Leonard H van den Berg

University Medical Center Utrecht, Utrecht, Utrecht, Netherlands

Are you Leonard H van den Berg?

Claim your profile

Publications (420)2797.24 Total impact

  • Ruben P A van Eijk · Leonard H van den Berg

    No preview · Article · Jan 2016 · Neurology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The purported migrations that have formed the peoples of Britain have been the focus of generations of scholarly controversy. However, this has not benefited from direct analyses of ancient genomes. Here we report nine ancient genomes (∼1 ×) of individuals from northern Britain: seven from a Roman era York cemetery, bookended by earlier Iron-Age and later Anglo-Saxon burials. Six of the Roman genomes show affinity with modern British Celtic populations, particularly Welsh, but significantly diverge from populations from Yorkshire and other eastern English samples. They also show similarity with the earlier Iron-Age genome, suggesting population continuity, but differ from the later Anglo-Saxon genome. This pattern concords with profound impact of migrations in the Anglo-Saxon period. Strikingly, one Roman skeleton shows a clear signal of exogenous origin, with affinities pointing towards the Middle East, confirming the cosmopolitan character of the Empire, even at its northernmost fringes.
    Full-text · Article · Jan 2016 · Nature Communications
  • [Show abstract] [Hide abstract]
    ABSTRACT: Polyneuropathy associated with IgM monoclonal gammopathy (IgM-PNP) is a slowly progressive, sensorimotor neuropathy. It is assumed that complement activation contributes to IgM-PNP pathogenesis. We investigated whether innate differences in complement activity of the classical and mannose binding lectin (MBL) pathways are associated with IgM-PNP or its severity. We measured complement activity using ELISA and determinedMBL serumconcentrations andMBL gene polymorphisms in 83 patients and 83 healthy controls. We did not observe differences between IgM-PNP patients and healthy controls nor associations with different disease severities. Differences in innate complement activity are not likely to explain susceptibility to or severity of IgM-PNP.
    No preview · Article · Jan 2016
  • [Show abstract] [Hide abstract]
    ABSTRACT: Microglia are the resident mononuclear phagocytes of the central nervous system and have been implicated in the pathogenesis of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). During neurodegeneration, microglial activation is accompanied by infiltration of circulating monocytes, leading to production of multiple inflammatory mediators in the spinal cord. Degenerative alterations in mononuclear phagocytes are commonly observed during neurodegenerative diseases, yet little is known concerning the mechanisms leading to their degeneration, or the consequences on disease progression. Here we observed that the serotonin 2B receptor (5-HT2B), a serotonin receptor expressed in microglia, is upregulated in the spinal cord of three different transgenic mouse models of ALS. In mutant SOD1 mice, this upregulation was restricted to cells positive for CD11b, a marker of mononuclear phagocytes. Ablation of 5-HT2B receptor in transgenic ALS mice expressing mutant SOD1 resulted in increased degeneration of mononuclear phagocytes, as evidenced by fragmentation of Iba1-positive cellular processes. This was accompanied by decreased expression of key neuroinflammatory genes but also loss of expression of homeostatic microglial genes. Importantly, the dramatic effect of 5-HT2B receptor ablation on mononuclear phagocytes was associated with acceleration of disease progression. To determine the translational relevance of these results, we studied polymorphisms in the human HTR2B gene, which encodes the 5-HT2B receptor, in a large cohort of ALS patients. In this cohort, the C allele of SNP rs10199752 in HTR2B was associated with longer survival. Moreover, patients carrying one copy of the C allele of SNP rs10199752 showed increased 5-HT2B mRNA in spinal cord and displayed less pronounced degeneration of Iba1 positive cells than patients carrying two copies of the more common A allele. Thus, the 5-HT2B receptor limits degeneration of spinal cord mononuclear phagocytes, most likely microglia, and slows disease progression in ALS. Targeting this receptor might be therapeutically useful.
    No preview · Article · Jan 2016 · Acta Neuropathologica
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sporadic ALS is considered to be a complex disease with multiple genetic risk factors contributing to the pathogenesis. Identification of genetic risk factors that co-occur frequently could provide relevant insight into underlying mechanisms of motor neuron degeneration. To dissect the genetic architecture of sporadic ALS we undertook a large sequencing study in 755 apparently sporadic ALS cases and 959 controls, analyzing ten ALS genes: SOD1, C9orf72, TARDBP, FUS, ANG, CHMP2B, ATXN2, NIPA1, SMN1 and UNC13A. We observed sporadic cases with multiple genetic risk variants in 4.1% compared to 1.3% in controls. The overall difference was not in excess of what is to be expected by chance (binomial test, P = 0.59). We did however observe a higher frequency than expected of C9orf72 repeat carriers with co-occurring susceptibility variants (ATXN2, NIPA1, SMN1; P = 0.001), which is mainly due to the co-occurrence of NIPA1 repeats in 15% of C9orf72 repeat carriers (P = 0.006).
