several scientific sessions discussed in the meeting and each session produced consensus statements. The meeting started 20 years ago as Karolinska Stroke Update, but since 2014, it is a joint conference with ESO. Importantly, it provides a platform for discussion on the ESO guidelines process and on recommendations to the ESO guidelines committee on specific topics. By this, it adds a direct influence from stroke professionals otherwise not involved in committees and work groups on the guidelines procedure. The discussions at the conference may also inspire new guidelines when motivated. The topics raised at the meeting are selected by the scientific programme committee mainly based on recent important scientific publications. The ESO-Karolinska Stroke Update consensus statement and recommendations will be published every 2 years and it will work as implementation of ESO-guidelines

    Background: This year’s ESO-Karolinska Stroke Update Meeting was held in Stockholm on 13–15 November 2016. There were 10 scientific sessions discussed in the meeting and each session produced a consensus statement (Full version with background, issues, conclusions and references are published as web-material and at http://www.eso-karolinska.org/2016 and http://eso-stroke.org) and recommendations which were prepared by a writing committee consisting of session chair(s), secretary and speakers and presented to the 312 participants of the meeting. In the open meeting, general participants commented on the consensus statement and recommendations and the final document were adjusted based on the discussion from the general participants.

    Recommendations (grade of evidence) were graded according to the 1998 Karolinska Stroke Update meeting with regard to the strength of evidence. Grade A Evidence: Strong support from randomised controlled trials and statistical reviews (at least one randomised controlled trial plus one statistical review). Grade B Evidence: Support from randomised controlled trials and statistical reviews (one randomised controlled trial or one statistical review). Grade C Evidence: No reasonable support from randomised controlled trials, recommendations based on small randomised and/or non-randomised controlled trials evidence.

    Fulltekst (pdf)
    fulltext
  • 29. Aho, Leena
    et al.
    Karkola, Kari
    Juusela, Jari
    Alafuzoff, Irina
    Department of Neuroscience and Neurology, University of Kuopio Finland .
    Heavy alcohol consumption and neuropathological lesions: a post-mortem human study2009Inngår i: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 87, nr 12, s. 2786-2792Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Epidemiological studies have indicated that excessive alcohol consumption leads to cognitive impairment, but the specific pathological mechanism involved remains unknown. The present study evaluated the association between heavy alcohol intake and the neuropathological hallmark lesions of the three most common neurodegenerative disorders, i.e., Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and vascular cognitive impairment (VCI), in post-mortem human brains. The study cohort was sampled from the subjects who underwent a medicolegal autopsy during a 6-month period in 1999 and it included 54 heavy alcohol consumers and 54 age- and gender-matched control subjects. Immunohistochemical methodology was used to visualize the aggregation of beta-amyloid, hyperphosphorylated tau, and alpha-synuclein and the extent of infarcts. In the present study, no statistically significant influence was observed for alcohol consumption on the extent of neuropathological lesions encountered in the three most common degenerative disorders. Our results indicate that alcohol-related dementia differs from VCI, AD, and DLB; i.e., it has a different etiology and pathogenesis.

  • 30.
    Akel, Sarah
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för biologisk grundutbildning. Department of Clinical Neuroscience, University of Gothenburg/Sahlgrenska University Hospital.
    Evaluating Blood Biomarker Profiles in Adults with New-onset Seizures using Machine Learning2022Independent thesis Advanced level (degree of Master (Two Years)), 30 poäng / 45 hpOppgave
    Abstract [en]

    Around 1% of the population worldwide suffer from epilepsy, a condition which is characterized by recurring seizures. The development of reliable biomarkers for both prediction and targeted treatment of seizures is critical, as they can pave the way towards personalized therapy in epilepsy. In addition, sensitive biomarkers can be utilized for the detection of epilepsy in its early stages and allow for early treatment intervention. Various types of biomarkers have been studied in relation to epilepsy, with blood markers emerging as major candidates. Blood biomarkers offer the benefit of being cost and time efficient, in addition to being less invasive to sample in contrast to cerebrospinal fluid markers. Importantly, they can enhance patient diagnosis and prognosis when supplemented with other diagnostic methods, such as EEG. In this pilot study, five blood biomarkers of brain injury are studied in epilepsy, post-stroke epilepsy and single seizure patients. The aim is to analyze whether S100B, NSE, GFAP, NfL and tau are promising indicators of epilepsy after a first seizure in adults. The results present S100B as the most promising biomarker, with potential to predict early epilepsy.

    Fulltekst (pdf)
    fulltext
  • 31.
    Akerstedt, T.
    et al.
    Karolinska Inst, Clin Neurosci, Stockholm, Sweden.;Stockholm Univ, Stress Res Inst, Stockholm, Sweden..
    Lindberg, Eva
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Lungmedicin och allergologi.
    Theorell-Haglöw, Jenny
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Lungmedicin och allergologi.
    Gruber, G.
    Siesta Grp, Vienna, Austria..
    Schwarz, J.
    Stockholm Univ, Stress Res Inst, Stockholm, Sweden..
    The polysomnographical characteristics of women who have sought medical help for sleep problems - a large study of sleep macro and micro architeture2016Inngår i: Journal of Sleep Research, ISSN 0962-1105, E-ISSN 1365-2869, Vol. 25, s. 90-90Artikkel i tidsskrift (Annet vitenskapelig)
  • 32.
    Akgül, Özge
    et al.
    Izmir Democracy Univ, Fac Arts & Sci, Dept Psychol, Izmir, Turkiye..
    Fide, Ezgi
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye..
    Özel, Fatih
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Fysiologi och miljötoxikologi.
    Alptekin, Köksal
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Bora, Emre
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Akdede, Berna Binnur
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Yener, Görsev
    Dokuz Eylul Univ, Brain Dynam Multidisciplinary Res Ctr, Izmir, Turkiye.;Izmir Univ Econ, Fac Med, Dept Neurol, Izmir, Turkiye.;Dokuz Eylul Univ, Izmir Int Biomed & Genome Inst, Izmir, Turkiye.;Izmir Univ Econ, Fac Med, Dept Neurol, TR-35340 Izmir, Turkiye..
    Enhanced Punishment Responses in Patients With Schizophrenia: An Event-Related Potential Study2024Inngår i: Clinical EEG and Neuroscience, ISSN 1550-0594, E-ISSN 2169-5202, Vol. 55, nr 2, s. 219-229Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    It is well known that abnormal reward processing is a characteristic feature of various psychopathologies including schizophrenia. Reduced reward anticipation has been suggested as a core symptom of schizophrenia. The Monetary Incentive Delay Task (MID) is frequently used to detect reward anticipation. The present study aims to evaluate the amplitude and latency of event-related potential (ERP) P300 in patients with schizophrenia (SCH) compared to healthy controls during the MID task. Twenty patients with SCH and 21 demographically matched healthy controls (HC) were included in the study. ERP P300 amplitude and latency values were compared between groups using an MID task in which reward and loss cues were presented. Relations between P300 and clinical facets were investigated in the patient group. SCH group had enhanced mean P300 amplitudes and delayed peak latency in the punishment condition compared with HC. These higher responses were also associated with negative symptoms. SCH group showed altered reward processing as being more sensitive to loss of reward conditions as firstly evidenced by electrophysiological methods, possibly due to abnormality in various systems including social withdrawal, social defeat, and behavioral inhibition system.

