Showing papers on "Reflex published in 2004"

Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia

Abstract: Patients with chronic pain after whiplash injury and fibromyalgia patients display exaggerated pain after sensory stimulation. Because evident tissue damage is usually lacking, this exaggerated pain perception could be explained by hyperexcitability of the central nervous system. The nociceptive withdrawal reflex (a spinal reflex) may be used to study the excitability state of spinal cord neurons. We tested the hypothesis that patients with chronic whiplash pain and fibromyalgia display facilitated withdrawal reflex and therefore spinal cord hypersensitivity. Three groups were studied: whiplash (n=27), fibromyalgia (n=22) and healthy controls (n=29). Two types of transcutaneous electrical stimulation of the sural nerve were applied: single stimulus and five repeated stimuli at 2 Hz. Electromyography was recorded from the biceps femoris muscle. The main outcome measurement was the minimum current intensity eliciting a spinal reflex (reflex threshold). Reflex thresholds were significantly lower in the whiplash compared with the control group, after both single (P=0.024) and repeated (P=0.035) stimulation. The same was observed for the fibromyalgia group, after both stimulation modalities (P=0.001 and 0.046, respectively). We provide evidence for spinal cord hyperexcitability in patients with chronic pain after whiplash injury and in fibromyalgia patients. This can cause exaggerated pain following low intensity nociceptive or innocuous peripheral stimulation. Spinal hypersensitivity may explain, at least in part, pain in the absence of detectable tissue damage.

Effect of central and peripheral body fat distribution on sympathetic and baroreflex function in obese normotensives.

Abstract: BackgroundPrevious studies have shown that obesity is characterized by a sympathetic overactivity coupled with an insulin resistance state and a baroreflex impairment. The present study was set out to compare the effects of peripheral versus central obesity on sympathetic, metabolic and reflex funct

Chronic post-ischemia pain (CPIP): a novel animal model of complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) produced by prolonged hindpaw ischemia and reperfusion in the rat.

Abstract: A neuropathic-like pain syndrome was produced in rats following prolonged hindpaw ischemia and reperfusion, creating an animal model of complex regional pain syndrome-Type I (CRPS-I; reflex sympathetic dystrophy) that we call chronic post-ischemia pain (CPIP). The method involves placing a tourniquet (a tight fitting O-ring) on one hindlimb of an anesthetized rat just proximal to the ankle joint for 3 h, and removing it to allow reperfusion prior to termination of the anesthesia. Rats exhibit hyperemia and edema/plasma extravasation of the ischemic hindpaw for a period of 2–4 h after reperfusion. Hyperalgesia to noxious mechanical stimulation (pin prick) and cold (acetone exposure), as well as mechanical allodynia to innocuous mechanical stimulation (von Frey hairs), are evident in the affected hindpaw as early as 8 h after reperfusion, and extend for at least 4 weeks in approximately 70% of the rats. The rats also exhibit spontaneous pain behaviors (hindpaw shaking, licking and favoring), and spread of hyperalgesia/allodynia to the uninjured contralateral hindpaw. Light-microscopic examination of the tibial nerve taken from the region just proximal to the tourniquet reveals no signs of nerve damage. Consistent with the hypothesis that the generation of free radicals may be partly responsible for CRPS-I and CPIP, two free radical scavengers, N -acetyl- l -cysteine (NAC) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl (Tempol), were able to reduce signs of mechanical allodynia in this model.