    No preview · Article · Dec 2015 · Neurobiology of aging
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: To investigate possible effects of the C9orf72 repeat expansion before disease onset, we assessed brain morphology in asymptomatic carriers. Methods: Aiming to diminish the effects of genetic variation between subjects, apart from the C9orf72 repeat expansion, 16 carriers of the repeat expansion were compared with 23 noncarriers from the same large family with a history of amyotrophic lateral sclerosis (ALS). Cortical thickness, subcortical volumes, and white matter connectivity, as assessed from high-resolution T1-weighted and diffusion-weighted MRIs, were evaluated. For comparison, we included 14 C9orf72 carriers with ALS and 28 healthy, unrelated controls. Results: We found temporal, parietal, and occipital regions to be thinner (p < 0.05) and the left caudate and putamen to be smaller (p < 0.05) in asymptomatic carriers compared with noncarriers. Cortical thinning of the primary motor cortex and decreased connectivity of white matter pathways (global, corticospinal tract, and corpus callosum) were observed in patients with C9orf72-associated ALS, but not in asymptomatic carriers. Conclusions: Asymptomatic C9orf72 carriers show cortical and subcortical differences compared with noncarriers from the same family, possibly effects of the C9orf72 repeat expansion on the brain. Of note, changes in the primary motor regions and motor-related tracts were found exclusively in patients with ALS, indicating that such motor changes may be a disease phenomenon.
    No preview · Article · Oct 2015 · Neurology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Across-nation differences in the mean values for complex traits are common, but the reasons for these differences are unknown. Here we find that many independent loci contribute to population genetic differences in height and body mass index (BMI) in 9,416 individuals across 14 European countries. Using discovery data on over 250,000 individuals and unbiased effect size estimates from 17,500 sibling pairs, we estimate that 24% (95% credible interval (CI) = 9%, 41%) and 8% (95% CI = 4%, 16%) of the captured additive genetic variance for height and BMI, respectively, reflect population genetic differences. Population genetic divergence differed significantly from that in a null model (height, P < 3.94 × 10(-8); BMI, P < 5.95 × 10(-4)), and we find an among-population genetic correlation for tall and slender individuals (r = -0.80, 95% CI = -0.95, -0.60), consistent with correlated selection for both phenotypes. Observed differences in height among populations reflected the predicted genetic means (r = 0.51; P < 0.001), but environmental differences across Europe masked genetic differentiation for BMI (P < 0.58).
    No preview · Article · Sep 2015 · Nature Genetics
  • Huub Creemers · Sandra de Morée · Jan H Veldink · Frans Nollet · Leonard H van den Berg · Anita Beelen
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective To examine the longitudinal associations between caregiver strain and patients’ clinical and psychosocial characteristics as well as caregivers’ psychosocial characteristics. Methods At 4-month intervals during the 12 months study period, longitudinal data on caregiver strain and patient and caregiver factors potentially associated with caregiver strain were collected from 126 couples, who participated in a randomised controlled trial on the effectiveness of case management in amyotrophic lateral sclerosis (ALS). Caregiver strain was assessed with the Caregiver Strain Index (CSI). Patient and caregiver factors included sociodemographic characteristics, distress, coping style and perceived quality of care, as well as the patient's functional status and emotional functioning. Multilevel regression analyses were performed. Results Caregiver strain increased significantly during the study period (β=0.315 points/months, p<0.001) and was significantly associated with patient time-dependent factors functional status (β=−0.131 points/months, p<0.001) and emotional functioning (β=0.022 points/months, p=0.03), and caregiver time-dependent factors passive coping style (β=0.152 points/months, p=0.03), symptoms of anxiety (β=0.186 points/months, p<0.001) and perceived quality of care for the caregiver (β=−0.452 points/months, p<0.001). Conclusions Our study has identified that apart from the patient's physical disability and emotional well-being, a passive coping style of the caregiver, increased symptoms of anxiety and feeling less supported by the ALS-team impact on caregiver strain. The multidisciplinary teams involved with the care of patients with ALS need to be aware of these factors and increase their attention for the caregiver. This will help guide the development of evidence-based supportive interventions that focus on caregiver's coping style and avoiding distress. Trial registration number Netherlands Trial Register, number NTR1270.
    No preview · Article · Sep 2015 · Journal of neurology, neurosurgery, and psychiatry
