Home-Based Interventions may Increase Recruitment, Adherence, and Measurement of outcomes in Clinical Trials of Stroke Rehabilitation.

OBJECTIVE: This study aimed to investigate the completion rates of a home-based randomized trial, which examined home-based high-intensity respiratory muscle training after stroke compared with sham intervention. MATERIALS AND METHODS: Completion was examined in terms of recruitment (enrolment and retention), intervention (adherence and delivery of home-visits) and measurement (collection of outcomes). RESULTS: Enrolment was 32% and retention was 97% at post-intervention and 84% at follow-up. Adherence to the intervention was high at 87%. Furthermore, 83% of planned home-visits were conducted and 100% of outcomes were collected from those attending measurement sessions. CONCLUSION: This home-based randomized trial demonstrated high rates of enrolment, retention, adherence, delivery of home-visits, and collection of outcomes. Home-based interventions may help to improve completion rates of randomized trials.

Clinimetric properties of the pressure biofeedback unit method for estimating respiratory pressures.

OBJECTIVE: The Pressure Biofeedback Unit (PBU) is used to assess the transversus abdominis muscle activity in order to determine the effectiveness of segmental stabilization, but not to verify its accuracy for measuring the pressure values of breathing from transversus abdominis activation. The objective of this study was to cross-validate the PBU pressure evaluated in transversus abdominis muscle activation with the respiratory pressure assessed through manovacuometry in order to verify the extent to which the PBU can be used to indirectly evaluate the strength of the respiratory muscle in both men and women and verify the reliability of the methods. PARTICIPANTS: A total of 39 healthy subjects. METHODS: Manovacuometry and Pressure Biofeedback Unit tests were performed in three days each with three replications: 1) Maximal Inspiratory Pressure; 2) Maximal Expiratory Pressure; and 3) Pressure Biofeedback Unit. RESULTS: Both tests showed good reliability and low correlation between the Pressure Biofeedback Unit and Maximal Inspiratory Pressure (r = 0.40; p = 0.01) and Maximal Expiratory Pressure (r = 0.33; p = 0.04). High differences were observed between pressures and wide limits of agreement in Bland-Altman analysis. CONCLUSION: It seems that the Pressure Biofeedback Unit is not able to effectively predict the respiratory muscles' strength as routinely evaluated through the use of the manovacuometry presenting a low cross-validation and good reliability.

Twitch mouth pressure for detecting respiratory muscle weakness in suspicion of neuromuscular disorder.

Twitch mouth pressure using magnetic stimulation of the phrenic nerves and an automated inspiratory trigger is a noninvasive, non-volitional assessment of diaphragmatic strength. Our aims were to validate this method in patients with suspected neuromuscular disease, to determine the best inspiratory-trigger pressure threshold, and to evaluate whether twitch mouth pressure decreased the overdiagnosis of muscle weakness frequently observed with noninvasive volitional tests. Maximal inspiratory pressure, sniff nasal pressure, and twitch mouth pressure were measured in 112 patients with restrictive disease and suspected neuromuscular disorder. Esophageal and transdiaphragmatic pressures were measured in 64 of these patients to confirm or infirm inspiratory muscle weakness. Magnetic stimulation was triggered by inspiratory pressures of -1 and -5 cmH2O. The -5 cmH2O trigger produced the best correlation between twitch mouth pressure and twitch esophageal pressure (R2 = 0.86; P <0.0001). The best association of noninvasive tests to predict inspiratory muscle weakness was sniff nasal pressure and twitch mouth pressure. Below-normal maximal inspiratory pressure and sniff nasal pressure values suggesting inspiratory muscle weakness were found in 63/112 patients. Only 52 of these 63 patients also had abnormal twitch mouth pressure. In conclusion twitch mouth pressure measurement is a simple, noninvasive, nonvolitional technique which may help to select patients with suspected neuromuscular disorder for invasive inspiratory-muscle investigation.

Long-term facilitation of expiratory and sympathetic activities following acute intermittent hypoxia in rats.

