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The Lumbosacral spine: kinesiology, physical rehabilitation, and interventional pain medicine.


Interventional pain management is the discipline of medicine devoted to the diagnosis and treatment of pain related disorders by the application of interventional techniques for the management of subacute, chronic, persistent, and intractable pain, independently or in conjunction with other modalities of treatment [1]. Under image guidance, such techniques include needle placement for percutaneous (and "targeted") drug delivery or ablation of targeted nerves [2-4], as well as minimally invasive procedures such as implantable therapies and vertebral augmentation [2,3].

A series of recently published reports compare nonsurgical methods (including interventional pain medicine procedures and therapeutic exercise) to surgical approaches (discectomy or laminectomy) for the treatment of low back pain [5-8]. The data set for these reports stemmed from the Spine Patient Outcomes Research Trial (SPORT) [9]. Subjects had low back pain secondary to one of three lumbar spine conditions: disc herniation, degenerative spondylolisthesis, and spinal stenosis. According to trial results, the nonsurgical treatment arms, taken as a group, were consistent with surgery outcomes in the randomized cohort for spondylolisthesis and spinal stenosis [5,7,8]. However, this was not the case in the observational cohort, where surgery produced better outcomes for all three conditions [6-8]. With apparent dichotomy concerning the benefits achieved among trial cohorts, SPORT has created ardent discussion in the medical community relative to the impact the trial may have on treatment decisions, and invites a synthesis of the literature on the roles of interventional pain medicine and physical rehabilitation to help restore quality of life for the low back pain patient.

In this article, neuro-musculoskeletal (kinesiology) principles are reviewed to examine the psycho-physical domains and pathomechanics of lumbosacral-related pain relative to select interventional techniques, based on the treatment algorithms developed by the International Spine Intervention Society [2]. Moreover, key therapeutic exercise concepts are highlighted. To this end, it is the aim of this article to serve as a crosswalk for spinal interventionalists (radiologists, interventional-trained physiatrists, and anaesthesiologists) and physical rehabilitation specialists (physiatrists, kinesiotherapists, athletic trainers, physical therapists, and rehabilitation nurses) to improve nonoperative treatment outcomes for patients with lumbosacral-related pain, as a result of a better understanding of the integrated roles of such professions along the continuum of care for the patient.


A review of the literature on kinesiology, neurology, pathophysiology/mechanics, pain psychology, and therapeutic exercise was conducted to examine interventional lumbosacral spine procedures in adults. The review included known textbooks, print journals, and the MEDLINE database from 1966 to the present. Articles were accepted based on the following 4 criteria:

1) The postulates identified by Bogduk [10] for spinal structures to be deemed a cause of back pain, as follows:

* A nerve supply to the structure.

* The ability of the structure to cause pain similar to that seen clinically in normal volunteers.

* The structure's susceptibility to painful diseases or injuries.

* Demonstration that the structure can be a source of pain in patients using diagnostic techniques of known reliability and validity.

2) Lumbosacral conditions in adults, mechanical or degenerative in nature.

3) Clinical practice guidelines to treat low back pain in interventional medicine.

4) Kinesiology and exercise science with respect to low back pain.

Spine Patient Outcomes Research Trial (SPORT)

The motivation for SPORT emerged from the lack of clinical consensus regarding the use of spine surgery [11]. Funded in part by the National Institutes of Health, this multicenter and multistate trial investigated surgical versus nonsurgical management for three conditions in the lumbar spine: intervertebral disc (IVD) herniation, spinal stenosis, and degenerative spondylolisthesis [5-9,11]). IVD herniation was defined as imaging evidence of protrusion, extrusion, or sequestered fragment with persistent radicular signs/symptoms (below the knee for lower lumbar herniations and into the anterior thigh for upper lumbar herniations) over a 6 week period [5,6]. Spinal stenosis was defined as narrowing of the central spinal canal, lateral recess, or intervertebral (neural) foramen [8]. Degenerative spondylolisthesis was defined as spinal stenosis due to forward slippage of either L4 on L5 or L3 on L4, with L4-L5 the most common level [7]. Results for patients in the randomized cohort suggest nonsurgical therapies achieve outcomes consistent with surgical treatments [5,7,8], but were not as effective in the observational cohort [6-8].

