Previous studies have reported increased brain deposits of iron in patients with chronic migraine (CM). This study aims to determine the relation between iron deposits and outcome after treatment ...with OnabotulinumtoxinA (OnabotA). Demographic and clinical data were collected for this study through a prospective cohort study including 62 CM patients treated with OnabotA in the Hospital Clínico Universitario de Santiago de Compostela (Spain). Demographic and clinical variables were registered. Selected biomarkers in plasma during interictal periods (calcitonin gene-related peptide (CGRP) and pentraxin-3 (PTX3)) and neuroimaging changes (iron deposits in the red nucleus (RN), substantia nigra (SN), globus pallidus (GP), and periaqueductal gray matter (PAG), and white matter lesions (WML)) were determined. Subjects were classified in responders (≥50% reduction in headache days) or non-responders (<50%). Responders to treatment were younger (mean age difference = 12.2; 95% confidence interval (CI): 5.4-18.9,
= 0.001), showed higher serum levels of CGRP (≥50 ng/mL) and PTX3 (≥1000 pg/mL) and smaller iron deposits in the GP and PAG (mean difference = 805.0; 95% CI: 37.9-1572.1 μL,
= 0.040 and mean difference = 69.8; 95% CI: 31.0-108.6 μL,
= 0.008; respectively). Differences in PAG iron deposits remained significant after adjusting for age (mean difference = 65.7; 95% CI: 22.8-108.6 μL,
= 0.003) and were associated with poor response to OnabotA after adjustment for clinical and biochemical variables (odds ratio (OR) = 0.963; 95% CI: 0.927-0.997,
= 0.041). We conclude that larger PAG iron deposits are associated with poor response to OnabotA in CM.
Introduction
Hospital‐associated deconditioning (HAD) or post‐hospital syndrome is well recognized as reduced functional performance after an acute hospitalization. Recommendations for the management ...of HAD are still lacking, partly due to a poor understanding of the underlying processes. We aimed to review existing data on risk factors, pathophysiology, measurement tools, and potential interventions.
Materials and methods
We conducted a systematic review from bibliographical databases in English, Spanish and French with keywords such as ‘post‐hospitalization syndrome’ or ‘deconditioning’. We selected studies that included people aged 60 years or older. Three researchers independently selected articles and assessed their quality.
Results
From 4421 articles initially retrieved, we included 94 studies. Most were related to risk factors, trajectories and measures, and focused on the physical aspects of deconditioning. Risk factors for HAD included age, nutritional status, mobility, and pre‐admission functional status, but also cognitive impairment and depression. Regarding interventions, almost all studies were devoted to physical rehabilitation and environmental modifications. Only one study focused on cognitive stimulation.
Discussion
In the last decade, studies on HAD have mostly focused on the physical domain. However, neurological changes may also play a role in the pathophysiology of HAD. Beyond physical interventions, cognitive rehabilitation and neurological interventions should also be evaluated to improve deconditioning prevention and treatment in the hospital setting.
Key points
Many studies have been devoted to HAD in the last decade, with some consistent findings.
Most studies have focused on the physical dimensions of HAD.
Few mechanistic and intervention studies have been conducted.
The cognitive and psychological dimensions of HAD remain understudied.
A consensus definition of HAD and a clear research agenda are needed.
Even though endothelial dysfunction is known to play a role in migraine pathophysiology, studies regarding levels of endothelial biomarkers in migraine have controversial results. Our aim was to ...evaluate the role of pentraxin 3 (PTX3) and soluble tumour necrosis factor-like weak inducer of apoptosis (sTWEAK) as potential biomarkers of endothelial dysfunction in chronic migraine (CM). We performed a case-control study including 102 CM patients and 28 control subjects and measured serum levels of markers of endothelial dysfunction (PTX3 and sTWEAK) and inflammation high-sensitivity C-reactive protein (hs-CRP) as well as brachial artery flow-mediated dilation (FMD) during interictal periods. Interictal serum levels of PTX3 and sTWEAK were higher in CM patients than in controls (1350.6 ± 54.8 versus 476.1 ± 49.4 pg/mL,
< 0.001 and 255.7 ± 21.1 versus 26.4 ± 2.6 pg/mL,
< 0.0001; respectively). FMD was diminished in CM patients compared to controls (9.6 ± 0.6 versus 15.2 ± 0.9%,
< 0.001). Both PTX3 and sTWEAK were negatively correlated with FMD (r = -0.508,
< 0.001 and r = -0.188,
= 0.033; respectively). After adjustment of confounders, PTX3 remained significantly correlated to FMD (r = -0.250,
= 0.013). Diagnosis of CM was 68.4 times more likely in an individual with levels of PTX3 ≥ 832.5 pg/mL, suggesting that PTX3 could be a novel biomarker of endothelial dysfunction in CM.
Background
Recently, amylin and its receptors were found in different structures involved in migraine pathophysiology. Here, we evaluate interictal concentrations of amylin and calcitonin ...gene-related peptide in peripheral blood as biomarkers for chronic migraine.
