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61.
  • Gustafson, Lars, et al. (författare)
  • A factor analytic approach to symptom patterns in dementia.
  • 2010
  • Ingår i: International Journal of Alzheimer's Disease. - : Hindawi Limited. - 2090-0252 .- 2090-8024.
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous publications have shown a high diagnostic sensitivity and specificity of three short clinical rating scales for Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VaD) validated against neuropathological (NP) diagnoses. In this study, the aim was to perform an exploratory factor analysis of the items in these clinical rating scales. The study included 190 patients with postmortem diagnoses of AD (n = 74), VaD (n = 33), mixed AD/VaD (n = 31), or FTD (n = 52). The factor analysis produced three strong factors. Factor 1 contained items describing cerebrovascular disease, similar to the Hachinski Ischemic Score. Factor 2 enclosed major clinical characteristics of FTD, and factor 3 showed a striking similarity to the AD scale. A fourth symptom cluster was described by perception and expression of emotions. The factor analyses strongly support the construct validity of the diagnostic rating scales.
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62.
  • Gustafson, Lars, et al. (författare)
  • The Accuracy of Short Clinical Rating Scales in Neuropathologically Diagnosed Dementia.
  • 2010
  • Ingår i: The American Journal of Geriatric Psychiatry. - : Elsevier. - 1545-7214 .- 1064-7481. ; Apr 7, s. 810-820
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:: The overall aim was to evaluate to what extent the diagnosis of dementia subtypes, obtained by three clinical rating scales, concurred with postmortem neuropathologic (NP) diagnosis of Alzheimer disease (AD), frontotemporal dementia (FTD), vascular dementia (VaD) and mixed AD/VaD. DESIGN:: A prospective longitudinal clinical work-up with postmortem NP examination. PARTICIPANTS:: Two hundred nine patients with dementia referred for clinical evaluation and follow-up. METHODS:: The diagnostic scores in a set of three short clinical rating scales for AD, FTD, and VaD were evaluated against NP diagnoses. RESULTS:: The sensitivity and specificity of the AD scale were 0.80 and 0.87, respectively, of the FTD scale 0.93 and 0.92, respectively, and of the Hachinski Ischemic Score (HIS, VaD diagnosis) 0.69 and 0.92, respectively. Cases with mixed AD/VaD generally presented a combination of high AD and ischemic scores. A preferred cutoff score of six was identified for both the AD and FTD scales. CONCLUSIONS:: All three clinical rating scales showed a high sensitivity and specificity, in close agreement with final NP diagnosis-for the HIS a moderate sensitivity. These scales may thus be considered good diagnostic tools and are recommended for clinical and research center settings.
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63.
  • Hagel, Sofia, et al. (författare)
  • Trends in 21st century Health Care Utilization in a Rheumatoid Arthritis Cohort Compared to the General Population
  • 2012
  • Ingår i: Arthritis and Rheumatism. - Hoboken, NJ : John Wiley & Sons. - 0004-3591 .- 1529-0131. ; 64:S10, s. S31-S32
  • Tidskriftsartikel (refereegranskat)abstract
    • Statement of purpose: To study twenty-first century trends in health care utilization by rheumatoid arthritis (RA) patients compared to the general population. Methods: Observational cohort study; using Swedish health care register data, we identified 3977 Region Skåne residents (mean age year 2001, 62.7 years and 73% women) consulting for RA (ICD-10 codes M05 or M06) in 1998-2001. We randomly sampled two referents from the general population per RA patient matched for age, sex, and area of residence. We calculated the year 2001-2010 trends for the annual ratio (RA cohort/referents) of the mean number of hospitalizations and outpatient clinic visits. Results: By the end of the 10-year period 62% of RA patients and 74% of referents were still alive and resident in the region. From 2001 to 2010 the ratio (RA cohort/referents) of the mean number of hospitalizations for men and women decreased by 27% (p=0.01) and 28% (p=0.004), respectively. The corresponding decrease was 29% (p=0.005), and 16% (p=0.004) for outpatient physician care, 34% (p=0.009) and 18% (p=0.01) for nurse visits, and 34% (p=0.01) and 28% (p=0.004) for physiotherapy (Figure 1 and 2). Figure 1.Health care utilization during the first decade of the twenty-first century by patients in a closed rheumatoid arthritis cohort and their matched referents from the general population. The y-axes show the mean number of visits per subject per calendar year. Figure 2.Health care utilization during the first decade of the twenty-first century by patients in a closed rheumatoid arthritis cohort and their matched referents from the general population. The y-axes show the mean number of visits per subject per calendar year. Conclusions: During the twenty-first century, coinciding with increasing use of earlier and more active RA treatment including biological treatment, the overall inpatient and outpatient health care utilization by a cohort of RA patients decreased relative to the general population.
