Influence of transcutaneous electrical nerve stimulation conditions on disynaptic reciprocal Ia inhibition and presynaptic inhibition in healthy adults

This study investigated the influence of stimulus conditions of transcutaneous electrical nerve stimulation (TENS) on disynaptic reciprocal Ia inhibition (RI) and presynaptic inhibition (D1 inhibition) in healthy adults. Eight healthy participants received TENS (stimulus frequencies of 50, 100, and 200?Hz) over the deep peroneal nerve and tibialis anterior (TA) muscle in the resting condition for 30?min. At pre- and post-intervention, the RI from the TA to the soleus (SOL) and D1 inhibition of the SOL alpha motor neuron were assessed by evoked electromyography. The results showed that RI was not changed by TENS at any stimulus frequency condition. Conversely, D1 inhibition was significantly changed by TENS regardless of the stimulus frequency. The present results and previous studies pertaining to RI suggest that the resting condition might strongly influence the lack of pre- vs. post-intervention change in the RI. Regarding the D1 inhibition, the present results suggest that the effect of TENS might be caused by post-tetanic potentiation. The knowledge gained from the present study might contribute to a better understanding of fundamental studies of TENS in healthy adults and its clinical application for stroke survivors.     

The effect of carbonic anhydrase inhibition on electrical self stimulation of the brain during hypoxia.

The effect of carbonic anhydrase inhibition on electrical self stimulation of the brain during hypoxia. Rats implanted with electrodes in the lateral hypothalamus were trained to self stimulate. Eighteen animals were injected with carbonic anhydrase inhibitor and eighteen with saline one hour prior to exposure to 8% oxygen for two hours. The performance of both groups declined in hypoxia. One hour following the onset of 8% oxygen, the animals that received the drug responded at a significantly higher rate than controls. Another group of 9 rats that had been prepared with arterial catheters was exposed to 8% oxygen before and after being treated with the drug. Arterial samples showed that the treated animals had a significantly lower pH than the controls both in air and hypoxia.     

Treatment of spinal spasticity by electrical stimulation

We present the results and the methodology of trials using transcutaneous electrical stimulation. The aim of our work was to decrease spasticity in 44 patients with traumatic damage to the spinal cord; 35 non-electrically stimulated spastics were used as controls. Both groups were randomly selected from inpatients in the Paraplegic Department at the Hospital Rehabilitation Centre. This electrical stimulation procedure leads to a long-lasting reduction in spasticity, an increased range of passive and active movements, the facilitation of lost functions, an improvement in breathing, an increase in pulmonary capacity, the reappearance of some neurological reflexes, and a diminution of supersensitivity to skin irritation. Blood pressure and neurogenic bladder functions were restored to normal. In addition to clinical observations, we investigated muscle force and the electromyogram; other measurements used in the trials involved the use of a specially adapted neurological hammer, a pendulum test, spirometry, cystometry, sphincterometry and biochemical estimations.     

Mechanisms of spinal cord electrical stimulation action on autonomic functions

The method of transcutaneous electrical stimulation of the spinal cord (ESSC) has recently begun to be actively used for both experimental studies of human motor functions and the rehabilitation of motor function in patients with spinal cord pathology. The spinal cord is the most important center of the regulation of vital functions, and ESSC affects as spinal locomotor networks as the visceral system too, which should be taken into account for the development of an improved method of rehabilitation and its use in experiments on healthy volunteers. We present a review of studies on the possible mechanisms of ESSC effects on the peripheral and cerebral circulation, cardiovascular, respiratory, excretory, and digestive systems of mammals.     

The effect of gastric electrical stimulation on canine gastric slow waves

This study determined the most efficient parameters of low-frequency/long-pulse gastric electrical stimulation (GES) required to entrain gastric slow waves and also evaluated the effect of entrainment and high-frequency, short-pulse GES on gastric electrical activity (GEA). Nine dogs were fitted with stimulation wires along the greater curvature. Entrainment was observed in six or seven animals, with long-pulse GES at six cycles per minute (cpm), at various combinations of current and pulse width and was directly related to the energy delivered. Entrainment was observed in four to seven animals, with GES at 12 cpm, and the maximal driven frequency was 6 cpm. Entrainment did not significantly increase the dominant power of GEA. High-frequency, short-pulse GES, using pulse trains of 14 Hz, 5 mA, and 330 micros, with 0.1 s on and 5 s off, and pulse trains of 40 Hz, 10 mA, and 330 micros, with 2 s on 3 s off, did not affect variables of GEA. We conclude that acute low-frequency GES but not high-frequency, short-pulse GES can entrain slow waves; the power of slow waves is not affected by either type of stimulation.     

