BACKGROUND

The natural history of low back pain has been reported to be quite favorable in some studies and is often quoted to patients as such. It has been reported that 40–50% of patients are symptom free within 1 week and up to 90% have resolution of symptoms without medical attention in 6–12 weeks.^1–4 However, recent studies suggest that lumbar axial pain is a more significant condition characterized by acute exacerbations and variable periods of remission. Deyo and Tsui-Wu⁵ reported 33.2% of patients with low back pain reported symptoms with a duration of less than 1 month, with 33% reporting pain for 1–5 months and 32.7% reporting pain for longer than 6 months. Recurrence rates from 60–85% have been reported in the first 2 years following an acute episode of low back pain.^6,7 More recently, Von Korff et al.⁸ observed that over a 2-year follow-up period, 44% report chronic symptoms (defined as more than 90 days of back pain in the previous 6 months). In this study, most patients were experiencing low levels of back pain with 20% rating their pain as 4 or greater on a 0–10 scale; 13% rated their current pain as 5 or greater and only 8% reported pain of 6 or greater. Furthermore, Von Korff et al.⁸ reported that 15–20% of primary care patients with low back pain show moderate to severe activity limitations during a 1-year follow-up period after the initial episode has resolved.

PATHOPHYSIOLOGY

Descriptions of the treatment for low back pain dates to Hippocrates (460–370 BC), with the reporting of joint manipulation and the use of traction.⁹ It often is theorized that the onset of low back pain is associated with bipedal ambulation and that this transformation in the mechanics of locomotion is the inciting evolutionary event that has made the lumbar spine susceptible to a relatively accelerated rate of degenerative disease. Degeneration is universal to the structures that comprise the basic functional spinal unit, which is composed of two adjacent vertebral bodies, the intervertebral disc, and the two zygapophyseal (Z-) joints at the same segment functioning as a tri-joint complex. As humans age, endure various micro- and macrotraumas, and undergo changes in body habitus that alter and unevenly distribute biomechanical forces on the lumbar spine, there is a natural progression of degeneration of the lumbar motion segment with corresponding anatomic, biomechanical, radiologic, and clinical findings.¹⁰ It is this evolution that provides the insight into the root cause of lumbar spinal pain syndromes.

The posterior elements of the lumbar spinal functional unit bear less weight than the anterior elements in all positions. During sitting, the anterior elements bear over 90% of the forces transmitted through the lumbar spine, whereas during standing, this fraction decreases to approximately 80%.¹⁰ As the degenerative process progresses, the relative anterior to posterior force transmission approaches 50%.¹⁰ The spine functions best within a realm of static and dynamic stability. The bony architecture and associated specialized soft tissue structures, especially the intervertebral disc, provide static stability. Dynamic stability, however, is accomplished via a system of muscular and ligamentous supports which act in concert during various functional, occupational, and avocational activities. The overall mechanical effect of these structures maintains the histologic integrity of the tri-joint complex. The net shear and compressive forces must be maintained below respective critical minimums in order to maintain the integrity of the tri-joint articulation. Persistent, recurrent, nonmechanical and/or excessive forces to the motion segment beyond minimal thresholds leads to microtrauma to the disc and Z-joints, which triggers and continues the degenerative process.¹⁰ This degenerative cascade, as described by Kirkaldy-Willis,¹⁰ is the widely accepted pathophysiologic model describing the degenerative process and ensuing spinal segment dysfunction as it affects the lumbar spine and its individual motion segments. This process is described as occurring in three phases in a progressive longitudinal manner over time. These phases are a continuum with a gradual transition rather than three distinct, clearly definable stages. Although the etiology of spinally mediated lumbar axial pain is variable and not always clearly definable, there are a finite number of potentially painful structural components of the lumbar spine, and the aforementioned degenerative cascade provides insight on the process by which these components develop pathology and can become symptomatic.

BASIC SCIENCE EVIDENCE OF INFLAMMATORY MECHANISMS IN DISCOGENIC-MEDIATED PAIN SYNDROMES

The anterior elements of the lumbar spine, most notably the intervertebral disc, are currently thought to be the primary source of the vast majority of spinally mediated lumbar axial pain syndromes. Several theories cite a traumatically induced acute annular tear as the inciting pathologic event. Others theorize the natural result of aging is the sole etiology of pathology of the lumbar disc. However, these models do not explain spontaneously occurring annular tears and disc degeneration in the young. Therefore, the cause of lumbar disc disease is most likely multifactorial. Various genetic, environmental, autoimmune, inflammatory, traumatic, infectious, toxin-induced, and other factors may alone, or in various combinations, result in the initiation and progression of degeneration of the intervertebral disc in a way that has not yet been elucidated. However, to some degree, the basic science literature has been able to elucidate the inflammatory mechanisms of discogenic mediated lumbar axial pain syndromes. In 1987, McCarron et al.¹¹ published a study in which they reported on the incitation of an inflammatory response upon injection of autologous nucleus pulposus into the epidural space of dogs. In addition, they reported that a delay in the treatment of this inflammatory process could result in tissue fibrosis and cellular damage. In 1990, Saal et al.¹² demonstrated significantly increased level of PLA₂, the rate-limiting enzyme in the arachidonic acid cascade, activity in lumbar HNP further demonstrating the inflammagenic properties of nuclear material. In 1996, further study helped elucidate the biochemical factors by which the nucleus pulposus elicits an inflammatory process. Takahashi et al.¹³ demonstrated the presence of inflammatory cytokines, including IL-1a+b, IL-6, TNF, GMCSF, and L-B4, in herniated nucleus pulposus (HNP). Kang et al.¹⁴ reported increased levels of MMPs, nitric oxide, IL-6, and PGF₂ in the culture media of HNP. These properties may in part be explained by the fact that the nucleus pulposus, a remnant of the embryonic notochord, is sheltered from the bloodstream during embryologic development and may therefore be construed as an antigen upon presentation to the immune system when entering the ventral aspect of the epidural space.¹⁵ Subsequently, epidural steroid injections (ESI) have become commonly employed interventions in treating spinally mediated lumbar axial pain syndromes thought to be potentially due to an inflammatory mechanism based on the aforementioned basic science literature as it pertains to specific discogenic induced spinal syndromes.

