HF TENS reduces substance P, which is increased in dorsal root ganglia neurons in animals after tissue injury. Thus, one consequence of activation of inhibitory pathways by TENS is to reduce excitation and consequent neuron sensitization in the spinal cord.īoth HF and LF TENS have effects at the site of stimulation. The reduction in glutamate is prevented by blockade of δ-opioid receptors. HF TENS also reduces central neuron sensitization, and release of the excitatory neurotransmitters glutamate and substance P in the spinal cord dorsal horn in animals with inflammation. Furthermore, in people with fibromyalgia and osteoarthritis, there is a reduction in pressure pain thresholds not only at the site of stimulation, but also at sites outside the area of application, implicating a reduction in central excitability. In parallel, there is a reduction in both primary and secondary hyperalgesia by both LF and HF TENS. In animals with peripheral inflammation or neuropathic pain, enhanced activity of dorsal horn neurons (i.e., central sensitization) to both noxious and innocuous stimuli is reduced by both HF and LF TENS.
In animals without tissue injury, both LF and HF TENS reduce dorsal horn neuron activity. Thus, LF TENS uses classical descending inhibitory pathways involving the PAG-RVM pathway activating opioid, GABA, serotonin and muscarinic receptors to reduce dorsal horn neuron activity and the consequent pain. In addition, LF TENS does not produce analgesia in opioid tolerant people and animals but HF TENS does. This opioid mediated effect of LF TENS has been confirmed in human subjects. Further, the reduction in hyperalgesia by LF TENS is prevented by blockade of GABAA, serotonin 5-HT2A and 5-HT3, and muscarinic M1 and M3 receptors in the spinal cord, and is associated with increased release of serotonin. The reduction in hyperalgesia by LF TENS is prevented by blockade of µ opioid receptors in the spinal cord or the RVM or spinal cord, and by synaptic transmission in the ventrolateral PAG. Thus, HF TENS produces analgesia by activating endogenous inhibitory mechanisms in the central nervous system involving opioid GABA, and muscarinic receptors. However, blockade of serotonin or noradrenergic receptors in the spinal cord has no effect on the reversal of hyperalgesia produced by HF TENS. Furthermore, the reduction in hyperalgesia produced by HF TENS is prevented by blockade of muscarinic receptors (M1 and M3) and GABAA receptors in the spinal cord. This opioid-mediated analgesia produced by HF TENS has been confirmed in human subjects. The analgesia produced reduction in hyperalgesia by HF TENS is prevented by blockade of opioid receptors in the RVM or spinal cord, or synaptic transmission in the ventrolateral PAG.
HF TENS increases the concentration of β-endorphins in the bloodstream and cerebrospinal fluid, and methionine-enkephalin in the cerebrospinal fluid, in human subjects. Neurotransmitters & receptors that mediate TENS analgesia This article offers a concise review of the basic science mechanisms for TENS as well as an up to date critique of current clinical research for TENS. We will also highlight advances from Randomized Controlled Trials (RCT) published in the last 5–7 years, which are not included in the systematic reviews. Findings of systematic reviews of TENS for pain management in the last 7 years will be presented. We will summarize mechanisms of action, factors that influence TENS efficacy, and describe and critique the use of TENS for pain control in a variety of patient populations.
This article will provide a critical review of the latest basic science and clinical evidence for TENS. The parameters of pulse frequency, and pulse intensity are adjustable and linked to TENS efficacy. These small battery-powered devices deliver alternating current via cutaneous electrodes positioned near the painful area. Transcutaneous electrical nerve stimulation (TENS) is an inexpensive nonpharmacological intervention used in the treatment of acute and chronic pain conditions.
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