Amyloidoses are rare protein-misfolding disorders characterized by the deposition of insoluble fibrillar aggregates, leading to potentially life-threatening organ damage. These deposits can be systemic or localized. Systemic amyloidoses are often associated with monoclonal gammopathies, chronic inflammatory conditions, or have a hereditary origin. Treatment strategies primarily focus on reducing the production of amyloidogenic proteins-depending on the specific protein and its origin-through therapies such as chemotherapy, anti-inflammatory agents, or gene-silencing approaches. Early diagnosis is crucial to prevent progressive organ dysfunction. Over the past 25 years, significant advances in the diagnosis and therapeutic management of amyloidosis have been made. Amyloidosen sind seltene Erkrankungen, bei denen Proteine aufgrund einer Fehlfaltung als fibrilläre Aggregate abgelagert werden, was zu potenziell lebensbedrohlichen Organschäden führen kann. Die Ablagerungen können systemisch oder lokal auftreten. Systemische Amyloidosen können mit monoklonalen Gammopathien oder chronischen Entzündungen verbunden oder hereditär bedingt sein. Die Behandlung zielt in den meisten Fällen darauf ab, die Produktion der amyloidbildenden Proteine zu verringern – je nach zugrunde liegendem Protein und dessen Ursprung etwa durch Chemotherapie, antientzündliche Therapien oder Gen-Silencer. Eine frühe Diagnose ist entscheidend, um eine weitere Organschädigung zu verhindern. In den letzten 25 Jahren haben sich Diagnostik und Therapie von Amyloidose-Erkrankungen deutlich verbessert.
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Radiation-induced (radiculo)plexopathy [RI(R)P] is a debilitating delayed neurological adverse event occurring in cancer survivors years after the irradiation of the brachial or lumbar plexuses. No effective treatments have been identified to date. The objective of this work was to evaluate the effectiveness of the anti-VEGF bevacizumab in the treatment of RI(R)P. We retrospectively identified patients diagnosed with contrast-enhancing RI(R)P and treated with bevacizumab in the setting of an institutionally sponsored expanded access program over the last 10 years. Clinical, radiological, and neurophysiological records were reviewed. We identified nine patients manifesting with neurophysiological-confirmed RI(R)P (brachial plexopathy, 4; lumbosacral radiculoplexopathy, 5) after a median of 13 years from radiotherapy for their cancer. Symptoms included focal weakness, paresthesia, cramps, hypoesthesia, amyotrophy, and pain. Patients received bevacizumab at 7.5 mg/kg/q2 weeks for a median of six cycles (range, three to nine cycles). Clinical improvement was noted in three cases and clinical stabilization in two. Patients treated within 2 years since symptom onset appeared as most likely to benefit. Enhancement reduction on follow-up MRI was associated with the clinical benefit. Bevacizumab could be effective in the treatment of RI(R)P, particularly when patients are managed early in their disease. Further prospective clinical trials are warranted to validate these results.
Post-traumatic stress disorder (PTSD) is a severe stress-related psychiatric condition triggered by traumatic life-threatening events, characterized notably by an altered memory profile. Although clinically well-documented, no specific biomarker exists. This translational study identifies plasminogen activator inhibitor-1 (PAI-1) as a brain risk factor for PTSD, thereby supporting its potential as a blood-derived biomarker. Mice with genetically ablated PAI-1 were protected from developing a PTSD-like memory profile. Conversely, mice exhibiting PTSD-like cognitive impairment showed increased blood PAI-1 levels, correlating with their profile severity. In the brain, PAI-1 levels were specifically increased in the dorsal hippocampus, a key region for cognitive functions and in the etiology of PTSD. Finally, a longitudinal study of soldiers revealed that those developing PTSD symptoms exhibit rising blood PAI-1 levels over a 12-month period. Its significant association with various indicators of PTSD-related psychological distress attests to PAI-1's potential as a blood biomarker and brain therapeutic target for PTSD.