  • 33.
    Akgül, Özge
    et al.
    Izmir Democracy Univ, Dept Psychol, Fac Arts & Sci, Izmir, Turkiye..
    Fide, Ezgi
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye..
    Özel, Fatih
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Fysiologi och miljötoxikologi.
    Alptekin, Köksal
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Bora, Emre
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Akdede, Berna Binnur
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Dokuz Eylul Univ, Fac Med, Dept Psychiat, Izmir, Turkiye..
    Yener, Görsev
    Dokuz Eylul Univ, Dept Neurosci, Izmir, Turkiye.;Izmir Univ Econ, Fac Med, Dept Anat, Izmir, Turkiye.;Izmir Int Biomed & Genome Inst, Izmir, Turkiye..
    Reduced Reward Processing in Schizophrenia: A Comprehensive EEG Event-Related Oscillation Study2024Inngår i: Brain Topography, ISSN 0896-0267, E-ISSN 1573-6792, Vol. 37, nr 1, s. 126-137Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    It is well known that abnormal reward processing is a characteristic feature of various psychopathologies including schizophrenia (SZ). Reduced reward anticipation has been suggested as a core symptom of SZ. The present study aims to evaluate the event-related oscillations (EROs) delta, theta, alpha, beta, and gamma in patients with SZ during the Monetary Incentive Delay (MID) task, which elicits the neural activity of reward processing. Twenty-one patients with SZ and twenty-two demographically matched healthy controls were included in the study. EROs were compared between groups and correlation analyses were conducted to determine a possible relationship between clinical scores and ERO values. Compared with healthy controls, the SZ group had reduced (1) delta and theta amplitudes in the reward condition (2) total beta and non-incentive cue-related beta amplitudes, and (3) incentive cue-related frontal gamma amplitudes. These reductions can be interpreted as impaired dopaminergic neurotransmission and disrupted cognitive functioning in the reward processing of SZ. In contrast, SZ patients showed higher incentive cue-related theta and occipital gamma amplitudes compared to controls. These increments may reflect negative symptoms in SZ. Moreover, theta amplitudes showed a negative correlation with Calgary Depression Scale for Schizophrenia scores and a positive correlation with attentional impulsivity. This is the first study showing the impairments of SZ patients in EROs from delta to gamma frequency bands compared with healthy controls during reward anticipation. Being the first comprehensive study, our results can be interpreted as providing evidence for disrupted brain dynamics in the reward processing of SZ studied by EROs. It may become possible to help patients' wellness by improving our understanding of reward processing in schizophrenia and developing innovative rehabilitation treatments based on these findings.

  • 34.
    Alafuzoff, Irina
    et al.
    Department of Neuroscience and Neurology, University of Kuopio Finland .
    Aho, L
    Helisalmi, S
    Mannermaa, A
    Soininen, H
    Beta-amyloid deposition in brains of subjects with diabetes2009Inngår i: Neuropathology and Applied Neurobiology, ISSN 0305-1846, E-ISSN 1365-2990, Vol. 35, nr 1, s. 60-68Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    AIM:

    A causative association between diabetes mellitus (DM) and Alzheimer's disease (AD) has been suggested based on clinical and epidemiological studies. One hypothesis is that the link between DM and AD is related to the function of insulin-degrading enzyme (IDE), an enzyme that degrades not only insulin and pancreatic amylin but also beta-amyloid (Abeta). Thus, in diabetics, insulin and Abeta might compete for IDE and this might lead to an increase in Abeta. The objective of this study was to test the hypothesis that hyperinsulinaemia can elevate Abeta levels and thus contribute to AD pathology in humans.

    METHODS:

    Neuropathological examination was carried out employing conventional and immunohistochemical (IHC) methods of the brains obtained post mortem from 701 aged subjects.

    RESULTS:

    The loads of IHC/Abeta, silver stained neuritic plaques (NP) and neurofibrillary tangles (NFT) were significantly higher in subjects carrying the Apolipoprotein E e4 allele. In contrast, the loads of Abeta, NPs and NFT in the brains were not influenced by hyperglycaemia when comparing 134 diabetic with 567 non-diabetic subjects.

    CONCLUSIONS:

    We conclude that the hypothesis that hyperinsulinaemia would significantly elevate the Abeta load and thus increase the extent of AD pathology cannot be supported. Our result challenges the claim that DM is a direct risk factor of developing AD. Thus further studies on pathological lesions in demented diabetics should be conducted.

  • 35.
    Alafuzoff, Irina
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala Univ Hosp, Dept Pathol, S-75185 Uppsala, Sweden..
    Libard, Sylwia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Neuroonkologi och neurodegeneration. Uppsala Univ Hosp, Dept Pathol, S-75185 Uppsala, Sweden..
    Ageing-Related Neurodegeneration and Cognitive Decline2024Inngår i: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 25, nr 7, artikkel-id 4065Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Neuropathological assessment was conducted on 1630 subjects, representing 5% of all the deceased that had been sent to the morgue of Uppsala University Hospital during a 15-year-long period. Among the 1630 subjects, 1610 were ≥ 41 years of age (range 41 to 102 years). Overall, hyperphosphorylated (HP) τ was observed in the brains of 98% of the 1610 subjects, and amyloid β-protein (Aβ) in the brains of 64%. The most common alteration observed was Alzheimer disease neuropathologic change (ADNC) (56%), followed by primary age-related tauopathy (PART) in 26% of the subjects. In 16% of the subjects, HPτ was limited to the locus coeruleus. In 14 subjects (<1%), no altered proteins were observed. In 3 subjects, only Aβ was observed, and in 17, HPτ was observed in a distribution other than that seen in ADNC/PART. The transactive DNA-binding protein 43 (TDP43) associated with limbic-predominant age-related TDP encephalopathy (LATE) was observed in 565 (35%) subjects and α-synuclein (αS) pathology, i.e., Lewy body disease (LBD) or multi system atrophy (MSA) was observed in the brains of 21% of the subjects. A total of 39% of subjects with ADNC, 59% of subjects with PART, and 81% of subjects with HPτ limited to the locus coeruleus lacked concomitant pathologies, i.e., LATE-NC or LBD-NC. Of the 293 (18% of the 1610 subjects) subjects with dementia, 81% exhibited a high or intermediate level of ADNC. In 84% of all individuals with dementia, various degrees of concomitant alterations were observed; i.e., MIXED-NC was a common cause of dementia. A high or intermediate level of PART was observed in 10 subjects with dementia (3%), i.e., tangle-predominant dementia. No subjects exhibited only vascular NC (VNC), but in 17 subjects, severe VNC might have contributed to cognitive decline. Age-related tau astrogliopathy (ARTAG) was observed in 37% of the 1610 subjects and in 53% of those with dementia.

