[Changes in hemodynamics upon nociceptive stimulation, electrical stimulation of the septum of the brain and a combination of both].
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Electrical stimulation of the gastrointestinal (GI) tract, analogous to pacing the human heart, is an attractive idea. This is because these organs, like the heart, have their own natural pacemakers, and the electrical signals they generate can be altered by externally delivering certain types of electric currents via intraluminal or serosal electrodes to certain areas of the GI tract. A number of studies on animals have been accomplished successfully to treat a variety of disease models, including gastroparesis, dumping, and short bowel syndrome. Over the past 10 years or so, electrical stimulation of the GI tract has received increasing attention among researchers and clinicians because of new techniques, such as implantable devices, and promising results achieved in treatment of gastroparesis and morbid obesity. The objective of this article is to review the advances in electrical stimulation of the gastrointestinal tract. First the electrophysiology of the GI tract and history of GI electrical stimulation are introduced. Then various methods of electrical stimulation of the stomach and small bowel in healthy animals and models of GI diseases are reviewed. Finally clinical applications of electrical stimulation to GI disorders and their possible mechanisms are discussed.
We measured total peripheral motor conduction time by two different methods, magnetic stimulation and electrical stimulation, to reveal which is better in determining actual peripheral motor conduction time. In the upper extremities, the difference between magnetic stimulation and electrical stimulation was within a mean time of 1.39 +/- 0.8 msec, while that in the lower extremities was 2.3 +/- 1.1 msec. In any 4 extremities, total peripheral motor conduction time obtained by magnetic stimulation was significantly shorter than that measured by electrical stimulation employing conventional F-wave response. We conclude that stimulus sites 8.8 +/- 5.1 cm distal to spinal motoneurons in the upper extremities, and 10.5 +/- 5.3 cm distal in the lower extremities were stimulated by magnetic stimulation of the peripheral nerves. Electrical stimulation employing conventional F-wave measurement is superior to magnetic stimulation for actual total peripheral nerve conduction study.
Electrical stimulation of the thalamus has been widely used to test for the existence of monosynaptic input to cortical neurons, typically with stimulation currents that evoke cortical spikes with high probability. We stimulated the lateral geniculate nucleus (LGN) of the thalamus and recorded monosynaptically evoked spikes from layer 4 neurons in visual cortex. We found that with moderate currents, cortical spikes were evoked with low to moderate probability and their occurrence was modulated by ongoing sensory (visual) input. Furthermore, when repeated at 8-12 Hz, electrical stimulation of the thalamic afferents caused such profound inhibition that cortical spiking activity was suppressed, aside from electrically evoked monosynaptic spikes. Visual input to layer 4 cortical cells between electrical stimuli must therefore have derived exclusively from LGN afferents. We used white-noise visual stimuli to make a 2D map of the receptive field of each cortical simple cell during repetitive electrical stimulation in the LGN. The receptive field of electrically evoked monosynaptic spikes (and thus of the thalamic input alone) was significantly elongated. Its primary subfield was comparable to that of the control receptive field, but secondary (flanking) subfields were weaker. These findings extend previous results from intracellular recordings, but also demonstrate the effectiveness of an extracellular method of measuring subthreshold afferent input to cortex.
Electrical stimuli were applied to subjects' upper and/or lower gingivae around the right canines; (i) during maintained relaxation of masticatory muscles; (ii) at an active opening position; (iii) while clenching in an incisal edge-to-edge contact (IEC) position; and (iv) at the wide-open position. Reflex responses of the suprahyoid and jaw-closing muscles were obtained using surface electrodes. The electrical stimulation produced segmented reflex excitation(s) in the suprahyoid muscle and conventional reflex excitation and/or inhibition in the jaw-closing muscles when some background activity was maintained in the muscle(s). The excitatory reflex in the suprahyoid muscle responded to multiple site electrical stimulation which was delivered on both the upper and lower jaw simultaneously rather than to single site stimulation. Also, the responses depended on the intensity of the electrical stimulation. In particular, stronger intensities resulted in longer latencies. The results support the suggestions in our previous studies with mechanical stimuli, i.e. that the human jaw-opening reflex can be obtained only when some background activity is maintained in the jaw openers, perhaps due to low threshold afferent input, and that spatial summation may be effective for the reflex.
