Background

Pain is the most undermanaged vital sign in a clinical setting (Warfield & Kahn, 1995). Various pharmacological and non‐pharmacological treatment modalities are in practice to treat acute and chronic pain (Grabois, 2005). Several theories explain the pathophysiology of pain and these have led to the invention of devices using modern technology to relieve pain.

Lower back pain is one of the most common complaints in western society (Kartz, 2001; Steenstra et.al. 2006). Ninety percent of the population in the United States suffers from lower back pain at one or multiple points in time in their lifetime (Steenstra et.al. 2006). The average age ranges from 18‐65 yrs. (Andersson, 1999; Long et. al., 1996). The direct costs due to lower back pain in the United States are reaching $40 billion per year, while the overall related costs from lower back pain disability are estimated at $80 billion.

 

Although lower back pain is a common chronic pain syndrome, in most cases a specific diagnosis cannot be established. Lower back pain can arise due to spinal injury, spinal disc problems, osteoarthritis, spinal stenosis, compression fractures, spinal tumors etc. (Long and et. al., 1996). Constant pain due to the compression of the spinal nerves and muscle spasm can lead to a chronic state. These chronic pain conditions may have major effect on the body physiology, functional status, work productivity, treatment costs, and on mental status (Sinatra, 2005). Pain stimulates the adrenergic nervous system, increases heart rate, blood pressure, and causes arteriolar constriction (Terkelson et. al., 2005). Decreased physical activity due to lower back pain may increase the incidence of pulmonary infections, deep venous thromboembolism, mortality and morbidity. All of this negatively effects the quality of life in chronic lower back pain patients.

 

NSAIDS are generally used for acute lower back pain. Opioids are the alkaloid analgesics used for the treatment of moderate to severe pain conditions. These opioids work on the mu, kappa and alpha receptors in the central nervous system (Przewlocki&Przewlocka, 2001). Due to the wide presence of these receptors in the body, they not only suppress the noxious stimuli effects but also have undesirable side effects, including nausea, vomiting, drowsiness, itching, constipation and respiratory arrest (Cepeda et.al. 2003; DeSantana et.al. 2008). The opioids are metabolized in the liver and are excreted by the kidneys (DeSantana et.al. 2008). The burden on the liver in any injury includes correction of altered homeostasis, drug metabolism, and a wound healing process. The continued administration of high amounts of opioids can drain the resources of the liver. In those who have undergone surgical procedures, or in bodily injuries involving the liver, an alternative pain relief method other than opioids should be used. In recent years, patient controlled analgesia (PCA) has gained importance in the pain management field for its efficacy, early patient mobilization, decrease in post-operative complications, and decrease in medical costs. However, PCA is a skilled, invasive, infection prone procedure which needs continuous patient monitoring and also brings on added drug side effects (Macintyre, 2001; Sinatra, 2005).

 

The concerns arising from the use of analgesic medications have increased the interest in non-pharmacological therapies for lower back pain. The non-pharmacological treatment modalities for pain relief include heat, cold, acupuncture, electrotherapy, and massage (Godfrey, 2005). The cold treatment increases muscle relaxation time and hot treatment decreases the muscle force. Prolonged use of such methods has shown to cause tissue and nerve injury. The unintended injury can lead to hyperalgesia. The primary hyperalgesia occurs due to the tissue injury and secondary hyperalgesia due to the excess excitation of the central neurons (McLean, 1989; Ochoa &Yarnitsky, 1994; Sluka and Walsh, 2003). Among electrotherapy modalities are transcutaneous electrical nerve stimulation (TENS) with various pulse modulation, electro-acupuncture and percutaneous electrical nerve stimulation (PENS). Unfortunately, these modalities fall short with respect to duration and magnitude of analgesia.  TENS has been investigated for years in the treatment of many painful conditions, including lower back pain. The tenet of TENS is found in Wall and Melzack’s gate control theory which suggests that large nerve fiber activation can modulate pain sensation conducted in small fiber nerves, by gating or blocking the transmission within central nociceptive pain pathways (Binder & Baron, 2010; Melzack& Wolf, 1965). Although the use of TENS contributes a component in multidisciplinary treatment programs for lower back pain, especially for its low benefit-risk ration and limited contraindication profile is considered, studies of TENS has produced limited statistically significant results (Machado et.al. 2009; Maetzel, 2002; Marchand et.al. 1993).

Active Trigger Points (ATP’s) – Pathophysiology

As mentioned previously, despite the fact that lower back pain (LBP) is a common chronic pain syndrome, in most cases, a specific diagnosis cannot be established. One accepted explanation for LBP symptoms is that patients have myofascial pain syndrome, a condition characterized by painful Active Trigger Points (ATPs) in muscles (Hong & Simons, 1998). In the last 10-15 years, much clinical and basic science research into ATPs has been published, including epidemiological, diagnostic, therapeutic, and pathophysiological studies (Simons et.al. 2002, 1999, 1998, 1996, 1997, 1999).The pathogenesis of ATPs is probably related to sensitized sensory peripheral free nerve endings (nociceptors) associated with dysfunctional endplates (Hong & Simons, 1998). In a histological study a small nerve fiber was commonly found near the sensitive ATPs (Hong et.al, 1996). Therefore, the sensitive loci in the region of a muscle ATPs are probably related to sensitized nerve fibers (nociceptors).

 

Local pain could be explained by the tissue ischemia resulting from prolonged muscle contraction with accumulation of acids and chemicals such as serotonin, histamine, kinins, and prostaglandins (Travel&Rinzler, 1972).