The Effect of Spinal Cord Stimulation in Patients with Chronic Reflex Sympathetic Dystrophy: Two Years' Follow-up of the Randomized Controlled Trial

Abstract: Chronic reflex sympathetic dystrophy is a painful, disabling disorder for which no treatment with proven effect is available. We performed a randomized trial in a 2 to 1 ratio of patients, in which 36 patients were treated with spinal cord stimulation and physical therapy (SCS+PT), and 18 patients received solely PT. Twenty-four SCS+PT patients were given a permanent spinal cord stimulation system after successful test stimulation; the remaining 12 patients received no permanent system. We assessed pain intensity, global perceived effect, functional status, and health-related quality of life. Patients were examined before randomization, before implantation, and also at 1, 3, 6, 12, and 24 months thereafter. At 2 years, three patients were excluded from the analysis. The intention-to-treat analysis showed improvements in the SCS+PT group concerning pain intensity (-2.1 vs 0.0 cm; p < 0.001) and global perceived effect (43% vs 6% "much improved"; p = 0.001). There was no clinically important improvement of functional status. Health-related quality of life improved only in the group receiving spinal cord stimulation. After careful selection and successful test stimulation, spinal cord stimulation results in a long-term pain reduction and health-related quality of life improvement in chronic reflex sympathetic dystrophy.

Effect of static stretch training on neural and mechanical properties of the human plantar-flexor muscles.

Abstract: To determine the contributions of neural and mechanical mechanisms to the limits in the range of motion (ROM) about a joint, we studied the effects of 30 sessions of static stretch training on the characteristics of the plantar-flexor muscles in 12 subjects. Changes in the maximal ankle dorsiflexion and the torque produced during passive stretching at various ankle angles, as well as maximal voluntary contraction (MVC) and electrically induced contractions, were recorded after 10, 20, and 30 sessions, and 1 month after the end of the training program. Reflex activities were tested by recording the Hoffmann reflex (H reflex) and tendon reflex (T reflex) in the soleus muscle. Training caused a 30.8% (P < 0.01) increase in the maximal ankle dorsiflexion. This improved flexibility was associated (r(2) = 0.88; P < 0.001) with a decrease in muscle passive stiffness and, after the first 10 sessions only, with a small increase in passive torque at maximal dorsiflexion. Furthermore, both the H- and T-reflex amplitudes were reduced after training, especially the latter (-36% vs. -14%; P < 0.05). The MVC torque and the maximal rate of torque development were not affected by training. Although the changes in flexibility and passive stiffness were partially maintained 1 month after the end of the training program, reflex activities had already returned to control levels. It is concluded that the increased flexibility results mainly from reduced passive stiffness of the muscle-tendon unit and tonic reflex activity. The underlying neural and mechanical adaptation mechanisms, however, showed different time courses.

Anandamide-evoked activation of vanilloid receptor 1 contributes to the development of bladder hyperreflexia and nociceptive transmission to spinal dorsal horn neurons in cystitis.

Abstract: The role of anandamide in the development of inflammatory hyperalgesia and visceral hyperreflexia was studied in the rat urinary bladder. Animals were given intraperitoneal cyclophosphamide injection, which evokes painful hemorrhagic cystitis accompanied by increased bladder reflex activity. The vanilloid receptor 1 [transient receptor potential vanilloid 1 (TRPV1)] antagonist capsazepine, applied onto the serosal surface of bladders, significantly reduced the hyperreflexia. Mass spectrometric analysis revealed that cyclophosphamide injection significantly and persistently increased the anandamide content of bladder tissues. The increase in the anandamide content paralleled the development of reflex hyperactivity. Anandamide (1-100 μm), applied onto the serosal surface of naive bladders, increased the reflex activity in a concentration-dependent manner. Repeated anandamide applications did not produce desensitization of the response. The anandamide-evoked effect was blocked by capsazepine or by instillation of resiniferatoxin, the ultrapotent TRPV1 agonist, into the bladders 24 hr before the anandamide challenge. The cannabinoid 1 receptor antagonist SR141716A [ N -piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide] significantly increased the potency of anandamide in enhancing bladder reflex activity in naive but not in cyclophosphamide-injected animals. Application of the fatty acid amide hydrolyze inhibitor palmitoylisopropylamine onto the serosal surface of bladders also increased the reflex activity both in naive and cyclophosphamide-injected rats. This latter effect in naive animals was blocked by capsazepine and by resiniferatoxin pretreatment. Finally, intravesical instillation of anandamide (50 μm) increased c- fos expression in the spinal cord, which was reduced by capsazepine or by resiniferatoxin pretreatment. These results suggest that anandamide, through activating TRPV1, contributes to the development of hyperreflexia and hyperalgesia during cystitis.

