Application of Radiofrequency in Low Back Pain Treatment (Conservative Treatment) Part 1

Introduction

Chronic low back pain (LBP) has become a main cause of absenteeism and disability in industrialized societies and is a major health problem with enormous economic and costs (Andersson, 1999). As many as 80% of adults experience at least one episode of LBP during their lifetime. Only 5% of patients suffering from chronic LBP can find a specific cause such as disc herniation, spondylolisthesis, discitis or spondylitis. No definite evident causes were found in 95% patients with low back pain (Schwarze et al., 1995a, 1995b).

At present, the treatment of low back pain consists of therapies, both conservative and invasive, that are aimed at symptomatic relief. As the evidence-based medicine developed over the years, there are now much more accumulated data that inform us how to treat patients with chronic LBP. Unfortunately, many of the treatments used today are not strongly effective (Carragee 2005).

Application of radiofrequency in medicine

Radiofrequency (RF) is a minimally invasive, target-selective technique that has been in clinical use for more than decades and has been demonstrated to be successful for treating cardiac arrhythmias (Baszko et al., 2002), dysplasia (Shahee et al., 2009) and reducing pain in several chronic pain conditions including trigeminal neuralgia, chronic LBP, postherpetic neuralgia, complex regional pain syndrome, ischemic pain, cervicobrachialgia, postthoracotomy pain, occipital neuralgia, and cervical or lumbar radicular pain (Chao et al., 2008; Navani et al., 2006; Racz & Ruiz-Lopez 2006; Zhang et al., 2011). Focusing on pain management, RF can not only reach directly to the source of pain but also modulate the pain signal transmission.


Principles and mechanisms of radiofrequency

There are two major mechanisms of radiofrequency (RF) treatment: thermal (continuous) RF and non-thermal (pulsed) RF (PRF). Thermal RF caused by continuous current within frequencies between 300 Hz and 300 GHz generates both current and heat on exposed tissues. Since temperatures above 45°C result in nonselective destruction of both myelinated and nonmyelinated nerve fibers (Smith et al., 1981), the thermal RF procedure has limited applications and caused some adverse effects. Unlike continuous RF, PRF generates intermittent pulsed current which lowers the target tissue temperature to below 45°C and causes different neurobiological effects (Cahana et al., 2003).

For example, a marker for neuronal activity in the dorsal horn, c-Fos, has been reported to be expressed immediately and up to 7 days after PRF treatment in rat models (Higuchi et al., 2002; Van Zundert et al., 2005). The long lasting effect of c-Fos expression was caused by non thermal RF but inhibition of excitatory C-fiber responses was seen in long-term depression (Richebe et al., 2005). Continuous RF creates a longer blockade of synaptic transmission than PRF in an in vitro model even under similar temperature. Both RF and PRF treatments induce distance dependent tissue destruction under the stimulating needle, but the effect was more pronounced in the RF group (Cahana et al., 2003). Moreover, morphological study showed no pathological findings in the control and sham-operated groups, minimal morphological changes in the PRF group, and neuro-destruction in the continuous RF group (Erdine et al., 2005). All these findings together indicate that the use of PRF promises to be a safer, reversible and nondestructive approach to various chronic pain conditions.

Application of radiofrequency treatment in low back pain from different origins and mechanisms

Low back pain can originate from several sources, such as discs, ligaments, muscles, and sacroiliac joints, and another cause can be lumbar facet joint degeneration (Deyo & Weinstein 2001). Since all the pain signals were transmitted by nerves, applying treatment targeting the neuronal transmission pathway can reasonably relieve the pain. Here we review the anatomy, possible biomechanical mechanisms, clinical presentation and physical examination findings of different sources of low back pain. The diagnostic tools and image findings are discussed as well.

Discogenic low back pain

Considering the diagnosis of LBP, pure discogenic pain is thought to be less than 10% (Deyo & Weinstein 2001). However, in chronic persistent LBP patients, intervertebral disc (IVD) degeneration seemed to be the initial step and played the most important role (Carragee 2005). After IVD degeneration, the biomechanical status of the vertebral column changes, and the possibility of facet joint degeneration, spondylosis, spondylolisthesis and spinal stenosis increases as well.