EVOLUTION OF INTERVENTIONAL SPINE PROCEDURES

The initial reports of epidural injections almost a century ago reported the instillation of cocaine into the epidural space to treat lumbago and sciatica. In the early 1900s, epidural injection of local anesthetic was used to treat intractable sciatica.¹⁶ In 1952, Robecchi and Capra¹⁷ reported success with the first ESI in treating lumbar and associated sciatic pain. Presently, ESIs are a commonly utilized intervention in the management of spinally mediated lumbar axial syndromes both with and without associated radicular symptomatology. Several studies have shown that up to 40% of blind (nonfluoroscopically guided) ESIs may erroneously deliver the injectate superficially into the soft tissues or inadvertently deep into the subarachnoid space, which may result in serious complications.^18–21 Therefore, we strongly advise that any type of ESI be performed under real-time fluoroscopic guidance with contrast-enhanced visualization of flow within the epidural space to the target site prior to the injection of medication unless otherwise contraindicated. In 1972, Winnie et al. emphasized the importance of placing the medication as close to the site of pathology as possible for the clinician to optimize outcome. They demonstrated improvement in 80% of patients in whom corticosteroids were infused at the site of pathology.²² This logical concept must be considered when determining which of the three commonly utilized epidural access routes, transforaminal, interlaminar, or caudal, is utilized when performing an ESI.

EFFICACY OF TRANSFORAMINAL ESI FOR LUMBAR AXIAL PAIN SYNDROMES WITH RADICULAR INVOLVEMENT

The optimal route for injection of corticosteroids into the epidural space at the site of pathology in patients with discogenic-mediated lumbar axial pain syndromes with corroborative radicular involvement is via the transforaminal route. This approach allows the clinician to deliver the injectate, composed of a combination of 6–12 mg of betamethasone and 0.5–1 cc of 1% lidocaine, precisely to eradicate the known inflammatory response emanating from the potentially inflammagenic HNP focally on the specific inflamed nerve root sleeve (Fig. 92.1). The efficacy of this approach has been demonstrated in four different randomized, prospective, double-blind, controlled clinical trials. Riew et al.²³ reported results of a prospective, randomized, controlled, double-blinded study using fluoroscopically guided lumbar transforaminal injections in 55 patients with imaging evidence of nerve root compression and corroborative radicular symptoms. Twenty-eight patients received bupivacaine and betamethasone, and 27 received only bupivacaine. At follow-up (13–26 months) 33.3% of the bupivacaine group decided not to have surgery, versus 71.4% of the bupivacaine and betamethasone group. This difference in surgical rates was statistically significant (p<0.004). This controlled study demonstrates the beneficial effect of precisely delivered corticosteroids in obviating the need for operative treatment in patients with HNP and/or spinal stenosis. Kraemer et al.²⁴ published a study in which they reported long-term pain relief with transforaminal ESI in a study in which 49 patients with lumbar radicular pain were randomized into a corticosteroid group and control group. Karppinen et al.^25,26 reported on 160 consecutive patients with symptomatic herniated discs with no prior history of lumbar spine surgery randomized into either a corticosteroid group or normal saline group. Outcome measures obtained at 2 weeks, 3 months, and 6 months included pain relief, sick leave, medical costs, the Nottingham Health Profile, and the future requirement for surgical intervention. They reported that transforaminal ESI provided significant short- and long-term improvement in all of the aforementioned outcome measures. Thomas et al.²⁷ reported results of a prospective, randomized, controlled, double-blinded study comparing the relative effectiveness of fluoroscopically guided lumbar transforaminal ESIs versus blind interlaminar ESIs in patients with radicular pain. They demonstrated the superiority of transforaminal ESIs in all of a variety of outcome measures including finger-to-floor lumbar flexion, daily activity including work and avocational function, and Dallas pain scores. This direct comparison study underscores the importance of fluoroscopic guidance as well as delivering medication accurately and precisely to the site of a potential ongoing inflammatory response. In a non-blinded, randomized, prospective study by Butterman,²⁸ transforaminal ESIs provided efficacy measured by reducing symptomatology and disability and obviating surgery at a follow-up of up to 3 years in patients with large (>25% of the cross-sectional area of the spinal canal) symptomatic lumbar herniated discs. Butterman²⁸ also reported that in those patients who had short-term improvement or ineffectiveness of transforaminal ESIs and required surgical discectomy, there was no adverse affect in the outcome of that surgery from the temporal delay caused by the trial of transforaminal ESIs.