    Fulltekst (pdf)
    FULLTEXT01
  • 36.
    Alafuzoff, Irina
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk och experimentell patologi.
    Libard, Sylwia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk och experimentell patologi.
    Mixed Brain Pathology Is the Most Common Cause of Cognitive Impairment in the Elderly2020Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 78, nr 1, s. 453-465Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Systemic diseases, diabetes mellitus (DM), and cardiovascular disease (CaVD) have been suggested being risk factors for cognitive impairment (CI) and/or influence Alzheimer's disease neuropathologic change (ADNC).

    Objective: The purpose was to assess the type and the extent of neuropathological alterations in the brain and to assess whether brain pathology was associated with CaVD or DM related alterations in peripheral organs, i.e., vessels, heart, and kidney.

    Methods: 119 subjects, 15% with DM and 24% with CI, age range 80 to 89 years, were chosen and neuropathological alterations were assessed applying immunohistochemistry.

    Results: Hyperphosphorylated tau (HP tau) was seen in 99%, amyloid-beta (A beta) in 71%, transactive DNA binding protein 43 (TDP43) in 62%, and alpha-synuclein (alpha S) in 21% of the subjects. Primary age related tauopathy was diagnosed in 29% (more common in females), limbic predominant age-related TDP encephalopathy in 4% (14% of subjects with CI), and dementia with Lewy bodies in 3% (14% of subjects with CI) of the subjects. High/intermediate level of ADNC was seen in 47% and the extent of HPt increased with age. The extent of ADNC was not associated with the extent of pathology observed in peripheral organs, i.e., DM or CaVD. Contrary, brain alterations such as pTDP43 and cerebrovascular lesions (CeVL) were influenced by DM, and CeVL correlated significantly with the extent of vessel pathology.

    Conclusion: In most (66%) subjects with CI, the cause of impairment was "mixed pathology", i.e., ADNC combined with TDP43, alpha S, or vascular brain lesions. Furthermore, our results suggest that systemic diseases, DMand CaVD, are risk factors for CI but not related to ADNC.

  • 37.
    Alafuzoff, Irina
    et al.
    Department of Neuroscience and Neurology, University of Kuopio Finland .
    Thal, Dietmar R.
    Arzberger, Thomas
    Bogdanovic, Nenad
    Al-Sarraj, Safa
    Bodi, Istvan
    Boluda, Susan
    Bugiani, Orso
    Duyckaerts, Charles
    Gelpi, Ellen
    Gentleman, Stephen
    Giaccone, Giorgio
    Graeber, Manuel
    Hortobagyi, Tibor
    Höftberger, Romana
    Ince, Paul
    Ironside, James W.
    Kavantzas, Nikolaos
    King, Andrew
    Korkolopoulou, Penelope
    Kovács, Gábor G.
    Meyronet, David
    Monoranu, Camelia
    Nilsson, Tatjana
    Parchi, Piero
    Patsouris, Efstratios
    Pikkarainen, Maria
    Revesz, Tamas
    Rozemuller, Annemieke
    Seilhean, Danielle
    Schulz-Schaeffer, Walter
    Streichenberger, Nathalie
    Wharton, Stephen B.
    Kretzschmar, Hans
    Assessment of beta-amyloid deposits in human brain: a study of the BrainNet Europe Consortium2009Inngår i: Acta Neuropathologica, ISSN 0001-6322, E-ISSN 1432-0533, Vol. 117, nr 3, s. 309-320Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    beta-Amyloid (A-beta) related pathology shows a range of lesions which differ both qualitatively and quantitatively. Pathologists, to date, mainly focused on the assessment of both of these aspects but attempts to correlate the findings with clinical phenotypes are not convincing. It has been recently proposed in the same way as iota and alpha synuclein related lesions, also A-beta related pathology may follow a temporal evolution, i.e. distinct phases, characterized by a step-wise involvement of different brain-regions. Twenty-six independent observers reached an 81% absolute agreement while assessing the phase of A-beta, i.e. phase 1 = deposition of A-beta exclusively in neocortex, phase 2 = additionally in allocortex, phase 3 = additionally in diencephalon, phase 4 = additionally in brainstem, and phase 5 = additionally in cerebellum. These high agreement rates were reached when at least six brain regions were evaluated. Likewise, a high agreement (93%) was reached while assessing the absence/presence of cerebral amyloid angiopathy (CAA) and the type of CAA (74%) while examining the six brain regions. Of note, most of observers failed to detect capillary CAA when it was only mild and focal and thus instead of type 1, type 2 CAA was diagnosed. In conclusion, a reliable assessment of A-beta phase and presence/absence of CAA was achieved by a total of 26 observers who examined a standardized set of blocks taken from only six anatomical regions, applying commercially available reagents and by assessing them as instructed. Thus, one may consider rating of A-beta-phases as a diagnostic tool while analyzing subjects with suspected Alzheimer's disease (AD). Because most of these blocks are currently routinely sampled by the majority of laboratories, assessment of the A-beta phase in AD is feasible even in large scale retrospective studies.