Anatomy and pathogenesis of disc and its degeneration

The IVD is composed of a tough outer ring, the annular fibrosus (AF), a gelatinous inner core, the nucleous pulposus (NP), and the adjacent vertebral endplate (VE). The axial loading force of IVD was support by posterior two facet joints. The healthy IVD is avascular and its nutritional supply depends on diffusion via the AF and VE. Symptomatic degeneration of the IVD is thought to be the leading causes of chronic back pain.

In a normal disc, the NP is devoid of nerve fibers, while the outer AF and VE contain nerve fibers. The nerve supply of the IVD is from branches of sympathetic trunk and sinuvertebral nerves (Fig. 1). The sinuvertebral nerves run ventral to the nerve root, back to the spinal canal and divide the posterior longitudinal ligament and ventral dural branches. The anterior part of IVD was supplied by branches through the anterior longitudinal ligament which is from the sympathetic trunk. The lateral and ventral aspects of IVD are supplied by branches of rami communicantes (Fig. 1).

Because the IVD was supply by the sympathetic trunk, somatosensory nerves and their communicating network through multiple segments, discogenic back pain is always hard to localize and seemed to be a visceral pain (Bogduk et al., 1981) and RF applying to the target nerves of IVD is much more complicated than other parts of the spinal column (Bogduk et al., 1981; Brown et al., 1997; Edgar 2007).

Schematic illustration of the lumbosacral intervertebral disc innervation.

Fig. 1. Schematic illustration of the lumbosacral intervertebral disc innervation.

During IVD degeneration, increase neuronal activity is found in inner NP which is the possible mechanism of painful disc (Freemont et al., 1997; Coppes et al., 1997; Hurri & Karppinen 2004; Peng et al., 2006; Peng et al., 2009; Freemont et al., 2002; Freemont 2009). Nociceptive neuropeptides just like calcitonin gene-related peptide and substance P, which are present within the nerve fibers in the outer AF and dorsal root ganglion (DRG), may likely play a role in discogenic pain transmission (Brown et al., 1997; Ohtori et al., 2002). It is believed that most afferent fibers from the low lumbar discs travel in the sinuvertebral nerve, pass through the ramus communicantes and lumbar sympathetic chain, and finally enter the spinal cord through the L2 ramus communicantes and L2 spinal nerve roots (Nakamura et al., 1996a; 1996b).

Since most nerve fibers that innervate the disc emanate from the sympathetic nervous system (Bogduk et al., 1981; Nakamura et al., 1996a; 1996b), RF targeting discogenic low back pain can reasonably apply through two locations. One is thermal RF lesioning causing nerve fiber destruction within the inner disc and the other is sensory modulation targeting the DRG of L2, the level at which the sympathetic nerve fibers leave the spinal cord.

Clinical presentation, physical examination

There are no typical physical examination findings of painful IVD and most of the findings appear in other types of LBP. Diagnosis of discogenic LBP is based on these non-specific past histories and physical examinations as well as the image study. Generally speaking, most of the discogenic back pain is not localized. It seemed to be visceral pain because of its characteristics and nerve supply (Bogduk et al., 1981). Most patients experience typical features including persistent nociceptive low back (more than six months), groin with or without leg pain which worsens with axial loading or flexion of painful segment, and pain relief when lying down. Moreover, there are nerve roots lying just posteriorly to the disc margin. So some patients with discogenic LBP experience some referred pain. For example, painful IVDs for upper lumbar segment typically cause referred pain to the anterior aspect of thigh and lower lumbar segments and sometimes cause referred pain down to the posterior thigh and leg (Ohnmeiss et al, 1999a; 1999b)

Image diagnosis and discography

Before the development of computed tomography (CT) and magnetic resonance imaging (MRI), discography had been used to diagnose possible disc pathology (Lindblom, 1951). However, it was thought to be obsolete because of its complications and efficacy for diagnosis after the invention of CT and MRI (Walsh et al., 1990). There are many benefits of CT and MRI for disc pathology diagnosis. They provide clear three dimensional images of the spinal column and can be reconstructed to view different aspects. Moreover, some unusual pathology can be found during CT and MRI study combined with contrast enhancement (Maus, 2010).

