Nonsurgical Management of Shoulder Pain in Rotator Cuff Tears: Ultrasound-Guided Biceps Tenotomy Combined With Corticosteroid Injection.

Traditionally, the management of rotator cuff tears in elderly individuals has involved surgical intervention, specifically biceps tenotomy. However, surgical procedures come with inherent medical risks and significant financial costs. As an alternative, ultrasound-guided biceps tenotomy combined with corticosteroid has emerged as a highly effective, well-tolerated, and cost-efficient option. This article aims to describe the procedural technique of nonsurgical management using ultrasound-guided biceps tenotomy combined with corticosteroid injection.

Safety and Efficacy of Pulmonary Rehabilitation for Long COVID Patients Experiencing Long-Lasting Symptoms.

Due to the high prevalence and persistence of long COVID, it is important to evaluate the safety and efficacy of pulmonary rehabilitation (PR) for patients who experience long-lasting symptoms more than six months after initial COVID-19 onset. Enrolled patients were admitted for a four-week in-patient-PR due to long COVID symptoms (n = 47). The safety of PR was confirmed by the absence of adverse events. Symptom-related outcomes were evaluated pre- and post-PR with significant score changes for: 6 min walking distance (61 [28 to 103] m), quality of life (mental Short Form-12: 10 [6 to 13], and physical: 9 [6 to 12]), Montreal Cognitive Assessment (1 [0 to 3]), fatigue (MFI-20: -19 [-28 to -8]), dyspnea (DYSPNEA-12: -7 [-9 to -2] and mMRC; -1 [-1 to 0]), Nijmegen questionnaire (-8 [-11 to -5]), anxiety and depression (HADS:-4 [-5 to -2] and -2 [-4 to -1], respectively) and posttraumatic stress disorder checklist scale (-8 [-12 to -4]). At the individual level, the percentage of symptomatic patients for each outcome decreased, with a high response rate, and the number of persistent symptoms per patient was reduced from six at PR initiation to three at the end of the program. Our results show that in-PR is safe and efficient at decreasing long-lasting symptoms experienced by long COVID patients at more than six months after initial disease onset.

Time-Course of Changes in Multidimensional Fatigue and Functional Exercise Capacity and Their Associations during a Short Inpatient Pulmonary Rehabilitation Program.

This study aimed to assess the time-course of changes in multidimensional fatigue and functional exercise capacity and their associations during an inpatient pulmonary rehabilitation (PR) program. Seventy COPD patients from three centres were enrolled for a four-week PR program and were evaluated before (T0) and at the end of each week (T1, T2, T3, and T4). Weekly change in multidimensional fatigue was assessed by the multidimensional inventory questionnaire (MFI-20) and functional exercise capacity by the 6-minute walking distance (6MWD). Reaction time (RT) and heart rate variability (HRV) were also assessed as complementary markers of fatigue. HRV did not change during the study (all p > 0.05). MFI-20 score and RT decreased during the first part of the program (p < 0.001) and levelled off at T2 (all p > 0.05 compared with each preceding time). While 6MWD improved by almost 70% during the first part of the PR, it continued to increase, albeit at a greatly reduced pace, between T2 and T4 (p < 0.05). In parallel, a negative association was found between MFI-20 score and 6MWD at each evaluation time (r ranged from 0.43 to 0.71), with a significantly stronger T3 correlation compared with the other time periods (all p < 0.05). The strengthening of the association between fatigue and functional exercise capacity at T3, which occurred concomitantly with the slowdown of functional exercise capacity improvement, is consistent with a role for fatigue in the limitation of performance changes during PR. The limitation of fatigue during PR is thus an interesting aspect to improve the magnitude of performance changes.

Is bilateral corticospinal connectivity impaired in patients with chronic obstructive pulmonary disease?

