Stimulation Of Deep Peroneal Nerve Research Articles

Renal Nerve Activity and Arterial Depressor Responses Induced by Neuromodulation of the Deep Peroneal Nerve in Spontaneously Hypertensive Rats.

Hypertension is a main cause of death in the United States with more than 103 million adults affected. While pharmacological treatments are effective, blood pressure (BP) remains uncontrolled in 50–60% of resistant hypertensive subjects. Using a custom-wired miniature electrode, we previously reported that deep peroneal nerve stimulation (DPNS) elicited acute cardiovascular depressor responses in anesthetized spontaneously hypertensive rats (SHRs). Here, we further study this effect by implementing a wireless system and exploring different stimulation parameters to achieve a maximum depressor response. Our results indicate that DPNS consistently induces a reduction in BP and suggests that renal sympathetic nerve activity (RSNA) is altered by this bioelectronic treatment. To test the acute effect of DPNS in awake animals, we developed a novel miniaturized wireless microchannel electrode (w-μCE), with a Z-shaped microchannel through which the target nerves slide and lock into the recording/stimulation chamber. Animals implanted with w-μCE and BP telemetry systems for 3 weeks showed an average BP of 150 ± 14 mmHg, which was reduced significantly by an active DPNS session to 135 ± 8 mmHg (p < 0.04), but not in sham-treated animals. The depressor response in animals with an active w-μCE was progressively returned to baseline levels 14 min later (164 ± 26 mmHg). This depressor response was confirmed in restrained fully awake animals that received DPNS for 10 days, where tail-cuff BP measurements showed that systolic BP in SHR lowered 10% at 1 h and 16% 2 h after the DPNS when compared to the post-implantation baseline. Together, these results support the use of DPN neuromodulation as a possible strategy to lower BP in drug-resistant hypertension.

Abstract MP23: Arterial Depressor Responses Induced By Neuromodulation Of Deep Peroneal Nerve In Spontaneously Hypertensive Rats

Hypertension affects nearly half of the US population but only 43% achieved blood pressure control with medication alone. Medical devices for hypertension include implantable lead electrodes that stimulate the carotid baroreceptors with promising results, albeit with significant adverse complications. To address these limitations, we have proposed the use of deep peroneal nerve stimulation (DPNS), which elicited a depressor response in anesthetized, breathing supported, spontaneously hypertensive rats (SHR). In this study, we further define the electrical stimulation parameters that optimize the DPNS depressor response, and demonstrated that increasing the pulse duration from 0.15 ms to 1ms, of 1.0 mA pulses at 2 Hz for 10 sec, significantly reduced the mean arterial pressure (MAP) by 8±4 mmHg (p&lt;0.005; n=4) in this animal model. DPNS also caused an immediate increase in renal nerve activity (RNA; p&lt; 0.004, n=5), which may represent afferent sensory axons from the kidney, although this possibility needs to be further investigated. In a separate cohort of anesthetized SHR animals, breathing spontaneously, we demonstrated that optimal DPNS stimulation reduced the MAP from 121±3 to 108±4; p=0.02; n=10). To confirm if DPNS is able to evoke a depressor response in fully awake SHR animals, we developed a novel miniaturized wireless microchannel electrode (w-μCE) with a L-shaped microchannel, through which the DPN slides and locks into a recording/stimulation chamber, causing no discomfort to the animal during locomotion. Two weeks after implantation of the w-μCE neural stimulation device, animals were movement-retrained to received wireless DPNS for 10 min daily for 2 weeks. Blood pressure was measured by tail-cuff at baseline, 10 days after device implantation, and 1 and 2-hr 15 days after DPNS. After two weeks of DPNS, the acute neuromodulation treatment reduced the initial systolic BP of 154±20 mmHg to 127±7 and 119±2 mmHg at 1 and 2 hr; respectively (p&lt; 0.001, n=15-19 measurements; n=2 animals). These results provide evidence of the effectiveness and reliability of DPN neuromodulation as a possible treatment for drug-resistant hypertension.