Trigeminocardiac reflex. A clinical phenomenon or a new physiological entity

Abstract: The trigemino-cardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea or gastric hypermotility during stimulation of any of the sensory branches of the trigeminal nerve. The sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. This afferent pathway continues along the short internuncial nerve fibers in the reticular formatio to connect with the efferent pathway in the motor nucleus of the vagus nerve. Clinically, the trigemino-cardiac reflex has been reported to occur during craniofacial surgery, balloon-compression rhizolysis of the trigeminal ganglion, and tumor resection in the cerebellopontine angle. Apart from the few clinical reports, the physiological function of this brainstem-reflex has not yet been fully explored. From experimental findings, it may be suggested that the trigemino-cardiac reflex represents an expression of a central neurogenic reflex leading to rapid cerebrovascular vasodilatation generated from excitation of oxygen-sensitive neurons in the rostral ventrolateral medulla oblongata. By this physiological response, the adjustments of the systemic and cerebral circulations are initiated to divert blood to the brain or to increase blood flow within it. As it is generally accepted that the diving reflex and ischemic tolerance appear to involve at least partially similar physiological mechanisms, the existence of such endogenous neuroprotective strategies may extend the actually known clinical appearance of the TCR and include the prevention of other potentially brain injury states as well. This may be in line with the suggestion that the TCR is a physiological, but not a pathophysiological entity.

The origin of sympathetic outflow in heart failure: The roles of angiotensin II and nitric oxide

Abstract: The regulation of sympathetic nerve activity in chronic heart failure (CHF) has been an area of renewed investigation. Understanding the central mechanisms that are responsible for sympatho-excitation in this disease state may help in reducing the deleterious effects of chronic sympatho-excitation. This review will summarize our understanding of abnormal reflex control of the circulation in CHF. The roles of the arterial baroreflex, the chemoreflex, the cardiac sympathetic afferent reflex and the cardiopulmonary reflex are discussed. New experimental techniques that allow genetic manipulation of substances such as nitric oxide synthase in discrete areas of the brain aid in clarifying the role of NO in the modulation of sympathetic tone in the CHF state. Lastly, clinical implications of this work are discussed.

Spastic long-lasting reflexes in the awake rat after sacral spinal cord injury.

Abstract: Following chronic sacral spinal cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after sacral spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for recording EMG from segmental tail muscles. In normal and acute spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute spinal or normal rats. In acute spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

Central and peripheral contributions to fatigue in relation to level of activation during repeated maximal voluntary isometric plantar flexions

Abstract: This study aimed to investigate central and peripheral contributions to fatigue during repeated maximal voluntary isometric plantar flexions (MVCs). Changes in joint torque, level of activation (LOA), resting twitch amplitude (RT), electromyographic signals (EMG), and presynaptic inhibition of Ia afferents were investigated during 9 bouts of 10 MVCs. MVCs lasted for 2 s and were separated by 1 s. The interval between bouts was 10 s. Electrical stimulation was applied to the tibial nerve; at rest to evoke RTs, M waves, and two (1.5-s interval) H reflexes; with the soleus EMG at 30% of that during MVC to evoke M waves and two H reflexes; and during MVCs to measure LOA. Over the nine bouts, LOA decreased by 12.6% and RT by 16.2%. EMG root mean square during MVCs remained unchanged for the soleus and tibialis anterior muscles, but it decreased for medial gastrocnemius. Peripheral fatigue (decrease in RT) was positively correlated to LOA, whereas central fatigue (decrease in LOA) was not. Depression of both H reflexes suggests that presynaptic inhibition after the first bout was partly induced by homosynaptic postactivation depression of the Ia terminal. The H-reflex-to-M-wave ratio increased with fatigue in both passive and active states, with no change in the ratio of the second H reflex to the first, thereby indicating a decrease of presynaptic inhibition during fatigue. The results indicate that both central and peripheral mechanisms contributed to the fatigue observed during repeated MVCs and that the development of peripheral fatigue was influenced by the level of voluntary activation and initial plantar flexor torque.

