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This paper aims to analyze the contradictions between sustainability and social justice by examining the deaths caused by asbestos processing and the resulting environmental disasters in affected areas. In the first part, the author explores the contradictions between sustainable reforms and “performative environmentalism” as compared to integral ecology, which advocates an integrated and holistic approach to addressing political, social, economic, and environmental issues. Her analysis is grounded in a theoretical framework that argues sustainable development must be evaluated in its full complexity and contrasted with neoliberal simplification practices that prioritize efficiency and the economization of economically assessable resources. From this perspective, the second part of the paper discusses these issues through an Italian asbestos case study, viewed as an instance of social injustice conflicting with sustainability policies. The author outlines three main points demonstrating how sustainability governance can bypass any potential for social justice in situations involving asbestos processing. She explains that managing asbestos cases contributes to the normalization of environmental disasters and exacerbates the conflict between the right to work and the right to health. The incidents involving asbestos exemplify how sustainability is interpreted through a neoliberal lens.

Background This study aimed to identify mesocorticolimbic functional abnormalities in cluster headache (CH) patients, disentangling the roles of chronification and affective symptoms. Methods Using the monetary incentive delay fMRI task to directly engage these pathways, we investigated functional alterations in key regions of this network in chronic ( n  = 23) and episodic CH patients ( n  = 49) compared to a control group ( n  = 32). After processing the fMRI data, we extracted beta values from selected regions and for contrasts of interest and entered them into logistic regression models adjusted for potential confounders (such as depressive and anxiety symptoms and smoking habit) to test their association with the diagnoses (chronic CH and control subjects, episodic CH and control subjects). Results Results showed that chronic CH patients exhibited reduced ventral tegmental area (VTA) activity and a tendency towards significance ( p  = 0.056) for an increased medial prefrontal cortex (mPFC) responsiveness during reward anticipation, alongside a significant decrease in mPFC activity during reward outcomes. Episodic patients displayed abnormal mPFC activity across both reward phases, but coupled with intact VTA responses. Importantly, these functional abnormalities were not correlated to depressive and anxiety symptoms and smoking habits. Conclusions These findings suggest that chronic CH patients experience an imbalance in the VTA-mPFC pathway, while episodic patients may show early signs of this emerging dysfunction. Moreover, the observed reward processing alterations seem distinct from those associated with affective disorders, possibly highlighting unique mechanisms underlying the pathophysiology of CH.

Accurate and reproducible automated segmentation of human hippocampal subfields is of interest to study their roles in cognitive functions and disease processes. Multispectral structural MRI methods have been proposed to improve automated hippocampal subfield segmentation accuracy, but the reproducibility in a multicentric setting is, to date, not well characterized. Here, we assessed test–retest reproducibility of FreeSurfer 6.0 hippocampal subfield segmentations using multispectral MRI analysis pipelines (22 healthy subjects scanned twice, a week apart, at four 3T MRI sites). The harmonized MRI protocol included two 3D-T1, a 3D-FLAIR, and a high-resolution 2D-T2. After within-session T1 averaging, subfield volumes were segmented using three pipelines with different multispectral data: two longitudinal (“long_T1s” and “long_T1s_FLAIR”) and one cross-sectional (“long_T1s_FLAIR_crossT2”). Volume reproducibility was quantified in magnitude (reproducibility error—RE) and space (DICE coefficient). RE was lower in all hippocampal subfields, except for hippocampal fissure, using the longitudinal pipelines compared to long_T1s_FLAIR_crossT2 (average RE reduction of 0.4–3.6%). Similarly, the longitudinal pipelines showed a higher spatial reproducibility (1.1–7.8% of DICE improvement) in all hippocampal structures compared to long_T1s_FLAIR_crossT2. Moreover, long_T1s_FLAIR provided a small but significant RE improvement in comparison to long_T1s (p = 0.015), whereas no significant DICE differences were found. In addition, structures with volumes larger than 200 mm3 had better RE (1–2%) and DICE (0.7–0.95) than smaller structures. In summary, our study suggests that the most reproducible hippocampal subfield FreeSurfer segmentations are derived from a longitudinal pipeline using 3D-T1s and 3D-FLAIR. Adapting a longitudinal pipeline to include high-resolution 2D-T2 may lead to further improvements.