  • 38.
    Alam, Aftab
    et al.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Singh, Tanya
    Cardiff Univ, Sch Biosci, Cardiff, Wales.;Cardiff Univ, Neurosci & Mental Hlth Innovat Inst, Cardiff, Wales..
    Kayhanian, Saeed
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England.;Univ Cambridge, Cambridge Biomed Campus, Cambridge CB2 0QQ, England..
    Tjerkaski, Jonathan
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Garcia, Nuria Marco
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Carpenter, Keri L. H.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Patani, Rickie
    UCL, Inst Neurol, Queen Sq, London, England..
    Lindblad, Caroline
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Förvärvade hjärnskador. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Thelin, Eric P. P.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England.;Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden..
    Syed, Yasir Ahmed
    Cardiff Univ, Sch Biosci, Cardiff, Wales.;Cardiff Univ, Neurosci & Mental Hlth Innovat Inst, Cardiff, Wales..
    Helmy, Adel
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Modeling the Inflammatory Response of Traumatic Brain Injury Using Human Induced Pluripotent Stem Cell Derived Microglia2023Inngår i: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 40, nr 19-20, s. 2164-2173Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The neuroinflammatory response after traumatic brain injury (TBI) is implicated as a key mediator of secondary injury in both the acute and chronic periods after primary injury. Microglia are the key innate immune cell in the central nervous system, responding to injury with the release of cytokines and chemokines. In this context, we aimed to characterize the downstream cytokine response of human induced pluripotent stem cell (iPSC)-derived microglia when stimulated with five separate cytokines identified after human TBI. The iPSC-derived microglia were exposed to interleukin (IL)-1 & beta;, IL-4, IL-6, IL-10, and tumor necrosis factor (TNF) in the concentration ranges identified in clinical TBI studies. The downstream cytokine response was measured against a panel of 37 separate cytokines over a 72h time-course. The secretome revealed concentration-, time- and combined concentration and time-dependent downstream responses. TNF appeared to be the strongest inducer of downstream cytokine changes (51), followed by IL-1 & beta; (26) and IL-4 (19). IL-10 (11) and IL-6 (10) produced fewer responses. We also compare these responses with our previous studies of iPSC-derived neuronal and astrocyte cultures and the in vivo human TBI cytokine response. Notably, we found microglial culture to induce both a wider range of downstream cytokine responses and a greater fold change in concentration for those downstream responses, compared with astrocyte and neuronal cultures. In summary, we present a dataset for human microglial cytokine responses specific to the secretome found in the clinical context of TBI. This reductionist approach complements our previous datasets for astrocyte and neuronal responses and will provide a platform to enable future studies to unravel the complex neuroinflammatory network activated after TBI.

  • 39.
    Albrecht, Daniel S.
    et al.
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA..
    Forsberg, Anton
    Karolinska Inst, Dept Clin Neurosci, Ctr Psychiat Res, SE-17176 Stockholm, Sweden.;Stockholm Cty Council, SE-17176 Stockholm, Sweden..
    Sandstrom, Angelica
    Karolinska Inst, Dept Clin Neurosci, Nobels Vag 9, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, Stockholm, Sweden..
    Bergan, Courtney
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA..
    Kadetoff, Diana
    Karolinska Inst, Dept Clin Neurosci, Nobels Vag 9, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, Stockholm, Sweden.;Stockholm Spine Ctr, Stockholm, Sweden..
    Protsenko, Ekaterina
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA..
    Lampa, Jon
    Karolinska Inst, Rheumatol Unit, Dept Med, Karolinska Univ Hosp, Stockholm, Sweden..
    Lee, Yvonne C.
    Harvard Med Sch, Div Rheumatol, Brigham & Womens Hosp, Boston, MA USA.;Northwestern Univ, Div Rheumatol, Feinberg Sch Med, Chicago, IL 60611 USA..
    Hoglund, Caroline Olgart
    Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden..
    Catana, Ciprian
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA..
    Cervenka, Simon
    Karolinska Inst, Dept Clin Neurosci, Ctr Psychiat Res, SE-17176 Stockholm, Sweden.;Stockholm Cty Council, SE-17176 Stockholm, Sweden..
    Akeju, Oluwaseun
    Harvard Med Sch, Dept Anesthesia Crit Care & Pain Med, Massachusetts Gen Hosp, Boston, MA USA..
    Lekander, Mats
    Karolinska Inst, Dept Clin Neurosci, Nobels Vag 9, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, Stockholm, Sweden.;Stockholm Univ, Stress Res Inst, Stockholm, Sweden..
    Cohen, George
    Harvard Med Sch, Dept Rheumatol, Massachusetts Gen Hosp, Boston, MA USA..
    Halldin, Christer
    Karolinska Inst, Dept Clin Neurosci, Ctr Psychiat Res, SE-17176 Stockholm, Sweden.;Stockholm Cty Council, SE-17176 Stockholm, Sweden..
    Taylor, Norman
    Harvard Med Sch, Dept Anesthesia Crit Care & Pain Med, Massachusetts Gen Hosp, Boston, MA USA..
    Kim, Minhae
    Harvard Med Sch, Dept Rheumatol, Massachusetts Gen Hosp, Boston, MA USA..
    Hooker, Jacob M.
    Harvard Med Sch, Dept Rheumatol, Massachusetts Gen Hosp, Boston, MA USA..
    Edwards, Robert R.
    Harvard Med Sch, Dept Anesthesiol, Brigham & Womens Hosp, Boston, MA USA..
    Napadow, Vitaly
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA.;Harvard Med Sch, Dept Anesthesiol, Brigham & Womens Hosp, Boston, MA USA..
    Kosek, Eva
    Karolinska Inst, Dept Clin Neurosci, Nobels Vag 9, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neuroradiol, Stockholm, Sweden.;Stockholm Spine Ctr, Stockholm, Sweden..
    Loggia, Marco L.
    Harvard Med Sch, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Dept Radiol, Boston, MA USA..
    Brain glial activation in fibromyalgia: A multi-site positron emission tomography investigation2019Inngår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 75, s. 72-83Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Fibromyalgia (FM) is a poorly understood chronic condition characterized by widespread musculoskeletal pain, fatigue, and cognitive difficulties. While mounting evidence suggests a role for neuroinflammation, no study has directly provided evidence of brain glial activation in FM. In this study, we conducted a Positron Emission Tomography (PET) study using [C-11]PBR28, which binds to the translocator protein (TSPO), a protein upregulated in activated microglia and astrocytes. To enhance statistical power and generalizability, we combined datasets collected independently at two separate institutions (Massachusetts General Hospital [MGH] and Karolinska Institutet [KI]). In an attempt to disentangle the contributions of different glial cell types to FM, a smaller sample was scanned at KI with [C-11]-L-deprenyl-D2 PET, thought to primarily reflect astrocytic (but not microglial) signal. Thirty-one FM patients and 27 healthy controls (HC) were examined using [C-11]PBR28 PET. 11 FM patients and 11 HC were scanned using [C-11]-L-deprenyl-D2 PET. Standardized uptake values normalized by occipital cortex signal (SUVR) and distribution volume (V-T) were computed from the [C-11]PBR28 data. [C-11]-L-deprenyl-D2 was quantified using lambda k(3). PET imaging metrics were compared across groups, and when differing across groups, against clinical variables. Compared to HC, FM patients demonstrated widespread cortical elevations, and no decreases, in [C-11]PBR28 ITT and SUVR, most pronounced in the medial and lateral walls of the frontal and parietal lobes. No regions showed significant group differences in [C-11]-L-deprenyl-Ds signal, including those demonstrating elevated [C-11] PBR28 signal in patients (p's >= 0.53, uncorrected). The elevations in [C-11]PBR28 V-T and SUVR were correlated both spatially (i.e., were observed in overlapping regions) and, in several areas, also in terms of magnitude. In exploratory, uncorrected analyses, higher subjective ratings of fatigue in FM patients were associated with higher [C-11] PBR28 SUVR in the anterior and posterior middle cingulate cortices (p's < 0.03). SUVR was not significantly associated with any other clinical variable. Our work provides the first in vivo evidence supporting a role for glial activation in FM pathophysiology. Given that the elevations in [C-11]PBR28 signal were not also accompanied by increased [C-11]-deprenyl-D2 signal, our data suggests that microglia, but not astrocytes, may be driving the TSPO elevation in these regions. Although [C-11]-L-deprenyl-D2 signal was not found to be increased in FM patients, larger studies are needed to further assess the role of possible astrocytic contributions in FM. Overall, our data support glial modulation as a potential therapeutic strategy for FM.

