Deep tissue afferents, but not cutaneous afferents, mediate transcutaneous electrical nerve stimulation-Induced antihyperalgesia.

Abstract

UNLABELLED:

In this study we investigated the involvement of cutaneous versus knee joint afferents in the antihyperalgesia produced by transcutaneous electrical nerve stimulation (TENS) by differentially blocking primary afferents with local anesthetics. Hyperalgesia was induced in rats by inflaming one knee joint with 3% kaolin-carrageenan and assessed by measuring paw withdrawal latency to heat before and 4 hours after injection. Skin surrounding the inflamed knee joint was anesthetized using an anesthetic cream (EMLA). Low (4 Hz) or high (100 Hz) frequency TENS was then applied to the anesthetized skin. In another group, 2% lidocaine gel was injected into the inflamed knee joint, and low or high frequency TENS was applied. Control experiments were done using vehicles. In control and EMLA groups, both low and high frequency TENS completely reversed hyperalgesia. However, injection of lidocaine into the knee joint prevented antihyperalgesia produced by both low and high frequency TENS. Recordings of cord dorsum potentials showed that both low and high frequency TENS at sensory intensity activates only large diameter afferent fibers. Increasing intensity to twice the motor threshold recruits Adelta afferent fibers. Furthermore, application of EMLA cream to the skin reduces the amplitude of the cord dorsum potential by 40% to 70% for both high and low frequency TENS, confirming a loss of large diameter primary afferent input after EMLA is applied to the skin. Thus, inactivation of joint afferents, but not cutaneous afferents, prevents the antihyperalgesia effects of TENS. We conclude that large diameter primary afferent fibers from deep tissue are required and that activation of cutaneous afferents is not sufficient for TENS-induced antihyperalgesia.

PERSPECTIVE:

Transcutaneous electrical nerve stimulation (TENS) is an accepted clinical modality used for pain relief. It is generally believed that TENS analgesia is caused mainly by cutaneous afferent activation. In this study by differentially blocking cutaneous and deep tissue primary afferents, we show that the activation of large diameter primary afferents from deep somatic tissues, and not cutaneous afferents, are pivotal in causing TENS analgesia.

• Authors: Rajan Radhakrishnan, Kathleen A Sluka
• Journal: The journal of pain (J Pain) Vol. 6 Issue 10 Pg. 673-80 (Oct 2005) ISSN: 1526-5900 [Print] United States
• PMID: 16202960 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Anesthetics, Local
• Inflammation Mediators
• Kaolin
• Carrageenan
• Lidocaine

Topics

• Administration, Topical
• Afferent Pathways (drug effects, physiology)
• Anesthetics, Local (administration & dosage)
• Animals
• Arthralgia (chemically induced, physiopathology, therapy)
• Carrageenan (pharmacology)
• Hyperalgesia (chemically induced, physiopathology, therapy)
• Inflammation Mediators (pharmacology)
• Kaolin (pharmacology)
• Knee Joint (drug effects, innervation, physiopathology)
• Lidocaine (administration & dosage)
• Male
• Nerve Fibers, Myelinated (drug effects, physiology)
• Nociceptors (drug effects, physiology)
• Posterior Horn Cells (drug effects, physiology)
• Rats
• Rats, Sprague-Dawley
• Sensory Receptor Cells (drug effects, physiology)
• Skin (drug effects, innervation)
• Transcutaneous Electric Nerve Stimulation
• Treatment Outcome