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The topological structure of the wiring of the mammalian brain cortex plays an important role in shaping the functional dynamics of large-scale neural activity. Due to their central embedding in the network, high degree hub regions and their connections (often referred to as the 'rich club') have been hypothesized to facilitate intermodular neural communication and global integration of information by means of synchronization. Here, we examined the theoretical role of anatomical hubs and their wiring in brain dynamics. The Kuramoto model was used to simulate interaction of cortical brain areas by means of coupled phase oscillators-with anatomical connections between regions derived from diffusion weighted imaging and module assignment of brain regions based on empirically determined resting-state data. Our findings show that synchrony among hub nodes was higher than any module's intramodular synchrony (p < 10(-4), for cortical coupling strengths, λ, in the range 0.02 < λ < 0.05), suggesting that hub nodes lead the functional modules in the process of synchronization. Furthermore, suppressing structural connectivity among hub nodes resulted in an elevated modular state (p < 4.1 × l0(-3), 0.015 < λ < 0.04), indicating that hub-to-hub connections are critical in intermodular synchronization. Finally, perturbing the oscillatory behavior of hub nodes prevented functional modules from synchronizing, implying that synchronization of functional modules is dependent on the hub nodes' behavior. Our results converge on anatomical hubs having a leading role in intermodular synchronization and integration in the human brain.
    Preview · Article · Sep 2015 · BMC Neuroscience
  • [Show abstract] [Hide abstract]
    ABSTRACT: Clinical trials in MMN have often used ordinal-based measures that may not accurately capture changes. We aimed to construct a disability interval outcome measure specifically for MMN using the Rasch model and to examine its clinimetric properties. A total of 146 preliminary activity and participation items were assessed twice (reliability studies) in 96 clinically stable MMN patients. These patients also assessed the ordinal-based overall-disability sum-score (construct, sample-dependent validity). The final Rasch-built overall-disability scale for MMN (MMN-RODS(©) ) was serially applied in 26 patients with newly diagnosed or relapsing MMN, treated with IVIg (1-year follow-up; responsiveness study). The magnitude of change for each patient was calculated using the minimum-clinically-important-difference technique related to the individually obtained standard errors. A total of 121 items not fulfilling Rasch requirements were removed. The final 25-item MMN-RODS(©) fulfilled all Rasch model's expectations and showed acceptable reliability and validity including good discriminatory capacity. Most serially examined patients improved, but its magnitude was low, reflecting poor responsiveness. The constructed MMN-RODS(©) is a disease-specific, interval measure to detect activity limitations in patients with MMN and overcomes the shortcomings of ordinal scales. However, future clinimetric studies are needed to improve the MMN-RODS(©) 's responsiveness by longer observations and/or more rigorous treatment regimens. This article is protected by copyright. All rights reserved.
    No preview · Article · Aug 2015 · Journal of the Peripheral Nervous System
  • [Show abstract] [Hide abstract]
    ABSTRACT: Because dietary intake may influence pathophysiologic mechanisms in sporadic amyotrophic lateral sclerosis (ALS), the association between premorbid dietary intake and the risk of sporadic ALS will provide insight into which mechanisms are possibly involved in ALS pathophogenesis. To systematically determine the association between premorbid dietary intake and the risk of sporadic ALS. A population-based case-control study was conducted in a general community setting in the Netherlands from January 1, 2006, to September 30, 2011. Analysis was conducted April 1, 2013, to November 15, 2014. All patients with a new diagnosis of possible, probable (laboratory supported), or definite ALS according to the revised El Escorial criteria were included and multiple sources were used to ensure complete case ascertainment. Of 986 eligible patients, 674 gave informed consent and returned a complete questionnaire; 2093 controls randomly selected from the general practitioners' registers and frequency matched to the patients for sex and age were included. We studied the premorbid intake of nutrients in association with the risk of ALS by using a 199-item food frequency questionnaire adjusted for confounding factors and corrected for multiple comparisons while minimizing recall bias. Presymptomatic total daily energy intake in patients, reported as mean (SD), was significantly higher compared with controls (2258 [730] vs 2119 [619] kcal/day; P < .01), and presymptomatic body mass index (calculated as weight in kilograms divided by height in meters squared) was significantly lower in patients (25.7 [4.0] vs 26.0 [3.7]; P = .02). With values reported as odds ratio (95% CI), higher premorbid intake of total fat (1.14; 1.07-1.23; P < .001), saturated fat (1.43; 1.25-1.64; P < .001), trans-fatty acids (1.03; 1.01-1.05; P < .001), and cholesterol (1.08; 1.05-1.12; P < .001) was associated with an increased risk of ALS; higher intake of alcohol (0.91; 0.84-0.99; P = .03) was associated with a decreased risk of ALS. These associations were independent of total energy intake, age, sex, body mass index, educational level, smoking, and lifetime physical activity. No significant associations between dietary intake and survival were found. The combination of independent positive associations of a low premorbid body mass index and a high fat intake together with prior evidence from ALS mouse models transgenic for SOD1 and earlier reports on premorbid body mass index support a role for increased resting energy expenditure before clinical onset of ALS.