Studies have found that development of ATPs is dependent on an integrative mechanism in the spinal cord. When the input from nociceptors in an original receptive field persists (pain from ATPs), central sensitization in the spinal cord may develop, and the receptive field corresponding to the original dorsal horn neuron may be expanded (referred pain). Through this mechanism, new “satellite ATPs” may develop in the referred zone of the original trigger point (Hong & Simons, 1998).

Hyper-Stimulation analgesia of ATP’s

Common treatments of ATPs typically include minimal invasive intervention such as injections with local anaesthetics, corticosteroids, botulinum toxin, or dry needling (Lucas et.al. 2009).

 

A procedure, often described as “hyper-stimulation analgesia”, during which a localized, intense, low-rate electrical pulses are applied to small surface areas at ATPS’s locations to stimulate peripheral nerve endings (A δ fibers), thus causing the release of endogenous endorphins (Flowerdew&Gadsby, 1997; Sjolund, Terenius& Eriksson, 1977), has been investigated in several controlled studies, showing a positive response in 87% of patients (Flowerdew&Gadsby, 1997; Cheng &Pomeranz, 1987; Cheng &Pomeranz, 1980; Cheng, Pomeranz&McKibbin, 1980). Considerable evidence suggests that this type of neurostimulation analgesia is achieved by activating extra segmental antinociceptive mechanisms which accelerates the release of endogenous endorphins, serotonin, and cortisol (Sjolund, Terenius& Eriksson, 1977).

Identification of ATPs

The most common physical finding of ATPs has been considered the palpation of a hypersensitive nodule of muscle fibre of harder than normal consistency; identification of such nodule appears very dependent on the subjective experience of the physician. There is no accepted reference standard for the clinical diagnosis of ATPs, and data on the reliability of physical examination are conflicting. A 2009 review of nine studies examining the reliability of ATPs diagnosis found that physical examination could not be recommended as reliable for the diagnosis of ATPs (Lucas et.al. 2009).

 

The presence of active ATPs causes a localized decrease in skin resistance than the surroundings' area. The hypoxic state in the pain area increase nociceptors and other sensitizing substances in the area, and this biochemical changes induces greater blood flow and secretion from sweet glands via stimulation of the autonomic nervous system. These physiologic differences may account for acute variations in electrodermal measurements at the pathologic site. ATPs points are defined as small diameter (3-4mm) circumscribed low skin resistance area`s (Shultz, Driban&Swanik, 2007). Localized decrease in skin resistance is frequently associated with clinically active myofascial trigger points that are richly innervated by myelinated A δ fibers, the smallest in diameter (0.2–1.5 μm) and most commonly present myelinated axons in peripheral nerves. Their extremely small size prevents their identification by any imaging modality (Shultz, Driban&Swanik, 2007).

 

Electrical skin impedance measurements are considered to be vulnerable to certain sources of imprecision, including instrument error resulting from the size, pressure, and duration of probe application as well as local skin conditions such as variable thickness, hydration, and intactness of the stratum corneum (Shultz, Driban&Swanik, 2007; Nakatni, 1972).

Hyper-Stimulation analgesia of ATP’s
Common treatments of ATPs typically include minimal invasive intervention such as injections with local anaesthetics, corticosteroids, botulinum toxin, or dry needling (Lucas et.al. 2009).
 
A procedure, often described as “hyper-stimulation analgesia”, during which a localized, intense, low-rate electrical pulses are applied to small surface areas at ATPS’s locations to stimulate peripheral nerve endings (A δ fibers), thus causing the release of endogenous endorphins (Flowerdew&Gadsby, 1997; Sjolund, Terenius& Eriksson, 1977), has been investigated in several controlled studies, showing a positive response in 87% of patients (Flowerdew&Gadsby, 1997; Cheng &Pomeranz, 1987; Cheng &Pomeranz, 1980; Cheng, Pomeranz&McKibbin, 1980). Considerable evidence suggests that this type of neurostimulation analgesia is achieved by activating extra segmental antinociceptive mechanisms which accelerates the release of endogenous endorphins, serotonin, and cortisol (Sjolund, Terenius& Eriksson, 1977).
Identification of ATP’s
The most common physical finding of ATPs has been considered the palpation of a hypersensitive nodule of muscle fibre of harder than normal consistency, identification of such nodule appears very dependent on the subjective experience of the physician. There is no accepted reference standard for the clinical diagnosis of ATPs, and data on the reliability of physical examination are conflicting. A 2009 review of nine studies examining the reliability of ATPs diagnosis found that physical examination could not be recommended as reliable for the diagnosis of ATPs (Lucas et.al. 2009).
 
The presence of active ATPs causes a localized decrease in skin resistance than the surroundings' area. The hypoxic state in the pain area increase nociceptors and other sensitizing substances in the area and this biochemical changes induces greater blood flow and secretion from sweet glands via stimulation of the autonomic nervous system. These physiologic differences may account for acute variations in electrodermal measurements at the pathologic site. ATPs points are defined as small diameter (3-4mm) circumscribed low skin resistance area`s (Shultz, Driban&Swanik, 2007). Localized decrease in skin resistance is frequently associated with clinically active myofascial trigger points that are richly innervated by myelinated A δ fibers, the smallest in diameter (0.2–1.5 μm) and most commonly present myelinated axons in peripheral nerves. Their extremely small size prevents their identification by any imaging modality (Shultz, Driban&Swanik, 2007).
 
Electrical skin impedance measurements are considered to be vulnerable to certain sources of imprecision, including instrument error resulting from the size, pressure, and duration of probe application as well as local skin conditions such as variable thickness, hydration, and intactness of the stratum corneum (Shultz, Driban&Swanik, 2007; Nakatni, 1972).