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Perspectives on Modern Orthopaedics

Treatment of Chronic Discogenic Low Back Pain With Intradiskal Electrothermal Therapy

Wetzel, Todd F. MD; McNally, Thomas A. MD

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Journal of the American Academy of Orthopaedic Surgeons: January 2003 - Volume 11 - Issue 1 - p 6-11
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Thermal energy has been shown to induce tissue shrinkage in cadaveric1 and animal models2,3 and has been applied to treat peripheral joint instability. Saal and Saal4 hypothesized that thermal energy might have a role in the treatment of so-called internal disk disruption5,6 and, thus, in chronic low back pain. This proposition led to the development of a catheter to deliver intradiskal electrothermal therapy (IDET).4

Patients with chronic low back pain secondary to degenerative disk disease are difficult to treat effectively. The source or sources of the pain may be unclear or multiple in origin. Meticulous evaluation is key to determining optimal therapy; however, careful evaluation is complicated by the fact that some tests, such as diskography, are controversial in relation to their efficacy. IDET delivered via catheter is a new technology with reported potential use in patients with back pain and degenerative disk disease. To appreciate its role, it is important to understand the pathophysiology and diagnosis of, and the treatment options for, degenerative disk disease.

Pathophysiology of Disk Degeneration

Chronic low back pain is the most common cause of morbidity and chronic pain in the United States.7 Degenerative disk disease is a frequent etiology of this pain;5 however, the pathophysiology and actual origins of the pain are incompletely understood. One theory hypothesizes that small, posttraumatic peripheral tears of the anulus fibrosus lead to an acceleration in the dehydration of the intervertebral disk, with resultant fraying of the nucleus pulposus.8 Studies using annular trauma in a sheep model support this theory.9 Vascular ingrowth also has been observed in peripheral tears of the anulus.10 Nociceptors may accompany this vascular growth and account for the presence of sensory nerve supply in the inner anulus.

In the normal intervertebral disk, sensory nerves do not penetrate beyond the outer one third of the anulus fibrosus.11-13 In degenerative disk disease, however, an association has been demonstrated between ingrowth of nerves expressing substance P and disk degeneration. The extent of neoneuralization has been shown to be greatest at the painful levels.12 Coppes et al13 noted that disk degeneration and perhaps disk injury are associated with centripetal growth of nerve fibers in the disk, which would provide a morphologic basis for true discogenic pain. The findings of these histologic studies agree with those of clinical studies identifying the anulus fibrosus as a common source of the back pain.14,15

Diagnosis and Imaging

The clinical features of internal disk disruption, as described by the Task Force on Taxonomy of the International Association for the Study of Pain, include lumbar spinal pain, with or without referred pain, that is aggravated by movements that stress the symptomatic disk.16 The diagnosis of internal disk disruption begins with a thorough patient history, physical examination, and review of systems. Clinical characteristics remain somewhat controversial, but some authors have identified extension preference (ie, patient preference for postures that emphasize maintenance or exaggeration of physiologic lumbar lordosis) as suggestive of symptomatic degenerative disk disease.17 Plain radiographs, magnetic resonance imaging (MRI), and computed tomography (CT) are sensitive to degenerative changes but clinically are nonspecific.18,19 Because it is not possible to diagnose internal disk disruption on clinical grounds alone, the key to diagnosis is diskography.20

While the specificity of provocative diskography remains controversial,21-25 it can provide two types of information. The morphologic information regarding the stage of disk degeneration is of secondary importance because of the nonspecific nature of that information in a clinically relevant sense.18,19 The more important component, precise reproduction of the patient's presenting pain symptoms (concordance), makes the test clinically useful. Some studies have identified a high level of sensitivity and specificity, whereas others have disputed this claim.21-25 The innately subjective nature of diskography—concordance pain reproduction—can never completely be overcome. However, with strict attention paid to technique and scrupulous insistence on exact reproduction of the patient's pain, diskography may be clinically useful. Arguably, it is the only study whereby a painful degenerated disk can be identified.

Treatment Options

The literature on appropriate nonsurgical treatment is confusing. Some evidence exists supporting the efficacy of exercise therapy,26,27 but few definite conclusions can be drawn. Invasive options may be judiciously considered in patients who remain persistently symptomatic. Historically, the surgical treatment of patients with discogenic pain without frank herniation has been limited to lumbar arthrodesis, but this approach lacks consensus.28 In one retrospective series of 25 patients with positive diskography who refused surgery, 68% nonetheless improved.29 The efficacy of arthrodesis is supported by other studies, with a rather wide range of success rates (39% to 96%).30-36 However, these rates are difficult to compare directly because of differences in the criteria used to assess success and variations in the types of surgical procedures performed.