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64.
  • Hagel, Sofia, et al. (författare)
  • Trends in the first decade of 21st century healthcare utilisation in a rheumatoid arthritis cohort compared with the general population.
  • 2013
  • Ingår i: Annals of the Rheumatic Diseases. - London : BMJ Publishing Group. - 1468-2060 .- 0003-4967. ; 72:7, s. 1212-1216
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To study 21st century trends in healthcare utilisation by patients with rheumatoid arthritis (RA) compared with the general population. METHODS: Observational cohort study. Using Swedish healthcare register data, we identified 3977 Region Skåne residents (mean age in 2001, 62.7 years; 73% women) presenting with RA (International Classification of Diseases-10 codes M05 or M06) in 1998-2001. We randomly sampled two referents from the general population per RA patient matched for age, sex and area of residence. We calculated the year 2001-2010 trends for the annual ratio (RA cohort/referents) of the mean number of hospitalisations and outpatient clinic visits. RESULTS: By the end of the 10-year period, 62% of patients and 74% of referents were still alive and resident in the region. From 2001 to 2010, the ratio (RA cohort/referents) of the mean number of hospitalisations for men and women decreased by 27% (p=0.01) and 28% (p=0.004), respectively. The corresponding decrease was 29% (p=0.005) and 16% (p=0.004) for outpatient physician care, 34% (p=0.009) and 18% (p=0.01) for nurse visits, and 34% (p=0.01) and 28% (p=0.004) for physiotherapy. The absolute reduction in number of hospitalisations was from an annual mean of 0.79 to 0.69 in male patients and from 0.71 to 0.59 in female patients. The corresponding annual mean number of consultations in outpatient physician care by male and female RA patients changed from 9.2 to 7.7 and from 9.9 to 8.7, respectively. CONCLUSIONS: During the first decade of the 21st century, coinciding with increasing use of earlier and more active RA treatment including biological treatment, overall inpatient and outpatient healthcare utilisation by a cohort of patients with RA decreased relative to the general population.
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65.
  • Haglund, Mattias, et al. (författare)
  • A methodological study of locus coeruleus degeneration in dementing disorders
  • 2016
  • Ingår i: Clinical Neuropathology. - : Dustri-Verlag. - 0722-5091. ; 35:5, s. 287-294
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Degeneration of the locus coeruleus (LC) of the brain stem is a recognized phenomenon in Alzheimer's disease (AD), in dementia with Lewy bodies (DLB), and in Parkinson's disease with dementia (PDD). Prior studies have suggested that LC degeneration can be used to differentiate various dementing disorders histologically, but the paucity of methodological data may hamper systematic research on this nucleus. Purpose: The purpose of this study was to evaluate various approaches to quantifying LC degeneration in dementing disorders, and to inform future decisions regarding the most appropriate method for diagnostics and research. Methods: 105 LCs from brains of demented individuals with AD, DLB/PDD, vascular dementia (VaD), mixed dementia (AD+VaD), or frontotemporal lobar degeneration (FTLD) were examined, and the extent of LC degeneration was assessed using macroscopic evaluation, cell counting, and two degeneration scales. Scores were compared across diagnostic categories; diagnostic utility and intra- and interobserver reliability were assessed. Results: AD and DLB/PDD were associated with greater LC damage using either assessment method, significantly different from VaD and FTLD. Macroscopic appearance was informative, but cell counting was more sensitive and specific. The degeneration scales did not add significant diagnostic value over cell counting and were associated with greater observer variability. Conclusions: The LC degenerates in certain dementia subtypes, especially in AD and DLB/PDD. Macroscopic assessment of the LC postmortem can be used to differentiate between disorders associated with degeneration (AD, DLB/PDD) or sparing (VaD) of the LC, but counting LC cells in a representative pontine section is the most appropriate method by which to assess LC degeneration.