    Fulltekst (pdf)
    fulltext
  • 40.
    Al-Chalabi, Ammar
    et al.
    Kings Coll London, Dept Basic & Clin Neurosci, Maurice Wohl Clin Neurosci Inst, London, England..
    Andersen, Peter M.
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden..
    Chandran, Siddharthan
    Univ Edinburgh, Edinburgh, Midlothian, Scotland..
    Chio, Adriano
    Univ Torino, ALS Ctr, Rita Levi Montalcini Dept Neurosci, Turin, Italy..
    Corcia, Philippe
    CHU Tours, Ctr Competence SLA Federat Tours Limoges, Tours, France..
    Couratier, Philippe
    CHU Limoges, Ctr Competence SLA Federat Tours Limoges, Limoges, France..
    Danielsson, Olof
    Linkoping Univ, Dept Neurol, Linkoping, Sweden.;Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden..
    de Carvalho, Mamede
    Univ Lisbon, Fac Med, Inst Phys, Inst Mol Med, Lisbon, Portugal.;H Santa Maria CHLN, Dept Neurosci & Mental Hlth, Lisbon, Portugal..
    Desnuelle, Claude
    CHU Nice, Hop Pasteur 2, Nice, France..
    Grehl, Torsten
    Alfried Krupp Hosp, Essen, Germany..
    Grosskreutz, Julian
    Jena Univ Hosp, Hans Berger Dept Neurol, Jena, Germany..
    Holmoy, Trygve
    Kershus Univ Lorenskog, Lorenskog, Norway..
    Ingre, Caroline
    Karolinska Inst, Stockholm, Sweden..
    Karlsborg, Merete
    Bispebjerg Hosp, Dept Neurol, Copenhagen, Denmark..
    Kleveland, Grethe
    Sykehuset Innlandet, Avdeling Nevrologi Klin Nevrofysiol, Lillehammer, Norway..
    Christoph Koch, Jan
    Univ Med Gottingen, Dept Neurol, Gottingen, Germany..
    Koritnik, Blaz
    Univ Med Ctr Ljubljana, Inst Clin Neurophysiol, Ljubljana, Slovenia..
    KuzmaKozakiewicz, Magdalena
    Med Univ Warsaw, Dept Neurol, Warsaw, Poland..
    Laaksovirta, Hannu
    Univ Helsinki, Cent Hosp, Helsinki, Finland..
    Ludolph, Albert
    Univ Ulm, Dept Neurol, Ulm, Germany..
    McDermott, Christopher
    Univ Sheffield, Sheffield Inst Translat Neurosci, Sheffield, S Yorkshire, England..
    Meyer, Thomas
    Univ Med Berlin, ALS Outpatient Dept, Charite, Berlin, Germany..
    Ropero, Bernardo Mitre
    Sahlgrens Univ Hosp, Gothenburg, Sweden..
    Pardina, Jesus Mora
    Hosp San Rafael, ALS Unit, Madrid, Spain..
    Nygren, Ingela
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurologi.
    Petri, Susanne
    Hannover Med Sch, Dept Neurol, Hannover, Germany..
    Povedano Panades, Monica
    Univ Bellvitge, IDIBELL, Neurol Dept Hosp, Barcelona, Spain..
    Salachas, Francois
    Hop Salptriere, Paris, France..
    Shaw, Pamela
    Univ Sheffield, Sheffield Inst Translat Neurosci, Sheffield, S Yorkshire, England..
    Silani, Vincenzo
    Univ Milan, IRCCS Ist Auxol Italiano, Dept Neurol, Stroke Unit, Milan, Italy.;Univ Milan, IRCCS Ist Auxol Italiano, Neurosci Lab, Dept Pathophysiol & Transplantat,Ctr Neurotechnol, Milan, Italy..
    Staaf, Gert
    Lund Univ, Lund, Sweden..
    Svenstrup, Kirsten
    Bispebjerg Hosp, Dept Neurol, Copenhagen, Denmark..
    Talbot, Kevin
    Univ Oxford, Nuffield Dept, Clin Neurosci, Oxford, England..
    Tysnes, Ole-Bjorn
    Haukeland Univ Sjukehus, Bergen, Norway..
    Van Damme, Philip
    Univ Leuven, KU Leuven, Dept Neurosci Expt Neurol, Leuven, Belgium.;VIB Ctr Brain & Dis Res, Leuven, Belgium.;Univ Hosp Leuven, Dept Neurol, Leuven, Belgium..
    van der Kooi, Anneke
    Univ Amsterdam Ctr, Acad Med Ctr, Dept Neurol, Amsterdam, Netherlands..
    Weber, Markus
    Kantonssp St Gallen, ALS Clin, Neuromuscular Dis Ctr, St Gallen, Switzerland..
    Weydt, Patrick
    Univ Bonn, Dept Neurodegenerat Dis & Gerontopsychiatry, Bonn, Germany..
    Wolf, Joachim
    Diakonissen Hosp, Dept Neurol, Mannheim, Germany..
    Hardiman, Orla
    Trinity Coll Dublin, Trinity Biomed Sci Inst, Acad Unit Neurol, Dublin, Ireland..
    van den Berg, Leonard H.
    Univ Med Ctr Utrecht, Brain Ctr Rudolf Magnus, Dept Neurol, Utrecht, Netherlands..
    July 2017 ENCALS statement on edaravone2017Inngår i: Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, ISSN 2167-8421, E-ISSN 2167-9223, Vol. 18, nr 7-8, s. 471-474Artikkel i tidsskrift (Annet vitenskapelig)
    Fulltekst (pdf)
    fulltext
  • 41.
    Ali, Abir
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrin Onkologi.
    Grönberg, Malin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Federspiel, B.
    Dept Pathol, Copenhagen, Denmark..
    Hjortland, G. O.
    Dept Oncol, Oslo, Norway..
    Ladekarl, M.
    Dept Oncol, Aarhus, Denmark..
    Langer, S. W.
    Dept Oncol, Copenhagen, Denmark..
    Welin, Staffan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrin Onkologi.
    Knigge, U.
    Dept Surg C, Copenhagen, Denmark.;Dept Endocrinol PE, Copenhagen, Denmark..
    Sorbye, H.
    Dept Oncol, Bergen, Norway..
    Grimelius, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Experimentell och klinisk onkologi.
    Tiensuu Janson, Eva
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrin Onkologi.
    Expression of Mutated p53 Protein in Gastroenteropancreatic Neuroendocrine Carcinoma (WHO G3)2016Inngår i: Neuroendocrinology, ISSN 0028-3835, E-ISSN 1423-0194, Vol. 103, s. 43-43Artikkel i tidsskrift (Fagfellevurdert)
  • 42.
    Ali, Zafar
    et al.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Human Molecular Genetics Laboratory, National Institute for Biotechnology and Genetic Engineering (NIBGE), PIEAS, 38000 Faisalabad, Pakistan.
    Klar, Joakim
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik.
    Jameel, Mohammad
    Human Molecular Genetics Laboratory, National Institute for Biotechnology and Genetic Engineering (NIBGE), PIEAS, 38000 Faisalabad, Pakistan.
    Khan, Kamal
    Human Molecular Genetics Laboratory, National Institute for Biotechnology and Genetic Engineering (NIBGE), PIEAS, 38000 Faisalabad, Pakistan.
    Fatima, Ambrin
    Human Molecular Genetics Laboratory, National Institute for Biotechnology and Genetic Engineering (NIBGE), PIEAS, 38000 Faisalabad, Pakistan.
    Raininko, Raili
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Baig, Shahid
    Human Molecular Genetics Laboratory, National Institute for Biotechnology and Genetic Engineering (NIBGE), PIEAS, 38000 Faisalabad, Pakistan.
    Dahl, Niklas
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik.
    Novel SACS mutations associated with intellectual disability, epilepsy and widespread supratentorial abnormalities2016Inngår i: Journal of the Neurological Sciences, ISSN 0022-510X, E-ISSN 1878-5883, Vol. 371, s. 105-111Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We describe eight subjects from two consanguineous families segregating with autosomal recessive childhood onset spastic ataxia, peripheral neuropathy and intellectual disability. The degree of intellectual disability varied from mild to severe and all four affected individuals in one family developed aggressive behavior and epilepsy. Using exome sequencing, we identified two novel truncating mutations (c.2656C>T (p.Gln886*)) and (c.4756_4760delAATCA (p.Asn1586Tyrfs*3)) in the SACS gene responsible for autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS). MRI revealed typical cerebellar and pontine changes associated with ARSACS as well as multiple supratentorial changes in both families as likely contributing factors to the cognitive symptoms. Intellectual disability and behavioral abnormalities have been reported in some cases of ARSACS but are not a part of the characteristic triad of symptoms that includes cerebellar ataxia, spasticity and peripheral neuropathy. Our combined findings bring further knowledge to the phenotypic spectrum, neurodegenerative changes and genetic variability associated with the SACS gene of clinical and diagnostic importance.