Diaphragm dysfunction is an important and often unrecognized cause of dyspnea. The current gold standard, transdiaphragmatic twitch pressure (Pdi,tw), requires oesophageal and gastric balloon catheters and is infrequently used in routine care. We evaluated whether ultrafast ultrasound descriptors of costal diaphragm during bilateral phrenic magnetic stimulation can provide a noninvasive alternative for assessing diaphragm contractility. Thirty patients (19 men and 11 women) referred for suspected diaphragm dysfunction (median age 57 [42-63] years) underwent bilateral anterolateral magnetic stimulation with simultaneous ultrafast ultrasound and oesophageal/gastric pressure recordings. Peak diaphragm tissue velocity, acceleration and jerk were extracted. Associations with Pdi,tw were assessed using ridge regression. Diagnostic performance for detecting abnormal Pdi,tw (< 20 cmH2O) was evaluated using Bayesian receiver operating characteristic (ROC) analysis, including posterior mean AUC and 95% credible intervals. Agreement between predicted and measured Pdi,tw was assessed using Lin's concordance correlation coefficient and Passing-Bablok regression. Twenty four of 30 patients (80%) had abnormal Pdi,tw. Ultrafast ultrasound descriptors correlated with Pdi,tw (Spearman's ρ: velocity 0.77 [95% CI, 0.57-0.89], acceleration 0.70 [95% CI, 0.41-0.87], jerk 0.67 [95% CI, 0.43-0.85]; all p < 0.0001). The multivariable ridge model explained 66% of the variance in Pdi,tw and showed high agreement with measured values (Lin's concordance correlation coefficient = 0.87 [95% CI, 0.75-0.93]). Bayesian ROC analysis demonstrated strong discrimination of diaphragm dysfunction (AUC = 0.91; 95% credible interval [CrI], 0.76-0.98). Using the clinical threshold of 20 cmH2O, model-predicted Pdi,tw yielded a sensitivity of 75% and specificity of 100%. The optimal velocity threshold for discriminating abnormal Pdi,tw was 10.25 mm·ms-1 (95% CrI, 6.12-18.58 mm·ms-1). The corresponding thresholds for acceleration and jerk were 408.6 mm·ms-2 (95% CrI, 122.6-952.4) and 3073 mm·ms-3 (95% CrI, 1038.8-11541.4), respectively. Ultrafast ultrasound coupled with magnetic phrenic stimulation provides a feasible, noninvasive, nonvolitional assessment of diaphragm contractility. Diaphragm motion descriptors reliably predicted Pdi,tw and enabled accurate identification of diaphragm dysfunction. These findings support further clinical evaluation and warrant larger multicentre validation studies.
Cardiopulmonary exercise testing (CPET) assesses physiological responses to incremental exercise and identifies potential causes of exercise limitation. There have been several population-specific reference equations published, but none that span the human age range. It would be advantageous to have all-age global reference ranges. This task force aimed to derive Global Lung Function Initiative reference equations for peak oxygen uptake (V̇ O2 peak) and peak work rate (Wpeak) in healthy individuals. CPET data were collected retrospectively. Generalised additive models of location, shape and scale were used to develop reference ranges, including age, sex, height and weight as explanatory variables. The influence of geographic region, equipment, testing protocols and averaging methods for peak exercise data were also examined. Data from 5956 healthy individuals aged between 6 and 83 years across 17 sites in Europe, North and South America and Asia were analysed. There was substantial between-subject variability in both V̇ O2 peak and Wpeak, with wide confidence intervals across age groups. Heterogeneity in V̇ O2 peak was related to geographic region, metabolic cart type, and averaging methods for peak exercise values. Controlling for these variables improved model fit, but not sufficiently to be reliable predictors for reference ranges. Significant heterogeneity in CPET testing methodology and outcomes between sites precluded the development of reference ranges for V̇ O2 peak and Wpeak. This task force has developed a framework for prospective data collection with strictly standardised protocols and centralised data analysis to reduce variability and establish robust, clinically meaningful reference ranges for CPET outcomes.