The primary outcome measure for SPORT was health-related quality of life as determined by responses to well-established assessment tools. These instruments consisted of the SF-36 Health Survey and the Oswestry Disability Index [9]. Secondary outcome measures compared the overall economic value between the approaches to treatment. This included but was not limited to analysis of indirect costs. Such costs were derived from questions on occupation, degree of difficulty in work performance (either in a job or as a homemaker), job changes, and financial distress [9].

Approaches employed in the surgical treatment arm consisted of decompression of the involved nerve root by discectomy (open or micro) for IVD herniation [5,6]; posterior decompressive laminectomy in spinal stenosis [8]; and posterior decompressive laminectomy with or without bilateral single level fusion for degenerative spondylolisthesis [7]. At a minimum, nonsurgical methods consisted of physical therapy, education/counseling with home exercise instruction, and a nonsteroidal anti-inflammatory drug if tolerated. Interventional treatment options included epidural, facet joint, and trigger point injections [9].

Critical review of the SPORT study design focuses on trial methodology and biostatistical analysis [9,11]. Three prevailing concerns are, as follows: 1) the lack of a standardized nonsurgical treatment protocol; 2) the high number of cross-over between treatment arms; and 3) use of the intention-to-treat statistical metric in the analysis of outcome measures. Regardless of critique, however, based on the resultant outcome-similarities in the treatment arms in the randomized cohort, the Centers for Medicare and Medicaid Services convened a task force to examine the role of lumbar fusion for degenerative conditions [11], in particular, spondylolisthesis.

Due to its rich data set, SPORT has the potential to influence health care policy [11]. In this context, it is important that spinal interventionalists advance techniques from evidenced-based research. Moreover, as new treatment methods emerge and technologies are introduced for lumbosacral pain, it is important for researchers to continue clinical, rehabilitative, and biomedical research initiatives which challenge the status quo and pursue new ideas for the interventional management of lumbosacral-related pain [12].


Lumbosacral Kinesiology

Lumbar Intervertebral Disc (IVD)

The IVD tolerates compressive loads by converting the resultant force into circumferentially applied tension by a phenomenon known as hoop stress [13]. Specifically, water is incompressible and therefore the nucleus pulposus (i.e., approximately 70%-90% water) exerts pressure in all directions on the surrounding rings of the anulus fibrosus through a process known as radial expansion [13,14]. Subsequently, the anulus fibrosus incurs tension throughout an interlaced network of fibers as part of the hydraulic effect to oppose radial expansion [13,14]. To quantify the ability of the IVD to absorb and transmit compressive forces during various activities, Nachemson et al. [15] recorded intradiscal pressure through sensor-needles placed in the nucleus at the L3-L4 disc. Presented in Table 1 are selected measurements obtained from that classic study, as well as comparative intradiscal pressure measurements obtained at the L4-L5 disc by Wilke et al. [16].

Morphometric analysis of the IVD shows the nucleus is not a discreet feature all to its own but rather an area of greater hydration than the anular rings [14], and thus healthy discs are clearly discernable from arthritic, desiccated discs on T2-weighted magnetic resonance imaging (MRI) sequences [17]. Further, the location and form of the nucleus is subject to positional changes of the lumbar spine as evidenced by discography and MRI (see Table 1) [18-20], and it is this conformity that is often used to the advantage of physical rehabilitation professionals for patients with discogenic back pain [21]. Furthermore, the degree of IVD water content is dynamically related to the effects of aging, pathology, and/or positional changes. Investigators [22,23] have recently utilized positional or kinematic MRI to report in vivo changes to the water content and height of lumbar IVDs in different seated postures. Sagittal T2-weighted exams were performed using a water content calibration phantom taped to the subject's back. Interpretations revealed that an optimal balance in IVD water content/disc height was obtained with the least amount of lumbar strain at 135 [degrees] in thigh-trunk angle compared to the usual 90 [degrees] sitting position, with seated forward flexion the most detrimental [22,23]. The percentage of water content for the L4-L5 and L5-S1 discs, in the various positions studied compared to supine lying, are presented in Table 1.