Interrogating interneurone function using threshold tracking of the H reflex in healthy subjects and patients with motor neurone disease

ObjectiveThe excitability of the lower motoneurone pool is traditionally tested using the H reflex and a constant-stimulus paradigm, which measures changes in the amplitude of the reflex response. This technique has limitations because reflex responses of different size must involve the recruitment or inhibition of different motoneurones. The threshold-tracking technique ensures that the changes in excitability occur for an identical population of motoneurones. We aimed to assess this technique and then apply it in patients with motor neurone disease (MND). MethodsThe threshold-tracking approach was assessed in 17 healthy subjects and 11 patients with MND. The soleus H reflex was conditioned by deep peroneal nerve stimulation producing reciprocal Ia and so-called D1 and D2 inhibitions, which are believed to reflect presynaptic inhibition of soleus Ia afferents. ResultsThreshold tracking was quicker than the constant-stimulus technique and reliable, properties that may be advantageous for clinical studies. D1 inhibition was significantly reduced in patients with MND. ConclusionsThreshold tracking is useful and may be preferable under some conditions for studying the excitability of the motoneurone pool. The decreased D1 inhibition in the patients suggests that presynaptic inhibition may be reduced in MND. SignificanceReduced presynaptic inhibition could be evidence of an interneuronopathy in MND. It is possible that the hyperreflexia is a spinal pre-motoneuronal disorder, and not definitive evidence of corticospinal involvement in MND.

Stimulus Point Distribution in Deep or Superficial Peroneal Nerve for Treatment of Ankle Spasticity

To develop effective electrical stimulation treatment to reduce spasticity, we examined the optimal stimulus point of the common peroneal nerve. The locations of selective stimulus points for the deep peroneal nerve or superficial peroneal nerve fiber were examined in 25 healthy subjects in both legs (50 legs) using the ratio of the tibialis anterior (TA) to the peroneus longus (PL) M-wave amplitude (TA/PL ratio). In addition, we measured reciprocal Ia inhibition in ten healthy subjects. The amount of inhibition was determined from short-latency suppression of the soleus (Sol) H-reflex by conditioning stimuli to the deep or superficial peroneal nerve. The paired t-test was used for statistical analysis. The mean TA/PL ratio during deep peroneal nerve stimulation was significantly different from superficial peroneal nerve stimulation (p < 0.001). The mean stimulus point for the deep peroneal nerve was located 7 ± 5 mm distal and 3 ± 6 mm anterior from the distal edges of the head of fibula and was markedly different from the stimulus point for the superficial peroneal nerve (20 ± 7 mm distal and 12 ± 8 mm posterior). During deep peroneal nerve stimulation, the mean conditioned H-reflex was depressed to 83.8 ± 10.7% of the unconditioned value of the H-reflex. In contrast, during superficial peroneal nerve stimulation, the mean conditioned H-reflex increased to 105.3 ± 5.2%. These values were significantly different (p < 0.001). In the present study, we revealed a stimulus area of the deep peroneal nerve. Also, we observed the inhibitory effects of stimulation upon the deep peroneal nerve at individual stimulus point. Our results appear to indicate that localized stimulation of the deep peroneal nerve is more useful for the reduction of ankle spasticity.

Electrical stimulation of deep peroneal nerve mimicking acupuncture inhibits the pressor response via capsaicin-insensitive afferents in anesthetized rats

