Doctrina Parot. Cobertura mediática en periódicos españoles

Treballs Finals de Grau de Criminologia, Facultat de Dret, Universitat de Barcelona, Curs: 2013-2014, Tutor: Dr. Santiago Redondo IllescasEsta investigación se centra en el tratamiento mediático que se ha producido como consecuencia de la derogación de la Doctrina Parot. Se han analizado veinte noticias de los dos periódicos más leídos en España: diez de El Mundo y diez de El País, ambos en su formato digital. El objetivo de este estudio es observar si asocian el fenómeno a valores positivos, negativos o si, en cambio, exponen la información de forma objetiva. También se ha analizado el posicionamiento ideológico acerca de la derogación. Los resultados indican un dominio de información objetiva por parte de ambos periódicos. No obstante, en los casos en que no es así, El País asocia el fenómeno a valores positivos mientras que El Mundo lo hace a valores negativos. Por último, El País se posiciona a favor de la derogación de la Doctrina Parot mientras que El Mundo lo hace en contra

Temporal distribution of sleep onset REM periods and N3 sleep in the MSLT and night polysomnogram of narcolepsy type 1 and other hypersomnias

The presence of $>\geq$2 sleep onset REM periods (SOREMP) in the Multiple Sleep Latency Test (MSLT) and the previous night polysomnogram (PSG) is part of the diagnostic criteria of narcolepsy, with every SOREMP having the same diagnostic value, despite evidence suggesting that time of SOREMP appearance and their preceding sleep stage might be relevant. We studied the temporal distribution of SOREMPs and associated sleep stages in the MSLT of patients with narcolepsy type 1 (NT1) and other hypersomnias (OH).We reviewed consecutive five-nap MSLTs and their preceding PSG from 83 untreated adult patients with hypersomnolence and ?1 SOREMPs. Wake/N1(W/N1)-SOREMPs, N2-SOREMPs, and N3 sleep presence and time of appearance were analyzed.Thirty-nine patients had NT1 and 44 OH. There were 183 (78%) SOREMPs in patients with NT1 and 83 (31%) in OH. Sixty-seven percent of SOREMPs in NT1 were from W/N1, and 20% -none from wake-in OH (p < 0.001). Most patients (94%) with ?2 W/N1-SOREMPs had NT1 (specificity 95%, sensitivity 82%). In patients with NT1 but not in OH, W/N1-SOREMPs decreased throughout the day (from 79% in the 1st nap to 33% in the preceding night, p < 0.001), whereas N2-SOREMPs did not change. N3 sleep frequency in the 5th nap was higher in NT1 than in OH (28% vs. 7%, p:0.009). Nocturnal-SOREMP plus ?4 daytime SOREMPs, Wake-REM transitions, and REM followed by N3 were only seen in NT1.Measuring the sleep stage sequence and temporal distribution of SOREMP helps to identify patients with narcolepsy in the MSLT.Copyright © 2022 Elsevier B.V. All rights reserved

Serum metabolic biomarkers for synucleinopathy conversion in isolated REM sleep behavior disorder

Neurodegeneració; Malaltia de Parkinson; Marcadors predictiusNeurodegeneración; Enfermedad de Parkinson; Marcadores predictivosNeurodegeneration; Parkinson's disease; Predictive markersIsolated rapid eye movement (REM) sleep behavior disorder (iRBD) is a prodromal stage of Lewy-type synucleinopathies (LTS), which can present either with an initial predominant parkinsonism (Parkinson’s disease (PD)) or dementia (dementia with Lewy bodies (DLB)). To provide insights into the underlying pathogenic mechanisms, the lipoprotein and protein glycosylation profile of 82 iRBD patients, collected before and/or after their conversion to an overt LTS, and 29 matched control serum samples were assessed by nuclear magnetic resonance (NMR) spectroscopy. Data were statistically analyzed to identify altered metabolites and construct predictive models. Univariant analysis detected no differences between iRBD patients with an LTS compared to controls. However, significant differences were found when the analysis distinguished between iRBD patients that manifested initially predominant parkinsonism (pre-PD) or dementia (pre-DLB). Significant differences were also found in the analysis of paired iRBD samples pre- and post-LTS diagnosis. Predictive models were built and distinguished between controls and pre-DLB patients, and between pre-DLB and pre-PD patients. This allowed a prediction of the possible future clinical outcome of iRBD patients. We provide evidence of altered lipoprotein and glycosylation profiles in subgroups of iRBD patients. Our results indicate that metabolic alterations and inflammation are involved in iRBD pathophysiology, and suggest biological differences underlying the progression of LTS in iRBD patients. Our data also indicate that profiling of serum samples by NMR may be a useful tool for identifying short-term high-risk iRBD patients for conversion to parkinsonism or dementia.The study was funded by the Fondo de Investigación Sanitaria-Instituto de Salud Carlos III (FIS-ISCIII, Spain)-European Regional Development Fund (FEDER, E.U.) (PI13/01897 to M.V.), Ministerio de Economía y Competitividad (MINECO, Spain) (SAF2015-73997-JIN to A.L. and SAF2016-77541-R to M.V.), Fundació Bancària La Caixa (Junior Leader Fellowship LCF/BQ/PR19/11700005 to A.L. and Health Research Project HR17-00513 to M.V.) and CIBERNED (to M.V. and E.T.). A.L. was the recipient of a postdoctoral contract SAF2015-73997-JIN from MINECO (Spain) with co-funding from FEDER (E.U.) and is currently funded by the Junior Leader Program from Fundació Bancària La Caixa (grant LCF/BQ/PR19/11700005). H.X. is the recipient of a Radboud University Personal Ph.D. Grant

