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BACKGROUND: Simple basic visual perception may be restored by epiretinal electrical stimulation in patients that are blind due to photoreceptor loss. To stimulate ganglion cells, epiretinally flat platinum microelectrodes embedded in thin polyimide film were developed and tested in the cat. METHODS: After removal of the lens and the vitreous body a thin microfilm electrode array was implanted through a corneoscleral incision in the cat eye (n = 4). In two eyes no further attempt was made to fixate the tip of the electrode, which was pressed onto the retinal surface due to the tension of the curved polyimide film. In two eyes the tip of the electrode was fixed with cyanoacrylate adhesive. The exterior part of the microelectrode film was directed under the skin towards the forehead which allowed fixation of the microplug to a head fixation bolt. Retinal stimulation experiments were performed within 1 week after implantation. Success of stimulation was assessed by recording neuronal activities from areas 17 and 18. Retinal microelectrodes were removed 2 weeks or longer after implantation. RESULTS: Intraocular inflammation or retinal detachment were not observed after implantation of the microelectrode film. In two eyes the tip of the microelectrodes dislocated spontaneously within the first few days. The lowest threshold of electrical stimulation was 35 microA, corresponding to a charge transfer of 14 nC per phase. These values were ten times higher than those obtained by needle electrodes used in prior experiments. CONCLUSIONS: Intraocular implanted flat microelectrodes made of platinum and polyimide were well tolerated. Because of the flat configuration of the microelectrodes higher stimulation thresholds than for needle electrodes were found, indicating insufficient contact to the retinal surface. An alternative shape and fixation technique is required to minimise electrodes' threshold of stimulation.
While applying solutions of 5 mM QHCl, 2 M NaCl and HCl at pH 3.0 to three different ipsilateral portions, root, middle and tip of the tongue surface of the frog, reflex discharges were recorded from three main branches of the hypoglossal nerve. Reflex discharges in the hypoglossal branch were elicited mainly when the caudal two-thirds of the tongue was stimulated with the chemicals, whereas those in the genioglossal branch occurred predominantly when the rostral two-thirds of the tongue was stimulated. The intrinsic branch responded reflexly to stimulation of any portion of the tongue. The hypoglossal branch was also highly sensitive to mechanical stimulation of the tip of the tongue. Action potentials reflexly elicited by electrical stimulation of medial and lateral branches of the glossopharyngeal nerve were recorded from the following two of the three efferent branches simultaneously. Then it was revealed that the activity of the hypoglossal branch was induced by sensory inputs from low threshold fibers in the medial branch, whereas that of the genioglossal branch was mainly by the lateral branch. Latencies between the electrical stimulation of the afferent branches and the potential in the hypoglossal branch produced by stimulation of the medial branch had the shortest latency. This reflex are may functionally play a role in retracting the tongue quickly after capturing a prey at the tip of the frog tongue.
Animal experiments and clinical studies were made to examine the effectiveness of combined neuro-myo-stimulation (conjugated electric stimulation of the injured nerve and muscles and intact reflexogenic areas together with conventional electric stimulation of the nerve) in the treatment of compression ischemic injury to the nerves. The combined neuro-myo-stimulation used in 27 rabbits with experimental compression ischemic injuries to the peripheral nerves made it possible to reduce the time of the recovery of the movements and sensitivity of the paresthetic limb and to reduce vegetative trophic disturbances. This conclusion was supported on the use of the combined neuro-myo-stimulation in the treatment of 16 patients with different injuries to the peripheral nervous system, in whose genesis the main part was played by compression ischemic factors.
Intramuscular electrical muscle stimulation has been used to treat spinal curvature. Five single-channel implantable stimulators with two alternating outputs each output supplying electrical stimuli to one reference (+) and two active (-) platinum corkscrew electrodes inserted into the deep paraspinal musculature were implanted. Stimulation is applied daily during rest, and nightly, during sleep, through implanted electrodes, evoking muscle contractions which cause correction of the curvature. Arrest of rapid progression in five patients with single primary curve, treated up to almost four years, (44 months) was observed in 60%. In one case the implantable system was removed after 10 months of treatment.
