Wallerian degeneration of the distal portion of a cut nerve is considered irreversible. A possible reason for degeneration is lack of axon stimulation in the distal, cut nerves. We hypothesized greater rates of stimulation of distal nerve stumps would prolong time to action potential propagation failure, and uncut nerves would not be damaged by implanted nerve stimulators. We also hypothesized that action potentials measured from the body of the sciatic nerve would show similar response as motor-evoked potentials measured in the muscles innervated by branches of the sciatic nerve. We implanted a nerve stimulator onto distal cut sciatic nerves of rats and recorded motor-evoked potentials. Three groups were stimulated at 1 Hz (once per second), 0.1 Hz (once per 10 seconds), and 0.01 Hz (once per 100 seconds) respectively. Motor-evoked potentials progressively declined after nerve transection, failing faster at 1 Hz (26.8 hours +/- 108 minutes) and 0.1 Hz (22 hours +/- 66 minutes) compared with stimulation at 0.01 Hz (36.75 hours +/- 83 minutes). Intact axons were not damaged by implanted nerve stimulators. Action potentials recorded directly from nerves were equivalent to motor- evoked potentials. Failure of motor-evoked potential transmission in a transected nerve is accelerated by a greater rate of continuous stimulation of the distal stump.
"Several investigators have reported that a low-frequency electrical stimulation is a promise approach to accelerate nerve regeneration after injury2,12). However, a high frequency of electrical stimulation may increase failure of nerve regeneration16). Hence, these results cannot exclude potential beneficial effects of sacral nerve stimulation in other models of SCI with different treatment protocols, the disappointing outcomes in this study were limited by the treatment protocol. "
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study is to evaluate neuroprotective effect of sacral neuromodulation in rat spinal cord injury (SCI) model in the histological and functional aspects.
Twenty-one female Sprague Dawley rats were randomly divided into 3 groups : the normal control group (CTL, n=7), the SCI with sham stimulation group (SCI, n=7), and the SCI with electrical stimulation (SCI+ES, n=7). Spinal cord was injured by dropping an impactor from 25 mm height. Sacral nerve electrical stimulation was performed by the following protocol : pulse duration, 0.1 ms; frequency, 20 Hz; stimulation time, 30 minutes; and stimulation duration, 4 weeks. Both locomotor function and histological examination were evaluated as scheduled.
The number of anterior horn cell was 12.3±5.7 cells/high power field (HPF) in the CTL group, 7.8±4.9 cells/HPF in the SCI group, and 6.9±5.5 cells/HPF in the SCI+ES group, respectively. Both the SCI and the SCI+ES groups showed severe loss of anterior horn cells and myelin fibers compared with the CTL group. Cavitation and demyelinization of the nerve fibers has no significant difference between the SCI group and the SCI+ES group. Cavitation of dorsal column was more evident in only two rats of SCI group than the SCI+ES group. The locomotor function of all rats improved over time but there was no significant difference at any point in time between the SCI and the SCI+ES group.
In a rat thoracic spinal cord contusion model, we observed that sacral neuromodulation did not prevent SCI-induced myelin loss and apoptosis.
Journal of Korean Neurosurgical Society 12/2012; 52(6):509-12. DOI:10.3340/jkns.2012.52.6.509 · 0.64 Impact Factor
"Immobilization studies using MS at 50 to 100 Hz have shown to minimize the reduction of the cross-sectional area of muscle fiber and to restore mechanical properties (Kim et al., 2007). Stimulation of distal nerve stumps had similar action potential response between normal and muscle innervated (O'Gara et al., 2006). Although the response of ImP and bone mass by MS under such periphery nerve block conditions is still remained unknown, MS could serve as a mitigating agent to retain bone mass under chronic nerve damage conditions, e.g., spinal cord injury. "
[Show abstract][Hide abstract] ABSTRACT: Intramedullary pressure (ImP) and low-level bone strain induced by oscillatory muscle stimulation (MS) has the potential to mitigate bone loss induced by disuse osteopenia, i.e., hindlimb suspension (HLS). To test this hypothesis, we evaluated (a) MS-induced ImP and bone strain as function of stimulation frequency and (b) the adaptive responses to functional disuse, and disuse plus 1 and 20 Hz stimulation in vivo. Femoral ImP and bone strain generated by MS were measured in the frequencies of 1-100 Hz in four rats. Forty retired breeder rats were used for the in vivo HLS study. The quadriceps muscle was stimulated at frequencies of 1 and 20 Hz, 10 min/d for four weeks. The metaphyseal trabecular bone quantity and microstructure at the distal femur were evaluated using microCT, while bone formation indices were analyzed using histomorphometric technique. Oscillatory MS generated a maximum ImP of 45+/-9 mmHg at 20 Hz and produced a maximum matrix strain of 128+/-19 microepsilon at 10 Hz. Our analyses from the in vivo study showed that MS at 20 Hz was able to attenuate trabecular bone loss and partially maintain the microstructure induced by HLS. Conversely, there was no evidence of an adaptive effect of stimulation at 1 Hz on disused skeleton. The results suggested that oscillatory MS regulates fluid dynamics and mechanical strain in bone, which serves as a critical mediator of adaptation. These results clearly demonstrated the ability of MS in attenuating bone loss from the disuse osteopenia, which may hold potential in mitigating skeletal degradation imposed by conditions of disuse, and may serve as a biomechanical intervention in clinic application.
Journal of Biomechanics 01/2009; 42(2):140-5. DOI:10.1016/j.jbiomech.2008.10.018 · 2.75 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Autonomic consequences of seizures are common, but can be severe. We sought to define changes in autonomic activity from limbic cortical seizures and their impact on the heart.
We studied kainic acid (KA)-induced seizures in urethane-anesthetized rats using peripheral nerve, blood pressure (BP), and ECG recordings and echocardiography.
Seizures were associated with massive increases in parasympathetic (vagus nerves) and sympathetic (cervical sympathetic ganglion >renal nerve >splanchnic nerve) activity. Seizure-associated activity increases were greater than activity changes induced by nitroprusside or phenylephrine (each producing BP changes of >50 mmHg). Increases in c-fos expression were found in both sympathetic and parasympathetic medullary regions (as well as hypothalamic areas). Baroreceptor reflex function (tested with nitroprusside and phenylephrine) was impaired during seizures. Finally, a significant fraction of the animals died and the mechanism of death was defined through ECG, BP, and echocardiographic measures to be profound cardiac dilatation and bradyarrhythmia leading to hypoperfusion of the brain and ultimately hypoperfusion of the heart. Cardiovascular changes occur within seconds (or less) of autonomic nerve activity changes and death by these mechanisms takes minutes.
We propose that the massive parasympathetic and sympathetic outflow that occurs during a seizure gets compounded by respiratory distress (driving both autonomic nervous system divisions in the same direction) causing mechanical dysfunction, slowing the heart, and hypoperfusing the brain.
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