Respiratory muscle dysfunction is prevalent in congenital myopathies and often leads to respiratory failure. Ultrasound shear wave elastography (SWE) measures tissue elasticity and has been proposed as an alternative to invasive measures of respiratory muscle contractility. This study aims to evaluate SWE to assess respiratory muscle function in healthy individuals and congenital myopathy patients, while also determining SWE reliability. Shear wave velocity in the diaphragm, parasternal intercostal, sternocleidomastoid, external oblique, internal oblique, and transverse abdominal muscles was acquired in healthy participants and congenital myopathy patients during different maneuvers. Mouth pressure (Pmo) was acquired simultaneously with SWE acquisition. Furthermore, transdiaphragmatic pressure (Pdi) was acquired in healthy participants. All measurements were repeated by two observers to assess reliability. Twenty-one congenital myopathy patients and 20 healthy participants were included. Shear wave velocity did not differ between healthy participants and patients during any maneuver in any muscle, and Pmo and Pdi were not correlated with shear wave velocity. Intraobserver intraclass correlation coefficients (ICC) varied between 0.28-0.95 for healthy participants and 0.62-0.95 for patients. Interobserver ICC varied between 0.00 and 0.87 for healthy participants and 0.00-0.79 for patients. Test-retest ICC varied between 0.00-0.66 for healthy participants and 0.00-0.72 for patients. The absence of differences in shear wave velocity between healthy participants and patients, and the low reliability estimates, indicate that SWE of the respiratory muscles is not suitable in routine clinical care or research. The complex mechanical properties of the respiratory muscles introduce challenges that may require alternative SWE techniques.
Oropharyngeal dysphagia is a common geriatric syndrome associated with an increased risk of aspiration pneumonia, malnutrition, functional decline and mortality. Presentation of the neurogeriatric syndromology of dysphagia by integrating disease-specific neurological and transdiagnostic geriatric aspects, including diagnostic and therapeutic approaches. A literature review and analysis of current clinical guidelines were conducted. Dysphagia presents as a multietiological syndrome with heterogeneous clinical phenotypes identifiable by instrumental assessment, particularly flexible endoscopic evaluation of swallowing (FEES). Besides disease-specific neurological mechanisms, transdiagnostic factors, such as presbyphagia with reduced pharyngeal sensation, sarcopenia and decreased neuroplasticity play a crucial role. Multimodal therapeutic approaches have proven to be effective. In various neurological disorders, disease-specific treatment also leads to an improvement in swallowing function. Across different conditions, protective measures (e.g., nutritional therapy and oral hygiene) as well as rehabilitative interventions have been shown to be effective. Geriatric-specific adapted assessment tools and care pathways are required to improve clinical outcomes and quality of life. HINTERGRUND: Oropharyngeale Dysphagie ist ein häufiges geriatrisches Syndrom mit erhöhtem Risiko für Aspirationspneumonien, Mangelernährung, Funktionsverlust und Mortalität. Darstellung der neurogeriatrischen Syndromologie durch Integration erkrankungsspezifischer neurologischer sowie transdiagnostischer geriatrischer Aspekte, einschließlich Diagnostik und Therapie. Es erfolgten eine Literaturrecherche sowie eine Analyse aktueller nationaler und internationaler Leitlinien. Dysphagie ist ein multiätiologisches Syndrom mit heterogenen klinischen Phänotypen, die mithilfe instrumenteller Dysphagiediagnostik, insbesondere durch die Flexible Endoskopische Evaluation des Schluckens (FEES), differenziert erfasst werden können. Neben erkrankungsspezifischen neurologischen Pathomechanismen spielen transdiagnostische Faktoren wie Presbyphagie mit reduzierter pharyngealer Sensibilität, Sarkopenie sowie eine verminderte Neuroplastizität eine zentrale Rolle. Multimodale Therapieansätze erweisen sich als wirksam: Bei verschiedenen neurologischen Erkrankungen geht die spezifische Behandlung auch mit einer Verbesserung der Schluckfunktion einher. Erkrankungsübergreifend erweisen sich sowohl protektive Maßnahmen (z. B. Ernährungstherapie und optimierte Mundhygiene) als auch rehabilitative Interventionen als effektiv. Zur Verbesserung von klinischen Outcomes und Lebensqualität sind geriatriespezifisch adaptierte Bewertungsinstrumente sowie integrierte Versorgungskonzepte erforderlich.
