Electromyographic biofeedback improves upper extremity function: a randomized, single-blinded, controlled trial.

OBJECTIVE: To examine the effects of a 6-week surface electromyographic biofeedback intervention on the re-learning of upper extremity motor function in subjects with paretic upper extremity after stroke. DESIGN: A randomized controlled trial. SETTING: State Centre of Attention to Brain Injury, Madrid, Spain. PARTICIPANTS: Thirty-eight participants in the sub-acute post-stroke stage were recruited and randomly allocated into either the surface electromyographic biofeedback (sEMG-BFB) or sham biofeedback (BFB) groups. INTERVENTIONS: The sEMG-BFB group (n=19) received the intervention focused on re-learning scapulothoracic control during arm-reaching tasks involving shoulder abduction. The sham BFB group (n=19) received a sham intervention. OUTCOME MEASURES: Upper extremity motor function assessed using the Fugl-Meyer Assessment-Upper Extremity Scale (66 points), the glenohumeral active range of motion, and the electromyographic amplitude signal of the middle deltoid and upper trapezius muscles were collected at baseline, after the intervention, and at the one-month follow-up. RESULTS: Compared with the sham BFB group, the sEMG-BFB group experienced significant increases in upper extremity motor function after the intervention. The mean differences between groups were as follows: 4.79 points (95% CI 2.92 to 6.66) after the intervention; 6.55 points (95% CI 3.75 to 9.34) at the one-month follow-up; improved active range of motion 15.75 points (95% CI 6 to 30) after the intervention and electromyographic activity in the upper trapezius muscle changed in favour of the sEMG-BFB. CONCLUSIONS: In the short term, a 6-week sEMG-BFB intervention effectively improved paretic upper limb motor function. Future research is needed to determine if the sEMG-BFB intervention has any long-term effects. Clinical trial number registration: NCT02974465 (ClinicalTrials.gov).

Absence of R-Ras1 and R-Ras2 causes mitochondrial alterations that trigger axonal degeneration in a hypomyelinating disease model.

Fast synaptic transmission in vertebrates is critically dependent on myelin for insulation and metabolic support. Myelin is produced by oligodendrocytes (OLs) that maintain multilayered membrane compartments that wrap around axonal fibers. Alterations in myelination can therefore lead to severe pathologies such as multiple sclerosis. Given that hypomyelination disorders have complex etiologies, reproducing clinical symptoms of myelin diseases from a neurological perspective in animal models has been difficult. We recently reported that R-Ras1-/- and/or R-Ras2-/- mice, which lack GTPases essential for OL survival and differentiation processes, present different degrees of hypomyelination in the central nervous system with a compounded hypomyelination in double knockout (DKO) mice. Here, we discovered that the loss of R-Ras1 and/or R-Ras2 function is associated with aberrant myelinated axons with increased numbers of mitochondria, and a disrupted mitochondrial respiration that leads to increased reactive oxygen species levels. Consequently, aberrant myelinated axons are thinner with cytoskeletal phosphorylation patterns typical of axonal degeneration processes, characteristic of myelin diseases. Although we observed different levels of hypomyelination in a single mutant mouse, the combined loss of function in DKO mice lead to a compromised axonal integrity, triggering the loss of visual function. Our findings demonstrate that the loss of R-Ras function reproduces several characteristics of hypomyelinating diseases, and we therefore propose that R-Ras1-/- and R-Ras2-/- neurological models are valuable approaches for the study of these myelin pathologies.

Functional and morphological alterations in a glaucoma model of acute ocular hypertension.

To study short and long-term effects of acute ocular hypertension (AOHT) on inner and outer retinal layers, in adult Sprague-Dawley rats AOHT (87mmHg) was induced for 90min and the retinas were examined longitudinally in vivo with electroretinogram (ERG) recordings and optical coherent tomography (OCT) from 1 to 90 days (d). Ex vivo, the retinas were analyzed for rod (RBC) and cone (CBC) bipolar cells, with antibodies against protein kinase Cα and recoverin, respectively in cross sections, and for cones, horizontal (HZ) and ganglion (RGC) cells with antibodies against arrestin, calbindin and Brn3a, respectively in wholemounts. The inner retina thinned progressively up to 7d with no further changes, while the external retina had a normal thickness until 30d, with a 20% thinning between 30 and 90d. Functionally, the a-wave showed an initial reduction by 24h and a further reduction from 30 to 90d. All other main ERG waves were significantly reduced by 1d without significant recovery by 90d. Radial sections showed a normal population of RBCs but their terminals were reduced. The CBCs showed a progressive decrease with a loss of 56% by 30d. In wholemount retinas, RGCs diminished to 40% by 3d and to 16% by 30d without further loss. Cones diminished to 58% and 35% by 3 and 7d, respectively and further decreased between 30 and 90d. HZs showed normal values throughout the study. In conclusion, AOHT affects both the inner and outer retina, with a more pronounced degeneration of the cone than the rod pathway.

Pelvic floor and abdominal muscle responses during hypopressive exercises in women with pelvic floor dysfunction.