Fig. 92.1 An AP view of a right L5 selective nerve sleeve injection (note the contrast dye hugging the inferior and medial aspect of the right L5 pedicle consistent with the anatomical location of the right L5 nerve root).

In addition to the aforementioned randomized clinical outcome studies, several prospective nonrandomized clinical trials on the efficacy of transforaminal ESI also strongly suggest the beneficial effects of transforaminal ESIs for HNP causing lumbar axial pain with corroborative radicular pain. For example, Weiner and Fraser²⁹ showed 21 out of 28 patients with a computed tomography (CT) documented HNP and corroborative lower extremity pain receiving a single transforaminal infusion of betamethasone and 1% Xylocaine injectate had moderate or complete pain relief not requiring surgery at an average of 3.4 years follow-up. Lutz et al.³⁰ reported on 69 patients, with an average of 22 weeks of symptoms, with magnetic resonance imaging (MRI) evidence of an HNP and radicular pain. Patients underwent an average of 1.8 transforaminal injections of betamethasone and 1% Xylocaine followed by a 6–12-week course of lumbar spine stabilization therapy. They reported a successful outcome, as defined by a 50% or greater reduction in pain and return to near-previous level of functioning, in 75% of patients at an average of 80 weeks follow-up. In a retrospective evaluation, Wang et al.³¹ demonstrated significant symptom improvement in both the short and long term and the avoidance of discectomy in 77% of patients with lumbar disc herniations treated with one to six transforaminal ESIs.

With respect to the interventional treatment of lumbar axial pain syndromes with corroborative radicular pain due to spinal stenosis, the previously stated Riew et al.²³ study reported on the effectiveness of transforaminal ESI as it incorporated spinal stenosis in addition to HNP as the underlying etiology to their subjects symptomatology. In addition, Delport et al.³² conducted a retrospective review of treating symptomatic spinal stenosis a subgroup of which underwent transforaminal ESI. They reported that of 140 subjects, over 70% had symptom improvement and were at least somewhat satisfied with their response, over 50% reported sustained improvement in their function, and only 29% of the 140 subjects ultimately underwent surgical decompression. Botwin et al.³³ conducted a prospective cohort outcome study assessing the efficacy of transforaminal ESIs in the treatment of symptomatic degenerative spinal stenosis. Thirty-four subjects were followed for 1 year. They reported that 75% of the patients had a successful long-term outcome as defined as >50% symptom reduction. They also reported more than 50% of the subjects improved standing and/or walking tolerance.

The aforementioned literature strongly suggests that transforaminal ESI should be the standard of care index interventional spine procedure for patients with spinally mediated lumbar axial pain syndromes associated with radicular involvement due to HNP and/or spinal stenosis when more conservative measures have failed. Furthermore, in the case of the majority of HNPs, the known phagocytic immunologic response and consequent benign anatomic natural history assists in the relatively high rate and long-term success of transforaminal ESIs.^34,35

CONCEPTUAL PATHOPHYSIOLOGIC MECHANISMS OF LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT DUE TO A DISCOGENIC-MEDIATED INFLAMMATORY RESPONSE

Some important inferences from the aforementioned literature on the successful long-term treatment of HNP-associated lumbar axial pain syndromes with corroborative radicular involvement may be extracted that, when combined with known previously stated basic science literature and lumbar spinal anatomy, suggest a possible utilization for transforaminal ESIs in the interventional treatment of discogenic-mediated lumbar axial pain without radicular involvement. The similarities in the basic ideologies by which the initial incorrect thought processes of compression as the sole mechanism of radicular pain due to HNP requiring discectomy as stated nearly a century ago by Mixter and Barr³⁶ mirror recent theory that motion segment instability and/or structural disc pathology is the sole mechanism of discogenic-mediated lumbar axial pain without radicular involvement. In the decades subsequent to Mixter and Barr’s³⁶ landmark article identifying HNP pathology as a key source of lumbar axial and radicular pain, there have been many attempts to identify the precise pathophysiologic mechanism of discogenic-mediated lumbar axial pain without radicular involvement. As stated earlier in this chapter, over the years, there have been key pieces of literature to suggest that a tear in the outer one-third of the anulus of the intervertebral disc may be the most common etiology of acute spinally mediated lumbar axial pain.^10,37 As with the painful sequelae of most degenerative spinal conditions, improvement and eventual remission within 6 weeks is the natural history. However, subacute symptoms can persist and the mechanism for this may be inflammatory in nature.³⁸ The basic science literature discussed earlier in this chapter has repeatedly and clearly demonstrated the inflammagenic properties of the intervertebral disc, particularly the nucleus pulposus when it is exposed to the ventral epidural space.^13–17,38 This literature lends credence to the mechanisms by which transforaminal ESI effectuate symptom relief on a molecular basis. Therefore, the possibility of a focally contained inflammatory response to a centrally or paracentrally contained herniated disc is entirely possible and may be instrumental in pain generation as well as inhibition of the natural healing processes known to exist. In fact, a contained HNP may chemically sensitize the posterior longitudinal ligament, resulting in axial pain in a fashion similar to that of inflammatory radicular pain due to an HNP sensitizing a nerve root. Furthermore, patients with internal disc disruption syndrome in which an annular fissure extends from the nucleus pulposus to the outer one-third of the anulus (which may or may not be associated with a HNP) and may pierce through the outer anulus and intermittently or consistently communicate microscopic amounts of nuclear material to the ventral epidural space ensuing in an intermittent and/or ongoing focal discogenic-induced inflammatory response (Fig. 92.2). This pathophysiologic model may explain why a randomized, prospective, double-blind clinical trial performed by Simmons et al.³⁹ failed to demonstrate a statistically significant benefit to intradiscal corticosteroid infusions when compared to placebo. The aforementioned hypothesis suggests the inflammatory response occurs in the ventral portion of epidural space on the floor of the spinal canal juxtapositioned to the afflicted intervertebral disc(s) rather than within nuclear material encased by the anulus fibrosus.

