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Isometric torque was generated about the knee joint by microstimulation of the cat L6 spinal cord using a single microelectrode. The torque responses varied with microstimulation location. Appreciable extension torque was generated by microstimulation in ventrolateral locations of the L6 spinal cord. Stimulation parameters (intensity, frequency and pulse-width) also influenced the extension torque. Specific stimulation parameters (100 microA intensity, 40 Hz frequency and 0.20 ms pulse-width) appear best suited for mapping the spinal cord based on knee joint torque responses. Low levels of cocontraction of the extensor and flexor could be achieved when extension torque was produced, but also varied with the stimulation locations. There are locations in the L6 ventral horn where microstimulation could evoke sustained extension for at least 4 min with only a slight change in torque. This study suggests the possibility of restoring lower limb function in patients with spinal cord injury above the lumbar level.

Neuroprosthetic techniques have been used to facilitate voiding via electrical stimulation for bladder management following spinal cord injury (SCI), but high urethral resistance has been a problem. This problem was investigated here in the chronic, spinal, male cat (C6-T1) using direct bladder and sacral nerve stimulation. Direct bladder stimulation was only conducted during terminal procedures with an open abdomen and with four hook electrodes inserted into the bladder wall. Sacral stimulation was conducted daily during the 10 weeks post-SCI and during terminal procedures. Stimulation was conducted with both implanted epidural electrode and surface electrodes over the sacral bone. Both of these sacral methods stimulated anterior and posterior roots. However, these sacral methods were generally ineffective for inducing voiding during the study. In three of the five animals investigated, stimulation did not empty the bladder. In the remaining two animals, the bladder was emptied with sacral stimulation, but only after return of bladder reflex activity, 2 to 4 weeks post-injury. When poor voiding occurred in spite of high bladder pressures, it indicates high urethral resistance. This was confirmed using video cystourethrography where the membranous urethra was observed to remain closed following stimulation. Direct bladder stimulation was then compared to sacral nerve stimulation during terminal procedures. Direct bladder stimulation induced voiding at a high rate both during and after stimulation, whereas sacral nerve stimulation with implanted electrodes induced voiding at a lower rate and only after stimulation. A simple urethral resistance measure, the ratio of bladder pressure to voiding rate, was lower with direct bladder stimulation than sacral nerve stimulation. Stimulation-facilitated voiding has also been associated with the development of bladder wall hypertrophy. This problem was investigated by evaluating bladder wall thickness postmortem in three groups of animals: the first group was the spinal-stimulated animals detailed above; the additional two groups were a spinal-nonstimulated but instrumented group maintained for 10 weeks following injury, and an intact group of animals. The stimulated spinal cats tended to have the thickest bladder wall followed by the nonstimulated spinal cats. The wall thickness of intact animals served as a control.

Recent reports have shown that electrical stimulation of the bladder wall or sacral nerves is effective for bladder management in the spinal cord injured (SCI) patient. However, less invasive methods are needed for electrode implantation. A modified percutaneous procedure for implanting needle electrodes in the sacral canal was evaluated. Stimulation with these electrodes were effective for inducing voiding with little residual volume after the recovery of bladder reflexes, 3 weeks after experimental spinal cord injury in the dog. An optimum electrode arrangement involved a single midline monopolar electrode located between sacral foramina L7 and S1. However, at low stimulating current, lateral electrodes adjacent to sacral nerves were more effective than midline electrodes for inducing voiding. Stimulation parameters that were effective for daily voiding were 10 pps, 1.5-5 mA, 0.3 ms pulse duration, and 2- to 3-second stimulation periods.

