Search

Purpose: This study aimed to non-invasively test the hypothesis that (a) short-term lower limb unloading would induce changes in the neural control of force production (based on motor units (MUs) properties) in the vastus lateralis muscle and (b) possible changes are reversed by active recovery (AR). Methods: Ten young males underwent 10 days of unilateral lower limb suspension (ULLS) followed by 21 days of AR. During ULLS, participants walked exclusively on crutches with the dominant leg suspended in a slightly flexed position (15°–20°) and with the contralateral foot raised by an elevated shoe. The AR was based on resistance exercise (leg press and leg extension) and executed at 70% of each participant's 1 repetition maximum, 3 times/week. Maximal voluntary isometric contraction (MVC) of knee extensors and MUs properties of the vastus lateralis muscle were measured at baseline, after ULLS, and after AR. MUs were identified using high-density electromyography during trapezoidal isometric contractions at 10%, 25%, and 50% of the current MVC, and individual MUs were tracked across the 3 data collection points. Results: We identified 1428 unique MUs, and 270 of them (18.9%) were accurately tracked. After ULLS, MVC decreased by 29.77%, MUs absolute recruitment/derecruitment thresholds were reduced at all contraction intensities (with changes between the 2 variables strongly correlated), while discharge rate was reduced at 10% and 25% but not at 50% MVC. Impaired MVC and MUs properties fully recovered to baseline levels after AR. Similar changes were observed in the pool of total as well as tracked MUs. Conclusion: Our novel results demonstrate, non-invasively, that 10 days of ULLS affected neural control predominantly by altering the discharge rate of lower-threshold but not of higher-threshold MUs, suggesting a preferential impact of disuse on motoneurons with a lower depolarization threshold. However, after 21 days of AR, the impaired MUs properties were fully restored to baseline levels, highlighting the plasticity of the components involved in neural control.

• Little is known about the consequences of disuse on the neural control of large muscles and how these can be reversed. • We studied changes in motor units properties in the vastus lateralis muscle after 10 days of unilateral lower limb suspension and after 21 days of active recovery. • A short period of muscle unloading reduces the discharge rate of lower- but not of higher-threshold motor units, suggesting a preferential impact of disuse on motoneurons with a lower depolarization threshold. • The restoration of neural control requires about twice the duration of the disuse period. This study aimed to non-invasively test the hypothesis that (a) short-term lower limb unloading would induce changes in the neural control of force production (based on motor units (MUs) properties) in the vastus lateralis muscle and (b) possible changes are reversed by active recovery (AR). Ten young males underwent 10 days of unilateral lower limb suspension (ULLS) followed by 21 days of AR. During ULLS, participants walked exclusively on crutches with the dominant leg suspended in a slightly flexed position (15°–20°) and with the contralateral foot raised by an elevated shoe. The AR was based on resistance exercise (leg press and leg extension) and executed at 70% of each participant's 1 repetition maximum, 3 times/week. Maximal voluntary isometric contraction (MVC) of knee extensors and MUs properties of the vastus lateralis muscle were measured at baseline, after ULLS, and after AR. MUs were identified using high-density electromyography during trapezoidal isometric contractions at 10%, 25%, and 50% of the current MVC, and individual MUs were tracked across the 3 data collection points. We identified 1428 unique MUs, and 270 of them (18.9%) were accurately tracked. After ULLS, MVC decreased by 29.77%, MUs absolute recruitment/derecruitment thresholds were reduced at all contraction intensities (with changes between the 2 variables strongly correlated), while discharge rate was reduced at 10% and 25% but not at 50% MVC. Impaired MVC and MUs properties fully recovered to baseline levels after AR. Similar changes were observed in the pool of total as well as tracked MUs. Our novel results demonstrate, non-invasively, that 10 days of ULLS affected neural control predominantly by altering the discharge rate of lower-threshold but not of higher-threshold MUs, suggesting a preferential impact of disuse on motoneurons with a lower depolarization threshold. However, after 21 days of AR, the impaired MUs properties were fully restored to baseline levels, highlighting the plasticity of the components involved in neural control. [Display omitted] [ABSTRACT FROM AUTHOR]