Considering radiation exposure, MRI seems better than CT except for bony structure evaluation and determination of pre-existing metal material inside the body. T2-weighted sequence MRI can provide detailed information of disc pathology included disc height and morphology change, herniation of nucleous pulposus, spinal canal or neuroforamen stenosis, hydration of disc and with gadolinium enhancement, some inflammation pathology or neogrowth can be detected (Maus, 2010).

However, the clinical symptoms and outcome of disc degeneration cannot be predicted even if MRI can identify signal changes in the discs themselves and surrounding soft tissues (Keller et al., 2011). Moreover, MRI also provides adjacent vertebrae end plate signal change and annular tear which is thought to be strongly associated with disogenic LBP (Carragee & Hannibal 2004; Zhou & Abdi 2006).

Because painful IVD was found to increase neuronal activity in its inner layer (Freemont et al., 1997; Coppes et al., 1997; Freemont et al., 2002), a direct increase in intradiscal pressure may cause more pain. Besides, during degeneration or trauma, the tough annular ring AF becomes weaker and then tears as fissure formation. When the intradiscal pressure increases, the force is transferred to the outer area of AF through the fissure which is always located in the posterior part of the disc and causes pain; so, provocative discography is thought to be useful to find the "exact" pain source. In summary, discography provokes pain through the following mechanisms: 1) Increase in intradiscal pressure during the injection of contrast material. Mechanical stretching of the annular fibers of the painful disc may stimulate the overgrowth of nerve endings. 2) Chemical irritation of the surrounding nerve endings within the disc.

The interpretation of discogram findings includes the degree of pain generation during the procedure in each disc, and the appearance of contrast medium in the disc. Sachs et al. described the Dallas grading system using the CT discogram appearance (Sachs et al., 1987). The ‘Modified Dallas Discogram Description’ was finalized in the 1990′s and is the ‘Gold Standard’ for the CT classification of anular tears (Fig. 2). Based on their article, they divided the CT discogram finding into six degrees: Grade 0: the contrast medium within the inner NP margin. Grade 1 to grade 3 indicates the contrast medium leaking to inner, middle, or outer layer of AF. Grade 4 indicates the circumferential spread greater than 30 degrees. Grade 5 tear describes either a grade 3 or grade 4 radial tear that has completely ruptured the outer layers of the disc and is ‘leaking’ contrast medium from the disc into the epidural space (Fig. 2).

The Modified Dallas Discogram

Fig. 2. The Modified Dallas Discogram

The degree of pain mainly depends on the Numeric Rating Scale (NRS), the reproduction of concordant pain and comparison of normal adjacent discs. According to the guidelines of the International Association for the Study of Pain (IASP) and the International Spine

Intervention Society (ISIS), they suggest at least two adjacent levels should be tested as controls during the provocative discography procedures. The criteria of discogenic pain is listed in table 1 (Kallewaard et al., 2010). However, because the discography is done without direct visualization of the disc structure and multiple combined pathologies of the lower back in most of the patients suffering from chronic LBP, the diagnosis made by provocative discography is controversial (Wichman, 2007). Wichman summarized three reasons causing controversy about discography for the diagnosis of discogenic LBP, namely, techniques, the disc pathology itself and symptom interpretation (Wichman, 2007).

Diagnosis

Diagnostic criteria

Absolute discogenic pain

Reproduce concordant pain in diseased level during procedures

NRS at least 7

The pain develops less than 15 psi above the opening pressure

Stimulation of the two adjacent discs is not painful

Highly probable discogenic pain

Reproduce concordant pain in diseased level during procedures

NRS at least 7

The pain develops less than 15 psi above the opening pressure

Stimulation of the one of the adjacent discs is not painful

Discogenic pain

Reproduce concordant pain in diseased level during procedures

NRS at least 7

The pain develops less than 50 psi above the opening pressure

Stimulation of the two adjacent discs is not painful

Possible discogenic pain

Reproduce concordant pain in diseased level during procedures

NRS at least 7

The pain develops less than 50 psi above the opening pressure

Stimulation of the one of the adjacent discs is not painful, and stimulation of another disc is painful at a pressure greater than 50 psi above the opening pressure, and the pain is discordant