As for other movements, axial rotation and/or side-bending will result in torsional forces applied to the lumbar IVDs, and resisted by the nature of the rings of the anulus fibrosus [13,14]. A patterned layer of obliquely oriented fibers, composed of both collagen and elastin characterizes these rings [14]. It is the histological combination and fiber alignment that provides the tensile strength and resilience of the anulus fibrosus during torsion. However, the fiber orientation also contributes to the relative weakness of the IVD to resist torsion, as anatomically only half of the total fibers are properly aligned to allow for taut resistance to a particular direction of rotation [13]. To help remedy this "design flaw" by acting to stabilize the lumbar spine during rotation, the facet joints and interspinous ligaments act to mechanically restrict the amount of torsion that could otherwise develop in the IVD [13,24]. Thus, axial rotation, side-bending, and forward bending are dependent upon the kinematics of joint coupling, in which the direction of either lumbar flexion/extension or side-bending governs the direction of rotation of a functional spinal unit (FSU) [13,14].

Neural Canal and Intervertebral Foramina

A lumbar FSU, or motion segment (see Figure 1), describes the basic functional structure protecting the neural elements (i.e., the conus medullaris, the cauda equina, and the spinal nerve roots) and permitting lumbar movement, and consists of two adjacent vertebrae along with the interconnecting soft tissue [13]. Thus, each motion segment is comprised of three joints: one anterior inter-body joint (the flexible interspace formed at the superior and inferior vertebral endplates and the IVD) and two posterior articular facet (zygapophysial) joints. In the lumbar spine there are five motion segments, with L1-L2 the most cranial and L5-S1 the most caudal. Within a FSU there are three fibro-osseous passageways, the neural canal and, bilaterally, the intervertebral foramen [13,14]. Irritation or impingement of the neural elements at these openings-brought on by segmental motion-may cause neuropathic pain and/or radiculopathy in the presence of underlying histopathological processes or instability. For example, the usual defects associated with a motion segment are either spondylolysis (defect of the pars interarticularis) or spondylolisthesis (slippage of the superior vertebral body of the FSU) with or without instability. In regard to spondylolisthesis, there are six types: congenital, isthmic (associated defect of the pars interarticularis), degenerative, traumatic, pathological, and post-surgical. It is noteworthy to reiterate, however, that only degenerative spondylolisthesis was included in SPORT.

The neural canal is made up of the vertebral arch and the ligamentum flavum, and the posterior longitudinal ligament. The ligamentum flavum spans the laminae between adjacent vertebral arches (see the illustration accompanying Table 2), and is the site of percutaneous interlaminar access into the canal. Deformity to this ligamentous structure or the IVD during trunk extension or axial load can account for changes in cross-sectional area (CSA) of the thecal sac, as evidenced by kinematic MRI studies in the axial-loaded, supine position [25], and in different upright, seated positions [26] (see Table 1).

The intervertebral foramina are formed by the inferior notch and superior notch of two adjacent pedicles and are vertically oblong in design (see Figure 1). Located within the superior aspect of the foramen are the dorsal root ganglion (DRG) and the ventral nerve root. In general, intervertebral foramina size will increase with lumbar flexion and decrease with lumbar extension (see Table 1) [27]. Moreover, analysis of 1 mm thick slices of lumbar transforaminal histological specimens-obtained from microtome using a cryosectional technique and subsequent analysis with an experimental high-resolution MRI sequence-has given investigators a detailed look of the transforaminal neural tissue in situ [28]. The study described the parasagittal appearance of a collection of small neural fascicles that form the proximal 2-6 mm of lumbar spinal nerves, and helps to explain the absence of a distinct solid spinal nerve immediately distal to the DRG and ventral root landmarks on views performed with the current state-of-the-art, "clinical" MRI equipment/sequences [28]. The fascicles are centrally located in the lateral aspect of the intervertebral foramen and have a closer relationship with adjacent IVDs and the ligamentum flavum than do the spinal nerve roots [28]. As to the associative clinical/rehabilitative implications of this study, consider that it is these neural fascicles that are the possible sites of entrapment or irritation by either the IVD or ligamentum flavum with flexion or extension, respectively.