The beneficial effects of prophylactic noninvasive ventilation (NIV) after extubation in patients without hypercapnia are uncertain. Our objective was to assess the effects of prophylactic NIV on reintubation among patients without hypercapnia at the time of extubation. Post hoc analysis of two multicenter clinical trials including high-risk patients (i.e., patients older than 65 years or with underlying cardiac/respiratory disease). Our analysis focused on the 829 patients without hypercapnia (PaCO2 ≤ 45 mmHg), the day of extubation who received NIV alternating high-flow nasal cannula (HFNC) oxygen or HFNC alone after extubation. The primary outcome was the proportion of patients who required reintubation within seven days following extubation. We used G-computation to robustly estimate the marginal causal effect of treatment on the risk of reintubation. After extubation, 540 patients (65%) received NIV + HFNC while 289 (35%) received HFNC alone. The reintubation rate at day 7 was 11.8% [95% CI 9.4-14.8%] with NIV + HFNC versus 17.6% [95% CI 13.7-22.5%] with HFNC alone (difference, - 5.8% [95% CI - 11.2 to -0.8%]; p = 0.021). Using G-computation, NIV + HFNC was more effective than HFNC alone in reducing the risk of reintubation, with an estimated difference of - 5.6% [95% CI - 11.0 to - 0.5%]. Reintubation rates were also significantly lower with NIV + HFNC than with HFNC alone at 48 h, 72 h, and until ICU discharge. For high-risk patients, but without hypercapnia on the day of extubation, the use of prophylactic NIV alternating with HFNC after extubation significantly decreases the risk of reintubation as compared to HFNC alone.
Dyspnoea is frequent in mechanically ventilated patients and contributes to substantial distress and a heightened risk of post-traumatic stress disorder. It attests to respiratory-related brain suffering that must be actively managed. This is particularly challenging in noncommunicative patients, hence the interest of electroencephalographic surrogates. This study aims at characterizing the effects of opioids, proposed to relieve dyspnoea, on respiratory-related cortical activity in mechanically ventilated patients. In a 16-bed intensive care unit (ICU) over a 4-month period, we consecutively included eighteen mechanically ventilated patients with self-reported dyspnoea (visual analog scale -VAS-, communicative patients) or an observation-derived suspicion of respiratory-related brain suffering (noncommunicative patients, respiratory distress observation scores -RDOS-) persisting despite ventilator settings optimisation. Participants underwent electroencephalographic (EEG) recordings before and after administration of intravenous opioids. Respiratory-related cortical activity was assessed using covariance-based connectivity analysis, preinspiratory potentials (PIPs), and time-frequency analysis (TFA) time-locked to inspiration. To disentangle respiratory-specific from general effects of opioids, TFA was also computed from randomly selected EEG segments. Opioids reduced dyspnoea evaluated by VAS and RDOS without significant sedation. EEG covariance analysis showed changes in brain state in 15 of 18 patients. PIP occurrence was variable and not modulated by opioids. TFA revealed statistically significant opioid-induced modulations in low beta and high beta power bands time-locked to inspiration, not observed in randomly timed analyses hence a specific effect of opioids on respiratory-related cortical networks. Opioids can relieve dyspnoea in mechanically ventilated ICU patients and modulate respiratory-related cortical activity beyond their general effects on cortical electrogenesis. This suggests that their effects on breathing control are not limited to brainstem mechanisms.