The effect of anodal/cathodal biphasic electrical stimulation on insulin release

We studied the effects of electrical stimulation on insulin release from rat insulinoma (INS-1) cells. The anodal/cathodal biphasic stimulation (ACBPS) electrical waveform resulted in a voltage- and stimulation duration-dependent increase in insulin release. ACBPS elicited insulin release both in the presence and absence of glucose. Basal and ACBPS-induced insulin secretion could be inhibited by mitochondrial poisons and calcium channel blockers, indicating that insulin release was dependent on adenosine triphosphate (ATP) and the influx of calcium. ACBPS parameters that released insulin caused no detectable plasma membrane damage or cytotoxicity, although temporary morphological changes could be observed immediately after ACBPS. ACBPS did not alter the plasma membrane transmembrane potential but did cause pronounced uptake of MitoTracker Red into the mitochondrial membrane, indicating an increased mitochondrial membrane potential. While the ATP:ADP ratio after ACBPS did not change, the guanosine triphosphate (GTP) levels increased and increased GTP levels have previously been associated with insulin release in INS-1 cells. These results provide evidence that ACBPS can have significant biological effects on cells. In the case of INS-1 cells, ACBPS promotes insulin release without causing cytotoxicity.     

Effects of transcutaneous electrical spinal cord stimulation on stepping patterns during walking

Effects of transcutaneous electrical spinal cord stimulation (tESCS) on the parameters of stepping movements in healthy subjects were investigated during two kinds of activity: walking on a moving treadmill belt (active treadmill) as well as pushing the treadmill belt by effort of the legs (passive treadmill). It was found that the total interference electromyogram (EMG) activity during stepping performance on a passive treadmill was 1.5–2 times higher than during stepping on an active treadmill. In addition, the amplitude of angular displacement of the hip joint and ankle was 2.5 times and 1.7 times higher, respectively, during passive vs. active treadmill, while the duration of stepping cycle decreased by 19%. Although the muscles were exposed to different load and the parameters of motion on the active and passive treadmill were different, tESCS caused an increase in the total EMG activity in 96% of cases both on the active and on the passive treadmill. In both cases, the stepping cycle period decreased by 4–43% in all subjects. These results suggest that tESCS can affect voluntary stepping patterns under conditions of different afferent control.     

Electrical stimulation in multiple sclerosis. Comparison of transcutaneous electrical stimulation and epidural spinal cord stimulation

Forty-nine multiple sclerosis patients with bladder symptoms and/or walking disability were subjected to a therapeutic trial with electrical spinal cord stimulation and transcutaneous electrical stimulation, a second aim being to compare these two treatments. A clear subjective improvement in bladder symptoms was achieved in the majority of the cases, and this was substantiated by objective parameters. In a proportion of cases a more moderate improvement seems to have been achieved in a variety of symptoms. Transcutaneous electrical stimulation seems to be a useful selection procedure for later electrical spinal cord stimulation.     

Alternating stimulation of synergistic muscles during functional electrical stimulation cycling improves endurance in persons with spinal cord injury

Therapeutic effects of functional electrical stimulation (FES) cycling for persons with spinal cord injury (SCI) are limited by high rates of muscular fatigue. FES-cycling performance limits and surface mechanomyography (MMG) of 12 persons with SCI were compared under two different stimulation protocols of the quadriceps muscles. One strategy used the standard “co-activation” protocol from the manufacturer of the FES cycle which involved intermittent simultaneous activation of the entire quadriceps muscle group for 400 ms. The other strategy was an “alternation” stimulation protocol which involved alternately stimulating the rectus femoris (RF) muscle for 100 ms and the vastus medialis (VM) and vastus lateralis (VL) muscles for 100 ms, with two sets with a 400 ms burst. Thus, during the alternation protocol, each of the muscle groups rested for two 100 ms “off” periods in each 400 ms burst. There was no difference in average cycling cadence (28 RPM) between the two protocols. The alternation stimulation protocol produced longer ride times and longer virtual distances traveled and used lower stimulation intensity levels with no differences in average MMG amplitudes compared to the co-activation protocol. These results demonstrate that FES-cycling performance can be enhanced by a synergistic muscle alternation stimulation strategy.     

Stretch reflex inhibition using electrical stimulation in normal subjects and subjects with spasticity

The effect of electricallys timulating the tibialis anterior muscle on the stretch reflex of the soleus muscle in normal subjects and subjects with spasticity is investigated. Stimulation of the tibialis anterior just prior to the onset of a mechanical disturbance, which causes a stretch in the soleus, inhibits the stretch reflex of the soleus in normal subjects and may inhibit clonus in subjects with spasticity.     