Cervical spinal cord injury by a low-impact trauma as an unnoticed cause of cardiorespiratory arrest

Background: Cardiorespiratory arrest (CA) secondary to traumatic cervical spinal cord injury can occur in minor accidents with low-impact trauma and may be overlooked as the cause of CA in patients admitted in the coronary care unit. Case summary: We present two patients admitted to the coronary care unit because of suspected CA of cardiac origin. Both patients were found in CA with asystole, one after collapsing in a shopping mall and falling down a few steps and the other in the street next to his bicycle. They underwent early pharmacologically induced coma and hypothermia precluding neurological examination. Both patients remained in coma after rewarming, with preserved brainstem reflexes but absent motor response to pain. One patient had post-anoxic myoclonus in the face without limb involvement. In both patients, median nerve somatosensory evoked potentials demonstrated bilateral absence of thalamocortical N19 responses and abnormal cervicomedullary junction potentials (N13 wave). Extensive diagnostic work-up did not find a cardiac cause of the CA, pulmonary thromboembolism, or intracranial haemorrhage. In both patients, cervical spinal cord injury was diagnosed incidentally 5 and 6 days after CA, when a brain magnetic resonance imaging performed to assess post-anoxic brain injuries detected spinal cord hyperintensities with fracture and luxation of the odontoid. Both patients died 11 and 8 days after CA. Discussion: Low-impact traumatic cervical spinal cord injury should be considered in the diagnostic work-up of patients with CA of unknown cause

Serum MicroRNAs Predict Isolated Rapid Eye Movement Sleep Behavior Disorder and Lewy Body Diseases

Background: Isolated rapid eye movement sleep behavior disorder (IRBD) is a well-established clinical risk factor for Lewy body diseases (LBDs), such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Objective: To elucidate whether serum microRNA (miRNA) deregulation in IRBD can antedate the diagnosis of LBD by performing a longitudinal study in different progression stages of IRBD before and after LBD diagnosis and assessing the predictive performance of differentially expressed miRNAs by machine learning-based modeling. Methods: Using genome-wide miRNA analysis and real-time quantitative polymerase chain reaction validation, we assessed serum miRNA profiles from patients with IRBD stratified by dopamine transporter (DaT) single-photon emission computed tomography into DaT-negative IRBD (n = 17) and DaT-positive IRBD (n = 21), IRBD phenoconverted into LBD (n = 13), and controls (n = 20). Longitudinally, we followed up the IRBD cohort by studying three time point serum samples over 26 months. Results: We found sustained cross-sectional and longitudinal deregulation of 12 miRNAs across the RBD continuum, including DaT-negative IRBD, DaT-positive IRBD, and LBD phenoconverted IRBD (let-7c-5p, miR-19b-3p, miR-140, miR-22-3p, miR-221-3p, miR-24-3p, miR-25-3p, miR-29c-3p, miR-361-5p, miR-425-5p, miR-4505, and miR-451a) (false discovery rate P < 0.05). Age- and sex-adjusted predictive modeling based on the 12 differentially expressed miRNA biosignatures discriminated IRBD and PD or DLB from controls with an area under the curve of 98% (95% confidence interval: 89-99%). Conclusions: Besides clinical diagnosis of IRBD or imaging markers such as DaT single-photon emission computed tomography, specific miRNA biosignatures alone hold promise as progression biomarkers for patients with IRBD for predicting PD and DLB clinical outcomes. Further miRNA studies in other PD at-risk populations, such as LRRK2 mutation asymptomatic carriers or hyposmic subjects, are warranted. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Cortical gray matter progression in idiopathic REM sleep behavior disorder and its relation to cognitive decline