Muscles and Ligaments

Fascia and muscles for dynamic stabilization and movement of the lumbar spine, as well as ligamentous support, are outlined in Table 2. This section will place emphasis on neuro-musculoskeletal principles, by focusing on the kinematics of the lumbar multifidus muscles. In the lumbar spine, the paired multifidi are found bilaterally along the transverse processes and spinous processes of the vertebral bodies. The segmental and independent origin of the L1 through L4 multifidi arise from the mamillary process of each respective superior articular process (SAP), whereas the deep fibers become contiguous with facet joint capsules [29,30]. The L1-L4 multifidi insert on the laminae (multifidi short fibers) or spinous processes (multifidi long fibers) spanning two vertebral levels above their origins [30]. The L5 laminar multifidi originate just above the S1 foramen [30]. Due to their independent attachments, lumbar multifidus muscles are designed to act in concert on individual laminae/spinous processes to stabilize the associated FSU [29,30], and are typically most active during trunk extension and axial rotation.

The lumbar multifidus acting directly on a particular vertebral segment is innervated by the spinal nerve of that vertebral segment, the medial branch of the respective dorsal ramus of spinal nerves L1 through L5 [31]. This anatomical and neuro-physiological relationship can greatly impact the body mechanics of individuals with localized low back pain. Sonography has allowed researchers to show differences in lumbar multifidus size (implying relative muscle health and activity) during different body postures in healthy subjects and patients with low back pain [32]. Results showed an inverse relationship in postures incurring maximal contraction of the muscle in these two groups (see Table 1). In healthy subjects, lumbar multifidus CSA increases from prone lying to standing, with a gradual decrease from 25 [degrees] forward stooping to 45 [degrees] forward stooping. In patients with low back pain, 25 [degrees] forward stooping incurred greatest multifidus CSA, suggesting an altered role in stabilization of the lumbar spine [32]. Moreover, in healthy subjects, a post fatigue effect of the paraspinal muscles has been shown to modify the flexion-relaxation phenomenon, as seen by electromyography (EMG), and thus shift load bearing to passive structures earlier than the phenomenon is normally induced (approximately 45 degrees forward bending) [33]. In this context, it is noteworthy to mention that this "shift" in the flexion-relaxation phenomenon can further accelerate under conditions of low back pain.

Lumbar Facet/Zygapophysial Joints

The two posterior articular joints, the facet or zygapophysial joints, of the FSU are formed by the articulating joint surface orientations of the SAPs (posteromedially) and the inferior articular processes (IAPs) (anterolaterally) [13,34]. The lumbar facet joints carry 20%-40% of the load on the lumbar spine, although degenerative discs may transfer more load to these joints thereby increasing this ratio [35]. One mechanical advantage inherent to the skewed orientation of facet joints is that they interlock to resist forward displacement and/or rotation of the top vertebral body [34], either independently or in combination during forward bending. However, the resultant shear forces during forward bending or forward stooping are also resisted by the interspinous ligament and abdominal muscles [24].

Sacroiliac (SI) Joint

Among weight-bearing joints, SI joint alignment with the paired innominate bones (ilium, ischium, and pubis) and the sacrum is remarkable. The joint is positioned in such a way that transfer of weight and ground reaction forces run obliquely through the joint line rather than crossing the joint space transversely [36]. The trabecular patterns in the innominate bones and femora transmit these forces to/from the acetabulae in standing positions or walking, and via the ischial tuberosities in sitting positions [36]. Moreover, the SI joint is innervated by a complex neural network, with variable patterns of pain referral [37].