KEY POINTS: During moderate and high levels of quadriceps force production, the ipsilateral motor cortex is concomitantly activated with the contralateral motor cortex throughout the corpus callosum to generate the motor command. Chronic obstructive pulmonary disease (COPD) patients display a structurally impaired corpus callosum that may explain the reduced motor command in this population, which in turn contributes to COPD-related muscle weakness of the knee extensors. The study aimed to determine whether bilateral connectivity was impaired and ipsilateral activation was lowered during unilateral strength production of the knee extensors. Our results indicate impaired bilateral connectivity but preserved ipsilateral activation in patients during unilateral isometric contractions of 50% of maximum voluntary strength. The preservation of ipsilateral activation during force production despite impaired bilateral connectivity is consistent with a reorganization of bilateral motor network function that drives unilateral strength production. ABSTRACT: The contralateral primary motor cortex (M1) is not the only brain area implicated in motor command generation. During moderate and high levels of quadriceps force production, the ipsilateral M1 is concomitantly activated. Such activation is mediated by the corpus callosum, the main component of bilateral connectivity. Structural damage to the corpus callosum has been observed in chronic obstructive pulmonary disease (COPD) patients, which might reduce ipsilateral activation and contribute to the lower motor command associated with COPD muscle weakness. We thus aimed to determine whether bilateral connectivity and ipsilateral activation were impaired in COPD. Twenty-two COPD patients and 21 healthy age-matched controls were evaluated by transcranial magnetic stimulation, at rest and during 50% of maximal voluntary isometric contraction (MVIC) of the dominant vastus lateralis muscle. Bilateral connectivity was determined by the ipsilateral silent period (iSP) during 50% MVIC. Ipsilateral activation was determined as the increase in ipsilateral excitability from rest to 50% MVIC. As expected, COPD patients had significantly lower MVIC (-25%, p = 0.03). These patients also showed a significantly lower iSP (-53%, p < 0.001) compared to controls. The ipsilateral excitability was increased in patients and controls (×2.5 and ×3.5, respectively, p < 0.001) but not differently between groups (p = 0.84). Despite impaired bilateral connectivity in COPD, ipsilateral activation was not increased. Reorganization in the patients' interhemispheric pathways could explain the preserved ipsilateral activation.

Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness.

BACKGROUND: Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness. METHODS: Twenty-two patients with quadriceps weakness (COPDMW), 18 patients with preserved quadriceps strength (COPDNoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VAperipheral) and transcranial magnetic (VAcortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions. RESULTS: COPDMW exhibited lower VAcortical and lower MEP/Mmax compared with COPDNoMW (p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VAcortical and MEP/Mmax. CONCLUSIONS: COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.

Psychoactive medications in chronic obstructive pulmonary disease patients: From prevalence to effects on motor command and strength.

INTRODUCTION: In chronic-obstructive pulmonary disease (COPD) patients, the peripheral muscle weakness is partly due to reduced motor command. The psychoactive medications, which are often prescribed in COPD, are mainly inhibitory and thus may contribute to motor command reduction. The aims were to characterize and quantify the use of these drugs and determine their effects on cortical excitability and inhibition and thus on motor command and muscle weakness in these patients. METHODS: First, a prevalence study was conducted on 421 COPD patients. Second, cortical excitability, inhibition and voluntary activation were assessed in 40 patients (15 under psychoactive medications vs. 25 controls) by transcranial magnetic stimulation of the rectus femoris. Quadriceps maximal isometric strength was also assessed. RESULTS: About 48% of the patients were taking psychoactive medication. Benzodiazepines (21%) and antidepressants (13.5%) were the most prescribed. Patients with medications tended to be younger and isolated (p < 0.05). They also showed impaired cortical inhibition and decreased cortical excitability (+36%, p = 0.02). Voluntary activation was reduced (-3.6%, p = 0.04) but quadriceps strength was comparable between groups. CONCLUSIONS: Psychoactive medications are prevalent in COPD patients. Patients under these medications exhibited brain impairment and reduced motor command. Paradoxically, voluntary strength was unaltered.

Impact of Chronic Obstructive Pulmonary Disease on Cognitive and Motor Performances in Dual-Task Walking.