Excitability changes in human forearm corticospinal projections and spinal reflex pathways during rhythmic voluntary movement of the opposite limb

Abstract: Rhythmic movements brought about by the contraction of muscles on one side of the body give rise to phase-locked changes in the excitability of the homologous motor pathways of the opposite limb. Such crossed facilitation should favour patterns of bimanual coordination in which homologous muscles are engaged simultaneously, and disrupt those in which the muscles are activated in an alternating fashion. In order to examine these issues, we obtained responses to transcranial magnetic stimulation (TMS), to stimulation of the cervicomedullary junction (cervicomedullary-evoked potentials, CMEPs), to peripheral nerve stimulation (H-reflexes and f-waves), and elicited stretch reflexes in the relaxed right flexor carpi radialis (FCR) muscle during rhythmic (2 Hz) flexion and extension movements of the opposite (left) wrist. The potentials evoked by TMS in right FCR were potentiated during the phases of movement in which the left FCR was most strongly engaged. In contrast, CMEPs were unaffected by the movements of the opposite limb. These results suggest that there was systematic variation of the excitability of the motor cortex ipsilateral to the moving limb. H-reflexes and stretch reflexes recorded in right FCR were modulated in phase with the activation of left FCR. As the f-waves did not vary in corresponding fashion, it appears that the phasic modulation of the H-reflex was mediated by presynaptic inhibition of Ia afferents. The observation that both H-reflexes and f-waves were depressed markedly during movements of the opposite indicates that there may also have been postsynaptic inhibition or disfacilitation of the largest motor units. Our findings indicate that the patterned modulation of excitability in motor pathways that occurs during rhythmic movements of the opposite limb is mediated primarily by interhemispheric interactions between cortical motor areas.

Cerebellar ataxia with bilateral vestibulopathy: description of a syndrome and its characteristic clinical sign

Abstract: We report four patients with the syndrome of cerebellar ataxia with bilateral vestibulopathy (CABV) and, using search coil oculography, we validate its characteristic clinical sign, namely impairment of the visually enhanced vestibulo-ocular reflex (VVOR) or doll's head reflex. In our four patients, CABV began in the sixth decade of life; they are still ambulant and self-caring 8-20 years after onset. The cause of CABV in our four patients is unknown. None has a family history of cerebellar or vestibular disease; spinocerebellar ataxia (SCA) 1, 2, 3, 6, 7 and Friedreich's ataxia were excluded by genetic testing. Three of the four have a sensory peripheral neuropathy but none has extrapyramidal or significant autonomic problems, and none has gluten sensitivity. We measured eye rotations in response to head-on-trunk head rotations and in response to head-and-trunk (en bloc) rotations. Horizontal smooth pursuit (SP), vestibulo-ocular reflex (VOR) and VVOR gains were measured in response to head rotations at 0.1, 0.3, 0.6 and 1.0 Hz. The optokinetic reflex (OKR) was tested by measuring optokinetic nystagmus slow phase velocity during constant 50 degrees /s rotation of the subject in light. The results showed that CABV patients had impairment of all three compensatory eye movement reflexes, the VOR, the OKR and SP. During VVOR testing, as the frequency of head rotation increased from 0.1 to 1.0 Hz, eye velocity failed to match head velocity, gaze velocity increased, and gaze position errors developed, which were corrected with bursts of saccades, the basis of the clinical sign of an impaired VVOR.

Possible contributions of CPG activity to the control of rhythmic human arm movement.

