Reflex Mechanisms Research Articles

The Digital Linguistics: Three Breakthroughs in Speech Sound and the Adaptation/Exploitation of Sign Reflex Mechanisms for Linguistic Processing

The Digital Linguistics: Three Breakthroughs in Speech Sound and the Adaptation/Exploitation of Sign Reflex Mechanisms for Linguistic Processing

Inhalation of electronic cigarette aerosol induces reflex bronchoconstriction by activation of vagal bronchopulmonary C-fibers.

The electronic cigarette (e-cig) has been suggested as a safer alternative to tobacco cigarettes. However, the health effects of e-cigs on the airways have not been fully investigated. Nicotine, the primary chemical constituent of the e-cig aerosol, has been shown to stimulate vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit vigorous pulmonary defense reflexes, including airway constriction. In this study, we investigated the bronchomotor response to e-cig inhalation challenge in anesthetized guinea pigs and the mechanisms involved in regulating these responses. Our results showed that delivery of a single puff of e-cig aerosol into the lung triggered immediately a transient bronchoconstriction that sustained for >2 min. The increase in airway resistance was almost completely abolished by a pretreatment with either intravenous injection of atropine or inhalation of aerosolized lidocaine, suggesting that the bronchoconstriction was elicited by cholinergic reflex mechanism and stimulation of airway sensory nerves was probably involved. Indeed, electrophysiological recording further confirmed that inhalation of e-cig aerosol exerted a pronounced stimulatory effect on vagal bronchopulmonary C-fibers. These effects on airway resistance and bronchopulmonary C-fiber activity were absent when the e-cig aerosol containing zero nicotine was inhaled, indicating a critical role of nicotine. Furthermore, a pretreatment with nicotinic acetylcholine receptor antagonists by inhalation completely prevented the airway constriction evoked by e-cig aerosol inhalation. In conclusion, inhalation of a single puff of e-cig aerosol caused a transient bronchoconstriction that was mediated through cholinergic reflex and triggered by a stimulatory effect of nicotine on vagal bronchopulmonary C-fiber afferents.

Local regulatory mechanism to coordinate colorectal motility in rats.

The presence of a fecal pellet in the colorectum causes ascending contraction and descending relaxation, propelling the pellet aborally. However, random occurrence of the reflexes at multiple sites would disturb sequential excretion of the pellets, resulting in inefficient defecation. Hence, we postulated that a regulatory mechanism to coordinate peristaltic motility initiated at adjacent portions of the colorectum may exist. Colorectal motility was recorded with balloons located at 2 cm, 5 cm and 7 cm from the anus in vivo in anesthetized rats. The presence of a balloon in the colorectum inhibited motility of the oral side and enhanced motility of the anal side. Both the ascending inhibitory and descending facilitatory actions were unaffected by cutting the pelvic nerves, suggesting little contribution of the lumbosacral defecation center. In contrast, disrupting the continuity of the enteric nervous system abolished the local reflex mechanism. The ascending inhibitory pathway operated in a condition in which facilitatory input from the lumbosacral defecation center was fully activated by intrathecal injection of ghrelin. We also found that functional impairment of the local reflex pathways was evident in rats that recovered from 2,4,6‐trinitrobenzensulfonic acid‐induced colitis. These results demonstrate that an intrinsic regulatory mechanism to coordinate peristaltic motility initiated at adjacent portions exists in the rat colorectum. The regulation may be beneficial to propel multiple pellets efficiently. In addition, impairment of the local regulatory mechanism might be involved in postinflammatory dysmotility in the colorectum.

High-intensity muscle metaboreflex activation attenuates cardiopulmonary baroreflex-mediated inhibition of muscle sympathetic nerve activity.