Sleep has traditionally been conceptualized as a state of cognitive disconnection, yet emerging evidence indicates that decision-making capacities persist across sleep stages. Here, we elucidate the computational mechanisms underlying real-time lexical decision-making during polysomnographically-verified sleep, using facial electromyography and hierarchical drift diffusion modeling in both healthy individuals and participants with narcolepsy. We found that lexical decision-making was preserved during N1 and lucid REM sleep, but relied on distinct computational strategies: in N1 sleep, both enhanced sensory-motor processing and increased evidence accumulation supported decisions about words, whereas in lucid REM sleep, lexical decisions were driven exclusively by evidence accumulation processes. Cross-state comparisons revealed two fundamental principles: (1) Selective preservation-during N1 sleep, lexical decisions for words were maintained while those for pseudowords were selectively impaired, indicating that cognitive resources during sleep are preferentially allocated to meaningful stimuli; (2) Parallel strategic adaptations-during lucid REM sleep, participants increased their decision thresholds, requiring more evidence before responding, which helped maintain accuracy even though the efficiency of evidence accumulation was reduced. Our findings demonstrate that, rather than a passive decline, sleep involves dynamic and state-specific reconfiguration of the computational mechanisms underlying decision-making, with important implications for understanding consciousness and cognitive flexibility.
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Narcolepsy type 1 (NT1) is increasingly recognized as a multidimensional disorder in which psychiatric and psychosocial difficulties contribute to disability. Yet little is known about how these difficulties are perceived by patients compared with close informants. This study examined discrepancies between self-reported and informant-reported psychobehavioral symptoms in adults with NT1. Within the multicenter French NarcoScol-NarcoVitae cross-sectional case-control study, 174 adults with NT1 (18-58 years) and 126 age- and sex-matched non-relative controls completed the Adult Self-Report (ASR), a standardized measure of adult psychobehavioral problems. A close informant completed the parallel Adult Behavior Checklist (ABCL), yielding 97 NT1 and 96 control ASR-ABCL dyads. T-scores were computed for internalizing and externalizing scales, and the total problems score. Between-group differences (NT1 vs non-relative controls) and within-individual discrepancies between self- and informant-reported symptoms were analyzed. Narcolepsy severity (NSS), sleepiness (ESS), age at diagnosis, and a composite professional prognosis score were compared across concordant and discordant dyads. Patients with NT1 reported significantly higher psychiatric symptom severity than controls across all ASR scales, with 44.8% versus 19.1% in the clinical range for internalizing difficulties. Informants generally rated patients' symptom severity as lower than patients' self-reports, particularly for internalizing symptoms. Discordant dyads in which informants rated internalizing symptoms as more severe than patients were characterized by lower NT1 symptom burden (NSS). Concordant patient-informant evaluations were associated with a more favorable professional prognosis. Adults with NT1 report substantial psychobehavioral impairments that are not consistently identified by close informants, especially internalizing difficulties. This perception gap highlights the complementary value of patient and informant perspectives and calls for improved recognition of less visible symptoms within patients' close environment. NCT03765892.