  • 43.
    Alix, James J. P.
    et al.
    Univ Sheffield, Sheffield Inst Translat Neurosci, 385A Glossop Rd, Sheffield S10 2HQ, S Yorkshire, England.
    Neuwirth, Christoph
    Kantonsspital, Neuromuscular Dis Unit ALS Clin, St Gallen, Switzerland.
    Gelder, Lucy
    Univ Sheffield, Stat Serv Unit, Sheffield, S Yorkshire, England.
    Burkhardt, Christian
    Kantonsspital, Neuromuscular Dis Unit ALS Clin, St Gallen, Switzerland.
    Castro, Jose
    Univ Lisbon, Hosp Santa Maria, Fac Med, Inst Med Mol,Dept Neurosci, Lisbon, Portugal.
    de Carvalho, Mamede
    Univ Lisbon, Hosp Santa Maria, Fac Med, Inst Med Mol,Dept Neurosci, Lisbon, Portugal.
    Gawel, Malgorzata
    Med Univ Warsaw, Dept Neurol, Warsaw, Poland.
    Goedee, Stephan
    UMC Utrecht, Dept Neurol & Neurosurg, Brain Ctr Rudolf Magnus, Utrecht, Netherlands.
    Grosskreutz, Julian
    Jena Univ Hosp, Hans Berger Dept Neurol, Jena, Germany.
    Lenglet, Timothee
    Grp Hosp Pitie Salpetriere, APHP, Dept Neurophysiol, Paris, France.
    Moglia, Cristina
    Univ Torino, ALS Ctr Torino, Dept Neurosci Rita Levi Montalcini, Turin, Italy.
    Omer, Taha
    Biomed Sci Inst TBSI, Trinity Coll, Dublin, Ireland;Beaumont Hosp, Dublin, Ireland.
    Schrooten, Maarten
    Univ Hosp Leuven, Dept Neurol, Leuven, Belgium.
    Nandedkar, Sanjeev
    Natus Med Inc, 15 Dartantra Dr, Hopewell Jct, NY 12533 USA.
    Stålberg, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Barkhaus, Paul E.
    Milwaukee Vet Adm, Med Ctr, Milwaukee, WI USA;Med Coll Wisconsin, Milwaukee, WI 53226 USA.
    Furtula, Jasna
    Aarhus Univ Hosp, Dept Clin Neurophysiol, Aarhus, Denmark.
    van Dijk, Johannes P.
    Univ Ulm, Dept Orthodont, Ulm, Germany.
    Baldinger, Reto
    Kantonsspital, Neuromuscular Dis Unit ALS Clin, St Gallen, Switzerland.
    Costa, Joao
    Univ Lisbon, Hosp Santa Maria, Fac Med, Inst Med Mol,Dept Neurosci, Lisbon, Portugal.
    Otto, Marit
    Aarhus Univ Hosp, Dept Clin Neurophysiol, Aarhus, Denmark.
    Sandberg, Arne
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Klinisk neurofysiologi.
    Weber, Markus
    Kantonsspital, Neuromuscular Dis Unit ALS Clin, St Gallen, Switzerland.
    Assessment of the reliability of the motor unit size index (MUSIX) in single subject "round-robin" and multi-centre settings2019Inngår i: Clinical Neurophysiology, ISSN 1388-2457, E-ISSN 1872-8952, Vol. 130, nr 5, s. 666-674Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: The motor unit size index (MUSIX) is incorporated into the motor unit number index (MUNIX). Our objective was to assess the intra-/inter-rater reliability of MUSIX in healthy volunteers across single subject "round robin" and multi-centre settings.