Previous studies have shown that muscle sympathetic nerve activity (MSNA) is reduced during low- and mild-intensity dynamic leg exercise. It has been suggested that such inhibition is mediated by loading of the cardiopulmonary baroreceptors and that this effect is overridden by muscle metaboreflex activation with higher-intensity exercise. However, limited data are available regarding the interaction between the cardiopulmonary baroreflex and the muscle metaboreflex. Therefore, we tested the hypothesis that cardiopulmonary baroreflex-mediated inhibition of MSNA is attenuated during high-intensity muscle metaboreflex activation. In nine young men, MSNA (right peroneal nerve), mean arterial pressure (MAP), and thoracic impedance were recorded. Graded isolation of muscle metaboreflex activation was achieved via postexercise ischemia (PEI) following low (PEI-L)-, moderate (PEI-M)-, and high (PEI-H)-intensity isometric handgrip performed at 20, 30, and 40% maximum voluntary contraction, respectively. Lower-body positive pressure (LBPP, +10 Torr) was applied at rest and during PEI, to load the cardiopulmonary baroreceptors. Handgrip exercise elicited intensity-dependent increases in MSNA and MAP that were maintained during PEI, indicating a graded muscle metaboreflex activation. LBPP at rest significantly decreased MSNA burst frequency (BF: -36.7 ± 4.7%, mean ± SE, P < 0.05), whereas MAP was unchanged. When LBPP was applied during PEI, MSNA BF decreased significantly at PEI-L (-40.0 ± 9.2%, P < 0.05) and PEI-M (-27.0 ± 6.3%, P < 0.05), but not at PEI-H (+1.9 ± 7.1%, P > 0.05). These results suggest that low- and moderate-intensity muscle metaboreflex activation does not modulate the inhibition of MSNA by cardiopulmonary baroreceptor loading, whereas high-intensity metaboreflex activation can override cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow. NEW & NOTEWORTHY The interaction between the sympathoinhibitory influence of cardiopulmonary baroreflex and sympathoexcitatory effect of skeletal muscle metaboreflex is not completely understood. In the current study, light- to moderate-intensity muscle metaboreflex activation did not modulate the suppression of muscle sympathetic nerve activity by cardiopulmonary baroreceptor loading, whereas high-intensity muscle metaboreflex activation attenuated the cardiopulmonary baroreflex-mediated inhibition of muscle sympathetic nerve activity. These results provide important information concerning the neural reflex mechanisms regulating sympathetic vasomotor outflow during exercise.

Feedforward neural control of toe walking in humans.

Activation of ankle muscles at ground contact during toe walking is unaltered when sensory feedback is blocked or the ground is suddenly dropped. Responses in the soleus muscle to transcranial magnetic stimulation, but not peripheral nerve stimulation, are facilitated at ground contact during toe walking. We argue that toe walking is supported by feedforward control at ground contact. Toe walking requires careful control of the ankle muscles in order to absorb the impact of ground contact and maintain a stable position of the joint. The present study aimed to clarify the peripheral and central neural mechanisms involved. Fifteen healthy adults walked on a treadmill (3.0kmh-1 ). Tibialis anterior (TA) and soleus (Sol) EMG, knee and ankle joint angles, and gastrocnemius-soleus muscle fascicle lengths were recorded. Peripheral and central contributions to the EMG activity were assessed by afferent blockade, H-reflex testing, transcranial magnetic brain stimulation (TMS) and sudden unloading of the planter flexor muscle-tendon complex. Sol EMG activity started prior to ground contact and remained high throughout stance. TA EMG activity, which is normally seen around ground contact during heel strike walking, was absent. Although stretch of the Achilles tendon-muscle complex was observed after ground contact, this was not associated with lengthening of the ankle plantar flexor muscle fascicles. Sol EMG around ground contact was not affected by ischaemic blockade of large-diameter sensory afferents, or the sudden removal of ground support shortly after toe contact. Soleus motor-evoked potentials elicited by TMS were facilitated immediately after ground contact, whereas Sol H-reflexes were not. These findings indicate that at the crucial time of ankle stabilization following ground contact, toe walking is governed by centrally mediated motor drive rather than sensory driven reflex mechanisms. These findings have implications for our understanding of the control of human gait during voluntary toe walking.

Bladder underactivity after prolonged stimulation of somatic afferent axons in the tibial nerve in cats.

To establish an animal model of bladder underactivity induced by prolonged and intense stimulation of somatic afferent axons in the tibial nerve. In seven cats under α-chloralose anesthesia, tibial nerve stimulation (TNS) of 30-min duration was repeatedly (3-8 times) applied at 4-6 times threshold (T) intensity for inducing a toe twitch to produce bladder underactivity determined by cystometry. Naloxone (1 mg/kg, i.v.) was administered to examine the role of opioid receptors in TNS-induced bladder underactivity. After prolonged (1.5-4 h) and intense (4-6T) TNS, a complete suppression of the micturition reflex occurred in six cats and an increase in bladder capacity to about 150% of control and a decrease in the micturition contraction amplitude to 50% of control occurred in one cat. The bladder underactivity was maintained for at least 1-1.5 h. Naloxone reversed the bladder underactivity, but an additional 30-min TNS removed the naloxone effect. The results indicate that prolonged and intense activation of somatic afferent axons in the tibial nerve can suppress the central reflex mechanisms controlling micturition. This animal model may be useful for examining the pathophysiology of neurogenic bladder underactivity and for development of new treatments for underactive bladder symptoms.