AIM: To measure the neuromuscular activation of the pelvic floor and abdominal muscles concurrently with vaginal closure forces induced during a hypopressive exercise (HE) and to identify the contribution of the HEs sequences (posture and maneuver) in the muscle's activation. METHODS: A cross-sectional study design was employed. Sixty-six women who had participated in a physical therapy program focused on HEs were recruited. Pelvic floor muscle (PFM) activation was measured using surface electromyography (sEMG) in supine and in the orthostatic position, and vaginal closure force was measured through vaginal dynamometry in supine. Activation of the abdominal, gluteal, and hip adductor muscles was measured using sEMG. Maximum effort voluntary contractions (MVCs) of the PFMs and reference contractions of the abdominal and hip muscles were acquired for normalization purposes. A HE was then performed in a supine position with one leg raised, then in an orthostatic position. RESULTS: During the supine HE, the peak PFM sEMG amplitude was 74.4% to 86.5% (49.6%-109.6%) of MVC, the peak vaginal closure force was between 51.2% and 55.7% (95.5%-382.9%) of MVC, and the muscles of the lateral abdominal wall were activated between 25.4% and 35.3% of the reference contraction. During the orthostatic HE, PFM activation was 61.4% (40.1%-105.6%) of MVC, and the lateral abdominal wall muscles contracted at 22.8% of the reference activation level. CONCLUSIONS: The PFMs, abdominal, gluteal, and adductor muscles are activated during the performance of a HE. The activation level of the PFMs and abdominal muscles is likely insufficient to result in strength gains; however, they could have an endurance effect.

Implications on older women of age- and sex-related differences in activation patterns of shoulder muscles: A cross-sectional study.

We conducted a cross-sectional study to assess differences in neuromotor attributes of shoulder muscles between age groups in both sexes and to better understand functional disorders in older women. Twenty young (20-42 years old), 20 middle-aged (43-67), and 20 older (> 68) adults participated in a comparative surface-electromyography study of five muscles. We identified age-related differences in women, especially in scapula stabilizer muscles. There was a tendency for both sexes of delayed onset times with increasing age, excepting the upper trapezius muscle in females. The results highlight the importance of understanding musculoskeletal aging in women to adequately guide physical therapeutic approaches.

Protective myoelectric activity at performing upper limb neurodynamic test 1 in breast cancer survivors. A cross-sectional observational study.

Myoelectric activity and range of motion during ULNT1 were recorded in 62 breast cancer (BC) survivors who had axillary lymph node dissection (n = 30) or sentinel lymph node biopsy (n = 32) within the previous 18 months, and 63 age-matched healthy women. BC survivors' symptoms were reproduced by ULNT1 and exhibited greater myoelectric activity in the biceps brachii than healthy women (MD (95% CI): 21,26 (10,83-31,70)). No differences between the axillary lymph node dissection and sentinel lymph node biopsy groups (MD (95% CI): 8,47 (-7,84-24,79)) were found. Myoelectric activity in the triceps brachii was greater in the sentinel lymph node biopsy group (MD (95% CI): 2,70 (-2,06-7,60)). BC survivors exhibited less shoulder and elbow range of motion during ULNT1 than healthy women. Increased upper limb nerve mechanosensitivity in BC survivors was associated with a greater protective muscle response during ULNT1.

Effect of leg dominance, gender and age on sensory responses to structural differentiation of straight leg raise test in asymptomatic subjects: a cross-sectional study.

STUDY DESIGN: Cross-sectional study. OBJECTIVES: To assess the effect of structural differentiation on sensory responses of asymptomatic individuals to standard neurodynamic tests of straight leg raise (SLR) and to evaluate the relevance of leg dominance, gender, and age. BACKGROUND: SLR test is a well-known neurodynamic test among physical therapists; no studies to date have investigated the influence of gender, age, and leg dominance to the sensory responses of this neurodynamic test and its structured differentiating maneuver. METHODS: Thirty (16 women) asymptomatic individuals enrolled in this study. Dominancy test was performed for each participant. Pain intensity using visual analogue scale (VAS), symptoms location in a body chart, nature of symptoms evoked, and hip range of motion (ROM) were recorded and compared at ankle neutral position (N-SLR) and dorsiflexion (DF-SLR) in both legs at the point of pain tolerance during SLR (P2). In addition, hip ROM was recorded at the onset of pain (P1). RESULTS: There was a statistically significant sex main effect for P1 and P2 between N-SLR and DF-SLR (p < 0.05). Mean hip ROM during the SLR was more than 10° greater in women than men. There was no statistically significant interaction between leg dominance and age group in N-SLR, DF-SLR, and VAS. Pain intensity was moderate for each SLR test. Symptoms most often described were stretch (96.7%), followed by tightness (70%) in the posterior thigh and leg. CONCLUSIONS: SLR hip ROM is influenced by sex in asymptomatic individuals, leading to a greater hip ROM in SLR in women. Age and limb dominance are not relevant to SLR hip ROM or pain intensity.

CSPalpha-deficiency causes massive and rapid photoreceptor degeneration.

Cysteine string protein (CSP) alpha is an abundant synaptic vesicle protein that contains a DNA-J domain characteristic of Hsp40-type cochaperones. Previous studies showed that deletion of CSPalpha in mice leads to massive lethal neurodegeneration but did not clarify how the neurodegeneration affects specific subpopulations of neurons. Here, we analyzed the effects of the CSPalpha deficiency on tonically active ribbon synapses of the retina and the inner ear. We show that CSPalpha-deficient photoreceptor terminals undergo dramatic and rapidly progressive neurodegeneration that starts before eye opening and initially does not affect other retinal synapses. These changes are associated with progressive blindness. In contrast, ribbon synapses of auditory hair cells did not exhibit presynaptic impairments in CSPalpha-deficient mice. Hair cells, but not photoreceptor cells or central neurons, express CSPbeta, thereby accounting for the lack of a hair-cell phenotype in CSPalpha knockout mice. Our data demonstrate that tonically active ribbon synapses in retina are particularly sensitive to the deletion of CSPalpha and that expression of at least one CSP isoform is essential to protect such tonically active synapses from neurodegeneration.