Fig. 92.2 Authors’ rendition of the pathophysiologic model by which an intermittent or continual posterior discogenic inflammatory response may occur in the ventral portion of the epidural space due to leakage of nuclear inflammogens.

EFFICACY OF TRANSFORAMINAL ESI FOR LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT

To date, there have been only two nonrandomized, retrospective studies reporting on the outcome of transforaminal ESI on spinally mediated lumbar axial pain due to discogenic pathology without imaging evidence of nerve root involvement. One is a subgroup reported by Rosenberg et al.⁴⁰ stating greater than 50% pain reduction after one year in 59% of patients. The other study reported by Manchikanti et al.⁴¹ on patients with spinally mediated lumbar axial pain treated by one of three interventions: (1) blind interlaminar ESI, (2) fluoroscopically guided caudal ESI, and (3) fluoroscopically guided transforaminal ESI, states that superior short- and long-term pain relief is achieved via the transforaminal route. This conclusion makes anatomical sense as transforaminal ESIs likely distribute injectate more focally to the ventral epidural space when compared to interlaminar and caudal route and therefore are more target specific when attempting the deliver medication to a possible focal posterior discogenic-induced inflammatory response.

We are in no way suggesting that transforaminal ESI should be utilized for low back pain in general. However, based on the previously described history of spinal disorders, spinal anatomy, basic science literature, inferences from the current class I evidence in the interventional treatment of HNP and ensuing inflammatory radicular pain, and some preliminary retrospective data, as well as our own anecdotal experience, transforaminal ESIs may be a possible spinal intervention in the treatment of discogenic-mediated lumbar axial pain. Certainly, further study is required in the form of randomized, double-blinded, placebo-controlled clinical trials to elucidate the role, if any, of transforaminal ESIs in the treatment of discogenic-mediated lumbar axial pain without radicular involvement.

As previously implied, the best route for infusion of corticosteroids into the ventral epidural space in patients with a potential component of focal posterior discogenic inflammatory response is the transforaminal route. In many cases, the specific level of discogenic pathology has not yet been elucidated at the algorithmic point of consideration of ESIs for the treatment of lumbar axial pain thought to be potentially due to a discogenic inflammatory etiology. In fact, more than one segmental level may be contributing to inflammation in the ventral aspect of the lumbar epidural space. Therefore, unless imaging strongly suggests one segment, the S1 transforaminal ESI is recommended (Figs 92.3, 92.4). This route allows the clinician to mechanically drive the corticosteroid injectate, typically 12–18 mg of betamethasone, diffusely along the floor of the lumbar spinal canal via a pressure effect utilizing 3–5 cc of 1% lidocaine in an attempt to quell potential inflammation along the ventral epidural space incited by leakage of nuclear material. In those patients where one-level disease is strongly suspected, a smaller volume of local anesthetic may be infused after the corticosteroid dose at the foraminal level below the suspected level to deliver the corticosteroids in the cephalad direction more focally on the ventral aspect of the spinal canal at the posterior aspect of the suspicious intervertebral segment. In cases where a nonhealing annular tear(s) exists communicating nuclear material to the ventral epidural space, mediation of the inflammatory response may create a more optimal environment for spontaneous healing of the annular tear.

Fig. 92.3 An AP view of a left S1 transforaminal ESI (note the outline of the left S1 root sleeve inferior and medial to the left S1 pedicle as well as the degree of dispersion of contrast dye upon cephalad flow into the inferior portion of the lumbar spinal canal with maintenance of ipsilateral flow cephalad to the L4 level).

Fig. 92.4 A lateral view of the S1 transforaminal ESI demonstrating relative ventral flow of contrast dye on the floor of the spinal canal flowing cephalad to the L4 level.