Fluorescent Based Tracing of Sensory Nerve Subtypes in Brainstem

Processing vagal and trigeminal afferent inputs in the brainstem is essential for regulating reflexes including those from the respiratory tract. Afferent nerves can be categorized into several subtypes depending on the ganglionic origin of cell bodies (placodal vs. neural crest), conduction velocity and response patterns to stimuli. These various nerve subtypes convey different types of information which is integrated at the brainstem to control respiratory reflexes. Vagal afferent nerve subtypes express particular ion channels/receptors which are stimulated by various stimuli resulting in different information being relayed to the brainstem. For example, stimulation of vagal jugular C‐fiber nociceptors evokes cough, whereas stimulation of vagal nodose C‐fiber nociceptors inhibits cough. Vagal afferents are known to innervate the nucleus of the solitary tract in the dorsal medulla. However, the innervation patterns may vary depending on the subsets of vagal afferents. The variation makes it difficult to understand how distinct peripheral vagal afferent inputs are processed in the central nervous system.In the current study, we focused on developing a neuroanatomical map of various sensory afferent nerve subtypes using a transgenic mouse model system. Cre‐LoxP reporter system allows us to target the specific ion channel/receptor positive sensory nerve subtypes enabling tracking of afferent nerve subtypes throughout medulla. Transient receptor potential vanilloid 1 (Trpv1), tachykinin 1 (Tac1) and 5‐hydroxytriptamine receptor 3 (5HT3) Cre strains were bred with Floxed Ai9 ROSA tdTomato; thus, expressing red fluorescent specific to Trpv1, Tac1 and 5HT3 positive cells. Mice (6 to 8‐week‐old) were euthanized and tissue was collected. Brainstem were cryosectioned at 30 μm thickness and slide mounted sequentially. Additionally, we used a passive tissue clearing technique (CLARITY‐PACT) to visualize the sensory nerve projections in dissected whole medulla. Images were taken using Nikon Eclipse microscope and Olympus FV1200 confocal microscope. The 3D images were processed with Imaris software.As a result, we were able to identify each sensory nerve subtype in the medulla and define their projections to different regions of medulla ‐ these include the nucleus of solitary tract (NTS), paratrigeminal nucleus (Pa5) and spinal trigeminal tract (sp5). While brainstem projection of the Trpv1, Tac1 and 5ht3 Cre/Rosa strains showed similarities in gross regional expression, the patterns of these projections were distinct depending on the strains. For example, Trpv1‐tdTomato projections were found in the commissural NTS but not the medial NTS, whereas Tac1‐tdTomato projections were largely absent from the commissural NTS but were abundantly present in the medial NTS. The only overlap of Trpv1 and Tac1 projections was not in the NTS, but rather in Pa5 and sp5, suggesting that vagal jugular C‐fiber nociceptors may terminate in Pa5 as opposed to the NTS. The cleared whole medulla from each strain were consistent with the medulla sections and were used to yield 3D maps of the sensory afferent nerve projections. Based on these observations, a genetic tool using Cre‐LoxP reporter system allowed us to define the neuronal circuitry of major vagal sensory afferent nerve subtypes. This information may be useful to study functionalities of each sensory nerve subtypes to better understand the mechanism of respiratory reflexes.Support or Funding InformationNIH Common Fund SPARC OT2This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Neural pathways involved in infection-induced inflammation: recent insights and clinical implications.