Urethral activity was investigated in the awake chronic spinal-injured canine using urodynamic recordings, video cystofluoroscopy, and urethral pressure recordings without anesthesia. Bladder contractions and voiding were induced by electrical stimulation with epidural electrodes inserted into the sacral canal. Urethral pressure remained elevated during stimulation and for 1-3 s afterward. Poststimulation voiding occurred with three different patterns: 1) pulsatile voiding in which squirting of urine was associated with contractions in the membranous urethra; 2) "on and off" voiding in which pulsatile flow was interrupted for brief periods of time; and 3) steady-stream voiding in which nonpulsatile flow was followed by pulsatile flow. Viewing these voiding patterns with fluoroscopy indicated that the proximal membranous urethra was important in all of the patterns. We conclude that in the chronic spinal-injured canine the skeletal muscle within the membranous urethra (rhabdosphincter) is involved in responses to sacral stimulation and various voiding patterns.

Naloxone has been reported to facilitate detrusor activity by blocking the inhibitory action of the enkephalins. We tested the urodynamic effects of intravenous naloxone (0.4 to 0.8 mg.) in 15 patients with spinal cord injury via rapid fill carbon dioxide cystometry and perineal electromyography. Fourteen patients had suprasacral lesions (3 complete), while 1 had an incomplete lower cord lesion. The average interval from injury was 4.2 months. Most of the patients were managed with intermittent catheterization and most had chronic bacteriuria. Initially, 10 patients had detrusor areflexia and 5 had detrusor hyperreflexia (2 with dyssynergia). Of the 15 patients 14 had no neuropathic condition as noted on baseline electromyography. After naloxone injection no significant cystometrographic changes occurred but 11 patients (73 per cent) had decreased electromyographic activity. The vesicourethral pattern of the 2 patients with dyssynergia did not change after naloxone, even though the electromyographic response decreased in both. The patients showed no other effects of the naloxone administration. Contrary to other studies, naloxone seemed to diminish pelvic floor (electromyographic) activity but it did not change bladder (cystometrographic) function during bladder rehabilitation of spinal cord injury patients.

Various forms of electrical stimulation are being used more frequently for bladder and muscle rehabilitation following spinal injury. Fifteen patients with spinal cord injury underwent a four to eight week period of thigh muscle reconditioning by surface electrical stimulation. The accumulated effects of this program on bladder function were assessed by urodynamic evaluation before and after the test period. Seven patients had beneficial changes of either an increase in bladder capacity and/or a decrease in bladder pressure. Six patients had a decrease in bladder capacity and/or an increase in bladder pressure, although two of these six patients had resolution of spinal shock. Two patients with detrusor areflexia had no changes in pressure or capacity. There was no change in the basic urodynamic patterns, only the parameters of bladder capacity and pressure. Increasing the use of electrical stimulation for rehabilitation of the spinal cord population might alter bladder function, although not consistently. One should, therefore, be aware of these changes when setting up such rehabilitation programs.

Twelve spinal cord injured subjects participated in a study of the short-term effects on leg spasticity of electrical stimulation of the quadriceps. Spasticity was quantified through the use of a normalized relaxation index (R2n) obtained from the pendulum drop test both before and after measurement of isometric quadriceps torque in response to 20 minutes of cyclic electrical stimulation. Two or three baseline evaluations were made on each subject, tests being at least one day apart. By comparing the first prestimulus baseline assessment of spasticity with that obtained poststimulus, we obtained a measure of changes in spasticity brought about by fatiguing exercise. We found that spasticity significantly (p less than or equal to 0.005) decreased after stimulation. To investigate whether this change was due to electrical stimulation or was a function of the performance of the drop test itself (ie, passive range of motion of the knees), drop-to-drop variability during the pendulum drop test both before and after stimulation was assessed. A comparison was made of the R2n value of the last drop before stimulation to that of the first drop afterward, to assess the direct effect of stimulation on spasticity. Spasticity decreased significantly (p less than or equal to 0.05) during the leg ranging inherent in the drop test itself, particularly for subjects with shorter times postinjury. Spasticity also decreased significantly as a direct result of electrical stimulation. This latter change could be accounted for by an interaction of peak quadriceps torque and the initial measure of spasticity before stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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)