    Methods: Data were obtained from (i) a round-robin assessment in which 12 raters (6 with prior experience and 6 without) assessed six muscles (abductor pollicis brevis, abductor digiti minimi, biceps brachii, tibialis anterior, extensor digitorum brevis and abductor hallucis) and (ii) a multi-centre study with 6 centres studying the same muscles in 66 healthy volunteers. Intrafinter-rater data were provided by 5 centres, 1 centre provided only intra-rater data. Intrafinter-rater variability was assessed using the coefficient of variation (COV), Bland-Altman plots, bias and 95% limits of agreement.

    Results: In the round-robin assessment intra-rater COVs for MUSIX ranged from 7.8% to 28.4%. Inter-rater variability was between 7.8% and 16.2%. Prior experience did not impact on MUSIX values. In the multi-centre study MUSIX was more consistent than the MUNIX. Abductor hallucis was the least reliable muscle.

    Conclusions: The MUSIX is a reliable neurophysiological biomarker of reinnervation.

    Significance: MUSIX could provide insights into the pathophysiology of a range of neuromuscular disorders, providing a quantitative biomarker of reinnervation.

  • 44.
    Alm, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Blom Johansson: Logopedi.
    Streptococcal infection as a major historical cause of stuttering: data, mechanisms, and current importance2020Inngår i: Frontiers in Human Neuroscience, E-ISSN 1662-5161, Vol. 14, artikkel-id 569519Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Stuttering is one of the most well-known speech disorders, but the underlying neurological mechanisms are debated. In addition to genetic factors, there are also major non-genetic contributions. It is here proposed that infection with group A beta-hemolytic streptococcus (GAS) was a major underlying cause of stuttering until the mid-1900s when penicillin was introduced in 1943. The main mechanism proposed is an autoimmune reaction from tonsillitis, targeting specific molecules, for example within the basal ganglia. It is here also proposed that GAS infections may have continued to cause stuttering to some extent, to the present date, though more rarely. If so, early diagnosis of such cases would be of importance. Childhood cases with sudden onset of stuttering after throat infection may be particularly important to assess for possible GAS infection. The support for this hypothesis primarily comes from three lines of argument. First, medical record data from the 1930s strongly indicates that there was one type of medical event in particular that preceded the onset of childhood stuttering with unexpected frequency: diseases related to GAS throat infections. In particular, this included tonsillitis and scarlet fever, but also rheumatic fever. Rheumatic fever is a childhood autoimmune sequela of GAS infection, which was a relatively widespread medical problem until the early 1960s. Second, available reports of changes of the childhood prevalence of stuttering indicate striking parallels between stuttering and the incidence of rheumatic fever, with: (1) decline from the early 1900s; (2) marked decline from the introduction of penicillin in the mid 1940s; and (3) reaching a more stable level in the 1960s. The correlations between the data for stuttering and rheumatic fever after the introduction of penicillin are very high, at about 0.95. Third, there are established biological mechanisms linking GAS tonsillitis to immunological effects on the brain. Also, a small number of more recent case reports have provided further support for the hypothesis linking stuttering to GAS infection. Overall, it is proposed that the available data provides strong evidence for the hypothesis that GAS infection was a major cause of stuttering until the mid-1900s, interacting with genetic predisposition.

    Fulltekst (pdf)
    fulltext
  • 45.
    Alm, Per A.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Logopedi.
    Is it Thinking and not Feeling that influence variability of stuttering in social situations?: About stuttering and social cognition2015Inngår i: 10Th Oxford Dysfluency Conference, ODC 2014, 2015, s. 289-290Konferansepaper (Fagfellevurdert)
    Fulltekst (pdf)
    fulltext
  • 46.
    Alm, Per A.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Blom Johansson: Logopedi.
    Stuttering: A Disorder of Energy Supply to Neurons?2021Inngår i: Frontiers in Human Neuroscience, E-ISSN 1662-5161, Vol. 15, artikkel-id 662204Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Stuttering is a disorder characterized by intermittent loss of volitional control of speech movements. This hypothesis and theory article focuses on the proposal that stuttering may be related to an impairment of the energy supply to neurons. Findings from electroencephalography (EEG), brain imaging, genetics, and biochemistry are reviewed: (1) Analyses of the EEG spectra at rest have repeatedly reported reduced power in the beta band, which is compatible with indications of reduced metabolism. (2) Studies of the absolute level of regional cerebral blood flow (rCBF) show conflicting findings, with two studies reporting reduced rCBF in the frontal lobe, and two studies, based on a different method, reporting no group differences. This contradiction has not yet been resolved. (3) The pattern of reduction in the studies reporting reduced rCBF corresponds to the regional pattern of the glycolytic index (GI; Vaishnavi et al., 2010). High regional GI indicates high reliance on non-oxidative metabolism, i.e., glycolysis. (4) Variants of the gene ARNT2 have been associated with stuttering. This gene is primarily expressed in the brain, with a pattern roughly corresponding to the pattern of regional GI. A central function of the ARNT2 protein is to act as one part of a sensor system indicating low levels of oxygen in brain tissue and to activate appropriate responses, including activation of glycolysis. (5) It has been established that genes related to the functions of the lysosomes are implicated in some cases of stuttering. It is possible that these gene variants result in a reduced peak rate of energy supply to neurons. (6) Lastly, there are indications of interactions between the metabolic system and the dopamine system: for example, it is known that acute hypoxia results in an elevated tonic level of dopamine in the synapses. Will mild chronic limitations of energy supply also result in elevated levels of dopamine? The indications of such interaction effects suggest that the metabolic theory of stuttering should be explored in parallel with the exploration of the dopaminergic theory.