    No preview · Article · Aug 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Case-control studies have reported multiple genetic loci to be associated with sporadic brain arteriovenous malformations (AVMs) but most of these have not been replicated in independent populations. The aim of this study was to find additional evidence for these reported associations and perform a meta-analysis including all previously published results. We included 167 Dutch patients and 1038 Dutch controls. Case genotyping was performed by KASPar assays. Controls had been previously genotyped with a genome wide single nucleotide polymorphisms (SNP) array. Differences in genotype frequencies between cases and controls were estimated by χ(2) testing in Plink V.1.07. Meta-analysis was performed in RevMan V.5.3. In our case-control study we found no significant association with brain AVM (BAVM) for previously discovered SNPs near ANGPTL4, IL-1β, GPR124, VEGFA and MMP-3. The meta-analysis revealed a statistically significant association with BAVMs for the polymorphism rs11672433 near ANGPTL4 (OR 1.39; 95% CI 1.10 to 1.75, p value 0.005). The results of this study support a role for the previously identified SNP near ANGPTL4 in the pathogenesis of AVMs. Previously found associations with SNPs near IL-1β, GPR124, VEGFA and MMP-3 genes could not be substantiated in our replication cohort or in the meta-analysis. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    No preview · Article · Aug 2015 · Journal of neurology, neurosurgery, and psychiatry
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study aimed to "define responder" through the concept of minimum clinically important differences using the individually obtained standard-errors (MCID-SE) and a heuristic "external criterion" responsiveness method in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). One hundred and fourteen newly diagnosed or relapsing patients (GBS: 55, CIDP: 59) were serially examined (1-year follow-up). The inflammatory-Rasch-built overall disability scale (I-RODS), Rasch-transformed MRC sum-score (RT-MRC), and Rasch-transformed modified-INCAT-sensory scale (RT-mISS) were assessed. Being a responder was defined having a MCID-SE cut-off≥1.96. Also, the correlations between patients' scores on each scale and the EuroQoL health-status "thermometer" (external criterion) were determined (higher correlation indicated better responsiveness). In both diseases, the SEs showed a characteristic "U"-shaped dynamic pattern across each scales' continuum. The number of patients showing a meaningful change were higher for the I-RODS > RT-MRC > RT-mISS and were in GBS higher than CIDP patients. The MCID-SE concept using Rasch-transformed data demonstrated an individual pattern of 'being-a-responder' in patients with immune-mediated neuropathies and the findings were validated by the external criterion responsiveness method. The I-RODS showed greater responsiveness compared to the MRC and INCAT sensory scales and its use is therefore recommended in future trials in GBS and CIDP.
    No preview · Article · Jun 2015 · Journal of the Peripheral Nervous System
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate whether high innate activity of the classical and lectin pathways of complement is associated with multifocal motor neuropathy (MMN) and whether levels of innate complement activity or the potential of anti-GM1 antibodies to activate the complement system correlate with disease severity. We performed a case-control study including 79 patients with MMN and 79 matched healthy controls. Muscle weakness was documented with Medical Research Council scale sum score and axonal loss with nerve conduction studies. Activity of the classical and lectin pathways of complement was assessed by ELISA. We also determined serum mannose-binding lectin (MBL) concentrations and polymorphisms in the MBL gene (MBL2) and quantified complement-activating properties of anti-GM1 IgM antibodies by ELISA. Activity of the classical and lectin pathways, MBL2 genotypes, and serum MBL concentrations did not differ between patients and controls. Complement activation by anti-GM1 IgM antibodies was exclusively mediated through the classical pathway and correlated with antibody titers (p < 0.001). Logistic regression analysis showed that both high innate activity of the classical pathway of complement and high complement-activating capacity of anti-GM1 IgM antibodies were significantly associated with more severe muscle weakness and axonal loss. High innate activity of the classical pathway of complement and efficient complement-activating properties of anti-GM1 IgM antibodies are determinants of disease severity in patients with MMN. These findings underline the importance of anti-GM1 antibody-mediated complement activation in the pathogenesis and clinical course of MMN.