Acute hypoxaemic respiratory failure (ARF) is the leading cause of intensive care unit (ICU) admission among immunocompromised patients. However, contemporary data regarding the epidemiology, management, and outcomes of ARF in this population remain scarce. We aimed to identify predictors of mortality and intubation in immunocompromised patients admitted to the ICU with ARF. This retrospective observational study was conducted in 103 ICUs in 26 countries. Adults (≥18 years) with ARF and immunodeficiency were eligible for inclusion. Patient data, including information on the nature of underlying immunosuppression, the cause of ARF, and the oxygenation strategy, were obtained from electronic medical records or medical charts. The primary outcome was to report 30-day mortality and identify associated factors in patients with complete data for all variables. Cox proportional hazards models were used to identify variables associated with mortality, and differences between groups were compared with χ2 tests or two-sided Wilcoxon rank-sum tests, with p values of less than 0·05 considered significant. 9854 immunocompromised patients with ARF admitted to participating ICUs between Jan 1, 2017, and Dec 31, 2023, were included in the study. The median age was 64 years (IQR 54-71); 3941 (40·0%) patients were female and 5913 (60·0%) were male. The main causes of immunodeficiency were a haematological malignancy (4759 [48·3%] of 9854 patients) or solid malignancy (3818 [38·7%] patients). Infection was the leading cause of ARF (6610 [62·0%] of 9854 patients); 5288 (53·7%) patients had more than one contributing cause of ARF, and no cause was identified in 1490 (15·1%) patients. The median partial pressure of oxygen in arterial blood (PaO2)/fractional concentration of oxygen in inspired air (FiO2) ratio was 198 [IQR 141-208]. The 30-day mortality rate was 47·3% (4662 patients). Predictors of higher mortality were older age (hazard ratio 1·01 [IQR 1·00-1·02]), higher Charlson Comorbidity Index score (1·04 [1·01-1·07]), higher Frailty Index score (1·22 [1·16-1·28]), longer time from hospital to ICU admission (1·02 [1·01-1·03]), higher respiratory rate (1·02 [1·02-1·03]), coma at ICU admission (2·04 [1·72-2·43]), invasive fungal infection as cause of ARF (1·82 [1·45-2·28]), disease-specific infiltrates (1·73 [1·32-2·26]), unidentified cause of ARF (2·16 [1·74-2·68]), and use of vasoactive drugs (2·45 [2·10-2·86]) or renal replacement therapy (2·07 [1·74-2·48]). Protective factors included receipt of a solid organ transplant (0·62 [0·49-0·79]), systemic vasculitis or connective tissue disease (0·61 (0·47-0·78]), higher PaO2/FiO2 ratio (0·78 [0·72-0·84]), receipt of high-flow nasal oxygen therapy (0·78 [0·64-0·95]), and cardiogenic pulmonary oedema (0·67 [0·51-0·89]). In this large international cohort of immunocompromised patients with ARF, we identified key risk and protective factors for mortality and intubation. These findings could improve outcomes by informing timely clinical decisions, goals-of-care discussions, and management in this vulnerable population. Kirsten and Freddy Johansen Foundation and Groupe de Recherche en Réanimation Onco-Hématologique.
Glenzocimab, a platelet glycoprotein VI antagonist, is a novel agent that inhibits platelet activation and aggregation. Its safety was demonstrated in the ACTIMIS trial (Acute Ischemic Stroke Interventional Study; URL: https://www.clinicaltrials.gov; Unique identifier: NCT03803007) for patients with stroke receiving thrombolysis, with or without mechanical thrombectomy, and results suggested a reduction in intracranial hemorrhages and mortality. The ACTISAVE trial was designed as a confirmatory study to evaluate the efficacy and safety of glenzocimab in acute ischemic stroke. ACTISAVE (Acute Ischemic Stroke Study Evaluating Glenzocimab Used as Add-On Therapy Versus Placebo) was an international, randomized, double-blind, placebo-controlled phase 2/3 study in patients with stroke, treated by thrombolysis within 4.5 hours of symptoms onset with or without mechanical thrombectomy. The study was conducted at 54 primary and comprehensive stroke centers located in 10 countries. Patients were randomized 1:1 to glenzocimab (1000 mg-IV) or placebo. The primary outcome was the modified Rankin Scale (mRS) score of 4 to 6 at day 90. Key secondary outcome was the mRS score of 0 to 2 at day 90. Mortality, mRS shift, National Institutes of Health Stroke Scale score, quality of life, and safety outcomes were assessed. Between September 2021 and October 2023, 438 patients were randomized, 421 treated, and included as randomized in the primary analysis set. Median age was 73 (63-80) years, and 43% were female. Thrombolysis was performed 2.3 hours (median) after symptom onset and followed by mechanical thrombectomy in 36% of patients. The assigned treatment began a median of 1.2 (interquartile range, 0.8-1.6) hours after thrombolysis initiation. Prethrombolysis National Institutes of Health Stroke Scale score median was 9 (6-15). At day 90, there was no statistically significant difference in the primary outcome between the treatment groups: the incidence of poor outcome (mRS score 4-6 versus 0-3) was 21.6% in the glenzocimab group compared with 15.3% placebo group (odds ratio, 1.51 [95% CI, 0.90-2.54]; P=0.120). No statistically significant difference in secondary outcomes was observed. There were no major safety signals with any intracerebral hemorrhage occurring respectively in 60 (28.6%) and 63 (29.9%) patients in glenzocimab and placebo arms. ACTISAVE failed to confirm a beneficial effect of glenzocimab on mRS in patients with acute ischemic stroke treated by thrombolysis. URL: https://www.clinicaltrials.gov; Unique identifier: NCT05070260.