When two tasks are performed simultaneously, they compete for attentional resources, resulting in a performance decrement in one or both tasks. Patients with attention disorders have a reduced ability to perform several tasks simultaneously (e.g., talking while walking), which increases the fall risk and frailty. This study assessed the cognitive and motor performances of patients with COPD and healthy controls within a dual-task walking paradigm. A subobjective was to assess the impact of a pulmonary rehabilitation program on the dual-task performances in COPD. Twenty-five patients with COPD and 20 controls performed a cognitive task (subtraction) and a 15-m walking test separately (single-task; ST) and jointly (dual-task; DT). In addition, a subsample of 10 patients performed the same evaluations 5 weeks later after a pulmonary rehabilitation program following current recommendations. Cognitive and gait performances in ST showed no differences between patients with COPD and controls (all p > 0.05). However, COPD patients exhibited a greater increase in gait variability than controls in DT (4.07 ± 1.46% vs. 2.17 ± 0.7%, p < 0.001). The pulmonary rehabilitation program had no effect on the dual-task impairment for the subsample of patients (p = 0.87). This study provides evidence of insufficient attentional resources to successfully deal with DT in patients with COPD, and this was expressed through an exaggerated increase in gait variability in DT walking. Given the high risk of falls and disability associated with altered gait variability, dual-task training interventions should be considered in pulmonary rehabilitation programs.

Prevention of Crush Syndrome through Aggressive Early Resuscitation: Clinical Case in a Buried Worker.

UNLABELLED: Introduction Crush syndrome, of which little is known, occurs as a result of compression injury to the muscles. This syndrome is characterized by systemic manifestations such as acute kidney injury (AKI), hypovolemic shock, and hydroelectrolytic variations. This pathology presents high morbidity and mortality if not managed aggressively by prehospital care. Clinical Case A 40-year-old worker was rescued after being buried underground in a ditch for 19 hours. The patient was administered early resuscitation with isotonic solutions and monitored during the entire rescue operation. Despite having increased plasma levels of total creatine kinase (CK), the patient did not develop AKI or hydroelectrolytic variations. CONCLUSION: Aggressive early management with isotonic solutions before hospital arrival is an effective option for nephron-protection and prevention of crush syndrome. Mardones A , Arellano P , Rojas C , Gutierrez R , Oliver N , Borgna V . Prevention of crush syndrome through aggressive early resuscitation: clinical case in a buried worker. Prehosp Disaster Med. 2016;31(3):340-342.

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation.

STUDY OBJECTIVES: Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. METHODS: One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index < 15) had polysomnographic sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. RESULTS: A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). CONCLUSIONS: Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. CLINICAL TRIAL REGISTRATION: The study was registered at www.clinicaltrials.gov as NCT01679782.

Cortical implication in lower voluntary muscle force production in non-hypoxemic COPD patients.

Recent studies have shown that muscle alterations cannot totally explain peripheral muscle weakness in COPD. Cerebral abnormalities in COPD are well documented but have never been implicated in muscle torque production. The purpose of this study was to assess the neural correlates of quadriceps torque control in COPD patients. Fifteen patients (FEV1 54.1±3.6% predicted) and 15 age- and sex-matched healthy controls performed maximal (MVCs) and submaximal (SVCs) voluntary contractions at 10, 30 and 50% of the maximal voluntary torque of the knee extensors. Neural activity was quantified with changes in functional near-infrared spectroscopy oxyhemoglobin (fNIRS-HbO) over the contralateral primary motor (M1), primary somatosensory (S1), premotor (PMC) and prefrontal (PFC) cortical areas. In parallel to the lower muscle torque, the COPD patients showed lower increase in HbO than healthy controls over the M1 (p<0.05), PMC (p<0.05) and PFC areas (p<0.01) during MVCs. In addition, they exhibited lower HbO changes over the M1 (p<0.01), S1 (p<0.05) and PMC (p<0.01) areas during SVCs at 50% of maximal torque and altered motor control characterized by higher torque fluctuations around the target. The results show that low muscle force production is found in a context of reduced motor cortex activity, which is consistent with central nervous system involvement in COPD muscle weakness.