To assess the inhibitory modulation of blood pressure by stimulation of the deep peroneal nerve (DPN) and to determine the involvement of nociceptive fibers in the modulation. All the animals were divided into six groups (A-F). The rats in groups A and B received no pretreatment. The rats in groups C and D received subcutaneous injection of capsaicin or control vehicle, respectively, near the DPN for 2 days. Those in groups E and F had the DPN exposed to capsaicin or control vehicle, respectively, for 20 min. Subsequently, pressor responses were induced by stimulation of paraventricular nucleus (PVN) either electrically (groups A and C C-F) or chemically via injection of glutamate (group B). After two stable pressor responses (baseline), all groups were subject to 5-min DPN stimulation followed by PVN stimulation for 10 s. Arterial blood pressure, heart rate, and electrocardiogram were recorded. The pressor response was calculated as the difference in the mean arterial pressure (MAP) before and after PVN stimulation, and changes from baseline in pressor response after DPN stimulation were compared between the groups. Increases of MAP of 22.88±2.18 mm Hg and 20.32±5.25 mm Hg were induced by electrical (group A) or chemical (group B) stimulation of the PVN, respectively. These pressor responses were inhibited by stimulation of the DPN, and the MAP was reduced to 12.00±2.10 mm Hg in group A (n=6, P<0.01) and 7.00±2.85 mm Hg in group B (n=6, P<0.01). Subcutaneous injection of capsaicin (125 mg/kg) near the DPN in group C (n=7) had no effect on the inhibitory effect of DPN stimulation compared with the group D (n=9), and neither did blockade of nociceptive fibers with capsaicin in group E (n=6) compared with group F (n=8). Stimulation of the DPN mimicking acupuncture has an inhibitory effect on the pressor response, and the effect is mediated by capsaicin-insensitive afferent fibers in the DPN.

Poster 96 Superficial Versus Deep Peroneal Nerve Stimulation during Plantar Loading in Acute Stroke: A Case Report

Poster 96 Superficial Versus Deep Peroneal Nerve Stimulation during Plantar Loading in Acute Stroke: A Case Report

Role of nitric oxide in inhibitory effect of somatic afferent inputs on central pressor response

To investigate the role of nitric oxide in the inhibitory effect of somatic afferent input on the pressor response caused by electrical stimulation of the paraventricular nucleus of the hypothalamus (PVN). SD rats anesthetized by urethane were used in the study. Bipolar stainless stimulating electrode was inserted into PVN for electrical stimulation. Multi-barreled micropipettes were used for microinjection of L-NAME or normal saline into the lateral ventricle or amygdala. Deep peroneal nerve (DPN) was stimulated with electrical current pulses of 0.4 mA with duration of 0.5 ms at 4 Hz for 5 min. PVN was stimulated by electrical current pulses of 0.3 mA with duration of 0.5 ms at 80 Hz for 10 sec. Electrical stimulation of PVN increased mean arterial pressure. Stimulation of DPN significantly inhibited the pressor response induced by stimulation of PVN (P<0.01), with the inhibitory percentage of 43.27%. Microinjection of L-NAME (0.5 mol/L,10 microl) into the lateral ventricle of brain attenuated the inhibitory effect of DPN. The inhibitory percentage decreased from 47.73% to 12.49% (P<0.05). Microinjection of L-NAME (2 mol/L,100 nl) into amygdala reduced the inhibitory effect of DPN. The inhibitory percentage of stimulating DPN on the pressor response decreased from 50.71% to 25.30% (P<0.05). Nitric oxide in the brain and amygdala are involved in the inhibitory effect of somatic afferent input on central pressor response.

Soleus Stretch Reflex Inhibition in the Early Swing Phase of Gait Using Deep Peroneal Nerve Stimulation in Spastic Stroke Participants

Objectives. To investigate the feasibility of inhibiting the stretch reflex of the soleus muscle by a conditioning stimulus applied to the deep peroneal nerve in spastic stroke participants during the early swing phase of gait. Materials and Methods. This study investigated the effect of an electrical conditioning stimulus applied to the deep peroneal nerve on the magnitude at the peak of the soleus stretch reflex in the early swing phase of gait in six spastic stroke participants. Results. Five of the six participants showed a reduced stretch reflex of more than 80%. On average (n= 4), it was shown that maximal inhibition occurred at a conditioning-test interval of 114 ms and had a magnitude of more than 90% (p < 0.05). For all five participants investigated, there was a significant reduction in the sensitivity of the soleus stretch reflex after conditioning (p < 0.02). Conclusions. It is concluded that the inhibition of the soleus stretch reflex with an electrical conditioning stimulus applied to the deep peroneal nerve is feasible in the early swing phase of walking. This shows a potential for being used in the rehabilitation of walking by spastic stroke persons.