Abstract: There is extensive modulation of cutaneous and H-reflexes during rhythmic leg movement in humans. Mechanisms controlling reflex modulation (e.g., phase- and task-dependent modulation, and reflex reversal) during leg movements have been ascribed to the activity of spinal central pattern generating (CPG) networks and peripheral feedback. Our working hypothesis has been that neural mechanisms (i.e., CPGs) controlling rhythmic movement are conserved between the human lumbar and cervical spinal cord. Thus reflex modulation during rhythmic arm movement should be similar to that for rhythmic leg movement. This hypothesis has been tested by studying the regulation of reflexes in arm muscles during rhythmic arm cycling and treadmill walking. This paper reviews recent studies that have revealed that reflexes in arm muscles show modulation within the movement cycle (e.g., phase-dependency and reflex reversal) and between static and rhythmic motor tasks (e.g., task-dependency). It is concluded that reflexes are modulated similarly during rhythmic movement of the upper and lower limbs, suggesting similar motor control mechanisms. One notable exception to this pattern is a failure of contralateral arm movement to modulate reflex amplitude, which contrasts directly with observations from the leg. Overall, the data support the hypothesis that CPG activity contributes to the neural control of rhythmic arm movement.

Medullary substrate and differential cardiovascular responses during stimulation of specific acupoints.

Abstract: Electroacupuncture (EA) at P5–P6 acupoints overlying the median nerve reduces premotor sympathetic cardiovascular neuronal activity in the rostral ventral lateral medulla (rVLM) and visceral reflex...

Neuropeptide Y antagonism reduces reflex cutaneous vasoconstriction in humans.

Abstract: Previous studies have provided evidence of a non-noradrenergic contributor to reflex cutaneous vasoconstriction in humans but did not identify the transmitter responsible. To test whether neuropept...

Conversion of the modulatory actions of dopamine on spinal reflexes from depression to facilitation in D3 receptor knock-out mice.

Abstract: Descending monoaminergic systems modulate spinal cord function, yet spinal dopaminergic actions are poorly understood Using the in vitro lumbar cord, we studied the effects of dopamine and D2-like receptor ligands on spinal reflexes in wild-type (WT) and D3-receptor knock-out mice (D3KO) Low dopamine levels (1 μm) decreased the monosynaptic “stretch” reflex (MSR) amplitude in WT animals and increased it in D3KO animals Higher dopamine concentrations (10-100 μm) decreased MSR amplitudes in both groups, but always more strongly in WT Like low dopamine, the D3 receptor agonists pergolide and PD 128907 reduced MSR amplitude in WT but not D3KO mice Conversely, D3 receptor antagonists (GR 103691 and nafadotride) increased the MSR in WT but not in D3KO mice In comparison, D2-preferring agonists bromocriptine and quinpirole depressed the MSR in both groups Low dopamine (1-5 μm) also depressed longer-latency (presumably polysynaptic) reflexes in WT but facilitated responses in D3KO mice Additionally, in some experiments (eg, during 10 μm dopamine or pergolide in WT), polysynaptic reflexes were facilitated in parallel to MSR depression, demonstrating differential modulatory control of these reflex circuits Thus, low dopamine activates D3 receptors to limit reflex excitability Moreover, in D3 ligand-insensitive mice, excitatory actions are unmasked, functionally converting the modulatory action of dopamine from depression to facilitation Restless legs syndrome (RLS) is a CNS disorder involving abnormal limb sensations Because RLS symptoms peak at night when dopamine levels are lowest, are relieved by D3 agonists, and likely involve increased reflex excitability, the D3KO mouse putatively explains how impaired D3 activity could contribute to this sleep disorder

Intraoperative monitoring for tethered cord surgery: an update.