Effect of local depression of inhibition on electrical activity of the spinal cord

The dorsal cord, dorsal root, and focal potentials in response to peripheral nerve stimulation were investigated in rats with local depression of inhibition in the left or right half of the lumbar segments produced by the action of tetanus toxin. The investigation was carried out at the stage of poisoning when excitation of the neuron population with disturbed inhibition caused generalized excitation of spinal and bulbar motoneurons. Experiments on spinal animals showed that if a cutaneous nerve is stimulated on the side affected by the toxin these responses have a greater amplitude and a much longer duration than those evoked by stimulation of the opposite nerve or responses in healthy rats. The maximal increase in amplitude and duration of the negative component of the focal potential corresponding to the time of the increased P wave of the dorsal cord potential was found in the ventral quadrant on the side affected by the toxin. Besides evoked focal potentials, spontaneous rhythmic negative waves also were recorded in this area. The mechanisms of spread of seizure activity from the focus of depressed inhibition are discussed and the structures generating spreading seizure activity are identified.     

Role of endogenous opiates and extracellular K+ accumulation in the inhibition of frog spinal reflexes by electrical skin stimulation

Electrical skin stimulation of the hind limb (10-100 Hz, 30 s-5 min) at the intensity which leads only to the excitation of low threshold afferents depressed (for 1-30 min) the flexor reflex evoked in spinal frogs by nociceptive stimuli. The inhibition, which lasted for longer than 5 min was blocked by naloxone. Short-term poststimulation effects were associated with an increase of extracellular K+ concentration (delta [K]e) and were not blocked by naloxone. Enkephalins or morphine applied to the spinal cord surface increased the threshold for flexor reflexes while naloxone decrease their threshold. The stimulation was followed by short-term hyperpolarization of primary afferents (PAH; 1-5 min) and by depression of dorsal root potentials (DPRs) which had a similar time course to the delta [K]e, and were not blocked by naloxone. This period was frequently followed by longlasting PAH and enhancement of DRPs (5-30 min), which were abolished by naloxone. Superfusion of the isolated spinal cord with opioids produced PAH and enhanced DRPs evoked by nociceptive stimuli, while naloxone or increase of [K] in Ringer solution depolarized primary afferents and depressed DRPs. It is suggested that the antinociceptive effects of electrical stimulation of low threshold cutaneous afferents in spinal frogs involves at least two mechanisms. The short-term effect may result from delta [K]e, especially at high stimulus strength and is equally effective against noxious and non-noxious stimuli. The longlasting effects selectively affecting nociceptive transmission appear to be produced by endogenous opioids.     

Excessive reflexes in spinal cord injury triggered by electrical stimulation

Interaction of electrocutaneous stimulation with an impaired human motor control system may result in unstable reflex loops causing excessive spastic reactions. These contractions are usually excluded from analysis since the presence of spasm is one of the criteria commonly applied for discarding a contraction. They may, however, provide interesting information on the nature of spasticity. The dorsiflexor muscles of four SCI subjects were activated by means of surface electrical stimulation and the isometric ankle moment was measured. Short bursts of constant stimulation frequency at seven different frequencies (8, 12, 16, 20, 25, 33, 50 Hz) triggered spastic reactions in all subjects. The onset times of spastic activity during an electrically elicited contraction shortened with increased stimulation frequency. A stimulation burst may also have a spasticity reduction effect on a subsequent burst, indicating potential short term therapeutic effects of stimulation on spasticity in isometric conditions.     

Antinociceptive effect of spinal cholinergic stimulation: interaction with substance P

Activation of central muscarinic receptors results in an antinociceptive response in experimental animals. Employing intrathecal (i.t.) injection and radiant heat applied to a rat's tail as the experimental paradigm, a spinally-mediated antinociceptive response was obtained following injection of cholinergic agonists. Since "cholinergic' analgesia is mediated independently of the opiate system, the possibility was considered that this response was mediated through inhibition of the local release of substance P. Rats were prepared with indwelling i.t. catheters which terminated in the L2-L3 region of the spinal cord. I.t. injection of carbachol (0.05-5 micrograms) or neostigmine (1-10 micrograms), but not nicotine (0.5-10 micrograms) produced dose-related increases in tail flick latencies. Pretreatment with i.t. injection of atropine or hemicholinium-3 significantly inhibited the antinociceptive response to neostigmine. Spinal substance P levels were measured 30 min following 0.5 micrograms carbachol. Levels in the dorsal horn were reduced by 30% compared with saline controls. Levels in the ventral horn were unchanged by carbachol. These results support the role of endogenous spinal acetylcholine in pain modification and suggest an interaction with substance P neurons of the dorsal spinal cord.