Spinocerebellar ataxias type 1 (SCA1) is an autosomal dominant disease usually manifesting in adulthood. We performed a prospective 1-year longitudinal study in 14 presymptomatic mutation carriers (preSCA1), 11 ataxic patients, and 21 healthy controls. SCA1 patients had a median disease duration of 6 years (range 2–16) and SARA score of 7 points (range 3.5–20). PreSCA1 had an estimated time before disease onset of 9.7 years (range 4–30), and no signs of ataxia. At baseline, SCA1 patients significantly differed from controls in SARA score (Scale for Assessment and Rating of Ataxia), cognitive tests, and structural MRI measures. Significant volume loss was found in cerebellum, brainstem, basal ganglia, and cortical thinning in frontal, temporal, and occipital regions. PreSCA1 did not differ from controls. At 1-year follow-up, SCA1 patients showed significant increase in SARA score, and decreased volume of cerebellum (− 0.6%), pons (− 5.5%), superior cerebellar peduncles (− 10.7%), and midbrain (− 3.0%). Signs of disease progression were also observed in preSCA1 subjects, with increased SARA score and reduced total cerebellar volume. Our exploratory study suggests that clinical scores and MRI measures provide valuable data to monitor and quantify the earliest changes associated with the preclinical and the symptomatic phases of SCA1 disease.

Background Despite hypothalamus has long being considered to be involved in the pathophysiology of cluster headache, the inconsistencies of previous neuroimaging studies and a limited understanding of the hypothalamic areas involved, impede a comprehensive interpretation of its involvement in this condition. Methods We used an automated algorithm to extract hypothalamic subunit volumes from 105 cluster headache patients (57 chronic and 48 episodic) and 59 healthy individuals; after correcting the measures for the respective intracranial volumes, we performed the relevant comparisons employing logist regression models. Only for subunits that emerged as abnormal, we calculated their correlation with the years of illness and the number of headache attacks per day, and the effects of lithium treatment. As a post-hoc approach, using the 7 T resting-state fMRI dataset from the Human Connectome Project, we investigated whether the observed abnormal subunit, comprising the paraventricular nucleus and preoptic area, shows robust functional connectivity with the mesocorticolimbic system, which is known to be modulated by oxytocin neurons in the paraventricular nucleus and that is is abnormal in chronic cluster headache patients. Results Patients with chronic (but not episodic) cluster headache, compared to control participants, present an increased volume of the anterior–superior hypothalamic subunit ipsilateral to the pain, which, remarkably, also correlates significantly with the number of daily attacks. The post-hoc approach showed that this hypothalamic area presents robust functional connectivity with the mesocorticolimbic system under physiological conditions. No evidence of the effects of lithium treatment on this abnormal subunit was found. Conclusions We identified the ipsilateral-to-the-pain antero-superior subunit, where the paraventricular nucleus and preoptic area are located, as the key hypothalamic region of the pathophysiology of chronic cluster headache. The significant correlation between the volume of this area and the number of daily attacks crucially reinforces this interpretation. The well-known roles of the paraventricular nucleus in coordinating autonomic and neuroendocrine flow in stress adaptation and modulation of trigeminovascular mechanisms offer important insights into the understanding of the pathophysiology of cluster headache.

Polymorphonuclear neutrophils (PMN) in atherosclerotic plaques have been identified only recently, and their contribution to plaque development is not yet fully understood. In this study, production of elastase, interleukin (IL)-8 and vascular endothelial growth factor (VEGF) by PMN was investigated in subjects with carotid stenosis undergoing carotid endarterectomy (CEA). The study enrolled 50 patients (Pts) and 10 healthy subjects (HS). Circulating PMN (cPMN) isolated from venous blood (in both Pts and HS) and from plaques (pPMN, in Pts) were cultured, alone or with 0.1 μM fMLP. Elastase, IL-8 and VEGF mRNA were analyzed by real-time PCR. In CEA specimens, PMN were localized by immunohistochemistry. In both Pts cPMN and pPMN, IL-8 mRNA was higher at rest but lower after fMLP (P<0.01 vs HS), and VEGF mRNA was higher both at rest and after fMLP (P<0.01 vs HS), while elastase mRNA was not significantly different. On the contrary, protein production was always higher in cPMN of HS with respect to values measured in cells of Pts. In CEA specimens, CD66b+ cells localized to areas with massive plaque formation close to neovessels. Pts with soft and mix plaques, as defined by computed tomography, did not differ in cPMN or pPMN IL-8, VEGF or elastase mRNA, or in intraplaque CD66b+ cell density. However, Pts with soft plaques had higher white blood cell count due to increased PMN. In Pts with carotid plaques, both circulating and intraplaque PMN produce IL-8, VEGF and elastase, which are crucial for plaque development and progression. These findings suggest mechanistic explanations to the reported correlation between PMN count and cardiovascular mortality in carotid ATH.