Background: Idiopathic Rapid eye movement sleep behavior disorder (IRBD) is recognized as the prodromal stage of the alpha-Synucleinopathies. Although some studies have addressed the characterization of brain structure in IRBD, little is known about its progression. Objective: The present work aims at further characterizing gray matter progression throughout IRBD relative to normal aging and investigating how these changes are associated with cognitive decline. Methods: Fourteen patients with polysomnography-confirmed IRBD and 18 age-matched healthy controls (HC) underwent neuropsychological, olfactory, motor, and T1-weighted MRI evaluation at baseline and follow-up. We compared the evolution of cortical thickness (CTh), subcortical volumes, smell, motor and cognitive performance in IRBD and HC after a mean of 1.6 years. FreeSurfer was used for CTh and volumetry preprocessing and analyses. The symmetrized percent of change (SPC) of the CTh was correlated with the SPC of motor and neuropsychological performance. Results: IRBD and HC differed significantly in the cortical thinning progression in regions encompassing bilateral superior parietal and precuneus, the right cuneus, the left occipital pole and lateral orbitofrontal gyri (FWE corrected, p < 0.05). The Visual form discrimination test showed worse progression in the IRBD relative to HC, that was associated with gray matter loss in the right superior parietal and the left precuneus. Increasing motor signs in IRBD were related to cortical thinning mainly involving frontal regions, and late-onset IRBD was associated with cortical thinning involving posterior areas (FWE corrected, p < 0.05). Despite finding olfactory identification deficits in IRBD, results did not show decline over the disease course. Conclusion: Progression in IRBD patients is characterized by parieto-occipital and orbitofrontal thinning and visuospatial loss. The cognitive decline in IRBD is associated with degeneration in parietal regions

Comparing the accuracy and neuroanatomical correlates of the UPSIT-40 and the Sniffin' Sticks test in REM sleep behavior disorder

Background: Olfactory impairment increases the risk of developing neurodegenerative diseases in patients with idiopathic REM sleep behavior disorder (IRBD). Knowing the test properties of distinct olfactory measures could contribute to their selection for clinical or research purposes. Objective: To compare the accuracy in distinguishing IRBD patients from controls with the University of Pennsylvania Smell Identification Test (UPSIT-40) and Sniffin' Sticks Extended test, and to assess the gray-matter volume correlates of these tests. Method: Twenty-one patients with IRBD and 27 healthy controls were assessed using both olfactory tests. Independent logistic regressions were computed with diagnosis as a dependent variable and olfactory measures as predictive variables. Receiver operating characteristic curves were computed for each olfactory subtest. Diagnostic accuracy for IRBD was calculated according to the resulting optimal cut-off score. Structural MRI data, acquired with a 3T scanner, were analyzed with voxel-based morphometry. Results: Patients differed from controls in all olfactory measures. The Sniffin-Identification correctly classified 89.1% of cases; the UPSIT-40, 85.4%; the Sniffin-Discrimination, 82.6%; the Sniffin-Total, 81.8%; and the Sniffin-Threshold, 77.3%. Respective AUROC, optimal cut-off, sensitivity, and specificity for each test were: 0.902, ≤26, 85.7%, and 85.2% for the UPSIT-40; 0.884, ≤29, 89.5%, and 76.0% for the Sniffin-Total; 0.922, ≤11, 90.5%, and 88.0% for the Sniffin-Identification; 0.739, ≤4, 73.7%, and 76.0% for the Sniffin-Threshold; and 0.838, ≤11, 85.7%, and 76.0% for the Sniffin-Discrimination. UPSIT-40 scores correlated with gray-matter volumes in orbitofrontal regions in anosmic patients. Conclusions: UPSIT-40 and Sniffin' Identification showed similar discrimination accuracy, but only the UPSIT-40 showed structural correlates (p ≤ .05 FDR-corrected)

HLA and microtubule-associated protein tau H1 haplotype associations in anti-IgLON5 disease