IntroductionLeprosy is an infectious disease that remains with a high number of new cases in developing countries. Household contacts have a higher risk for the development of the disease, but the neural impairment in this group is not well elucidated yet. Here, we measured the chance of occurrence of peripheral neural impairment in asymptomatic leprosy household.MethodsContacts who present anti-PGL-I IgM seropositivity, through electroneuromyography (ENMG) evaluation. We recruited 361 seropositive contacts (SPC) from 2017 to 2021, who were subjected to an extensive protocol that included clinical, molecular, and electroneuromyographic evaluations.ResultsOur data revealed a positivity of slit skin smear and skin biopsy qPCR of 35.5% (128/361) and 25.8% (93/361) respectively. The electroneuromyographic evaluation of the SPC showed neural impairment in 23.5% (85/361), with the predominance of a mononeuropathy pattern in 62.3% (53/85). Clinical neural thickening was observed in 17.5% (63/361) of seropositive contacts, but among the individuals with abnormal ENMG, only 25.9% (22/85) presented neural thickening in the clinical exam.DiscussionOurs results corroborates the need to make the approach to asymptomatic contacts in endemic countries more timely. Since leprosy in its early stages can present an indolent and subclinical evolution, serological, molecular, and neurophysiological tools are essential to break the disease transmission chain.

Abstract Background ETB has been reported to regulate neurogenesis and vasoregulation in foetal development. Its dysfunction was known to cause HSCR, an aganglionic colonic disorder with syndromic forms reported to associate with both small heads and developmental delay. We therefore asked, "is CNS maldevelopment a more general feature of ETB mutation?" To investigate, we reviewed the micro-CT scans of an ETB −/− model animal, sl/sl rat, and quantitatively evaluated the structural changes of its brain constituents. Methods Eleven neonatal rats generated from ETB +/− cross breeding were sacrificed. Micro-CT scans were completed following 1.5% iodine-staining protocols. All scans were reviewed for morphological changes. Selected organs were segmented semi-automatically post-NLM filtering: TBr, T-CC, T-CP, OB, Med, Cer, Pit, and S&I Col. Volumetric measurements were made using Drishti rendering software. Rat genotyping was completed following analysis. Statistical comparisons on organ volume, organ growth rate, and organ volume/bodyweight ratios were made between sl/sl and the control groups based on autosomal recessive inheritance. One-way ANOVA was also performed to evaluate potential dose-dependent effect. Results sl/sl rat has 16.32% lower body weight with 3.53% lower growth rate than the control group. Gross intracranial morphology was preserved in sl/sl rats. However, significant volumetric reduction of 20.33% was detected in TBr; similar reductions were extended to the measurements of T-CC, T-CP, OB, Med, and Pit. Consistently, lower brain and selected constituent growth rates were detected in sl/sl rat, ranging from 6.21% to 11.51% reduction. Lower organ volume/bodyweight ratio was detected in sl/sl rats, reflecting disproportional neural changes with respect to body size. No consistent linear relationships exist between ETB copies and intracranial organ size or growth rates. Conclusion Although ETB −/− mutant has a normal CNS morphology, significant size reductions in brain and constituents were detected. These structural changes likely arise from a combination of factors secondary to dysfunctional ET-1/ET-3/ETB signalling, including global growth impairment from HSCR-induced malnutrition and dysregulations in the neurogenesis, angiogenesis, and cerebral vascular control. These changes have important clinical implications, such as autonomic dysfunction or intellectual delay. Although further human study is warranted, our study suggested comprehensive managements are required for HSCR patients, at least in ETB −/− subtype.