Methods
We prospectively recruited patients with episodic migraine, chronic migraine and healthy controls. Interictal amylin and calcitonin gene-related peptide levels were assessed in blood samples using enzyme linked immunosorbent assay.
Results
We assessed plasma samples from 58 patients with episodic migraine (mean age 37.71 ± 10.47, 87.9% female), 191 with chronic migraine (mean age 46.03 ± 11.93, 95% female), and on 68 healthy controls (mean age 43.58 ± 11.08 years, 86% female). Body mass index was 25.94 ± 4.53 kg/m2 for migraine patients and 25.13 ± 4.92 kg/m2 for healthy controls (p = 0.0683). Interictal plasma amylin levels were higher in chronic migraine patients (47.1 pg/mL) than in the episodic migraine patients (28.84 pg/mL, p < 0.0001) and healthy controls (24.74 pg/mL, p < 0.0001). Plasma calcitonin gene-related peptide levels were increased (20.01 pg/mL) in chronic migraine patients when compared to healthy controls (11.37 pg/mL, p = 0.0016), but not to episodic migraine patients (18.89 pg/mL, p = 0.4369). Applying a cut-off concentration of 39.68 pg/mL plasma amylin, the sensitivity to differentiate chronic migraine from healthy controls was 57.6% and the specificity was 88.2%. Variables such as age, analgesic overuse, depression, allodynia, use of preventive medication or a history of aura did not influence the plasma concentrations of amylin or calcitonin gene-related peptide.
Conclusion
Interictal plasma amylin levels are higher in patients with chronic migraine and may serve as a diagnostic biomarker for chronic migraine.
Frontotemporal dementia (FTD) is the second most common cause of early-onset neurodegenerative dementia. Several studies have focused on early imaging changes in FTD patients, but once subjects meet ...full criteria for FTD diagnosis, structural changes are generally widespread.
This study aims to determine the earliest structural brain changes in asymptomatic MAPT MUTATION carriers.
This is a cross-sectional multicenter study comparing global and regional brain volume and white matter integrity in a group of MAPT mutation preclinical carriers and controls. Participants belong to multiple generations of six families with five MAPT mutations. All participants underwent a medical examination, neuropsychological tests, genetic analysis, and a magnetic resonance scan (3T, scout, T1-weighted image followed by EPI (BOLD), MPRAGE, DTI, FLAIR, and ASL sequences).
Volumes of five cortical and subcortical areas were strongly correlated with mutation status: temporal lobe (left amygdala, left temporal pole), cingulate cortex (left rostral anterior cingulate gyrus, right posterior cingulate), and the lingual gyrus in the occipital lobe. We did not find significant differences in whole brain volume, white matter hyperintensities volume, and white matter integrity using DTI analysis.
Temporal lobe, cingulate cortex and the lingual gyrus seem to be early targets of the disease and may serve as biomarkers for FTD prior to overt symptom onset.
Coping with dementia requires an integrated approach encompassing personal, health, research, and community domains. Here we describe “Walking the Talk for Dementia,” an immersive initiative aimed at ...empowering people with dementia, enhancing dementia understanding, and inspiring collaborations. This initiative involved 300 participants from 25 nationalities, including people with dementia, care partners, clinicians, policymakers, researchers, and advocates for a 4‐day, 40 km walk through the Camino de Santiago de Compostela, Spain. A 2‐day symposium after the journey provided novel transdisciplinary and horizontal structures, deconstructing traditional hierarchies. The innovation of this initiative lies in its ability to merge a physical experience with knowledge exchange for diversifying individuals' understanding of dementia. It showcases the transformative potential of an immersive, embodied, and multi‐experiential approach to address the complexities of dementia collaboratively. The initiative offers a scalable model to enhance understanding, decrease stigma, and promote more comprehensive and empathetic dementia care and research.
To evaluate the effect of natalizumab on progression of brain atrophy in multiple sclerosis (MS) patients and to search for a clinical or radiological marker of progression of brain atrophy.
We ...retrospectively recorded demographic and clinical data, as well as the corpus callosum index (CCI) using MRI, in MS patients treated with natalizumab for 1-4 years.
In the study population (n = 29), baseline mean CCI was 0.37 ± 0.04 and final CCI 0.36 ± 0.04. 17 patients did not develop brain atrophy during follow-up. There was no statistically significant relationship between progression of atrophy and clinical and radiological parameters.
Natalizumab may have a neuroprotective effect.
Freezing of gait (FOG) is a motor disturbance usually appearing in advanced Parkinson's disease (PD). Cognitive and executive function seems to play an important role in this phenomenon.
To ...investigate if cognitive and kinematic parameters correlate with FOG in PD patients without dementia.