Although the immune and nervous systems have long been considered independent biological systems, they turn out to mingle and interact extensively. The present review summarizes recent insights into the neural pathways activated by and involved in infection-induced inflammation and discusses potential clinical applications. The simplest activation concerns a reflex action within C-fibers leading to neurogenic inflammation. Low concentrations of pro-inflammatory cytokines or bacterial fragments may also act on these afferent nerve fibers to signal the central nervous system and bring about early fever, hyperalgesia and sickness behavior. In the brain, the preoptic area and the paraventricular hypothalamus are part of a neuronal network mediating sympathetic activation underlying fever while brainstem circuits play a role in the reduction of food intake after systemic exposure to bacterial fragments. A vagally-mediated anti-inflammatory reflex mechanism has been proposed and, in turn, questioned because the major immune organs driving inflammation, such as the spleen, are not innervated by vagal efferent fibers. On the contrary, sympathetic nerves do innervate these organs and modulate immune cell responses, production of inflammatory mediators and bacterial dissemination. Noradrenaline, which is both released by these fibers and often administered during sepsis, along with adrenaline, may exert pro-inflammatory actions through the stimulation of β1 adrenergic receptors, as antagonists of this receptor have been shown to exert anti-inflammatory effects in experimental sepsis.

Neuroreflex control of cardiovascular function is impaired after acute poisoning with chlorpyrifos, an organophosphorus insecticide: Possible short and long term clinical implications

Although it is well-established that severe poisoning by organophosphorus (OP) compounds strongly affects the cardiorespiratory system, the effects of sub-lethal exposure to these compounds on the neural control of cardiovascular function are poorly explored. The aim of this study was to evaluate the effects of acute sub-lethal exposure to chlorpyrifos (CPF), a commonly used OP insecticide, on three basic reflex mechanisms involved in blood pressure regulation, the peripheral chemoreflex, the baroreflex and the Bezold-Jarisch reflex. Adult male Wistar rats were injected intraperitoneally with a single dose of CPF (30 mg/kg) or saline (0.9%). 24 h after injections, cardiovascular reflexes were tested in awake rats. Potassium cyanide (KCN) and phenylbiguanide (PBG) were injected intravenously to activate the chemoreflex and the Bezold-Jarisch reflex, respectively. The baroreflex was activated by phenylephrine and sodium nitroprusside infusions. Blood samples were taken for measurements of butyrylcholinesterase (BChE) activity while acetylcholinesterase (AChE) activity was measured in brainstem samples. Animals treated with CPF presented signs of intoxication such as ataxia, tremor, lacrimation, salivation, tetany, urination and defecation. The hypertensive and the bradycardic responses of the chemoreflex as well as the hypotensive and bradycardic responses of the Bezold-Jarisch reflex were attenuated in CPF treated animals (P < 0.05). Concerning the baroreflex responses, CPF treatment reduced the bradycardia plateau, the range and the gain of the reflex (P < 0.05). Plasma BChE and brainstem AChE were both reduced significantly after CPF treatment (P < 0.05). Our results showed that acute sub-lethal exposure to CPF impairs the cardiovascular responses of homeostatic and defensive cardiovascular reflexes. These effects are associated with a marked inhibition of plasma BChE and brainstem AChE.

Characterizing the transcutaneous electrical recruitment of lower leg afferents in healthy adults: implications for non-invasive treatment of overactive bladder

BackgroundAs a potential new treatment for overactive bladder (OAB), we investigated the feasibility of non-invasively activating multiple nerve targets in the lower leg.MethodsIn healthy participants, surface electrical stimulation (frequency = 20 Hz, pulse width = 200 μs) was used to target the tibial nerve, saphenous nerve, medial plantar nerve, and lateral plantar nerve. At each location, the stimulation amplitude was increased to define the thresholds for evoking (1) cutaneous sensation, (2) target nerve recruitment and (3) maximum tolerance.ResultsAll participants were able to tolerate stimulation amplitudes that were 2.1 ± 0.2 (range = 2.0 to 2.4) times the threshold for activating the target nerve.ConclusionsNon-invasive electrical stimulation can activate neural targets at levels that are consistent with evoking bladder-inhibitory reflex mechanisms. Further work is needed to test the clinical effects of stimulating one or more neural targets in OAB patients.