Magnetically and electrically elicited blink reflexes were studied in 11 normal subjects and in 5 patients with partial peripheral facial nerve palsy. Both methods were able to elicit a reproducible blink reflex. In both groups the latencies of the magnetically elicited reflexes were equal to those that followed electrical stimulation. The magnetic stimulation technique offered 2 advantages over the electrical stimulation: (1) it was less painful and therefore better tolerated and (2) the coil position in the middle of the forehead was sufficient to elicit a bilateral blink reflex because the windings of the stimulation coil excited both supraorbital nerves simultaneously. This bilateral response enables one to reduce the number of stimuli and can be used in the examination of patients that have peripheral facial nerve palsies without the concomitant impairment of the reflex pathway in the brainstem. The magnetic technique can also elicit a blink reflex at stimulation points distant from the supraorbital notch. This finding offers an alternative explanation of the late responses of facial muscles following transcranial magnetic stimulation of the motor cortex.
Various electrical stimuli were tested for their ability to suppress or relieve severe tinnitus. Stimulation was applied transdermally by electrodes placed on the preauricular and postauricular regions and on the two mastoids. Of the 50 patients tested, only 14 (28%) obtained relief that met the criterion of a reduction in the tinnitus by 40% or more. When relief was obtained, it usually extended for several hours into the poststimulation period. There was only one positive response (2%) in the placebo trial, which was administered to all patients. It was concluded that transdermal electrical stimulation such as that used in this research is not a practical therapeutic procedure for the relief of tinnitus.
Electrical stimulation is an effective and well-tolerated treatment for overactive bladder. Initial work in animals indicated the potential of this treatment, and early clinical experience in Europe further supported its likely efficacy. Although the mechanism of action of electrical stimulation remains unproven in humans, it is believed to be a neuromodulating therapy which affects the neural signaling that controls continence. There is also strong evidence that electrical stimulation affects striated muscle. The therapy can cause hypertrophy of skeletal muscle fibers, possibly by the recruitment of faster-conducting motor units, which would not normally be recruited during voluntary efforts. In addition, electrical stimulation can alter the expression of myosin isoforms, favoring a conversion to type I muscle. Despite our incomplete understanding of the mechanism of action of electrical stimulation, clinical devices have been developed quickly. Case series have been reported throughout Europe. These were followed by controlled clinical trials in the United States. There is good evidence that the use of vaginal electrical stimulators can reduce the occurrence of symptoms of overactive bladder in about half of the patients treated. Multiple uses of nonimplanted stimulation, including thigh stimulation, anal stimulation, and direct pelvic muscle stimulation, have been reported. In these trials, it is common for objective findings to be poorly correlated with subjective reports of improvements or cure. Patients frequently report that the urge-to-leak time improves, but this is difficult to measure objectively. The use of nonimplanted devices is effective and well tolerated, and should precede the use of implanted devices. A direct comparison with other effective methods of treatment for overactive bladder is warranted.
OBJECTIVES/HYPOTHESIS: Electrical stimulation of the posterior cricoarytenoid muscle, when paced with inspiration, offers a physiological approach to restore ventilation in bilateral laryngeal paralysis without any of the disadvantages associated with conventional treatment. STUDY DESIGN: A prospective study of six patients. METHODS: The patients were successfully implanted with an Itrel II stimulator (Medtronic, Inc). In postoperative sessions, stimulated vocal fold abduction, patient ventilation, and voice were assessed and compared with preoperative values. RESULTS: The optimum stimulus paradigm was a 1- to 2-second train of 1-millisecond pulses delivered at a frequency of 30 to 40 Hz and amplitude of 2 to 7 V. Posterior cricoarytenoid stimulation produced a large dynamic abduction (3.5-7 mm) in three patients and moderate abduction (3 mm) in a fourth patient. The fifth patient showed a large but delayed response of 4 mm to stimulation with some lateralization of the vocal fold. In the sixth patient, stimulated abduction was noted on device implantation but was lost postoperatively. All five patients with stimulated abduction postoperatively met the ventilatory criteria for decannulation, and three patients subsequently had decannulation. Long-term stimulation of the posterior cricoarytenoid muscle had no appreciable effect on voice quality. CONCLUSIONS: Electrical stimulation of the posterior cricoarytenoid muscle shows potential as an improved therapy for bilateral vocal fold paralysis.