    Fulltekst (pdf)
    FULLTEXT01
  • 47.
    Alm, Per A
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Dreimanis, Karolina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Neuropathic pain: transcranial electric motor cortex stimulation using high frequency random noise: Case report of a novel treatment2013Inngår i: Journal of Pain Research, E-ISSN 1178-7090, Vol. 6, s. 479-486Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES: Electric motor cortex stimulation has been reported to be effective for many cases of neuropathic pain, in the form of epidural stimulation or transcranial direct current stimulation (tDCS). A novel technique is transcranial random noise stimulation (tRNS), which increases the cortical excitability irrespective of the orientation of the current. The aim of this study was to investigate the effect of tRNS on neuropathic pain in a small number of subjects, and in a case study explore the effects of different stimulation parameters and the long-term stability of treatment effects.

    METHODS: THE STUDY WAS DIVIDED INTO THREE PHASES: (1) a double-blind crossover study, with four subjects; (2) a double-blind extended case study with one responder; and (3) open continued treatment. The motor cortex stimulation consisted of alternating current random noise (100-600 Hz), varying from 0.5 to 10 minutes and from 50 to 1500 μA, at intervals ranging from daily to fortnightly.

    RESULTS: One out of four participants showed a strong positive effect (also compared with direct-current-sham, P = 0.006). Unexpectedly, this effect was shown to occur also for very weak (100 μA, P = 0.048) and brief (0.5 minutes, P = 0.028) stimulation. The effect was largest during the first month, but remained at a highly motivating level for the patient after 6 months.

    DISCUSSION: The study suggests that tRNS may be an effective treatment for some cases of neuropathic pain. An important result was the indication that even low levels of stimulation may have substantial effects.

    Fulltekst (pdf)
    fulltext
  • 48.
    Almqvist Téran, Nicolas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurokirurgi.
    Loayza, Richard
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurokirurgi.
    Wikström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Ericson, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurokirurgi.
    Abu Hamdeh, Sami
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurokirurgi.
    Svedung Wettervik, Teodor
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Neurokirurgi.
    Posterior Fossa Volume and Dimensions: Relation to Pathophysiology and Surgical Outcomes in Classic Trigeminal Neuralgia2023Inngår i: World Neurosurgery, ISSN 1878-8750, E-ISSN 1878-8769, Vol. 179, s. e397-e403Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: A small posterior fossa (PF) has been hypothesized to explain the increased incidence of trigeminal neuralgia (TN) in females and could make microvascular decompression (MVD) more challenging. The aim of this study was to investigate the association between the PF volume and dimensions in relation to biological sex, type of neurovascular conflict (NVC), and outcome after MVD in classic TN.

    METHODS: In this observational study, 84 patients with TN operated on with MVD with a preoperative head computed tomography(CT) scan were included. Eighty-two adults without TN who had undergone head CT for other reasons were included as controls. PF volume and dimensions (x-axis, y-axis, and z-axis) were evaluated on the CT scans. For the patients with TN, Barrow Neurological Institute (BNI) grade was evaluated 6 months after MVD.

    RESULTS: There was no difference in PF volume or dimensions between the patients with TN and controls. Women showed a smaller volume and narrower (x-axis) PF than men, but these differences did not manifest when comparing patients with TN and controls within each sex. Patients with an NVC involving the superior cerebellar artery had a narrower (x-axis) and shorter (y-axis) PF than did patients with an NVC resulting from other arteries. PF volume or dimensions were not associated with BNI grade after MVD.

    CONCLUSIONS: PF anatomy was related to the NVC type but did not differ between patients with TN and controls and was not related to the surgical outcome after MVD.

    Fulltekst (pdf)
    fulltext
  • 49.
    Alping, P.
    et al.
    Karolinska Inst, Stockholm, Sweden..
    Burman, Joachim
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurologi.
    Fink, K.
    Karolinska Inst, Stockholm, Sweden..
    Gunnarsson, M.
    Orebro Univ Hosp, Orebro, Sweden..
    Lycke, J.
    Univ Gothenburg, Gothenburg, Sweden..
    Nilsson, P.
    Lund Univ, Lund, Sweden..
    Salzer, J.
    Umea Univ, Umea, Sweden..
    Vrethem, M.
    Linkoping Univ, Linkoping, Sweden..
    Langer-Gould, A.
    Kaiser Permanente Southern Calif, Pasadena, CA USA..
    Svenningsson, A.
    Karolinska Inst, Stockholm, Sweden..
    Frisell, T.
    Karolinska Inst, Stockholm, Sweden..
    Piehl, F.
    Karolinska Inst, Stockholm, Sweden..
    Baseline characteristics from the COMBAT-MS study: Initial analyses suggest main driver for therapy choice is geographic location2017Inngår i: Multiple Sclerosis Journal, ISSN 1352-4585, E-ISSN 1477-0970, Vol. 23, s. 714-714Artikkel i tidsskrift (Annet vitenskapelig)
  • 50.
    Alping, P.
    et al.
    Danderyd Hosp, Karolinska Inst, Clin Neurosci, Stockholm, Sweden..
    Svenningsson, A.
    Danderyd Hosp, Karolinska Inst, Clin Sci, Stockholm, Sweden..
    Salzer, J.
    Umea Univ, Pharmacol & Clin Neurosci, Umea, Sweden..
    Burman, Joachim
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurologi. Uppsala Univ, Neurosci, Uppsala, Sweden..
    Dahle, C.
    Linkoping Univ, Clin & Expt Med, Linkopin, Sweden..
    Fink, K.
    Danderyd Hosp, Karolinska Inst, Clin Neurosci, Stockholm, Sweden..
    Hillert, J.
    Danderyd Hosp, Karolinska Inst, Clin Neurosci, Stockholm, Sweden..
    Lycke, J.
    Univ Gothenburg, Clin Neurosci & Rehabil, Gothenburg, Sweden..
    Landtblom, A-M
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurologi.
    Martin, C.
    Danderyd Hosp, Karolinska Inst, Clin Sci, Stockholm, Sweden..
    Nilsson, P.
    Lund Univ, Neurol, Lund, Sweden..
    Walentin, F.
    Orebro Univ Hosp, Neurol, Orebro, Sweden..
    Olsson, T.
    Danderyd Hosp, Karolinska Inst, Clin Neurosci, Stockholm, Sweden..
    Frisell, T.
    Karolinska Inst, Med Solna, Stockholm, Sweden..
    Piehl, F.
    Danderyd Hosp, Karolinska Inst, Clin Neurosci, Stockholm, Sweden..
    Rituximab in multiple sclerosis; data from the swedish MS registry.2016Inngår i: Multiple Sclerosis Journal, ISSN 1352-4585, E-ISSN 1477-0970, Vol. 22, nr suppl. 3, s. 49-49Artikkel i tidsskrift (Fagfellevurdert)
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