Even when it is relatively certain that the pain is discogenic in origin (ie, is not muscular or from facet arthropathy), determining the appropriate therapy is a challenge. There is a wide gap between nonsurgical care (short periods of bed rest for exacerbations, medications, and physical therapy) and surgical care (anterior, posterior, or combined procedures). IDET has been proposed as a possible treatment between these extremes.

Intradiskal Electrothermal Therapy

The theoretic basis for IDET is that targeted thermal energy is designed to shrink collagen fibrils, cauterize granulation tissue, and coagulate nerve tissue in the posterior anulus fibrosus.4,37 Several studies investigating the use of thermal energy have demonstrated tissue shrinkage in peripheral joints. Hayashi et al1 applied various temperatures to cadaveric shoulder capsules. Above 65°C, the authors discovered shrinkage of the specimen and, histologically, hyalinization of the collagen.1 These results were corroborated by Obrzut et al2 in glenohumeral capsular tissue from sheep. Shortening of 14% from pretreatment resting length was shown after thermal lesions of 80°C; in concordance with the results of Hayashi et al,1 tissue shrinkage was not present at temperatures below 65°C.

Further studies regarding the mechanism and action of IDET, including biomechanical and histologic evaluation, still are required. One recent study by Kleinstueck et al38 on temperature distribution and biomechanical effects of IDET on 13 fresh-frozen human lumbar cadaveric specimens did not demonstrate temperature production high enough to cause nociceptive cell death. On the surface, this appears to discredit the theory of deafferentation as a factor in pain reduction. This is consistent with the clinical finding of delayed (1 to 3 months) improvement in pain.

Kleinstueck et al38 also investigated the biomechanical effects of IDET on vertebral motion. It is plausible that the heated catheter denatures and shrinks the collagen fibrils, thus stabilizing the motion segment. In this cadaveric study, there was an increase in motion at the IDET-treated levels. This investigation, however, did not take into account the effects of healing (scarring) that would occur in vivo. Healing may result in stiffening and stabilization of the motion segment over a period of time consistent with the clinical relief of pain (1 to 3 months). Others39 have noted a similar triad of biologic repair in the therapeutic effect (maintenance of shrinkage, secondary scarring and thickening, and destruction of sensory fibers). Gross pathology before and after treatment demonstrates shrinkage of nuclear matrix (Fig. 1).

Figure 1 A,
Figure 1 A,:
Gross pathology cadaveric intervertebral disk specimen before electrothermal treatment. B, The same specimen after 15-minute intradiskal electrothermal treatment. Note the shrinkage of the nuclear matrix.

Indications for IDET

In most studies published to date, good candidates for IDET meet the following criteria: low back pain of at least 3 months' duration, with or without nonradicular referred pain; failure of 3 months of nonsurgical care; no prior surgery at the intervertebral levels to be treated; and degenerative lumbar disk disease evident on MRI and concordant diskography. Given the nature of diskography and the inability to completely eliminate all subjectivity inherent in this diagnostic procedure, the importance of a meticulous evaluation before intervention, including appreciation of possible confounding variables, cannot be overestimated. Patients with marked stenosis, spinal deformity (eg, spondylolisthesis or scoliosis), or neurologic deficit, or who are pregnant or have other confounding medical conditions, are not considered candidates. From a technical point of view, patients with a notable loss of disk height are not appropriate candidates for IDET; in many, the increased degree of nuclear disorganization further serves to make intradiskal navigation difficult.


The procedure is done in an outpatient setting with biplanar fluoroscopy, using local anesthetic and conscious intravenous sedation. Utilizing a standard posterolateral Lyman Smith approach, the disk is cannulated and the thermal catheter positioned along the posterior anulus. Final catheter position is verified with biplanar fluoroscopic views (Fig. 2), and then thermal treatment is delivered. The temperature of the catheter is initially 65°C and is increased by 1° every 30 seconds until the target temperature (80° to 90°) is reached and maintained for 4 to 6 minutes (Fig. 3). Patients are observed for a short period, usually 1 to 2 hours, then discharged.