Chapter 11 - Skin vasoconstriction as a heat conservation thermoeffector

Cold exposure stimulates heat production and conservation to protect internal temperature. Heat conservation is brought about via reductions in skin blood flow. The focus, here, is an exploration of the mechanisms, particularly in humans, leading to that cutaneous vasoconstriction. Local skin cooling has several effects: (1) reduction of tonic nitric oxide formation by inhibiting nitric oxide synthase and element(s) downstream of the enzyme, which removes tonic vasodilator effects, yielding a relative vasoconstriction; (2) translocation of intracellular alpha-2c adrenoceptors to the vascular smooth-muscle cell membrane, enhancing adrenergic vasoconstriction; (3) increased norepinephrine release from vasoconstrictor nerves; and (4) cold-induced vasodilation, seen more clearly in anastomoses-rich glabrous skin. Cold-induced vasodilation occurs in nonglabrous skin when nitric oxide synthase or sympathetic function is blocked. Reflex responses to general body cooling complement these local effects. Sympathetic excitation leads to the increased release of norepinephrine and its cotransmitter neuropeptide Y, each of which contributes significantly to the vasoconstriction. The contributions of these two transmitters vary with aging, disease and, in women, reproductive hormone status. Interaction between local and reflex mechanisms is in part through effects on baseline and in part through removal of the inhibitory effects of nitric oxide on adrenergic vasoconstriction.

НОРМОБАРИЧЕСКАЯ ПЕРИОДИЧЕСКАЯ ГИПОКСИЯ ПОВЫШАЕТ ОРТОСТАТИЧЕСКУЮ РЕЗИСТЕНТНОСТЬ КРЫС ПОСЛЕ МОДЕЛИРОВАННОЙ НЕВЕСОМОСТИ

The effects of adaptation to periodic normobaric hypoxia (PNH) on the intensity of orthostatic reactions were studied after long-term simulated microgravity in Wistar rats. It was established that exposure of animals to PNH prior to the simulated microgravity attenuates the orthostatic hypotension and increases orthostatic tolerance after simulated microgravity. It was assumed that the decrease in the intensity of hemodynamic orthostatic responses is a result of the positive cross-adaptation that occurs due to stabilization of the central intersystem reflex mechanisms, mediated both chemo- and baroreceptor regulation implemented on the new functional level.

Correlation of head‐up tilt table test time interval with future risk of recurrent syncope

Head-up tilt table test (HUTT) is widely used for the investigation of syncope and presyncope. Time required for positive response has a probable relationship to the sensitivity of neural reflex mechanism underlying syncope. We evaluated patients with history of syncope. Group A included patients with recurrent syncope defined as two or more episodes of syncope and group B included those with one episode of syncope. Time required for the test to become positive in both the groups was analyzed. Patients with positive HUTT were followed for 1 year. Of 80 patients, 68 eligible study patients were divided into group A (32.35%) and group B (67.65%). HUTT was positive in 41 patients (positivity rate=60.29%). Positivity rate was 100% in group A and 41.3% in group B. Median time interval for positive response in groups A and B were 12.5 and 30.0 minutes, respectively. An inverse association was found between recurrent syncope and time interval for positive response (R=-0.282, P=0.002). Time interval of less than 19.5 minutes for positive response had 94.5% sensitivity and 97.89% specificity for recurrent syncope. On follow-up, positive association was found between time interval for positive response less than 19.5 minutes and future recurrence of syncope (odds ratio=22.75, 95% confidence interval=4.37-118.34, P=0.000). HUTT time interval of less than 19.5 minutes for positive response predicted future recurrence of syncope. Hence, it may serve as an important predictor of future recurrence of syncope.

Sinus bradycardia and syncope: what pathophysiological mechanism and what management of the patient?

Sick sinus syndrome (SSS) can be diagnosed only when there is a clear correlation between symptoms and sinus node dysfunction. In the absence of such correlation, the mechanism of undocumented intermittent symptoms such as syncopal spells in patients with permanent mild sinus bradycardia remains uncertain. Some clinical data suggest that a reflex mechanism is likely to be involved in many patients with syncope and sinus bradycardia: the course of syncopal recurrences is very variable from patient to patient and transient loss of consciousness does not recur in more than half of unpaced patients during an observation period of several years. The results of some studies seem to confirm a reflex mechanism as the cause of syncope in most cases: in patients with SSS and syncope the prevalence of positive response to tilt testing was high (~60%) and significantly higher than in patients with SSS without syncope and in other control groups. However, a depressed sinus node automaticity, roughly expressed by very prolonged sinus node recovery time, suggests a role of sinus node dysfunction in the origin of syncope. Patients with permanent mild sinus bradycardia and syncope as an isolated symptom should undergo tilt testing and electrophysiological study. In the presence of positive tilt test without very prolonged sinus node recovery time, the patient should be managed as the patients with neurally mediated syncope and normal sinus rate.