    Full-text · Article · Jun 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: The objectives of the current study were to provide an overview of the outcome measures (OMs) applied in clinical trials in MMN and to determine the responsiveness of a core set of selected OMs as part of the PeriNomS study. The following OMs were serially applied in 26 patients with newly diagnosed or relapsing MMN, receiving intravenous-immunoglobulin (assessments: T0/T3/T12 months): 14 muscle-pairs MRC scale, the Neuropathy-Impairment-Scale motor-subset, a self-evaluation scale, grip strength, and MMN-RODS(©) . All data, except the grip strength, were subjected to Rasch analyses before determining responsiveness. For grip strength, responsiveness was examined using a combined anchor- (SF-36 question-2) and distribution-based (½xSD) minimum clinically important difference (MCID) techniques, determining the proportion of patients exceeding both identified cut-offs. For the remaining scales, the magnitude of change for each patient on each scale was determined using the MCID related to the individual standard errors (responder definition: MCID-SE≥1.96). Overall, a great assortment of measures has been used in MMN trials with different responsiveness definitions. For the selected OMs, responsiveness was poor and only seen in 1/4-1/3 of the patients, the grip strength being more responsive. Despite the efforts taken to standardize outcome assessment, further clinimetric responsiveness studies are needed in MMN. This article is protected by copyright. All rights reserved.
    No preview · Article · Jun 2015 · Journal of the Peripheral Nervous System
  • L. Vlam · M. Stam · W. de Jager · E.A. Cats · L H van den Berg · W L van der Pol
    [Show abstract] [Hide abstract]
    ABSTRACT: Multifocal motor neuropathy (MMN) and progressive muscular atrophy (PMA) are associated with IgM monoclonal gammopathy or the presence IgM anti-GM1-antibodies. To further investigate the pathophysiology of MMN and PMA we determined concentrations of 16 mainly B-cell associated inflammatory markers in serum from 25 patients with MMN, 55 patients with PMA, 25 patients with amyotrophic lateral sclerosis (ALS) and 50 healthy controls. Median serum concentrations of the 16 tested cytokines and chemokines were not significantly increased in patients with MMN or patients with PMA, irrespective of the presence of IgM monoclonal gammopathy or high IgM anti-GM1 antibodies. These results argue against a systemic B-cell mediated immune response underlying the pathogenesis of MMN and PMA. Copyright © 2015. Published by Elsevier B.V.
    No preview · Article · Jun 2015 · Journal of neuroimmunology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Our objective was to compare the effects of cognitive behavioural therapy (CBT) and usual care (UC) on quality of life (QoL) in psychologically distressed patients with ALS and their caregivers. We conducted a multicentre randomized controlled trial (RCT). In 16 weeks, patient-carer pairs received five to 10 CBT sessions plus usual care (UC) or UC alone. Outcome measures were SF-36 Mental Component Summary (MCS), ALSAQ-40 Emotional Functioning (EF), Hospital Anxiety and Depression Scale (HADS) and Caregiver Strain Index (CSI). Assessments took place at baseline, four, seven and 10 months. The steering committee decided to stop the trial prematurely and analyse the data due to: 1) slow recruitment (15 patients over 42 months); and 2) the low demand for joint patient-carer CBT sessions. Caregivers, however, expressed an unanticipated demand for individual psychological support. Patients’ ALSAQ-40-EF and caregivers’ SF-36-MCS were significantly better in CBT than UC (p < 0.05). CSI was significantly lower in the CBT than the UC (p < 0.05). In conclusion, CBT might be beneficial to patients and caregivers. The stringent eligibility criteria limited participation rate and consequently the generalizability of results. Future studies should further examine the impact of CBT interventions for patients with ALS and their caregivers.
    Full-text · Article · Jun 2015 · Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: How hexanucleotide (GGGGCC) repeat expansions in C9ORF72 cause amyotrophic lateral sclerosis (ALS) remains poorly understood. Both gain- and loss-of-function mechanisms have been proposed. Evidence supporting these mechanisms in vivo is, however, incomplete. Here we determined the effect of C9orf72 loss-of-function in mice. We generated and analyzed a conditional C9orf72 knockout mouse model. C9orf72(fl/fl) mice were crossed with Nestin-Cre mice to selectively remove C9orf72 from neurons and glial cells. Immunohistochemistry was performed to study motor neurons and neuromuscular integrity, as well as several pathological hallmarks of ALS, such as gliosis and TDP-43 mislocalization. In addition, motor function and survival were assessed. Neural-specific ablation of C9orf72 in conditional C9orf72 knockout mice resulted in significantly reduced body weight but did not induce motor neuron degeneration, defects in motor function, or altered survival. Our data suggest that C9orf72 loss-of-function, by itself, is insufficient to cause motor neuron disease. These results may have important implications for the development of therapeutic strategies for C9orf72-associated ALS. This article is protected by copyright. All rights reserved. © 2015 American Neurological Association.
    Full-text · Article · Jun 2015 · Annals of Neurology