The persistence of quadriceps weakness represents a major concern following anterior cruciate ligament reconstruction (ACLR). The underlying adaptations occurring in the activity of spinal motoneurons are still unexplored. This study examined the discharge patterns of large populations of motor units (MUs) in the vastus lateralis (VL) and vastus medialis muscles following ACLR. Nine ACLR individuals and 10 controls performed unilateral trapezoidal contractions of the knee extensor muscles at 35%, 50% and 70% of the maximal voluntary isometric force (MVIF). High‐density surface electromyography (HDsEMG) was used to record the myoelectrical activity of the vasti muscles in both limbs. HDsEMG signals were decomposed with a convolutive blind source separation method and MU properties were extracted and compared between sides and groups. The ACLR group showed a lower MVIF on the reconstructed side compared to the contralateral side (28.1%; P < 0.001). This force deficit was accompanied by reduced MU discharge rates (∼21%; P < 0.05), lower absolute MU recruitment and derecruitment thresholds (∼22% and ∼22.5%, respectively; P < 0.05) and lower input–output gain of motoneurons (27.3%; P = 0.009). Deficits in MU discharge rates of the VL and in absolute recruitment and derecruitment thresholds of both vasti MUs were associated with deficits in MVIF (P < 0.05). A strong between‐side correlation was found for MU discharge rates of the VL of ACLR individuals (P < 0.01). There were no significant between‐group differences (P > 0.05). These results indicate that mid‐ to long‐term strength deficits following ACLR may be attributable to a reduced neural drive to vasti muscles, with potential changes in excitatory and inhibitory synaptic inputs. Key points: Impaired expression and control of knee extension forces is common after anterior cruciate ligament reconstruction and is related to high risk of a second injury.To provide novel insights into the neural basis of this impairment, the discharge patterns of motor units in the vastus lateralis and vastus medialis were investigated during voluntary force contractions.There was lower knee extensor strength on the reconstructed side with respect to the contralateral side, which was explained by deficits in motor unit discharge rate and an altered motoneuronal input–output gain. Insufficient excitatory inputs to motoneurons and increased inhibitory afferent signals potentially contributed to these alterations.These results further our understanding of the neural underpinnings of quadriceps weakness following anterior cruciate ligament reconstruction and can help to develop effective rehabilitation protocols to regain muscle strength and reduce the risk of a second injury. [ABSTRACT FROM AUTHOR]

We adopt Bidirectional Long Short-Term Memory (BiLSTM) neural network and Wavelet Scattering Transform with Support Vector Machine (WST-SVM) classifier for detecting speech impairments of patients at the early stage of central nervous system disorders (CNSD). The study includes 339 voice samples collected from 15 subjects: 7 patients with early stage CNSD (3 Huntington, 1 Parkinson, 1 cerebral palsy, 1 post stroke, 1 early dementia), other 8 subjects were healthy. Speech data is collected using voice recorder from Neural Impairment Test Suite (NITS) mobile app. Features are extracted from pitch contours, Mel-frequency cepstral coefficients (MFCC), Gammatone cepstral coefficients (GTCC), Gabor (analytic Morlet) wavelet and auditory spectrograms. 94.50% (BiLSTM) and 96.3% (WST-SVM) accuracy is achieved for solving healthy vs. impaired classification problem. The developed method can be applied for automated CNSD patient health state monitoring and clinical decision support systems as well as a part of Internet of Medical Things (IoMT).

Brief airway occlusion produces a potent reflex inhibition of inspiratory muscles that is thought to protect against aspiration. Its duration is prolonged in asthma and obstructive sleep apnea. We assessed this inhibitory reflex (IR) in chronic obstructive pulmonary disease (COPD). Reflex responses to brief (250 ms) inspiratory occlusions were measured in 18 participants with moderate to severe COPD (age 73 ± 11 yr) and 17 healthy age-matched controls (age 72 ± 6 yr). We compared the incidence and properties of the IR between groups. Median eupneic preocclusion electromyographic activity was higher in the COPD group than controls (9.4 µV vs. 5.2 µV, P = 0.001). Incidence of the short-latency IR was higher in the COPD group compared with controls (15 participants vs. 7 participants, P = 0.010). IR duration for scalenes was similar for the COPD and control groups [73 ± 37 ms (means ± SD) and 90 ± 50 ms, respectively] as was the magnitude of inhibition. IRs in the diaphragm were not detected in the controls but were present in 9 participants of the COPD group (P = 0.001). The higher incidence of the IR in the COPD group than in the age-matched controls may reflect the increased inspiratory neural drive in the COPD group. This higher drive counteracts changes in chest wall and lung mechanics. However, when present, the reflex was similar in size and duration in the two groups. The relation between the IR in COPD and swallowing function could be assessed. [ABSTRACT FROM AUTHOR]