Lung-protective ventilation is the current standard for mechanical ventilation of patients with acute respiratory distress syndrome (ARDS). Traditionally, this approach has focused on the controlled phase of mechanical ventilation, but emerging data suggest that how patients are managed during assisted ventilation may also impact clinical outcomes. Experimental and observational clinical data indicate that excessive respiratory effort may further damage already injured lungs and may also lead to diaphragm myotrauma. Conversely, insufficient effort and prolonged passive ventilation are associated with diaphragm atrophy and dysfunction. Recent non-invasive techniques to monitor respiratory drive and effort at the bedside have facilitated the development of a new strategy to protect both the lungs and the diaphragm. The lung- and diaphragm-protective (LDP) ventilation framework highlights the need to better integrate ventilation and sedation strategies to facilitate timely and safe spontaneous breathing. This new paradigm has driven the development of emerging supportive and therapeutic modalities, such as diaphragm neurostimulation and partial neuromuscular blockade. Clinical trials are needed to evaluate the impact of LDP strategies on patient-centered outcomes, using designs that account for the possibility of heterogeneity of treatment effect in the ARDS population. In this review, we summarize the physiological background for the LDP framework, as well as the current clinical evidence evaluating this strategy.
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Unilateral diaphragmatic dysfunction can cause exertional and postural dyspnoea, along with sleep-related breathing disturbances. Diaphragm plication alleviates daytime symptoms, but its effects on sleep have not been evaluated in detail. We analysed prospectively collected observational data in 12 patients undergoing surgical plication for unilateral diaphragmatic dysfunction. Standardised pre- and postoperative assessments included ratings of exertional dyspnoea, orthopnoea and antepnoea (D-VAS), quality of life (VSRQ), spirometry (sitting and supine), transdiaphragmatic twitch pressures, and polysomnography (PSG). Sleep-disordered breathing was evaluated using standard PSG indices including the obstructive apnoea-hypopnoea index (oAHI), measured globally and during REM. Following plication, dyspnoea decreased and orthopnoea and antepnoea were nearly abolished (p = 0.0123 and p = 0.0001, respectively). VSRQ improved (p = 0.0078). Supine vital capacity rose from 52.5% to 75.0% predicted (p = 0.0010), and supine VC drop decreased from 15.1% to 2.65% (p = 0.0068). Twitch pressures increased significantly. oAHI decreased from 15.5 to 8.5 events·h⁻¹ (not significant after multiplicity correction). REM AHI decreased from 43.0 [24.5-66.9] to 19.0 [11.5-23.3] events·h⁻¹ (p = 0.0020), and REM hypopnoea index from 19.5 to 11.0 (p = 0.0098). Strong correlations were found between REM AHI changes and both FRC and expiratory reserve volume (ERV). In patients with unilateral diaphragmatic dysfunction, diaphragm plication is associated with improved REM-related obstructive events. This may relate to lung volume restoration. These exploratory findings suggest that prospective studies are needed to determine the usefulness of systematic pre-post plication PSG for patient selection and outcome evaluation.