Cooperative Oxygen Sensing by the Kidney and Carotid Body in Blood Pressure Control.

Oxygen sensing mechanisms are vital for homeostasis and survival. When oxygen levels are too low (hypoxia), blood flow has to be increased, metabolism reduced, or a combination of both, to counteract tissue damage. These adjustments are regulated by local, humoral, or neural reflex mechanisms. The kidney and the carotid body are both directly sensitive to falls in the partial pressure of oxygen and trigger reflex adjustments and thus act as oxygen sensors. We hypothesize a cooperative oxygen sensing function by both the kidney and carotid body to ensure maintenance of whole body blood flow and tissue oxygen homeostasis. Under pathological conditions of severe or prolonged tissue hypoxia, these sensors may become continuously excessively activated and increase perfusion pressure chronically. Consequently, persistence of their activity could become a driver for the development of hypertension and cardiovascular disease. Hypoxia-mediated renal and carotid body afferent signaling triggers unrestrained activation of the renin angiotensin-aldosterone system (RAAS). Renal and carotid body mediated responses in arterial pressure appear to be synergistic as interruption of either afferent source has a summative effect of reducing blood pressure in renovascular hypertension. We discuss that this cooperative oxygen sensing system can activate/sensitize their own afferent transduction mechanisms via interactions between the RAAS, hypoxia inducible factor and erythropoiesis pathways. This joint mechanism supports our view point that the development of cardiovascular disease involves afferent nerve activation.

Electroacupuncture Therapy for Auricular Paresthesia.

Background: The great auricular nerve (GAN) provides sensory innervation to the skin around the auricle. Although disorder of this nerve has been reported, great auricular neuralgia, as reported by Blumenthal in 1992, is uncommon. The authors report a case of auricular paresthesia that responded well to electroacupuncture treatment (EAT). Case: A man in his 60s was consulted in the clinic after a 6-month history of experiencing tingling sensations of the skin around the auricle. General degenerative deformity of the cervical spine was observed using computed radiography scans and magnetic resonance imaging; tactile hyperesthesia in the skin of the GAN area was also noted. This case was diagnosed as a disturbance of the great auricular nerve (mild neuralgia). As a potential treatment, EAT was administered near the affected nerve once per week for 6 weeks. Results: Visual analogue scale (VAS) measurements showed a marked decrease in the severity of this patient's symptoms, and the tactile hyperesthesia in the affected area had normalized. The main complaint, auricular paresthesia, had disappeared and had not recurred according to a check-up 15 months later. Conclusions: EAT was effective in the current case. It is hypothesized that EAT can reduce neural sensitivity via a reflex mechanism actuated by somatosensory input.

Baroreflex and neurovascular responses to skeletal muscle mechanoreflex activation in humans: an exercise in integrative physiology.

Cardiovascular adjustments to exercise resulting in increased blood pressure (BP) and heart rate (HR) occur in response to activation of several neural mechanisms: the exercise pressor reflex, central command, and the arterial baroreflex. Neural inputs from these feedback and feedforward mechanisms integrate in the cardiovascular control centers in the brain stem and modulate sympathetic and parasympathetic neural outflow, resulting in the increased BP and HR observed during exercise. Another specific consequence of the central neural integration of these inputs during exercise is increased sympathetic neural outflow directed to the kidneys, causing renal vasoconstriction, a key reflex mechanism involved in blood flow redistribution during increased skeletal muscle work. Studies in humans have shown that muscle mechanoreflex activation inhibits cardiac vagal outflow, decreasing the sensitivity of baroreflex control of HR. Metabolite sensitization of muscle mechanoreceptors can lead to reduced sensitivity of baroreflex control of HR, with thromboxane being one of the metabolites involved, via greater inhibition of cardiac vagal outflow without affecting baroreflex control of BP or baroreflex resetting. Muscle mechanoreflex activation appears to play a predominant role in causing renal vasoconstriction, both in isolation and in the presence of local metabolites. Limited investigations in older adults and patients with cardiovascular-related disease have provided some insight into how the influence of muscle mechanoreflex activation on baroreflex function and renal vasoconstriction is altered in these populations. However, future research is warranted to better elucidate the specific effect of muscle mechanoreflex activation on baroreflex and neurovascular responses with aging and cardiovascular-related disease.

