How can e-stim work to minimise pain?

Like everything to do with e-stim the theory behind how it does or could actually help minimise patient pain is controversial and open to debate. Two main theories have evolved; the Gate control theory and Opiate Mediated Control Theory. Other theories such as increased local vasodilation and a sensory analgesia effect have also been proposed. 

The Gate Control Theory

 A Theory of “pain” proposed by Ronald Mezlacxk and Patrick Wall in 1985 discussed a hypothetical gate mechanism that could open or close and exists within the spinal cord. Small nerve fibres (pain receptors) and large nerve fibres (somatosensory receptors) synapse on projection cells (P), which project up to the spinothalamic tract to the brain, and inhibitory interneurons (I) within the dorsal horn.

It is the interplay among all these connections which determines when a painful stimulus is transmitted to the brain:

1. (gate is closed) When no input comes is received, the inhibitory neuron prevents the projection neuron from sending signals to the brain.

2. (gate is closed) Normal somatosensory input occurs when there is increased large-fibre stimulation (or only large-fiber stimulation). Both the inhibitory neuron and the projection neuron are stimulated, but the inhibitory neuron prevents the projection neuron from sending signals to the brain.

3. (gate is open) Nociception (pain reception) occurs when there is increased small-fibre stimulation or only small-fiber stimulation. This inactivates the inhibitory neuron, and the projection neuron sends signals to the brain informing it of pain.

Further to this, there are also descending pathways from the brain that can ‘close the gate’ by inhibiting the projector neurons and therefore diminish pain perception.

E-stim, applies an electrical current to a painful area and as such the transmission of the

perception of pain. Small nerve fibres to the brain are inhibited by the activity of the large nerve and somatosensory nerve fibres (triggered by the electrical current), resulting in 'closing the gate' of the pain perception.

Picture sited from www.google.com/images

Video sited form http://www.youtube.com/

The video will give an advanced insight into the mechanisms of the Gate Theory of Pain.

Opiate Mediated Control Theory

The human body has its own naturally occurring opiate and they act as a natural pain suppressor. Opiates include Beta-endorphins produced in the pituitary gland and enkephalins, produced in the spinal cord that bind to specific receptor sites. These natural opiates can be aroused by stimulating the sensory nerves with the electrical current produced with e-stim and thus block the perception of pain.

Other Theories

Other theories involved with the e-stim and pain philosophy are that it helps to increase vasodilation to tissues that have been injured leading to a painful trigger point which can initiate local ischemia. A further theory involves e-stim being able to stimulate acupuncture points causing a sensory analgesia effect by challenging the pain evoked nerve impulses at the different levels of the nervous system.

References

Cameron MH. Physical Agents in Rehabilitation from Research to Practice. Philadelphia: WB Saunders Company; 1999:387-390.

Cramp FL, McCullough GR, Lowe AS, Walsh DM. Transcutaneous electric nerve stimulation: The effect of intensity on local and distal cutaneous blood flow and skin temperature in healthy subjects. Arch Phys Med Rehabil 2002 Jan;83(1):5-9.

Hecox B, Mehreteab TA, Weisburg J. Physical Agents: A Comprehensive Text for Physical Therapists. East Norwalk, Conn: Appleton & Lange; 1994:299-305.

Joodaki MR, Olyaei GR, Bagheri H. The effects of electrical nerve stimulation of the lower extremity on H-reflex and F-wave parameters. Electromyogr Clin Neurophysiol. 2001 Jan-Feb;41(1):23-8.

Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:1971-979.

Milne S, Welch V, Brosseau L, Saginur M, Shea B, Tugwell P, Wells G. Transcutaneous electrical nerve stimulation (TENS) for chronic low back pain (Cochrane Review). In: The Cochrane Library, 4, 2001.