  • No preview · Conference Paper · Jun 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: The Jamar dynamometer and Vigorimeter have been used to assess grip strength in immune-mediated neuropathies, but have never been compared with each other. Therefore, we performed a comparison study between these two devices in patients with immune-mediated neuropathies. Grip strength data were collected in 102 cross-sectional stable and 163 longitudinal (new diagnoses or changing condition) patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), gammopathy-related polyneuropathy (MGUSP), and multifocal motor neuropathy (MMN). Stable patients were assessed twice (validity/reliability studies). Longitudinal patients were assessed 3–5 times during one year. Responsiveness comparison between the two tools was examined using combined anchor-/distribution-based minimum clinically important difference (MCID) techniques. Patients were asked to indicate their preference for the Jamar or Vigorimeter. Both tools correlated highly with each other (ρ=0.86, p<0.0001) and demonstrated good intra-class correlation coefficients (Jamar [Right/Left hands]: ICC 0.997/0.96; Vigori: ICC 0.95/0.98). Meaningful changes were comparable between the two instruments, being higher in GBS compared to CIDP patients. In MGUSP/MMN poor responsiveness was seen. Significant more patients preferred the Vigorimeter. In conclusion, validity, reliability and responsiveness aspects were comparable between the Jamar dynamometer and Vigorimeter. However, based on patients’ preference, the Vigorimeter is recommended in future studies in immune-mediated neuropathies.
    No preview · Article · Jun 2015 · Journal of the Peripheral Nervous System

Publication Stats

13k Citations
2,797.24 Total Impact Points

Institutions

  • 1997-2016
    • University Medical Center Utrecht
      • • Department of Neurology
      • • Department of Neurosurgery
      Utrecht, Utrecht, Netherlands
  • 2014
    • Pfizer Inc.
      New York, New York, United States
  • 2009-2013
    • Netherlands Institute for Neuroscience
      Amsterdamo, North Holland, Netherlands
  • 1993-2012
    • Utrecht University
      • • Rudolf Magnus Institute
      • • Department of Neurology
      Utrecht, Utrecht, Netherlands
  • 2011
    • Mario Negri Institute for Pharmacological Research
      • Laboratory of Neurological Disorders
      Milano, Lombardy, Italy
  • 2003
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 1991-1992
    • Columbia University
      • Department of Neurology
      New York City, New York, United States