We investigated the associations with HLA and microtubule-associated protein tau (MAPT) H1 haplotype in anti-IgLON5 disease, a recently identified disorder characterized by gait instability, brainstem dysfunction, and a prominent sleep disorder in association with IgLON5 antibodies and pathologic findings of a novel neuronal-specific tauopathy. We compared the HLA alleles and MAPT H1/H1 genotype of 35 patients with anti-IgLON5 with healthy controls. The on-line server tool NetMHCIIpan 3.1 was used to predict the IgLON5 peptide binding to HLA Class II molecules. The HLA-DRB1*10:01-DQB1*05:01 haplotype was overrepresented in patients with anti-IgLON5 disease (OR = 54.5; 95% CI: 22.2-133.9, p < 0.0001). In addition, HLA-DQA was genotyped in 27 patients, and 25 (92.6%) of them had DQ molecules composed by DQA1*01 and DQB1*05 chains compared with 148/542 (27.3%) controls (OR = 43.9; 95% CI: 10.4-185.5, p < 0.0001). Patients DRB1*10:01 positive developed more frequently sleep or bulbar symptoms than those carrying other HLA alleles (70.0% vs 26.7%; p = 0.011). Prediction algorithms identified 2 IgLON5 peptides (1 located in the signal sequence) that showed strong binding to HLA-DRB1*10:01 and other HLA-DRB1, but not to HLA-DQA and HLA-DQB molecules. The MAPT H1/H1 homozygous genotype was present in 20/24 (83.3%) anti-IgLON5 Caucasian patients compared with 54/116 (46.5%) healthy controls (p = 0.0007). The robust association of anti-IgLON5 disease with distinct HLA Class II molecules supports a primary autoimmune origin. The significant association of MAPT H1 haplotype also suggests that an underlying neurodegenerative process could be involved in anti-IgLON5 disease

Neurodegenerative disorder risk in idiopathic REM sleep behavior disorder: study in 174 Patients.

Objective To estimate the risk for developing a defined neurodegenerative syndrome in a large cohort of idiopathic REM sleep behavior disorder (IRBD) patients with long follow-up. Methods Using the Kaplan-Meier method, we estimated the disease-free survival rate from defined neurodegenerative syndromes in all the consecutive IRBD patients diagnosed and followed-up in our tertiary referal sleep center between November 1991 and July 2013. Results The cohort comprises 174 patients with a median age at diagnosis of IRBD of 69 years and a median follow-up of four years. The risk of a defined neurodegenerative syndrome from the time of IRBD diagnosis was 33.1% at five years, 75.7% at ten years, and 90.9% at 14 years. The median conversion time was 7.5 years. Emerging diagnoses (37.4%) were dementia with Lewy bodies (DLB) in 29 subjects, Parkinson disease (PD) in 22, multiple system atrophy (MSA) in two, and mild cognitive impairment (MCI) in 12. In six cases, in whom postmortem was performed, neuropathological examination disclosed neuronal loss and widespread Lewy-type pathology in the brain in each case. Conclusions In a large IRBD cohort diagnosed in a tertiary referal sleep center, prolonged follow-up indicated that the majority of patients are eventually diagnosed with the synucleinopathies PD, DLB and less frequently MSA. IRBD represented the prodromal period of these conditions. Our findings in IRBD have important implications in clinical practice, in the investigation of the early pathological events occurring in the synucleinopathies, and for the design of interventions with potential disease-modifying agents

Disruption of posterior brain functional connectivity and its relation to cognitive impairment in idiopathic REM sleep behavior disorder

Background: Resting-state functional MRI has been proposed as a new biomarker of prodromal neurodegenerative disorders, but it has been poorly investigated in the idiopathic form of rapid-eye-movement sleep behavior disorder (IRBD), a clinical harbinger of subsequent synucleinopathy. Particularly, a complex-network approach has not been tested to study brain functional connectivity in IRBD patients. Objectives: The aim of the current work is to characterize resting-state functional connectivity in IRBD patients using a complex-network approach and to determine its possible relation to cognitive impairment. Method: Twenty patients with IRBD and 27 matched healthy controls (HC) underwent resting-state functional MRI with a 3T scanner and a comprehensive neuropsychological battery. The functional connectome was studied using threshold-free network-based statistics. Global and local network parameters were calculated based on graph theory and compared between groups. Head motion, age and sex were introduced as covariates in all analyses. Results: IRBD patients showed reduced cortico-cortical functional connectivity strength in comparison with HC in edges located in posterior regions (p <0.05, FWE corrected). This regional pattern was also shown in an independent analysis comprising posterior areas where a decreased connectivity in 51 edges was found, whereas no significant results were detected when an anterior network was considered (p <0.05, FWE corrected). In the posterior network, the left superior parietal lobule had reduced centrality in IRBD. Functional connectivity strength between left inferior temporal lobe and right superior parietal lobule positively correlated with mental processing speed in IRBD (r=.633; p=.003). No significant correlations were found in the HC group. Conclusion: : Our findings support the presence of disrupted posterior functional brain connectivity of IRBD patients similar to that found in synucleinopathies. Moreover, connectivity reductions in IRBD were associated with lower performance in mental processing speed domain