Electrical stimulation is a therapeutic modality available for the preservation of muscle function following peripheral nerve injury. Agrin, a synaptic basal lamina protein, induces accumulation of acetylcholine receptors (AChRs) and other molecules at the neuromuscular junction. Electrical stimulation of denervated muscle does not alter agrin and AChR distribution at abandoned synaptic sites, supporting the hypothesis that the existing aggregation of synaptic molecules, which may be necessary for successful reinnervation, is unaltered by electrical stimulation of denervated muscle.
Electrical stimulation studies have demonstrated that a "supplementary motor area" (SMA) exists in humans. However, its precise functional organization has not been well defined. We reviewed the extraoperative electrical stimulation studies of 15 patients with intractable epilepsy who were evaluated with chronically implanted interhemispheric subdural electrodes. SMA-type positive motor responses were elicited not only from the mesial portion of the superior frontal gyrus but also from its dorsal convexity, and from the paracentral lobule, cingulate gyrus, and precuneus. Sensory symptoms, that could not be attributed to stimulation of the primary sensory area, were elicited from the superior frontal and cingulate gyri in addition to the precuneus. Therefore, human SMA, as defined by electrical stimulation, is not always confined to the mesial portion of the superior frontal gyrus as described previously. It is also not strictly "motor" but "sensorimotor" in representation. We propose referring to this region as the "supplementary sensorimotor area" (SSMA). We observed a somatotopic organization within the SSMA with an order of lower extremity, upper extremity, and head from posterior to anterior. Sensory representation in an individual was either anterior or posterior to the positive motor representation but never both. There was a supplementary eye field within the head representation. A supplementary negative motor area was noted at the anterior aspect of the SSMA. No language area was demonstrated within the SSMA. The physiologic significance of the SSMA and functional consequences of its resection must be addressed in further studies.
Electrical stimulation of paralyzed muscles has been shown to affect their spasticity, especially in patients with hemiplegia. But little has been reported on the long-term effects of such stimulation on individuals with spinal cord injury. This paper documents initial quadriceps spasticity in 31 spinal cord injured subjects, and the effect of four to eight weeks of reconditioning using electrical stimulation. Spasticity was quantified through the use of a normalized relaxation index (R2n) obtained from a pendulum drop test. The reconditioning protocol consisted of twice daily 20-minute exercise sessions at least four hours apart, six days per week. Spasticity and stimulated quadriceps torque were measured during one to three evaluations performed at least one day apart at the beginning of the program, and at four and eight weeks. There was no significant difference in average initial measures of spasticity between left and right legs and no effect of time since injury on average R2n values. Significant differences were seen for right leg average baseline R2n values when grouped by lesion level or completeness. Quadriplegic individuals were more spastic than paraplegic individuals, and subjects with incomplete lesions were more spastic than those with complete lesions. These findings are interrelated since most of the quadriplegic subjects (14 of 16) had incomplete lesions. Most participants had increased spasticity after four weeks of reconditioning but not after eight weeks. However, only eight subjects completed eight weeks of reconditioning. Subjects who had the greatest increases in spasticity also had the greatest gains in stimulated torque, both after four and eight weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
Electrically stimulating the stomach to treat gastroparesis has been proposed by investigators for decades. With the development of techniques of implantable pacing devices and electrodes and promising preliminary results in chronic pacing studies, gastric electrical stimulation (GES) has received increasing attention recently among researchers and clinicians. A number of studies have been performed to investigate the effects of GES on gastric motility, gastric emptying, and gastrointestinal symptoms in both dogs and humans. Based on the frequency of the electrical stimulus used for chronic treatment of gastroparesis, gastric electrical stimulation can be classified into low-frequency stimulation (LFS) and high-frequency stimulation (HFS). Although some of the results are still controversial, the majority of these studies seem to indicate that LFS is able to normalize gastric dysrhythmias and entrain gastric slow waves and accelerate gastric emptying. On the other hand, HFS has no effect on gastric emptying but is able to significantly reduce symptoms of nausea and vomiting in gastroparetic patients. GES has provided an exciting new advance in the treatment of gastroparesis and management of upper gastrointestinal symptoms. This paper will review the available studies of GES in the treatment of gastroparesis and current status of this field.