The SI joint is structurally and functionally classified as a diarthrodial synovial joint [36,38-40]. However, the posterior synovial capsule is noted to be rudimentary at best and the anterior capsule is nothing more than a thickening of the anterior sacroiliac ligament [39]. Moreover, both the tortuous union of the auricular surfaces (i.e., the area forming the synovial joint) and the unique morphologic features created by the anterior and posterior sacroiliac ligaments, but chiefly by the stout interosseous ligaments, stabilize the joint by strictly limiting planar (gliding) movement [36,38]. In effect, it is the interosseous ligaments that constitute a fibrous synarthrosis through extensive attachments to the sacral and iliac tuberosities [36,38]. In addition, two accessory ligaments bilaterally are integral in helping to stabilize the SI joint. The sacrotuberous ligament fans out from the ischial tuberosity to the posterior superior iliac spine and the tuberosities of the sacrum; and the sacrospinous ligament, deep to the sacrotuberous ligament, attaches from the posterolateral aspects of the S3-S5 sacral body segments to the ischial spine [36].

Therefore, as a stress-relieving point about the spine and the pelvic girdle [39], functional movement occurs with respect to symmetrical and asymmetrical orientations [36,38], and with respect to lumbopelvic rhythm [36]. Symmetrical motion involves nutation and counternutation. Nutation denotes sacral base translation anteroinferiorly on the ilium [36,38], and is checked by the sacrotuberous and sacrospinous ligaments (e.g., in weight-bearing, anatomic position) [36]. Counternutation represents sacral base movement posteroinferior in relation to the ilium [36,38], and is checked by the longitudinal fibers of the interosseous ligament [39]. Asymmetrical motion is best depicted in unilateral leg stance, during which angular-momentum from influential force vectors cause pelvic torsion [36]. Lumbopelvic rhythm is the phenomenon of motion occurring around the axis of the hip joint that is best demonstrated in forward bending [37]. It is important to note that the SI joint and its ligamentous constituents are vulnerable to age-related changes and ankylosing [41,42], and this can eventually alter all described kinematics associated with the joint, all biomechanical forces that traverse the joint space, and likelihood of pain referral prevalence [37].

Psycho-Physical Domains

Pain Catastrophizing/Kinesiophobia

Pain-related fear may manifest as hypervigilance with a somatic focus, in which pain is believed to be a sign of bodily harm or damage, or an activity-avoidance behavior [43,44]. Pain catastrophizing [43] and fear of movement/(re)injury (also known as kinesiophobia) [44] are the terms given to each behavior, respectively. When present, in accordance with case presentation, strategies to manage or reduce kinesiophobia and/or pain catastrophizing should be considered integral components of exercise therapy programs implemented to restore functional activities secondary to reducing low back pain (e.g., interventional pain management including referral to pain psychology and physical rehabilitation specialists) [43,44]. Moreover, these behaviors help to conceptualize the term, "psycho-physical domains."

Broadly speaking, psycho-physical domains describe the different but interrelated measures of quality of life (psychological, physical, social and economic), which can become negatively affected by functional limitations due to pain and fatigue. For example, on one hand, physical and emotional energy must be spent on coping strategies; and on the other, pain-related signs/symptoms can make it difficult for patients to obtain the sleep architecture (pattern of sleep stages) necessary to rejuvenate during a restful night's sleep. To this point, notably, one pain research group (the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials) recently suggested that core outcome measures should consist of six domains: pain (including intensity and quality), physical functioning, emotional functioning, symptoms and side-effects, global improvement and satisfaction with treatment, and subject disposition [45].

In regard to physical activity, pain, and issues of employment, Fishbain et al. [46,47] looked at functional capacity based on the Dictionary of Occupational Titles and found statistical significance for employment capacity in eight job factors: stooping, climbing, balancing, crouching, feeling shapes, handling left and right, lifting, and carrying. Furthermore, the predictive validity for return to work using the above measurable job factors was confirmed for functional capacity evaluations in patients with low back pain [47]. Functional capacity evaluations are comprehensive physical assessments in patients of working age. Such data can be important when attempting to extrapolate treatment effects to the broader definition of psycho-physical domains relative to socioeconomic concerns [48].