Tremor's glove-an innovative electrical muscle stimulation therapy for intractable tremor in Parkinson's disease: A randomized sham-controlled trial

BackgroundMedically refractory resting tremor is a debilitating symptom of Parkinson's disease (PD) patients. In our pilot study, modulation of peripheral reflex mechanism by electrical muscle stimulation (EMS) temporarily suppressed tremor. ObjectivesTo investigate the efficacy of EMS, delivered using Tremor's glove, as a treatment of resting hand tremor. Patients and methodsThirty PD patients with medically refractory resting tremor were randomly allocated to a Tremor's glove group (n=15) or a sham glove group (n=15). Gloves were placed on the most tremulous hand for 30min per testing session. Demographics, clinical rating scales, and tremor parameters (RMS of angular velocity and angular displacement, peak magnitude, and frequency) were assessed before and during stimulation. Correlations with validated clinical rating scales were performed. ResultsThere were no statistically significant differences between groups in demographics, rating scales, or tremor parameters. During stimulation, significant reduction in RMS angular velocity (as percentage) in every axis and peak magnitude in axis (x-, y-) and UPDRS tremor score, were found with Tremor's glove compared to the sham groups (p<0.05, each). Significant moderate correlations were observed between a percentage reduction of RMS angular velocity in every axis and UPDRS tremor scores. Mean duration of tremor reduction after stimulation was 107.78±104.15s. No serious adverse events were observed. ConclusionIn this study, EMS-based Tremor's glove was effective in suppressing resting hand tremor in PD patients. Tremor's glove is light-weight with a good safety profile, making it a future potential therapeutic option for PD patients with medically refractory tremor.

S60 Clinical neurophysiology in movement disorders: Myoclonus

Myoclonus can be defined as abnormal short jerks caused by bursts of muscular activity or brief periods of inhibition. Myoclonus can be classified depending on their origin and pathophysiologic mechanism in cortical, cortical-subcortical, subcortical (including spinal) and peripheral myoclonus. From a topographic point of view, myoclonus can be generalized, segmentary or focal. Myoclonus can be spontaneous, induced by action, or induced by an external stimulus (reflex). Clinical Neurophysiology is a key step in this diagnostic process. The battery of tests that can be performed in the study of myoclonus include EEG, somatosensory evoked potentials (SSEPs), multi-muscle surface EMG and back-averaging of the EEG signal using the EMG as trigger. If reflex myoclonus is suspected, it might be necessary to average EMG activity using the triggering stimulus in order to demonstrate the reflex mechanism. EEG and back-averaging are useful in the study of cortical myoclonus. Epileptiform activity preceding the muscle jerks can be sometimes observed in the EEG, while the back-averaging should show a cortical spike preceding the jerk with a latency compatible with cortico-spinal conduction times. EEG can also provide specific information about the etiology of the myoclonus (suggesting a metabolic encephalopathy or a myoclonic epilepsy, for instance). High amplitude (giant) SSEPs can be observed in many patents with cortical myoclonus, and their presence is highly suggestive of a cortical origin. In some of them, a reflex response (enhanced C reflex) can be detected (and recorded) during the SSEPs. Surface EMG from different muscles gives valuable information about the duration and spatial spread of the myoclonus. Additionally, the timing and pattern of activation of the different muscles may also be useful to determine the origin (for instance, in reticular or propriospinal myoclonus).

Central pattern generator and feedforward neural network-based self-adaptive gait control for a crab-like robot locomoting on complex terrain under two reflex mechanisms

Although quite a few central pattern generator controllers have been developed to regulate the locomotion of terrestrial bionic robots, few studies have been conducted on the central pattern generator control technique for amphibious robots crawling on complex terrains. The present article proposes a central pattern generator and feedforward neural network-based self-adaptive gait control method for a crab-like robot locomoting on complex terrain under two reflex mechanisms. In detail, two nonlinear ordinary differential equations are presented at first to model a Hopf oscillator with limit cycle effects. Having Hopf oscillators as the basic units, a central pattern generator system is proposed for the waveform-gait control of the crab-like robot. A tri-layer feedforward neural network is then constructed to establish the one-to-one mapping between the central pattern generator rhythmic signals and the joint angles. Based on the central pattern generator system and feedforward neural network, two reflex mechanisms are put forward to realize self-adaptive gait control on complex terrains. Finally, experiments with the crab-like robot are performed to verify the waveform-gait generation and transition performances and the self-adaptive locomotion capability on uneven ground.