Electrical stimulation is known to cause activation in mammalian oocytes, possibly by eliciting an elevation in intracellular calcium (Ca2+). This study reports intracellular Ca2+ concentrations in mature rabbit oocytes using the Ca2+ indicator fura-2. Calcium levels were determined prior to, during, and after the administration of an electrical pulse (3.6 kV/cm for 60 microseconds). Baseline Ca2+ levels ranged from 30 to 90 nM. The intracellular Ca2+ transient evoked by a pulse, peaked at 11 sec, was highly variable in amplitude (40-300 nM) and returned to prepulse levels within 300 sec. Electrically stimulated oocytes did not exhibit repetitive Ca2+ transients. The size of the cytoplasmic Ca2+ rise was influenced by the duration of the pulse, the field strength and the concentrations of external Ca2+ rise was influenced by the duration of the pulse, the field strength and the concentrations of external Ca2+ (P less than 0.05). Oocytes electrically stimulated in the presence of 100 microM CaCl2, which evoked Ca2+ transients with a mean magnitude of 120 nM, activated at a higher rate (P less than 0.05) than oocytes stimulated in the presence of either higher or lower levels of external Ca2+. Although oocytes electrically shocked at 16-18 hr after administration of human chorionic gonadotropin (hphCG) activated at a lower rate than oocytes stimulated at 22-24 hphCG (P less than 0.05), their intracellular Ca2+ response to the pulse was similar (P less than 0.05). These results indicate that electrical pulse parameters and extracellular Ca2+ concentrations can be used to modulate intracellular Ca2+ levels and optimize oocyte activation rates.(ABSTRACT TRUNCATED AT 250 WORDS)
Electrical stimulation of the chick ciliary nerve leads to a frequency-dependent increase in the Na+-dependent high affinity uptake of [3H]choline (SDHACU) and its conversion to acetylcholine (ACh) in the nerve terminals innervating the iris muscle. The forces that drive this choline (Ch) uptake across the presynaptic membrane were evaluated. Depolarization with increased [K+] out or veratridine decreases Ch accumulation. In addition to the electrical driving force, energy is provided by the Na+ gradient. Inhibition of the Na,K-ATPase decreased the Ch taken up. Thus, changes in the rate of Ch transport are dependent on the electrochemical gradients for both Ch and Na+. Ch uptake and ACh synthesis were increased after a conditioning preincubation with high [K+] out or veratridine. As is the case for electrical stimulation, this acceleration of Ch uptake and ACh synthesis was strongly dependent on the presence of Ca++ in the incubation medium. Na+ influx through a TTX-sensitive channel also contributed to this acceleration. Inasmuch as membrane depolarization reduces the initial velocity of Ch uptake and ACh synthesis, their increases during electrical stimulation therefore cannot be the direct effect of the depolarization phase of the action potential. Instead they are the result of the ionic fluxes accompanying the presynaptic spike. It is concluded that stimulation of Ch uptake and ACh synthesis by nerve activity depends first, on the ACh release elicited by Ca++ influx after depolarization and second, on the activation of the Na,K-ATPase due to Na+ entry. Furthermore, it is suggested that the release of ACh after stimulation drives translocation of cytoplasmic ACh into a protected compartment (probably vesicular). This recompartmentation of intraterminal ACh stimulates ACh synthesis by mass action, allowing further accumulation of Ch.