Combinations of transcutaneous electrical stimulation (TES) and inhalation of nitrous oxide with oxygen have been used for surgical pain control and this report explored the possible synergism of these two treatments. During painful dental stimulation, 18 subjects gave pain reports while event-related potentials were recorded at vertex. Electrical stimulation was delivered bilaterally at the LI-4 acupuncture points on the hands at 20 Hz, mean = 9.65 mA intensity. Inhalation treatment was nitrous oxide 33% with oxygen. Testing was done on two days to permit evaluation of each treatment alone and their combination. Treatment sequence was counterbalanced. Base-to-peak amplitude and peak latency scores were derived for the event-related potentials under each testing condition. Both stimulation and inhalation treatments altered event-related potential scores and pain report. The combination treatment was significantly more effective than stimulation alone but was not significantly more effective than nitrous oxide alone. Nitrous oxide with oxygen alone reduced peak amplitude at 250 ms and 350 ms, as well as pain report. It increased peak latency at 100 ms. Transcutaneous electrical stimulation alone decreased peak amplitude and latency at 150 ms and increased peak latency at 350 ms. Decreased peak amplitude at 250 ms and increased peak latency at 150 ms were observed when inhalation was added to stimulation, and there was also a significant reduction in pain report. Nine control subjects were studied to demonstrate that analgesic changes were not due to repeated testing. These outcomes demonstrated no synergism between the stimulation and inhalation treatments. The data suggest that nitrous oxide blocks the effects of electrical stimulation at LI-4.
Chronic intermittent electrical stimulation (15 min on, 85 min off, seven times per day) eliminated endothelial dysfunction of pre-capillary arterioles in ischaemic rat ankle flexor muscles. Responses to acetylcholine were restored from constriction to dilation, and the reduced dilation to bradykinin was corrected by 1 week of stimulation. Administration of the NOS inhibitor N(omega)-nitro-L-arginine for 1 week impaired arteriolar reactivity in a similar way to ischaemia, and dilator function was likewise restored by chronic stimulation. This suggests that nitric oxide production in the microcirculation is depressed by chronic ischaemia and that chronic electrical stimulation can specifically reverse this deficit. Stimulation applied to ischaemic muscles for 2 weeks also increased the numbers of microvessels immunostained for alpha-smooth muscle actin and the numbers of eNOS-positive microvessels and capillaries. These findings help to elucidate the mechanism of the beneficial effect of exercise in the treatment of peripheral vascular diseases by showing that muscle activity can improve both function and structural capacity of the microvasculature.
Electrical stimulation to augment or maintain muscle performance has been well documented. The purpose of this preliminary report is to present the results of a single-case study conducted to determine the order of activation of skeletal muscle fibers as a result of electrical stimulation. The subject's quadriceps femoris muscles were electrically stimulated at 80% of maximal isometric torque. Pre-stimulation and immediate post-stimulation muscle biopsy samples were obtained, and a modification of the glucogen-depletion method was used to determine activation of muscle fibers. The pre-stimulation muscle biopsy sample demonstrated uniform periodic acid-Schiff (PAS)-positive staining in all fiber types, whereas the post-stimulation muscle biopsy sample showed glycogen depletion of type II muscle fibers. The most PAS-negative muscle fibers were type IIa skeletal muscle fibers. The results of this single-case study provide evidence that electrical stimulation, as described, selectively activates type II skeletal muscle fibers. The implication of this finding is that, in many chronic diseases, type II fibers are selectively and preferentially affected. Electrical stimulation may be a clinically viable technique to use in patients with type II fiber involvement.
We studied the effects of electrical stimulation of the skin on upper extremity spasticity in nine hemiparetic stroke subjects. The effects were quantified by comparing reflex torque responses elicited during ramp and hold angular perturbations of the elbow recorded before and after low-intensity skin stimulation. Electrical stimulation was applied to skin over the biceps muscle for a period of ten minutes at a 20 Hz frequency, pulse duration 0.1 ms, with an intensity level below motor threshold but above sensory threshold. In seven of the nine subjects, stimulation of skin over spastic muscle reduced peak torque responses in both flexors and extensors for at least 30 min. In these seven subjects there were significant increases in mean threshold angle for the onset of reflex torque so that a greater angular rotation was required to initiate the stretch reflex response. This shift occurred without change in reflex impedance. The origins of these long-term changes in reflex torque are unclear, but may reflect synaptic plasticity of spinal circuitry outside the stretch reflex loop.