Technique of performing transforaminal ESI

Transforaminal ESI absolutely requires fluoroscopic guidance in order for the site of pathology to be precisely targeted. The transforaminal route is the optimal access for delivering an injectate on the lumbar nerve sleeve and/or the ventral portion of the epidural space. Transforaminal ESIs are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. Real-time fluoroscopy is utilized to identify the pedicle corresponding to the foramina through which injectate is to be delivered. In patients with a transitional segment, either a lumbarized S1 vertebral body or sacralized L5 vertebral body, the interventional spine specialist will need to count the vertebral bodies beginning with L1 after the most caudal rib (T12) to establish that the appropriate pedicle is identified. Once the targeted pedicle is correctly identified, the c-arm should be rotated ipsilaterally until the superior articular process of the juxtapositioned caudal vertebral body comes into view and advances to the medial portion of the targeted pedicle on the created oblique view. The targeted pedicle should now take on an ovoid shape once the correct degree of rotation is achieved as opposed to the circular shape on a true anteroposterior (AP) image with the lumbar spinous processes in the midline. Then, a skin wheal utilizing a combination of 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate⁴² is raised just inferior to the midline portion of the targeted pedicle on the oblique image. A long-handled sponge clamp is utilized to guide a 20-gauge, 3.5 inch spinal needle through the raised skin wheal in a bull’s-eye manner (the needle hub concentrically outlines the needle tip (Fig. 92.5) just inferior to the midline portion of the targeted pedicle until a change in tissue resistance is appreciated or until the spinal needle hub abuts the skin. If the needle abuts skin prior to a change in tissue resistance, the 3.5 inch spinal needle is then utilized as an introducer and is positioned to align its tip to the midline portion of the targeted pedicle and a 25-gauge, 6 inch needle is guided through the index needle until a change in tissue resistance is appreciated. In either instance, the needle tip should then feel stable or locked into position if it has entered the targeted foramen. Verification of needle tip placement is achieved by rotating the c-arm in a manner that provides a true midline AP image. The needle tip is then slowly advanced to the six-o’clock position, proximated just inferior to the targeted pedicle. The lumbar spinal nerves exit the spinal canal just inferior and medial to the midposition of the corroborative pedicle on the AP image. Needle placement just superior to the spinal nerve and just inferior to the pedicle is confirmed by visualization of contrast medium centrally hugging the pedicle both inferiorly and medially as well as spreading cephalad along the ipsilateral ventral portion of the spinal canal, bathing the posterior aspect of the intervertebral discs as well as peripherally along the lumbar spinal nerve sleeve. Care must be taken and technique must be precise throughout needle advancement to maintain the bull’s-eye approach at all times via real-time fluoroscopy to prevent straying of the needle away from the targeted foramen. Inadvertent curvature of the needle outside the confines of the bull’s-eye approach may result in the needle tip hitting periosteum, such as the targeted pedicle if the needle tip strays superiorly, punctured viscus if the needle tip strays anteriorly towards the retroperitoneal and/or abdominal cavity, or punctured spinal nerve extraforaminally if the needle tip strays inferiorly. In some instances when performing a transforaminal ESI through the L5–S1 foramen, the targeted inferior aspect of the midline of the L5 pedicle may be accessible only by ipsilateral rotation due to one or a combination of a high-riding pelvis, significant loss of disc space height, large L5 transverse process, L5–S1 fusion, or a L5 on S1 spondylolisthesis. These obstacles can be overcome with a variable degree, depending on the severity of the aforementioned anatomical variations, of cranial to caudal tilt which will in effect move the pelvis inferiorly, creating direct access to the inferior portion of the targeted L5 pedicle. In cases of performing transforaminal ESI through the L5–S1 foramen in patients with a partially or completely sacralized L5 vertebral body, the approach is similar to that utilized when performing sacral transforaminal ESIs. When performing S1 transforaminal ESI, the skin wheal is raised superior and lateral to the targeted S1 pedicle. The needle is advanced through the skin wheal via a long-handled sponge clamp in the direction of the X-ray beam at a 45° angle to gently abut sacral periosteum just lateral to the S1 pedicle. Then, the needle is slightly withdrawn, reoriented inferiorly and medially, and slowly advanced, sliding to just inferior to the midline of the S1 pedicle into the targeted foramen. A slight suction or vacuum phenomena may be felt as the needle tip enters the targeted sacral foramen. A similar approach is utilized for L5–S1 transforaminal ESI in patients with partial or complete sacralization of the L5 vertebral body; however, the skin wheal is raised lateral and inferior to the targeted L5 pedicle and the needle too is advanced superiorly and medially after depth is achieved by contacting periosteum.

Fig. 92.5 An oblique view of a right L5 transforaminal ESI demonstrating the bull’s-eye approach to needle advancement visualized as a black dot with a thin concentric ring circumscribing the needle tip just inferior to the mid portion of the right L5 pedicle.

INTRADISCAL INJECTIONS OF BIOLOGICS FOR DISCOGENIC MEDIATED LUMBAR AXIAL PAIN SYNDROMES

Patients with discogenic mediated lumbar axial pain have, at least a component of, a structural anatomic lesion within the outer annulus of the intervertebral disc. This lesion may or may not communicate with the nucleus pulposus and is conceptually regarded as the inciting pathologic event that progresses over time and results in degeneration of the disc and, potentially, discogenic mediated pain. Intradiscal infusions of active biologics may represent the future in the prevention of this progression and repair of structural lesions within the intervertebral disc.