We conducted an observational cross-sectional study. Participants were classified in two groups: freezers and non-freezers. Clinical information was obtained by Hoehn and Yahr scale, Unified Parkinson's Disease Rating Scale and balance test of Short Physical Performance Battery. Cognitive function was evaluated using Minimental Examination and the Fuld Object Memory Evaluation; executive function was assessed with the Frontal Assessment Battery test. Battery kinematic parameters were assessed by means of gait speed, cadence, stride length and stride time.
Twenty-five participants with PD without dementia completed the evaluation. Statistical significant differences between freezers and non-freezers were found in global cognition (p = 0,02), memory (p = 0,04), executive function (p = 0,04), cadence (p = 0,02), stride length (p = 0,04) and stride time (p = 0,01).
Cognitive parameters may have an important contribution to the manifestation of freezing of gait in PD. These results may have important clinical implications for developing future non-pharmacological and cognitive interventions strategies targeted to PD patients with FOG.
Background
Hospital‐associated deconditioning (HAD) or post‐hospital syndrome is a multisystem decline that leads to poor functional performance after acute hospitalization. Although hospitalization ...is supposed to treat an acute condition and improve the overall outcome, HAD may be significant, especially in older people. Recommendations for the management of HAD still lack, partly due to the poor understanding of the underlying processes. We aim to review existing data on mechanisms, risk factors, natural history, measuring tools, and intervention in HAD, with a specific focus on brain health.
Method
We searched PubMed, sCielo and Cochrane database for relevant articles published between 1 January 2009 and 31 December 2019. Search terms were “post‐hospitalization syndrome” OR “deconditioning” OR “hospital‐associated functional decline” OR “pre‐existing frailty” OR “unrecognized vulnerability”. Three researchers independently selected papers according to title relevance and then re‐checked for relevance.
Results
We first selected 63 studies based on the title relevance and 14 of them were excluded after reviewing the . Research on this field has been mainly led from a physical perspective, in geriatrics or rehabilitation settings. 25 studies were related to mechanisms; 18 to risk factors and trajectories; 10 to measuring and predictive tools and 5 to interventions. Mechanisms referred to the inevitable change imposed by the hospitalization (e.g. reorganization of sensorimotor cortex, maladaptive cognitive schemas, vascular deconditioning) and to the own frail condition of the population at risk. Risk factors varied from older age to nutritional status, mobility or functional status before admission among others. Cognitive impairment, ability for ADLs and IADLs at admission and depression were also predictors of functional decline. Assessment of those items worked as a useful tool to identify vulnerable patients for HAD. Regarding interventions, all but one was devoted to physical rehabilitation and environmental modifications. Only one study focused on cognitive stimulation.
Conclusions
Several studies have focused on HAD in the last decade, with some consistent findings. Cognitive impairment, depression and neurological changes may have a role in hospital deconditioning pathophysiology and may be useful to identify patients and risk. Cognitive rehabilitation and neurological interventions should be evaluated as well in deconditioning prevention and treatment.
Abstract
Background
Hospital‐associated deconditioning (HAD) or post‐hospital syndrome is a multisystem decline that leads to poor functional performance after acute hospitalization. Although ...hospitalization is supposed to treat an acute condition and improve the overall outcome, HAD may be significant, especially in older people. Recommendations for the management of HAD still lack, partly due to the poor understanding of the underlying processes. We aim to review existing data on mechanisms, risk factors, natural history, measuring tools, and intervention in HAD, with a specific focus on brain health.
Method
We searched PubMed, sCielo and Cochrane database for relevant articles published between 1 January 2009 and 31 December 2019. Search terms were “post‐hospitalization syndrome” OR “deconditioning” OR “hospital‐associated functional decline” OR “pre‐existing frailty” OR “unrecognized vulnerability”. Three researchers independently selected papers according to title relevance and then re‐checked for abstract relevance.
Results
We first selected 63 studies based on the title relevance and 14 of them were excluded after reviewing the abstract. Research on this field has been mainly led from a physical perspective, in geriatrics or rehabilitation settings. 25 studies were related to mechanisms; 18 to risk factors and trajectories; 10 to measuring and predictive tools and 5 to interventions. Mechanisms referred to the inevitable change imposed by the hospitalization (e.g. reorganization of sensorimotor cortex, maladaptive cognitive schemas, vascular deconditioning) and to the own frail condition of the population at risk. Risk factors varied from older age to nutritional status, mobility or functional status before admission among others. Cognitive impairment, ability for ADLs and IADLs at admission and depression were also predictors of functional decline. Assessment of those items worked as a useful tool to identify vulnerable patients for HAD. Regarding interventions, all but one was devoted to physical rehabilitation and environmental modifications. Only one study focused on cognitive stimulation.
Conclusions
Several studies have focused on HAD in the last decade, with some consistent findings. Cognitive impairment, depression and neurological changes may have a role in hospital deconditioning pathophysiology and may be useful to identify patients and risk. Cognitive rehabilitation and neurological interventions should be evaluated as well in deconditioning prevention and treatment.
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