Background: ETB has been reported to regulate neurogenesis and vasoregulation in foetal development. Its dysfunction was known to cause HSCR, an aganglionic colonic disorder with syndromic forms reported to associate with both small heads and developmental delay. We therefore asked, "is CNS maldevelopment a more general feature of ETB mutation?" To investigate, we reviewed the micro-CT scans of an ETB-/- model animal, sl/sl rat, and quantitatively evaluated the structural changes of its brain constituents.Methods: Eleven neonatal rats generated from ETB+/- cross breeding were sacrificed. Micro-CT scans were completed following 1.5% iodine-staining protocols. All scans were reviewed for morphological changes. Selected organs were segmented semi-automatically post-NLM filtering: TBr, T-CC, T-CP, OB, Med, Cer, Pit, and S&I Col. Volumetric measurements were made using Drishti rendering software. Rat genotyping was completed following analysis. Statistical comparisons on organ volume, organ growth rate, and organ volume/bodyweight ratios were made between sl/sl and the control groups based on autosomal recessive inheritance. One-way ANOVA was also performed to evaluate potential dose-dependent effect.Results: sl/sl rat has 16.32% lower body weight with 3.53% lower growth rate than the control group. Gross intracranial morphology was preserved in sl/sl rats. However, significant volumetric reduction of 20.33% was detected in TBr; similar reductions were extended to the measurements of T-CC, T-CP, OB, Med, and Pit. Consistently, lower brain and selected constituent growth rates were detected in sl/sl rat, ranging from 6.21% to 11.51% reduction. Lower organ volume/bodyweight ratio was detected in sl/sl rats, reflecting disproportional neural changes with respect to body size. No consistent linear relationships exist between ETB copies and intracranial organ size or growth rates.Conclusion: Although ETB-/- mutant has a normal CNS morphology, significant size reductions in brain and constituents were detected. These structural changes likely arise from a combination of factors secondary to dysfunctional ET-1/ET-3/ETB signalling, including global growth impairment from HSCR-induced malnutrition and dysregulations in the neurogenesis, angiogenesis, and cerebral vascular control. These changes have important clinical implications, such as autonomic dysfunction or intellectual delay. Although further human study is warranted, our study suggested comprehensive managements are required for HSCR patients, at least in ETB-/- subtype. [ABSTRACT FROM AUTHOR]

Aims: To evaluate the microvascular and neural differences of the optic nerve head (ONH) between type 2 diabetes mellitus (T2DM) subjects and controls. Methods: This was a cross-sectional observational study. One hundred and eight eyes of 108 T2DM subjects with or without diabetic retinopathy (DR) (54 preclinical DR and 54 mild-to-moderate DR) were included. Fifty-two eyes of 52 healthy subjects were included as controls. The 4.5-mm Angio Disc scan mode and the ganglion cell complex scan mode were performed with all participants using AngioVue software 2.0 of the optical coherence tomography angiography (OCTA) device. Results: Regarding ONH radial peripapillary capillary (RPC) density, the peripapillary region was mainly significantly reduced in the No-DR (NDR) group. Moreover, the RPC density of the peripapillary region and the inside optic disc area were significantly reduced in the non-proliferative DR (NPDR) group. When compared to the controls, significantly reduced peripapillary capillary density in six sections was observed in the NPDR group. However, reduced density was observed in only two sections in the NDR group. The NPDR group had significantly increased focal loss volume (FLV) and reduced peripapillary RNFL thickness in the inferior nasal section compared to those in the controls, but similar changes were not observed in the NDR group. A regression model identified RPCs inside the optic disc as a significant parameter in early-stage DR detection. In the NPDR group, BCVA showed a significantly negative correlation with RPCs inside the optic disc and a significantly positive correlation with FLV. Conclusions: OCTA findings of the ONH area may provide evidence that microvascular changes occur preceding neural impairment in early-stage DR. However, further researches are still needed to support the statement. Reduced ONH perfusion inside the optic disc may be one of the crucial biomarkers in early-stage DR detection and is a possible sensitive visual acuity predictor in early-stage DR subjects. With the ONH mode, OCTA may be a more promising tool in DR screening. [ABSTRACT FROM AUTHOR]

Chronic consumption of tellurium results in heavy deposits of the metal in neuronal lysosomes. Acute exposure to tellurium produces noticeable toxic reactions, and long-term exposure may produce pathological changes. Previous studies have reported only mild neurological symptoms, and it is unclear as to how much functional brain damage results from uptake of the metal. The present study found rats, which had been exposed to a tellurium diet for five months, to be severely impaired in their ability to learn a sequence of behavioral tasks. The learning deficits remained severe even after exposure to tellurium had been terminated for three months. The results suggest long-term disturbance of motivational as well as discriminative capacity as a result of neural impairment. [ABSTRACT FROM AUTHOR]