Abstract: Object. Intraoperative neurophysiological recording techniques have found increasing use in neurosurgical practice. The development of new recording techniques feasible while the patient receives a general anesthetic have improved their practical use in a similar way to the use of digital recording, documentation, and video technology. This review intends to provide an update on the techniques used and their validity. Methods. Two principal methods are used for intraoperative neurophysiological testing during tethered cord release. Mapping identifies functional neural structures, namely nerve roots, and monitoring provides continuous information on the functional integrity of motor and sensory pathways as well as reflex circuitry. Mapping is performed mostly by using direct electrical stimulation of a structure within the surgical field and recording at a distant site, usually a muscle. Sensory mapping can also be performed with peripheral stimulation and recording within the surgical site. Monitoring of the motor system is achieved with motor evoked potentials. These are evoked by transcranial electrical stimulation and recorded from limb muscles and the external anal sphincter. The presence or absence of muscle responses are the parameters monitored. Sensory potentials evoked by tibial or pudendal nerve stimulation and recorded from the dorsal columns via an epidurally inserted electrode and/or from the scalp as cortical responses are used to access the integrity of sensory pathways. Amplitudes and latencies of these responses are then interpreted. The bulbocavernosus reflex, with stimulation of the pudendal nerve and recording of muscle responses in the external anal sphincter, is used for continuous monitoring of the reflex circuitry. Presence or absence of this response is the pertinent parameter that is monitored. Conclusions. Intraoperative neurophysiology provides a wide and reliable set of techniques for intraoperative identification of neural structures and continuous monitoring of their functional integrity.

Alteration of the spinal modulation of nociceptive processing in patients with irritable bowel syndrome.

Abstract: Background: Visceral hypersensitivity has been evidenced in patients with irritable bowel syndrome (IBS) but its mechanisms remain poorly elucidated. We investigated the spinal transmission of nociceptive signals in IBS patients by analysing the effects of rectal distensions on electromyographic recordings of the somatic nociceptive flexion (RIII) reflex, an objective index of spinal nociceptive processes. Methods: Fourteen IBS and 10 healthy volunteers were included in the study. Slow ramp (40 ml/min) and rapid phasic (900 ml/min, 10, 20, 30, and 40 mm Hg) rectal distensions were randomly performed while the RIII reflex evoked by electrical stimulation of the sural nerve at the ankle was continuously recorded from the ipsilateral biceps femoris. Results: In healthy volunteers, significant progressive inhibition of the RIII reflex was observed during slow ramp distension (61 (13)% of control values) while biphasic effects (facilitation and inhibition) were observed during rapid distensions. In contrast, in IBS patients, the RIII reflex was significantly facilitated during slow ramp distension (139 (15)% of control values) and inhibitions induced by rapid distensions were significantly reduced. Volumes of distension and rectal compliance were similar in both groups. Conclusions: Our results provide direct evidence that a hyperexcitability of spinal nociceptive processes is present in a large subgroup of IBS patients.

Mental stress inhibits pain perception and heart rate variability but not a nociceptive withdrawal reflex

Abstract: Aim: Do distraction from- or attention to sural nerve stimulation affect pain, heart rate variability, and a spinal withdrawal reflex? Material and methods: In 26 male volunteers, electrical stimulation at the distal cutaneous receptive field of the sural nerve elicited pain and a nociceptive withdrawal reflex. Intensity of pain was rated on a numeric rating scale. Electromyographic reflex responses were measured from biceps femoris muscle. Cardiac autonomic function was estimated by heart rate variability measures and was expressed in the time domain as mean of RR-intervals for normal heart beats (mean-RR) and standard deviation of all normal RR-intervals (SD-NN) and, in the frequency domain, where pure vagal activity was assessed by high frequency power (0.15–0.4 Hz). Low frequency power (0.04–0.15 Hz) reflects both parasympathetic and sympathetic control. Effect parameters were recorded before and during random distraction and attention. Distraction from sural nerve stimulation was induced by a mental arithmetic test, paced auditory serial addition task (PASAT), while attention was induced by concentrating on painful foot stimulation. Results: Paced auditory serial addition task decreased mean-RR and SD-NN, frequency domain parameters, as well as pain (P < 0.001). In contrast, PASAT did not change the spinal withdrawal reflex. Attention did not affect any effect parameter. Conclusion: Distraction by PASAT altered autonomic activity and inhibited pain but failed to affect withdrawal reflex responses, while attention had no effect on either parameter. Psychological distraction and attention may have different effects on noxious evoked pain perception and autonomic activity. Pain relief during PASAT probably involves supraspinal mechanisms.