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66.
  • Haglund, Mattias, et al. (författare)
  • Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia.
  • 2006
  • Ingår i: International Journal of Geriatric Psychiatry. - : John Wiley & Sons Inc.. - 1099-1166. ; 21:7, s. 681-687
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and purpose Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. Methods We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. Results CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. Conclusions Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA. Copyright (c) 2006 John Wiley & Sons, Ltd.
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67.
  • Haglund, Mattias, et al. (författare)
  • Cerebral amyloid angiopathy, white matter lesions and Alzheimer encephalopathy - A histopathological assessment
  • 2002
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : Karger. - 1420-8008. ; 14:3, s. 161-166
  • Tidskriftsartikel (refereegranskat)abstract
    • To test the hypothesis that the cerebral amyloid angiopathy (CAA) of Alzheimer's disease (AD) is quantitatively associated with white matter lesions (WML), the brains of 63 demented patients exhibiting varying degrees of Alzheimer encephalopathy (AE) were examined, along with those of 10 nondemented control cases. The ratio of amyloid-positive to amyloid-negative vessels in the leptomeninges of the frontal pole from each patient was calculated subsequent to microscopical examination, and the severity of WML was graded according to previously published criteria. In AD cases without a significant component of vascular dementia, the level of CAA was found to correlate with the degree of WML diagnosed and graded by neuropathology. Neither age nor severity of AE correlated significantly with WML. There may be several reasons for the conflicting results of this study vis-a-vis earlier investigations; the roles played by different methods of staining, CAA quantitation and patient subgroup selection are also discussed. Copyright (C)2002 S. Karger AG, Basel.
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68.
  • Haglund, Mattias, et al. (författare)
  • Differential deposition of amyloid beta peptides in cerebral amyloid angiopathy associated with Alzheimer's disease and vascular dementia.
  • 2006
  • Ingår i: Acta Neuropathologica. - : Springer. - 1432-0533. ; 111:5, s. 430-435
  • Tidskriftsartikel (refereegranskat)abstract
    • Cerebral amyloid angiopathy (CAA) caused by deposition of amyloid beta (A beta) peptides in the cerebrovasculature, involves degeneration of normal vascular components and increases the risk of infarction and cerebral hemorrhage. Accumulating evidence suggests that sporadic CAA is also a significant contributor to cognitive decline and dementia in the elderly. However, the mechanisms by which CAA arises are poorly understood. While neuronal sources of A beta peptides are sufficient to cause CAA in transgenic mice overexpressing the amyloid precursor protein, there is reason to believe that in aging man, vascular disease modulates the disease process. To better understand CAA mechanisms in dementia, we assessed the frontal cortex of 62 consecutive cases of Alzheimer's disease (AD), vascular dementia (VaD), and mixed dementia (MD) using immunohistochemistry with antibodies to A beta, smooth muscle actin and the carboxyl-terminal peptides to detect A beta(40) and A beta(42). While vascular A beta deposition was invariably associated with smooth muscle degeneration as indicated by absence of smooth muscle cell actin reactivity, VaD/MD cases exhibited markedly more vascular A beta(42) deposits and smooth muscle actin loss compared to AD cases with similar degrees of CAA and A beta(40) deposition. This suggests that distinct mechanisms are responsible for the differential deposition of A beta in CAA associated with AD and that associated with ischemic/cerebrovascular disease. It is plausible that experimental studies on the effects of cerebrovascular disease on A beta production and elimination will yield important clues on the pathogenesis of CAA.