AIM: Acute intermittent hypoxia (AIH) promotes persistent increases in ventilation and sympathetic activity, referred as long-term facilitation (LTF). Augmented inspiratory activity is suggested as a major component of respiratory LTF. In this study, we hypothesized that AIH also elicits a sustained increase in expiratory motor activity. We also investigated whether the expiratory LTF contributes to the development of sympathetic LTF after AIH. METHODS: Rats were exposed to AIH (10 × 6-7% O2 for 45 s, every 5 min), and the cardiorespiratory parameters were evaluated during 60 min using in vivo and in situ approaches. RESULTS: In unanesthetized conditions (n = 9), AIH elicited a modest but sustained increase in baseline mean arterial pressure (MAP, 104 ± 2 vs. 111 ± 3 mmHg, P < 0.05) associated with enhanced sympathetic and respiratory-related variabilities. In the in situ preparations (n = 9), AIH evoked LTF in phrenic (33 ± 12%), thoracic sympathetic (75 ± 25%) and abdominal nerve activities (69 ± 14%). The sympathetic overactivity after AIH was phase-locked with the emergence of bursts in abdominal activity during the late-expiratory phase. In anesthetized vagus-intact animals, AIH increased baseline MAP (113 ± 3 vs. 122 ± 2 mmHg, P < 0.05) and abdominal muscle activity (535 ± 94%), which were eliminated after pharmacological inhibition of the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG). CONCLUSION: These findings indicate that increased expiratory activity is also an important component of AIH-elicited respiratory LTF. Moreover, the development of sympathetic LTF after AIH is linked to the emergence of active expiratory pattern and depends on the integrity of the neurones of the RTN/pFRG.

Electrophysiological properties of rostral ventrolateral medulla presympathetic neurons modulated by the respiratory network in rats.

The respiratory pattern generator modulates the sympathetic outflow, the strength of which is enhanced by challenges produced by hypoxia. This coupling is due to the respiratory-modulated presympathetic neurons in the rostral ventrolateral medulla (RVLM), but the underlining electrophysiological mechanisms remain unclear. For a better understanding of the neural substrates responsible for generation of this respiratory-sympathetic coupling, we combined immunofluorescence, single cell qRT-pCR, and electrophysiological recordings of the RVLM presympathetic neurons in in situ preparations from normal rats and rats submitted to a metabolic challenge produced by chronic intermittent hypoxia (CIH). Our results show that the spinally projected cathecholaminergic C1 and non-C1 respiratory-modulated RVLM presympathetic neurons constitute a heterogeneous neuronal population regarding the intrinsic electrophysiological properties, respiratory synaptic inputs, and expression of ionic currents, albeit all neurons presented persistent sodium current-dependent intrinsic pacemaker properties after synaptic blockade. A specific subpopulation of non-C1 respiratory-modulated RVLM presympathetic neurons presented enhanced excitatory synaptic inputs from the respiratory network after CIH. This phenomenon may contribute to the increased sympathetic activity observed in CIH rats. We conclude that the different respiratory-modulated RVLM presympathetic neurons contribute to the central generation of respiratory-sympathetic coupling as part of a complex neuronal network, which in response to the challenges produced by CIH contribute to respiratory-related increase in the sympathetic activity.

Neuromuscular facilitation induced by muscarinic antagonists in the rat isolated diaphragm.

1. Atropine (EC50 = 87 microM), pirenzepine (447 microM), and AF-DX 116 (95.5 microM), but not 4-DAMP (at concentrations of up to 110 microM), produced neuromuscular facilitation and antagonized the oxotremorine-induced neuromuscular blockade in the rat isolated diaphragm. 2. Atropine, pirenzepine, and AF-DX 116 did not change the responses of curarized diaphragms to direct stimulation, or the twitch tension produced by retrograde injection of acetylcholine. 3. These results indicate that neuromuscular facilitation induced by muscarinic antagonists may depend on drug interaction with the M2 subtype of muscarinic autoreceptors to increase acetylcholine output in the neuromuscular junction.

Effects induced by bothropstoxin, a component from Bothrops jararacussu snake venom, on mouse and chick muscle preparations.

Bothropstoxin, a 13,700 mol. wt myotoxic phospholipase homologue isolated from the venom of Bothrops jararacussu and devoid of PLA2, proteolytic or hemolytic activities, inhibited muscle twitch tension, evoked either directly or indirectly through stimulation of the motor nerve in the mouse phrenic-diaphragm preparations. The compound action potential of the muscle was also abolished with a similar time course. In addition, the toxin (0.7 mM) evoked membrane depolarization which was inhibited in the presence of 10 mM Ca2+. In chick biventer cervicis muscle, the toxin (2 mM) induced a contracture that reached its maximum amplitude in 44.8 +/- 15.6 min (n = 6) and was not blocked by either d-tubocurarine or tetrodotoxin. The time to maximum amplitude was reduced to 5.5 +/- 1.0 min (n = 4) in nominally Ca(2+)-free Krebs solution and was completely abolished in Ca(2+)-free Krebs solution containing 1 mM EGTA.