Interventional Pain Medicine

Intervertebral Disc

Interventional treatment

The neuronal network associated with the neural canal is more pervasive along the anterior border of the canal. The archetypal example is the path taken by the sinuvertebral nerve-which penetrates and courses through the posterior longitudinal ligament into the outer third of the disc (see the figure accompanying Table 2). This nerve relays sensory information from the disc, as well as the posterior longitudinal ligament, via the sympathetic nervous system [49-51]. Spanning the length of the anterior border of the neural canal, the posterior longitudinal ligament provides biomechanical support to the spine in the sagittal plane. However, with a characteristic hourglass shape that is thinnest between the pedicles, the widest part of the ligament does not cover the posterolateral portion of the IVDs. As a result, because the anular rings are not reinforced in the posterolateral direction, the anulus fibrosus is susceptible to injury, and common injury mechanisms involve excessive, highly forceful IVD loading or axial rotation. The load required to cause mechanical failure to the spine falls in a range from 3,000 N to 10,000 N of compressive force [24], with such orders of magnitude of stress possible during end-range forward bending or improper lifting. In these classic scenarios, the anterior IVD is compressed and the intradiscal material is forced posterolaterally against the layers of the anulus fibrosus, which may, then, irritate the sinuvertebral nerve. If the nucleus pushes against the anular rings with enough force to cause outward deformity of the anulus fibrosus, the IVD is said to be bulging or protruding into the neural canal. Conversely, if the magnitude of the intradiscal pressure against the rings exceeds the capacity of the rings to maintain such force, the nucleus may extrude through the rings and invade the neural canal, the IVD is said to be herniated, and the disc material may sequester.

Mild cases of IVD herniation can reduce spontaneously as the hydrophillic nucleus is reabsorbed, allowing the involved sinuvertebral nerve and/or spinal nerve roots to recover from irritation [52]. Whereas, in more severe cases, bulging, protruding, or herniated IVDs may become neurocompressive on the thecal sac and/or spinal nerve roots and cause back pain with radicular symptoms. The most common levels of herniation are the L5-S1 disc and the L4-L5 disc [6,7,53,54], in extreme cases cauda equina syndrome can occur and is most frequently associated with L4-L5 or L3-L4/L4-L5 disc herniations [55]. Moreover, surgery may be indicated in patients who have progressive neurologic decline [56]. From an imaging perspective, if patient history includes one or more surgical resection(s) of herniated disc(s) (e.g., postoperative discectomy), MRI exams should be performed with contrast enhancement to differentiate scar tissue (which enhances with gadolinium) from possible recurrent IVD herniation. However, the disc may enhance due to IVD-intravascular uptake within approximately 30 minutes following administered gadolinium [57,58].

In terms of gross anatomy and pathophysiological relationships, trauma/irritation imposed on a spinal nerve from an abutting herniated disc is typically associated with the disc-level immediately above the level of the exit foramen for the nerve, since spinal nerve roots traverse the superior aspects (i.e., the inferior notch) of the intervertebral foramina. For example, in the case of an L4-L5 disc herniation, neurocompression may occur on the L5 spinal nerve along its course within the lateral recess of the neural canal. Therapeutic interventional techniques for IVD herniation include three methods for epidural steroid injections: the transforaminal (TFESI), interlaminar, and caudal approaches [2,3]. Respectively, for each of these three methods the needle enters into the superior aspect of the orifice of the intervertebral [exit] foramen; pierces the ligamentum flavum to enter the canal space (and subsequently, the epidural space); or is placed into the sacral hiatus to push injectate into the terminal caudal equina. Only the transforaminal and the interlaminar approaches are discussed here. Figure 2 shows "ideal" spread of the contrast media during a TFESI procedure, i.e., bathing both the canal space and the spinal nerve. Note: if the exit foramen exhibits stenosis to the degree that optimal TFESI needle placement is complicated, then a selective nerve block may result (not shown), with the intention to alleviate any irritability associated with the involved spinal nerve(s). Figure 3 shows an interesting interlaminar epidural steroid injection (as further described below).