In vitro studies have demonstrated a cellular response of intervertebral disc cells to exogenous bone morphogenetic protein (BMP). These studies have demonstrated improved disc height and signal changes on MRI suggestive of repair of the intervertebral disc following intradiscal administration of BMP to discs damaged via chemical and mechanical methods. In a rabbit model, Miyamoto et al.⁵⁶ demonstrated that intradiscal infusion of osteogenic protein −1 (OP-1, BMP-7) restored the biomechanical properties of the degenerated intervertebral disc. Furthermore, An et al.⁵⁷ demonstrated that infusion of OP-1 intradiscally resulted in increased disc height and proteoglycan content. In addition, Takegami et al.⁵⁸ reported that intervertbral disc cells exposed to interleukin-1 alpha lost no intrinsic ability to upregulate proteoglycan synthesis in response to OP-1 stimulation. In fact, he went on to describe that the reformed matrix was actually richer in proteoglycans than that prior to interleukin-1 alpha exposure. Interestingly, Yoon et al.⁵⁹ demonstrated that infusion of adenovirus carrying Lim Mineralization Protein − 1 increases disc production of proteoglycans as well as bone morphogenic proteins. In a rat model, Kawakami et al.⁶⁰ demonstrated both enhancement of the extracellular matrix as well as inhibition of pain-related behavior with intradiscal OP-1 injection into painful degenerated discs. Based on these initial in vitro studies, it has been proposed that intradiscal infusion of BMP to a degenerated dessicated disc may initiate repair of the disc, manifested clinically as reduction in lumbar pain and concomitant improvement of physical function and potentially manifested structurally as a radiographic increase in disc height and/or an increase in MRI disc signal intensity. This author is a principal investigator in a multicenter phase 1 study evaluating infusion of a BMP into single level symptomatic degenerative disc disease in humans.

Although transforaminal ESIs targeted on the floor of the spinal canal at a focal discogenic mediated inflammatory response holds promise for some patients episodic chemically induced discogenic pain as previously described (Fig. 92.2), randomized prospective double-blinded studies done by both Simmons et al.⁶¹ as well as Khot et al.⁶² have demonstrated no statistically significant benefit of intradiscal infusion of corticosteroids for discogenic pain diagnosed by provocative lumbar discography. Other biologics that have been reported upon but whose role has not yet been elucidated include infusions of hematopoietic precursor stem cells, methylene blue and ozone (O₃). For example, Haufe et al.⁶³ reported no reduction in discogenic pain at one year follow-up in patients who underwent intradiscal infusion of hematopoietic precursor stem cells harvested from the pelvic bone marrow. Peng et al.⁶⁴ demonstrated that 87% of patient with chronic discogenic pain who met inclusion criteria for lumbar interbody fusion surgery but were instead treated with intradiscal injection of methylene blue were able to report marked improvement in pain and physical function. In 2004, Muto et al⁶⁵ reported on 2200 patients treated with intradiscal oxygen-ozone injection reporting no side effects and a 75–80% success rate at 6 and 18 months. Buric et al⁶⁶ conducted a prospective case series reporting on chemonucleolysis via ozone injections in 30 patients with non-contained disc herniations. They stated 90% of patients had a statistically significant improvement in pain and function as measured by VAS and Roland Morris Disability Questionnaires. Of course, further study is required before any of the aforementioned intradiscal infusions of various biologics can be regarded as a generally acceptable or standard of care intervention for discogenic lumbar axial pain syndromes.