Fundamental and clinical neuroscience has benefited tremendously from the development of automated computational analyses. In excess of 600 human neuroimaging papers using Voxel-based Morphometry (VBM) are now published every year and a number of different automated processing pipelines are used, although it remains to be systematically assessed whether they come up with the same answers. Here we examined variability between four commonly used VBM pipelines in two large brain structural datasets. Spatial similarity and between-pipeline reproducibility of the processed gray matter brain maps were generally low between pipelines. Examination of sex-differences and age-related changes revealed considerable differences between the pipelines in terms of the specific regions identified. Machine learning-based multivariate analyses allowed accurate predictions of sex and age, however accuracy differed between pipelines. Our findings suggest that the choice of pipeline alone leads to considerable variability in brain structural markers which poses a serious challenge for reproducibility and interpretation. Four common processing pipelines tested on two Voxel-based Morphometry (VBM) datasets yield considerable variations in results, raising issues on the interpretability and robustness of VBM results.

Background Mindfulness practice has gained interest in the management of Chronic Migraine associated with Medication Overuse Headache (CM-MOH). Mindfulness is characterized by present-moment self-awareness and relies on attention control and emotion regulation, improving headache-related pain management. Mindfulness modulates the Default Mode Network (DMN), Salience Network (SN), and Fronto-Parietal Network (FPN) functional connectivity. However, the neural mechanisms underlying headache-related pain management with mindfulness are still unclear. In this study, we tested neurofunctional changes after mindfulness practice added to pharmacological treatment as usual in CM-MOH patients. Methods The present study is a longitudinal phase-III single-blind Randomized Controlled Trial (MIND-CM study; NCT03671681). Patients had a diagnosis of CM-MOH, no history of neurological and severe psychiatric comorbidities, and were attending our specialty headache centre. Patients were divided in Treatment as Usual (TaU) and mindfulness added to TaU (TaU + MIND) groups. Patients underwent a neuroimaging and clinical assessment before the treatment and after one year. Longitudinal comparisons of DMN, SN, and FPN connectivity were performed between groups and correlated with clinical changes. Vertex-wise analysis was performed to assess cortical thickness changes. Results 177 CM-MOH patients were randomized to either TaU group or TaU + MIND group. Thirty-four patients, divided in 17 TaU and 17 TaU + MIND, completed the neuroimaging follow-up. At the follow-up, both groups showed an improvement in most clinical variables, whereas only TaU + MIND patients showed a significant headache frequency reduction ( p  = 0.028). After one year, TaU + MIND patients showed greater SN functional connectivity with the left posterior insula (p-FWE = 0.007) and sensorimotor cortex (p-FWE = 0.026). In TaU + MIND patients only, greater SN-insular connectivity was associated with improved depression scores ( r = -0.51, p  = 0.038). A longitudinal increase in cortical thickness was observed in the insular cluster in these patients ( p  = 0.015). Increased anterior cingulate cortex thickness was also reported in TaU + MIND group (p-FWE = 0.02). Conclusions Increased SN-insular connectivity might modulate chronic pain perception and the management of negative emotions. Enhanced SN-sensorimotor connectivity could reflect improved body-awareness of painful sensations. Expanded cingulate cortex thickness might sustain improved cognitive processing of nociceptive information. Our findings unveil the therapeutic potential of mindfulness and the underlying neural mechanisms in CM-MOH patients. Trial Registration Name of Registry; MIND-CM study; Registration Number ClinicalTrials.gov identifier: NCT0367168; Registration Date: 14/09/2018