While bilateral flow of iodinated contrast media in the neural canal is frequently verified under fluoroscopically guided interlaminar epidural injections, anecdotal evidence suggests unilateral blockades under this method may be the result of a band of connective tissue known as the plica mediana dorsalis (Figure 3) [59]. The presence and spatial orientation of this tissue has been investigated by computed tomography (CT) epidurography [60-62]. Although findings of prevalence are inconclusive, when the tissue is present it is usually oriented in the mid-sagittal plane within the posterior epidural space [60]. In addition, it is suggested that this tissue may interfere with the placement of epidural catheters or leads [60], but does not usually pose any clinical significance. Interestingly, a greater concern of interference during epidural blockade or catheter/lead placement can be associated with the presence of intra-epidural tissue obstructions due to post-surgical, post-traumatic, and/or degenerative epidural scarring [63].

Low back pain without/with neurocompressive MRI evidence due to bulging, protruding, or herniated disc pathology may be evaluated by provocative discography; especially in the absence of the high-intensity-zone MRI marker, which strongly indicates the presence of nuclear material within the anular rings [64,65]. Discography is an interventional diagnostic procedure to determine if the IVD is the generator of pain [2,66] (see Figures 4 and 5), often performed after facetogenic pain is ruled out. A positive response at a tested IVD level is morphologically specific for radial anular fissures [10], or internal disc derangement. (It should be noted that while some authors argue discography accelerates disc degeneration [67], at this time the International Spine Intervention Society advocates inclusion of discography in the interventional spine armamentarium when properly administered, including patient selection--see the low back pain treatment algorithm, Figure 6.)

Because discogenic pain is mediated by nerve endings located mainly in the periphery of the anulus fibrosus [10,13,14,31], such as the sinuvertebral nerve [50,51], it is nociceptive in nature but may also have a sympathetic [nervous system] component as well. A technique for needle placement that has the lowest probability for producing radicular pain to minimize false-positives has been described [68]. The intent of the discogram procedure is to provoke pain symptoms as a result of increased intradiscal pressure from iodinated contrast media injected into the nucleus to distend the IVD under fluoroscopic guidance. End-feel of intradiscal injection and type of pain provoked and disc morphology are recorded. A loss of end-feel occurs when the anular rings do not retain the contrast media and the injected volume spills out of the IVD due to a complete tear in the anular rings. Pain is concordant if the procedure reproduces the exact everyday complaints of low back pain expressed by the patient. Post-discography CT scans provide detailed IVD morphology evidence and offer a differential diagnosis between torsion injuries versus internal disc disruption by the cross-sectional analysis of anular fissures [10,66].

With respect to future directions toward lumbar disc therapy, apart from the 24-hour diffusion of gadolinium (referred to as the "diffusion march") across the vertebral endplates and into the discs as confirmed by serial MRI [58], a prospective study on discography recently confirmed real-time (live fluoroscopy) intravascular uptake of iodinated contrast media-from the IVD to the surrounding vertebral column vascular supply and the inferior vena cava [69]. The investigators in the discography study observed a 14.3% intravascular uptake incidence in the studied patient population [69]. Collectively, these two studies have broad implications: as evidence of such IVD vascularization may facilitate solutions to delivery challenges of bioengineering designs such as IVD tissue scaffolds [70-72], mesenchymal stem cell therapy [73,74], or biomolecules to act as biochemical mediators within the disc [75], and thus serve to help heal the nucleus or deranged anular layers. (Note: a fluoroscopic image of intravascular uptake captured by this author during a lumbar discogram is shown in Figure 7.)