Table 1. Diagnostic criteria of discogenic pain by discography

Treatment choices of radiofrequency applying to discogenic low back pain

RF applying to the disc itself included transdiscal biacuplasty (Baylis Medical Inc., Montreal, Canada), intradiscal electrothermal therapy (IDET) with spinecath (OratecInterventions, Inc., Menlo Park, CA) and disctrode (Radionics RFG-3C,Valleylab, Tyco Healthcare Group LP 5920 Longbow Drive, Boulder, Colorado 80301-3299 USA) (Karasek & Bogduk 2000; Saal JA & Saal JS, 2000, 2002; Davis et al., 2004; Kapural & Mekhail 2006; Andersson et al., 2006; Kvarstein et al., 2009; Tsou et al., 2010). The spinecath and disctrode are flexible catheters with a distal thermocoil. When it is introduced into the annulus, the distal part should ideally be along the internal aspect of the posterior annulus. Local denervation effect is caused by heating of the distal portion of the catheter. The other two major mechanisms of IDET are intradiscal pressure reduction and enhancement of the annular healing process (Saal JA & Saal JS, 2000). However, two prospective studies have shown the opposite efficacy results using IDET for discogenic LBP patients (Pauza et al., 2004; Freeman et al., 2005). There are limited prospective studies mentioning transdiscal RF annuloplasty and their effects are uncertain (Helm et al., 2009).

The other choice of the RF target for discogenic LBP is the L2 DRG, which is based on the natural history of discogenic LBP and was not easily confirmed. With regard to discogenic pain, Nakamura et al. proposed that the main afferent pathway of pain from the lower intervertebral discs is through the L2 spinal nerve root, presumably via sympathetic afferents from the sinuvertebral nerve (Helm et al., 2009). Therefore, discogenic pain should be regarded as visceral pain due to its neural pathway. Nakamura et al. believe that the nerve fibers in the sinuvertebral nerve originate from the rami communicans of the sympathetic nerves (Nakamura et al., 1996b). RF lesioning to cervical DRG has been proved effective in a select group of patients with cervical brachialgia (van Kleef et al., 1996; Van Boxem et al., 2011). However, because of the side effects and possible complications of neuropathic pain, PRF was applied to cervical DRG treatment. In contrast, DRG lesioning for lumbosacral radicular pain was thought to be less effective (Geurts et al., 2003). Since the DRG of L2 was thought to be the main trunk of the lower back sensory afferent pathway, some clinical retrospective studies of PRF showed effectiveness for chronic LBP with highly suspect disc origins or unspecific LBP with or without radicular pain (Tsou et al., 2010; Nagda et al., 2011).

Neurogenic low back pain

Spinal nerves are protected in the spinal canal before they penetrate out of the neuroforamen. However, during the degeneration and aging process, the bony structure and soft tissue such as ligaments surrounding the nerves see hypertrophic change which possibly compromises the neuronal structure including nerve roots and their low back branches. Most patients with spondylosis, spinal stenosis and spondylolisthesis with or without radicular symptoms suffer from symptoms of back pain (Singh et al., 2005). Before the radicular symptoms are displayed, the narrowing canals compress the nerves and more or less cause local inflammatory and mechanical mechanism of back pain. Singh et al. divided two groups of patients with spinal stenosis; one group was congenital and young, while the other was degenerated and elderly. Since the pain is possibly from inflammation or mechanical stress directed to the nerves, neuronal modulation or temporary blocks are suitable for those without severe spinal stenosis or not suitable for surgical intervention. The clinical presentation of neurogenic LBP always combined both low back symptoms and neurogenic claudication with or without radicular pain (Singh et al., 2005). Diagnosis of neurogenic LBP depends on clinical presentation and dynamic lateral lumbar X ray imaging. Pedicle width narrowing and neuroforamen compromise can be seen on CT or MRI. The treatment choices for neurogenic pain before shifting to surgery includes epidural neuroforamen steroid injection (Benny & Azari 2011) selective nerve block (Thackeray et al., 2010) and RF for adjacent DRG (Van Boxem et al., 2011).

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