The role of bladder-to-urethral reflexes in urinary continence mechanisms in rats

Abstract: Urethral closure mechanisms during passive increments in intravesicular pressure (P(ves)) were investigated using microtip transducer catheters in urethane-anesthetized female rats. After a block of reflex bladder contractions by spinal cord transection at T8-T9, abruptly raising P(ves) to 20, 40, or 60 cmH(2)O for 2 min induced a bladder pressure-dependent contractile response in a restricted portion of the middle urethra (12.5-15 mm from the urethral orifice) that was abolished by cutting the pelvic nerves bilaterally. In pelvic nerve-intact rats, the bilateral transection of either the pudendal nerves, the nerves to the iliococcygeous/pubococcygeous muscles, or the hypogastric nerves significantly reduced (49-74%) the urethral reflex response induced by passive P(ves) increases, and combined transection of these three sets of nerves totally abolished the urethra-closing responses. In spinal cord-intact rats, similar urethral contractile responses were elicited during P(ves) elevation (20 or 40 cmH(2)O) and were also eliminated by bilateral pelvic nerve transection. After spinal cord and pelvic nerve transection, leak point pressures, defined as the pressure inducing fluid leakage from the urethral orifice during passive P(ves) elevation by either bladder pressure clamping in 2.5-cmH(2)O steps or direct compression of the bladder, were significantly lowered by 30-35% compared with sham-operated (spinal cord-transected and pelvic nerve-intact) rats. These results indicate that 1) passive elevation of P(ves) can elicit pelvic afferent nerve-mediated contractile reflexes in the restricted portion of the urethra mediated by activation of sympathetic and somatic nerves and 2) bladder-to-urethral reflexes induced by passive P(ves) elevation significantly contribute to the prevention of stress urinary incontinence.

Altered neurotransmitter control of reflex vasoconstriction in aged human skin.

Abstract: Cutaneous vasoconstriction (VC) in response to cooling is attenuated in older humans; however, mechanisms underlying this functional decline remain unclear. The present study tested the hypothesis that the contributions of noradrenaline (NA) and sympathetic cotransmitters to reflex-mediated cutaneous VC are altered with age. In 11 young (18–26 years) and 11 older (61–77 years) men and women, forearm skin blood flow was monitored at three sites using laser Doppler flowmetry (LDF) while mean skin temperature was lowered from 34 to 30.5°C using a water-perfused suit. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed as percentage change from baseline (%ΔCVCbase). Solutions of yohimbine + propranolol (Y + P), bretylium tosylate (BT), and lactated Ringer solution were infused via intradermal microdialysis at each LDF site to antagonize α- and β-adrenoceptors, block sympathetic release of NA and cotransmitters, and act as control, respectively. During cooling, VC was attenuated at the control site in older subjects compared to young subjects (−16 ± 3 versus−34 ± 4%ΔCVCbase, P 0.9 versus baseline). BT completely blocked VC in both age groups. Cutaneous VC in young subjects is mediated by both NA and sympathetic cotransmitter(s); however, reflex VC in aged skin is attenuated compared to young and appears to be mediated solely by NA.

Postural effects on pharyngeal protective reflex mechanisms.

Abstract: Study Objectives Pharyngeal muscle dilators are important in obstructive sleep apnea pathogenesis because the failure of protective reflexes involving these muscles yields pharyngeal collapse. Conflicting results exist in the literature regarding the responsiveness of these muscles during stable non-rapid eye movement sleep. However, variations in posture in previous studies may have influenced these findings. We hypothesized that tongue protruder muscles are maximally responsive to negative pressure pulses during supine sleep, when posterior tongue displacement yields pharyngeal occlusion.

AT1 receptor mRNA antisense normalizes enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.

Abstract: Previous studies showed that the cardiac sympathetic afferent reflex (CSAR) is enhanced in dogs and rats with chronic heart failure (CHF) and that central ANG II type 1 receptors (AT1R) are involve...