Background Accumulating evidence suggests that migraine patients present abnormal brain responses to salient sensory and emotional stimuli. However, it is still unclear whether this is a generalized or domain-specific phenomenon. Employing a well-validated fMRI paradigm, we investigated pain empathic reactivity across two domains: observation of physical pain (noxious stimulation) and affective pain (facial expressions). On the basis of a generalized hyperexcitability/hyperreactivity in migraine, we hypothesized abnormal responses to both dimensions of pain empathy. Methods We collected fMRI and psychometric data from 21 migraine patients and matched controls. Univariate and multivariate neuroimaging analyses were utilized to examine domain-specific dysregulations in (a) neural reactivity in meta-analytically defined shared regions of pain-empathy processing, and (b) whole-brain neurofunctional signatures of physical and affective pain empathy (VPS, Zhou et al., 2020). Logistic regression models and machine learning-based classification were employed to determine differences between groups (migraine or control). Results Migraine patients exhibit increased neural responses during empathy for physical pain in the bilateral inferior frontal gyrus (slightly more pronounced on the right side), with alterations on the right significantly associated with the pain experienced during the attack. On the whole-brain level, the predictive accuracy of the VPS for physical pain empathy was shown to be significantly higher for patients as compared to controls, reaching 100% accuracy. Across analyses, we did not find evidence of altered empathy processing for affective pain. Conclusions Contrary to our hypothesis, our results indicate that migraine patients present a domain-specific increased brain responsivity, localized in the bilateral inferior frontal gyrus but also extending to subtle whole brain patterns, during empathy for physical pain stimuli, but not during empathy for affective pain. Based on the evidence that the neural pathways for empathy for physical pain and experimental pain robustly overlap, these results indicate a specific hyperresponsivity of the pain pathways, with the inferior frontal gyrus likely playing a regulatory role in modulating pain-related processes. Finally, the results underscore the translational application potential of neuroaffective multivariate signatures as neuromarkers for pathological dysregulations in affective and pain-related processes.

Background Chronic migraine with medication overuse headache (CM-MOH) is a disabling neurological condition. CM-MOH is associated with functional impairment and high prevalence of psychiatric comorbidities. Neuroimaging research showed alterations in large-scale brain networks in chronic pain disorders. Among these, the so-called “triple network model” -Default Mode Network (DMN), Salience Network (SN), and Central Executive Network (CEN)- has garnered attention for its critical role in cognitive and emotional regulation. Dysregulation within and between these networks has been implicated in various chronic pain, substance abuse, and affective disorders. However, the role of triple network functional connectivity alterations in CM-MOH remains poorly understood. This study aims to investigate alterations in functional connectivity (FC) both within and between the triple networks and whole brain, and to explore how these neural changes relate to the clinical and psychiatric characteristics of CM-MOH. Methods This case-control study, 91 patients with CM-MOH and 35 healthy controls underwent clinical, neuropsychological, and resting-state fMRI assessments as part of the CM-MIND study. Patients were classified by type of medication overuse (triptans, NSAIDs, polyabusers). FC within and between the DMN, SN, and CEN, as well as whole-brain FC, was analyzed. Associations with clinical and psychiatric features (including allodynia, medication intake, anxiety, and depression) were examined using between-group comparisons and regression analyses. Results Compared to healthy controls, CM-MOH patients exhibited increased extra-network DMN and SN FC with sensorimotor regions, most pronounced in triptan abusers who also showed CEN-motor alterations. Moreover, SN nodes were associated with reduced global and local efficiency. Allodynia severity was associated with increased SN-sensorimotor and decreased DMN intra-network FC, while higher anxiety correlated with reduced DMN-amygdala/putamen FC. Migraine chronification and higher medication intake were linked to increased DMN and SN FC with temporal-occipital regions. Notably, polyabusers showed SN - CEN disconnection and concurrently enhanced coupling of both networks with temporo-occipital regions as an effect of medication intake. Conclusions Our results suggest that CM-MOH involves maladaptive connectivity of the triple network model. Alterations in FC, mainly in SN and DMN, and in CEN to a lesser extent, might be associated with migraine chronification and pain embodiment, while altered CEN interactions might be associated with medication overuse.