Electrical stimulation of the rat heart sarcolemmal membranes with a square wave current was found to increase Ca2+-ATPase activity. This activation of the enzyme was dependent upon the voltage of the electric current, frequency of stimulation and duration of stimulation of the sarcolemmal membranes. The increase in Ca2+-ATPase was reversible upon terminating the electrical stimulation. The activation of sarcolemmal Ca2+-ATPase due to electrical stimulation was markedly depressed when the reaction was carried out at high pH (7.8 to 8.2), low pH (6.6 to 7.0), high temperatures (45 to 50 degrees C) and low temperatures (17 to 25 degrees C) of the incubation medium. Ca2+-antagonists, verapamil and D-600, unlike other types of inhibitors such as propranolol and ouabain, were found to reduce the activation of sarcolemmal Ca2+-ATPase by electrical stimulation. These results support the view that Ca2+/Mg2+ ATPase may be involved in the gating mechanism for opening Ca2+-channels in the sarcolemmal membrane upon excitation of the cardiac muscle.
Electrical stimulation is a commonly used clinical tool, but subject and patient comfort is still a major problem retarding its widespread application. Stimulus waveform in combination with pulse duration can play a major part in subject comfort. An asymmetric balanced biphasic square waveform was perceived as comfortable and was clinically effective in stimulating wrist flexor and extensor muscles. Subjects preferred the square waveforms over a paired spike monophasic waveform. In the larger quadriceps muscle group, a symmetric biphasic square wave was perceived as more comfortable than either a monophasic paired spike or any of three medium frequency waveforms. There seemed to be, however, a small subpopulation of subjects who consistently preferred the medium frequency waveforms. Medium frequency stimulation should be tried for those patients who have considerable difficulty adapting to the sensory input inherent with the use of surface electrical stimulation.
Electrical stimulations of low voltage, frequency and short duration of time are suitable for amphibian muscle to induce localized muscular exercise in an intact animal. The pattern of changes in the muscle chemical components on chronic exposure to repeated electrical stimulations suggested the onset of regulation on muscle metabolism leading to carbohydrate sparing process and muscular hypertrophy. The applicability of this procedure to prevent the muscle wasting in atrophic and dystrophic muscles is suggested.
Electrical stimulation of advanced tadpoles of Rana breviceps for 24 hr with 3 microA current after hindlimb amputation through shank and ankle slightly increased the number of perfect regenerates as compared to controls. When amputation was made through thigh in tadpoles of the same stage regeneration failed in all cases of the controls but 24 hr stimulation of these tadpoles after similar operation with 3 and 10 microA currents induced fair degree of regeneration in 9 and 40% cases, respectively.
Electrical stimulation as a treatment for tinnitus seems to be effective in about 50% of patients with tinnitus of various causes. Electrical stimulation as a treatment for tinnitus is safe, if delivered within the parameters described in this article.
The effects of ethanol (EtOH) on potassium and electrically stimulated acetylcholine (ACh) release were compared in rat cerebral cortical slices in vitro. ACh was measured by pyrolysis - gas-liquid chromatography (GLC). Paired samples were incubated with and without 0.11 M EtOH. In the potassium stimulation experiments, cortical slices were serially incubated for three 45-min periods in normal incubation medium followed by two periods in medium containing either 15 or 27 mM K+. In the electrical stimulation experiments, the cortical slices were similarly incubated for three 30-min periods without stimulation followed by two periods of electrical (10 HZ) stimulation. ACh output rose 20% at 15 mM K+ and 160% at 27 mM K+. Ethanol had no effect on spontaneous ACh release and did not influence the ACh response to high K+ stimulation. Electrical stimulation approximately doubled the ACh output but EtOH reduced electrically stimulated ACh relese by 50--80%. These findings are compatible with the view that EtOH acts primarily on Na+ influx during the action potential.
Electrical field stimulation (9 V, 1.0 ms, 4 Hz) of isolated segments of rat tail arteries and dog coronary arteries inhibits contractile responses to exogenous norepinephrine and elevated potassium concentration. This inhibitory effect of electrical stimulation is blocked by various agents that alter oxygen metabolism: superoxide dismutase, catalase, glutathione, ascorbate, and dimethyl sulfoxide. The observations suggest that the inhibitory effect is due to an action of oxygen free radical metabolites that are generated by the electrical stimulation of the oxygen-rich buffer. These free radical metabolites have two actions: 1) they oxidize drugs in the experimental system, and 2) they exert a direct inhibitory action on vascular smooth muscle.