PATHOPHYSIOLOGY OF Z-JOINT-MEDIATED LUMBAR AXIAL PAIN SYNDROMES

The lumbar Z-joint is the primary posterior element structure thought to be a potential etiology of spinally mediated lumbar axial pain. The rationale is derived from conclusions drawn from the conceptual model of the lumbar spine degenerative cascade as initially described by Kirkaldy-Willis,¹⁰ as previously reported within this chapter, as well as properties intrinsic to the Z-joint. As outlined earlier in this chapter, the posterior elements take on more axial load in certain positions (standing) as well as with increasing age. Anatomically, the Z-joint is a true diarthrodial joint with articular and subchondral cartilage, a small meniscus, a capsule, and a fluid-filled synovium encased in synovial lining. The initiating event that is thought to implicate the Z-joint as an etiology of lumbar axial pain is synovitis and the resultant synovial reaction which occurs as a result of the shift in axial loading from the anterior elements to the posteriorly situated Z-joints due to the temporally related incompetence of the intervertebral disc. On the other hand, it is theorized that the aforementioned initiating pathology to the synovial capsule can result in a younger population when induced by sudden, unexpected flexion–extension moments as occurs commonly in motor vehicle trauma. The Z-joints are able to accommodate the increased load up to a critical maximum at which point synovial pathology ensues leading to eventual progressive destruction of the cartilaginous articular surface when facet joint weight bearing exceeds the critical maximum. Acute, recurrent, and/or chronic inflammation can result in these synovial joints filling with fluid and distending. This distention may result in pain perception because of mechanical and/or chemical stimulation of the richly innervated synovial capsule. Evidence suggests that the Z-joint’s synovial capsule has a complex innervation provided by small, C-type pain fibers.⁶⁷ Furthermore, the majority of mechanosensitive somatosensory units found within the Z-joint were discovered to be group III high-threshold, slow-conduction units, which are thought to mediate nociception.^68–70 Therefore, the Z-joint can result in nociception by osteochondral and/or capsular mechanisms similar to those found in other extensively studied degenerated joints, such as the hip or knee. Capsular laxity can result and the accompanying subluxation can stretch and/or tear the richly innervated capsule leading to one or a combination of inflammatory or structural lumbar axial pain syndromes emanating from the lumbar Z-joint. Another potential mechanism for nociception arising from lumbar Z-joint has not been recognized until recently. In most diarthrodial joints, prolonged immobilization can lead to a cascade of joint changes. These may include, among other things, capsular stiffness leading to contracture, decrease in synovial fluid production, and tightening of para-articular muscles, all leading to joint rigidity. In some cases, complete ankylosis may accompany extreme inactivity, immobilization, and inhibition of function. In such cases, mechanical loads applied to the rigid joints typically can produce pain, which may be related to capsular stretching/tearing, synovial irritation from cartilage fragmentation due to poor nutrition, and/or muscle spasm from sudden stretching of immobilized, debilitated muscle. In chronic lumbar axial pain conditions, patients often splint segments of the lumbar spine, and the chronic immobilization may lead to nociception. Stretching the involved joint–muscle complex is the obvious physiologic therapeutic modality. Unfortunately, pain and fear-avoidance may prevent some pain-sensitive patients from complying with such logical medical advice. Nevertheless, the Z-joint can be the source of pain associated with these mechanisms, particularly after chronic persistent or chronic episodic lumbar axial pain conditions have produced disability for longer than 6 months.⁷¹

Technique of performing lumbar intra-articular Z-joint interventions

Lumbar intra-articular Z-joint injections are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. Real-time fluoroscopy is utilized to rotate the c-arm ipsilaterally until the medial and lateral edges of the targeted Z-joint are clearly visualized. Local anesthesia is achieved by infiltrating the skin, creating a skin wheal raised just medial to the midline or inferior aspect of the joint with a combination of approximately 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate.⁴² Real-time fluoroscopy is utilized to advance a 22-gauge, 3.5 inch spinal needle in a bull’s-eye fashion so that the needle tip abuts the lateral edge of the middle to inferior portion of the Z-joint. The spinal needle is then slightly withdrawn and directed just medially into the capsule of the targeted Z-joint. Approximately 0.1–0.3 cc of contrast can be utilized to verify needle placement, visualized by the presence of an hourglass-shaped arthrogram or portion thereof (Figs 92.6–92.8). Once needle tip confirmation is achieved, a combination of 0.5–0.8 cc of betamethasone and 0.2–0.5 cc of 1% lidocaine can be injected, dependent on the degree of compromise of the synovial capsule and the ensuing capacity to accommodate an infusion of volume.

Fig. 92.6 An oblique view demonstrating a medial to lateral approach to the right L4–5 Z-joint. The needle tip is directed toward the inferior portion of the joint space. (Note that rotation must be adequate in order to clearly visualize the edges of the inferior articular process of L4 and superior articular process of L5.)

Fig. 92.7 An infusion of 0.2 cc of contrast dye demonstrates filling of the joint space and visualization of the right L4–5 Z-joint partial arthrogram.

Fig. 92.8 An oblique view of a left L4–5 intra-articular Z-joint injection with visualization of a classic hourglass arthrogram pattern filling the superior and inferior capsules.

CONTRAINDICATIONS AND COMPLICATIONS OF INTERVENTIONAL SPINE PROCEDURES

Contraindications to interventional spine procedures include possible pregnancy (secondary to the potential adverse effects of fluoroscopic radiation on the fetus), hypersensitivity to any component of the injectate, bacteremia, full anticoagulation, and bleeding diathesis. Other concerns are elevations of serum glucose levels in diabetics, elevations of blood pressure in hypertensive patients, and fluid retention in congestive heart failure patients. The use of aspirin and other NSAIDs have not been demonstrated to predispose patients to any significant bleeding while receiving ESIs.⁸⁷

Potential complications of fluoroscopically guided interventional spine procedures include increased pain, hypersensitivity reactions, dural puncture, subarachnoid injection, anaphylaxis, infection, unmasking of preexisting systemic infection, epidural abscess, increased pain, fever, epidural bleeding and/or hematoma, bladder dysfunction with urinary retention, weakness, permanent neural element damage via penetrating trauma, intravascular injection resulting in local anesthetic toxicity such as seizure, cardiac arrhythmia or arrest, and death. However, these events are quite rare. Botwin et al.⁸⁸ reported no major complications and less than a 10% rate of minor complications, all of which resolved without hospitalization, in 207 patients undergoing 322 fluoroscopically guided lumbar transforaminal ESIs.