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69.
  • Haglund, Mattias, et al. (författare)
  • Hippocampus and basal ganglia as potential sentinel sites for ischemic pathology after resuscitated cardiac arrest
  • 2019
  • Ingår i: Resuscitation. - : Elsevier. - 0300-9572. ; 139, s. 230-233
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims of the study: Neurological impairment after resuscitated cardiac arrest (CA) remains a significant unmet medical need. Brain ischemia associated with CA and subsequent reperfusion is evident as two fundamentally different types of damage on neuropathological examination: frank necrosis (involving all cell types) and selective eosinophilic neuronal death (SEND). These types of damage are not only dissimilar in micromorphology, but also differently detectable with clinical brain imaging methods. In a previous study, SEND was reported in most patients surviving the initial CA. This study was undertaken to further characterize and map SEND in an expanded dataset. Methods: A cohort of 46 cases was included from an observational study on targeted temperature management (TTM) of resuscitated CA. Six brain and brain stem regions and 21 subregions were examined, and SEND severity was tested for correlation with time to ROSC. Representativity of all regions vis-à-vis global SEND was assessed, to investigate whether any particular region could be used as a “sentinel site” for overall damage. Results: The thalamus, the CA4 subregion of the hippocampus and the Purkinje cell layer of the cerebellum were the most severely affected subregions. Involvement of the hippocampus, cerebellum, cortex or basal ganglia indicated presence of SEND in other regions. There was a significant correlation between time to ROSC and SEND. Conclusion: There are regional differences in SEND distribution. Cases free of SEND in the hippocampus or basal ganglia are unlikely to have significant SEND in other regions, suggesting that these regions could be used as “sentinel sites” for global SEND in future studies.
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70.
  • Haglund, Mattias, et al. (författare)
  • Locus ceruleus degeneration is ubiquitous in Alzheimer's disease: possible implications for diagnosis and treatment.
  • 2006
  • Ingår i: Neuropathology. - : Wiley-Blackwell. - 0919-6544. ; 26:6, s. 528-532
  • Tidskriftsartikel (refereegranskat)abstract
    • Degeneration of the locus ceruleus (LC) and decreased cortical levels of norepinephrine are common findings in Alzheimer's disease (AD), but their significance is unknown. Because the noradrenergic system is accessible to pharmacological intervention, the role of LC degeneration and noradrenergic dysfunction in the pathogenesis and clinical manifestations of AD needs clarification. Hypothetically, loss of noradrenergic innervation could cause microvascular dysfunction and manifest as ischemia. The objectives of this study were to develop a scale for assessment of LC degeneration and to determine whether degeneration of the LC correlates quantitatively with either duration of clinical dementia, overall severity of AD pathology or with measures of ischemic non-focal white matter disease (WMD) in AD. This report is a pathological follow-up of a clinical longitudinal dementia study of 66 consecutive cases of AD without admixture of vascular dementia (VaD) from the Lund Longitudinal Dementia Study, neuropathologically diagnosed between 1990 and 1999. Ten cases of VaD were included for comparative purposes. No correlation between degree of LC degeneration and duration of dementia, AD or WMD severity was found. LC degeneration was significantly more severe in the AD group than in the VaD group. Even though LC degeneration was not associated with WMD or the severity of AD pathology in this AD material, we suggest that clinical studies on the consequences of noradrenergic dysfunction are warranted. Treatment augmenting noradrenergic signaling is available and safe. The marked difference in the level of LC degeneration between AD and VaD cases suggests that LC degeneration could be used as a diagnostic marker of AD.
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