Convergent inputs to neurones in the nucleus paragigantocellularis lateralis in the cat

Extracellular recordings were made in the nucleus paragigantocellularis (PGL) of the cat in response to stimulation of the hypothalamic perifornical defence area (HPDA), dorsal periaqueductal grey matter (PAG), nucleus raphe obscurus (Rob), deep peroneal nerve (DPN), and superficial peroneal nerve (SPN). Stimulation of the HPDA, dorsal PAG and SPN evoked excitatory responses whilst the prevalent response to stimulation of Rob was inhibition. However, most of the defence-reaction-related neurones showed little response to stimulation of DPN. Of 53 cells tested 48 (91%) received convergent inputs from two or more sites of stimulation. These findings are discussed in relation to the integrative function of PGL in cardiovascular control.

ROLES OF OPIOID PEPTIDES OF PAG IN ANALOGOUS ELECTRO-ACUPUNCTURE INHIBITION OF EXPERIMENTAL ARRHYTHMIA: ANALYZED BY SPECIFIC ANTISERA MICROINJECTION

Using specific antisera microinjected into periaqueductal grey (PAG), we further studied the mechanism of the analogous electroacupuncture, deep peroneal nerve stimulation (DPNS), inhibition on the experimental arrhythmia, hypothalamic stimulation-induced ventricular extrasystoles (HVE). Neither normal serum nor anti-leu-enkephalin antiserum interfered with DPNS inhibition; anti-dynorphin A (1-8) tended to attenuate the inhibition; and anti-beta-endorphin antiserum blocked it. The results provided further evidence for the hypothesis that beta-endorphin in PAG plays an important role in the neural circuit of DPNS inhibition on HVE.

EDITORIAL: HIGHLIGHTS OF THE FORTHCOMING 1ST INTERNATIONAL SYMPOSIUM ON ACUPUNCTURE &amp; ELECTRO-THERAPEUTICS TO CELEBRATE 10TH ANNIVERSARY OF ACUPUNCTURE &amp; ELECTROTHERAPEUTICS RESEARCH, THE INTERNATIONAL JOURNAL. 1) Stress &amp; Immunity and Effects of Stimulation of Deep Peroneal Nerve at St. 36 on Ventricular Arrythmia, Heart Disease &amp; Sudden Death. 2) New Simple Accurate and Inexpensive Imaging Technique of Internal Organs and Cancer

EDITORIAL: HIGHLIGHTS OF THE FORTHCOMING 1ST INTERNATIONAL SYMPOSIUM ON ACUPUNCTURE &amp; ELECTRO-THERAPEUTICS TO CELEBRATE 10TH ANNIVERSARY OF ACUPUNCTURE &amp; ELECTROTHERAPEUTICS RESEARCH, THE INTERNATIONAL JOURNAL. 1) Stress &amp; Immunity and Effects of Stimulation of Deep Peroneal Nerve at St. 36 on Ventricular Arrythmia, Heart Disease &amp; Sudden Death. 2) New Simple Accurate and Inexpensive Imaging Technique of Internal Organs and Cancer

INHIBITORY EFFECT OF ANAL0G0US ELECTRO-ACUPUNCTURE ON EXPERIMENTAL ARRYTHMIA

Rabbits were used to study the inhibitory effect of analogous electro-acupuncture on the experimental arrhythmias, i.e. hypothalamic stimulation-induced ventricular extrasystole (HVE). The result revealed that HVE, which was due to an increased cardiac sympathetic activity, could be inhibited by deep peroneal nerve stimulation with an electrical current of low frequency and low intensity. Such effect is related to endogenous opioid peptides and serotonin in the arcuatus area, the periaqueductal gray and and the medial medulla. The acupuncture correction of arrhythmias may have the same mechanism.