Figure 2
Figure 2:
Lateral (A) and anteroposterior (B) intraoperative fluoroscopic views showing position of the catheter (arrows) during IDET procedure. This 36-year-old woman had intractable lumbosacral back pain and could sit for no more than 5 minutes without severe pain. She was unresponsive to 12 months of active physical therapy and medications. Provocative diskography was positive at L5-S1 with negative rostral control levels. Diskography revealed internal disk disruption but no full-thickness annular tearing.
Figure 3
Figure 3:
Temperature distribution through the annular wall. A, Ideal position of the intradiskal electrothermal catheter (white arrowhead) is along the posterior anulus fibrosus across the midline. The diagram indicates temperature distribution at various points (A, B, C) in the posterior anulus at the target temperature. The temperature is 38° in the epidural space. The dark portion of the catheter represents the heating element. B, Temperature tracing generated during lesioning. Tracing T corresponds to the temperature of the intranuclear catheter abutting the posterior anulus. Tracing C reflects the outer annular temperature obtained by placing a sensor in the outer anulus on the side opposite the catheter introduction.

Early clinical experience has shown that patients may have an increase in back pain for the first week, then return to their baseline pain level. Improvement in symptoms generally does not occur until 6 weeks after the procedure. During this time, symptoms are treated with nonsteroidal anti-inflammatory drugs. Rehabilitation and reconditioning are started after 8 to 12 weeks to facilitate healing and maintain the presumptive tissue shrinkage. Activities that raise intradiskal pressure, such as prolonged unsupported sitting, should be avoided.

Clinical Results

Clinical studies to date suggest a therapeutic effect from the use of IDET. In a series of 25 patients, Saal and Saal4 reported reduction of two points in the visual analog pain scale (VAS) in 80% of patients and improvement in sitting tolerance and decrease or discontinuation of pain medication in 72%. They defined a successful functional outcome as at least a seven-point increase in the Medical Outcomes Study 36-Item Short Form (SF-36); this was achieved in 77% of patients with single-level disease and in 75% of patients with two or more symptomatic degenerated disks. At the 2-year follow-up of 55 patients treated with IDET, the mean decrease in VAS was 3.2, and the mean increase in the SF-36 physical function subscale was 20.37

In a cohort of 35 patients treated with IDET, Karasek and Bogduk40 reported that 60% demonstrated benefit at 1 year. They also compared the outcomes of the 35 patients with those of 17 patients who underwent a physical rehabilitation program. (The 17 patients treated nonsurgically were considered candidates for IDET but had been denied coverage by insurance carriers.) Analysis of the two subgroups based on improvement in VAS showed that 23% of the patients in the IDET-treated group reduced their pain level to zero at 1 year. However, because of the relatively small sample size, the authors noted that this absolute success rate of 23% carries a 95% confidence interval of 16%. Additionally, there is inherent bias in the control group because treatment was denied, potentially imparting a negative outcome bias to the group. At 3 months, only 1 of 17 in the control group had improved symptomatically, with no mean improvement in VAS pain scores or increase in functional activity for the group.

Thompson and Eckel41 reported 6-month follow-up data in an industry-sponsored multicenter study of 170 patients. The mean decrease in VAS was 2.6; the mean increase in the SF-36 among six subscales was 19.1. The authors also noted increases in sitting, standing, and walking tolerance. A multicenter prospective control cohort study of 78 patients reported by Wetzel et al42 demonstrated similar results. All patients had failed nonsurgical care and had low back pain with or without nonradicular referred pain, one or two levels of degenerative disease, and a positive concordant diskography. Of the 75% of patients who reached the 2-year follow-up, 88% reported they would undergo IDET again; 61% were working without restriction (versus 23% before treatment).


Of all the IDET procedures done, there has been only one reported case of cauda equina syndrome caused by device malpositioning.43 This could have been avoided by biplanar confirmation of the catheter location before initiating the heating cycle. Theoretic complications include nerve root injury, cerebrospinal fluid leak, and diskitis. A 5% incidence of transient paresthesias, presumably resulting from needle position, has been reported.42 Efforts are underway to compile data on complications at various centers. There have been no reported cases of diskitis to date.


Chronic discogenic low back pain is difficult to treat. Nonsurgical care is the rule for most patients. When this fails, IDET may offer an alternative between the extremes of continued nonsurgical therapy and lumbar spinal fusion. Preliminary data are encouraging, with reported therapeutic success rates of 60% to 80%. Given the limitations of study design in reports to date, however, additional clinical data continue to be collected.


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