Chronic indirect electrical stimulation of adult mammalian skeletal muscle brings about a transformation from the fast-twitch to the slow-twitch type. Underlying this transformation there is a sequence of profound changes in the expression of proteins involved in all the major molecular systems of the muscle. These include qualitative changes in the expression of myosin light and heavy chain isoforms. The time course of these changes has been studied in some detail at the protein level, both during chronic stimulation and during the recovery process that follows the cessation of stimulation. Here we report on the use of cDNA probes to study corresponding changes in myosin heavy chain (MHC) and light chain (MLC) mRNAs in rabbit fast-twitch muscles during continuous electrical stimulation at 10 Hz and during the first 12 days of recovery after cessation of 6 weeks of stimulation. At an early stage of the response to stimulation, fast MHC mRNA is replaced by slow MHC mRNA. During recovery this process occurs in reverse but takes longer. Broadly similar changes are seen for MLC mRNAs, although the time course is somewhat different. These experiments contribute to a growing body of evidence that many of the protein changes induced by chronic stimulation are the result of regulatory events that take place at a pre-translational level.
Procedures are described for determining trace quantities of Pt released into brain tissue directly beneath cortical surface stimulation electrodes. Implanted electrodes (1.1 mm Pt discs) were stimulated for 4.5 h, 9 h and 36 h (4 X 9 h/day) with balanced biphasic pulses (20 micro C/cm2 or 100 micro C/cm2 per phase, 50 Hz), following which tissue 0-2 mm beneath stimulation electrodes and the encapsulating tissue adherent to electrodes was excised and analyzed for Pt. A time-dependent increase in Pt concentration was observed between 4.5 h (4-20 ng Pt/stimulation site) and 9 h (50-339 ng Pt/site) of stimulation at 100 micro C/cm2 with nearly all of the Pt located in the encapsulating tissue associated with the electrodes. Somewhat less Pt was observed in the 36 h samples, and it was almost equally distributed between the encapsulating tissue of the electrodes and the first millimeter depth of underlying brain tissue. Little or no Pt was found at electrode sites receiving 20 micro C/cm2 pulses. Control brain tissue samples as well as samples of blood, CSF and kidney were negative for Pt. The findings indicate that the rate of Pt dissolution gradually decreases during in vivo stimulation, and that dissolved Pt may slowly move away from stimulation sites, possibly by diffusion or fluid exchange.
Electrical stimulation of the nerve to the gracilis muscle following its transposition around the anal canal creates an artificial sphincter capable of actively opposing intrarectal pressure. Not all patients have an available or suitable gracilis. This paper describes the anatomic basis for the use of the long head of the biceps femoris as a potential electrically stimulated neoanal sphincter. The muscle was found to have an adequate length and a suitable arc of rotation for transposition around the anal canal. In 75 percent of thighs studied the neurovascular anatomy of the long head of the biceps femoris was compatible with its utilization in this manner as an alternative to the gracilis.
Although neuromuscular electrical stimulation (NMES) can increase the ability of muscle to exert force, the means by which this is accomplished seem to be different from those associated with voluntary exercise. The aim of the study was to determine whether the recruitment order of motor units elicited by over-the-muscle electrical stimulation is different from that achieved with voluntary activation of muscle. This difference was tested by comparing muscle twitch responses that were elicited by Hoffmann reflexes (H-reflexes) and direct motor responses (M-responses) and by examining the effect of submotor NMES on the twitch force associated with H-reflexes. Because H-reflexes represent the summed activity of many motor units, in a manner that is consistent with volitional activation, variation in the time to peak twitch force indicates changes in the population of motor units that contribute to the response. The results demonstrated that the percutaneous application of submotor NMES to the limbs of human subjects causes a faster-contracting population of motor units to be activated during a test H-reflex. Consequently, it seems that the application of NMES preferentially activates faster-contracting motor units, perhaps those that are normally only active at high exercise intensities under voluntary conditions.
The [14C]-2-deoxyglucose (2-DG) autoradiographic technique was used to study how auditory-related metabolic activity changes with deafness, and how chronic electrical stimulation of the deafened system may modify these changes. Guinea pigs were deafened by administration of kanamycin and ethacrynic acid. After nine weeks of deafness, the basal unstimulated uptake of 2-DG in the inferior colliculus (IC) was lower than in normal hearing control animals. 100 microA of acute cochlear electrical stimulation significantly increased 2-DG uptake in normal hearing animals but did not evoke a significant increase in four or nine week deafened animals. Electrically elicited 2-DG uptake in the IC is therefore depressed by prolonged deafness. In a second series of experiments, after four weeks of deafness, animals were chronically electrically stimulated via a cochlear implant 2.5-3.5 h a day, five days a week for five weeks at 100 microA. Acute cochlear electrical stimulation following this chronic stimulation significantly increased 2-DG uptake in the contralateral IC over unstimulated levels. This suggests that some depressive effects of profound deafness on the auditory brain stem may be reduced or reversed with chronic electrical stimulation by a cochlear implant.