PHYSICAL REHABILITATION

Physical rehabilitation is a key modality on the treatment of patients with spinally mediated lumbar axial pain. Physical therapy programs prescribed specifically to address the primary site of injury and secondary sites of dysfunction can provide a means of treatment with or without adjuvant medications and interventional spine procedures. Back schools and other training programs that are not job specific have not been shown to be statistically effective; however, programs that integrate the job requirements into the training program show statistical significant results.⁸⁹ Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days following an acute episode may be indicated to help calm down initial pain symptoms and relieve fatigue. Rest for longer periods of time has not been shown to be beneficial, and may be harmful, potentially causing deconditioning, loss of bone density, decreased intradiscal nutrition, loss of muscle strength and flexibility, and increased segmental stiffness.⁹⁰ Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief, but protracted courses of passive treatments become counter-productive as they place the patient in a dependent role instead of participating in an active, function maximizing rehabilitation program. One of the most important components of any back care program is education. Education should include an explanation of the natural history of an acute, subacute, and chronic disc injury. In addition, education should include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. The greatest successes in health education can be seen in two great medical problems, heart disease⁹¹ and cancer.⁹² Education has had a direct effect on decreasing the prevalence of smoking, from 40% of the population in 1965 to 29% in 1987.⁹³ An education-based low back paradigm is inexpensive and begins with providing reassuring information to the patient. The seeds of the educational approach exist in back schools, functional restorative programs, and innovative prevention and rehabilitation strategies. LaCroix found that 94% of patients with a good understanding of their condition returned to work, whereas only 33% of patients with a poor understanding of their condition returned to employment.⁹⁴ Reassurance that activity is helpful promotes return to function. Back school provides information on spine anatomy and function and was found to be one of only three interventions identified by the Quebec Task Force on Spinal Disorders as effective for patients in randomized, controlled trials.⁹⁵ Myofascial manual techniques may be employed to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, then an active, dynamic, outpatient lumbar spine stabilization rehabilitation program should be prescribed. In addition, rehabilitation of other associated components of the functional kinetic chain may be appropriate, as these structures may also be affected. A dynamic lumbar spine stabilization rehabilitation program is aimed at maintaining a neutral spine position throughout various daily activities. An extension bias is commonly employed to help reduce intradiscal pressure. This position allows for a balanced segmental force distribution between the intervertebral disc and Z-joints, provides functional stability with axial loading to help minimize the chance for acute dynamic overload upon the discs, minimizes tension on ligaments and fascia planes, and alleviates symptoms. Repetition is key in increasing flexibility, building endurance, and developing the required muscle motor programs that activate a series of key multimuscular contractions subconsciously that maintain the lumbar spine in a neutral position throughout static and dynamic activities. For athletes, the aforementioned program can be combined progressively with sport-specific polymetrics to help the lumbar spine maintain a neutral position during high-intensity, unpredictable, reaction-intensive sports. Another method for rehabilitation of athletes is to train them in maintaining a neutral spine position in the individual motions of their sport, then subsequently grouping these component motions into a new, safe, stable spine movement. Cardiovascular fitness training is an important component to a comprehensive rehabilitation program as it assists in providing the endurance necessary to prevent fatigue of the spine-stabilizing musculature.

CASE STUDIES

Case study 1

S.G. is a 36-year-old male with a history of occasional spontaneously resolving short-term (less than 1 week duration) low back pain episodes who presents to a spine specialist complaining of 12 weeks of worsening low lumbar axial pain initiated while lifting a heavy television set helping a friend move into a house. The patient states his symptoms are located across the width of the low back without lower extremity radiation. He qualifies his pain as a constant, deep, dull ache worsened with prolonged sitting, especially riding in his car, as well as with twisting motions when bent forward. The patient reports lumbar extension and staying active seem to provide some symptom mitigation. Physical examination reveals some tenderness and spasm to palpation over the bilateral low lumbar paraspinal musculature. Lumbar flexion is significantly limited due to worsening of the patient’s lumbar pain; however, lumbar extension alleviates the patient’s lumbar pain. In addition, the patient reported increasing lumbar pain with decreasing angle acuity during sustained hip flexion. Sacroiliac joint stress maneuvers and provocative maneuvers were not pain provoking. The lumbosacral spinal neurologic examination was normal. Plain films of the lumbar spine ordered by the patient’s primary care physician revealed moderate loss of disc height posteriorly at the L5–S1 segment. Physical therapy had been initiated 10 weeks previously with minimal improvement. The patient reports that mostly passive modalities had been employed in therapy for pain and spasm control, as several attempts at advancement to an active extension-biased McKenzie stabilization program proved too difficult due to pain provocation. An MRI of the lumbar spine was ordered, revealing focal degenerative disc desiccation at the L5–S1 segment with reactive endplate edema and a high-intensity zone lesion posteriorly (Figs 92.9, 92.10). A diagnosis of discogenic lumbar axial pain was made and the patient underwent two therapeutic bilateral S1 transforaminal ESIs. After the second procedure, the patient reported greater than 90% alleviation of his lumbar pain. Physical therapy was reinitiated, resulting in near-complete symptom resolution. The patient understood the key to obtaining long-term success with management of his disc disease included compliance with his home exercise program and proper lumbar spine mechanics during all activities. Although the patient continues to have occasional lumbar pain episodes, he reports that these episodes resolve within a few days with rest, activity modification and/or mild analgesics.

Fig. 92.9 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.

Fig. 92.10 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.