Physical rehabilitation considerations

When patients present with acute radiating low back pain that is mechanical in nature, the McKenzie protocol may help to abate radicular symptoms [21]. However, maintaining a neutral spine during daily activities helps to reduce the chance of IVD abutment on the intraspinal structures and spinal nerve roots. It is assumed that early recruitment of the core abdominal wall muscles (the dynamic stabilization muscles) before movement during a variety of functional tasks is commensurate with a stabilization role for the spine. Richardson et al. [76] published the first in vivo evidence of the biomechanical effects of two common therapeutic exercise approaches for patients with low back pain, with respect to efficient spinal stabilization and implications for lumbosacral load transfer. Using both EMG and real-time ultrasound imaging, the research team compared activation of the global abdominal muscles (i.e., the "brace pattern") to activation of the transversus abdominis only (i.e., the "draw-in pattern"). Of these two abdominal muscle patterns, activation of the transversus abdominis--the draw-in pattern--was found to have the greatest effect on reducing sacroiliac joint laxity (i.e., causing increased joint stiffness/stability) [76]. See Figure 8 for a representative diagram detailing the resulting joint reaction forces compared to the muscle force.

Although the work by Richardson et al. [76] supports low back pain exercise protocols which focus on enhancing the stabilization role of the transversus abdominis by precise contractions, independently of the other abdominal muscles, rather than general, whole-body exercise programs, exercise regimens which incorporate gentle stretching of the hamstring muscles and body mechanics training, as well as adjunctive manual therapy techniques, are vital to acquire satisfactory lumbopelvic rhythm to help maintain a neutral spine over the long term [77,78]. To this point, in a study which provided insight into the functional relationship between image-proven IVD herniation and SIJ dysfunction, Galm et al. [79] showed that physical therapy is more likely to reduce lumbarosacral pain in patients with disc herniation if those patients present with SI joint dysfunction that is successfully resolved by manual therapy techniques prior to physical therapy. Such outcomes speak to avoiding an incorrect indication for discectomy/nucleotomy, as well as avoiding discectomy/nucleotomy reoperation since SI joint dysfunction can be identified as the cause of pseudoradicular pain in 10%-23% of patients following such surgery [79]. It is important to emphasize here that the manual therapy techniques applied to treat SI joint dysfunction were conducted with the patient in the prone position (i.e., to reduce risks associated with spinal rotation for this patient population), whereas both mobilizing techniques without impulse and manipulative techniques with high-velocity impulses were performed. The interested reader may refer to Galm et al. [79] for further discussion of the manual therapy techniques employed.

Special note: it is recognized that joint manipulation may be a controversial topic; however, it is beyond the scope of this article to present an exhaustive list on the points/counterpoints of whether or not to include lumbosacral manipulation as a component of a therapy regimen for low back pain patients. Therefore, it is being explicitly stated by the author that precautions and/or contra-indications should be strictly followed in all cases of the lumbosacral conditions discussed here. The reader is directed to the February 2009 white paper issued by the American Physical Therapy Association on thrust joint manipulation for additional information [80].

Post-laminectomy Syndrome

Interventional treatment

When considering treatment for low back pain associated with post-laminectomy syndrome, or failed back surgery syndrome (FBSS), observational based studies support neuromodulation by route of spinal cord stimulation (SCS) as a viable alternative to reoperation [81-83]. Outcomes of SCS are best achieved in the treatment of neuropathic pain, including radiculopathy. Patients with FBSS often have some component of epidural fibrosis or arachnoiditis [3,84], conditions that respond favorably to stimulation-effects because of the neurogenic nature. Within the spinal cord, pain signals mediated by afferent nerves are conducted through fibers of the dorsal column pathway. Upon positioning and alignment of electrodes dorsomedially to the spinal cord (i.e., in the epidural fat overlying the dorsal column, see Figure 9), the gate-control theory asserts that stimulation closes the gate to pain transmission [3,85]. Presently, the first multi-center, randomized controlled-trial (the EVIDENCE trial, NCT01036529) is recruiting subjects with FBSS to compare the therapeutic effectiveness and cost effectiveness of SCS therapy to spine reoperation (discectomy, laminotomy, laminectomy, foraminotomy, foraminectomy, fusion with or without instrumentation) [86].

Physical rehabilitation considerations

While functional improvements associated with pain relief are routinely clinically documented in patients with SCS systems for analgesia, Buonocore et al. [87] recently introduced discussion of improved strength independent of the analgesic effects induced by SCS in a single case. It is important to keep in mind that case report interpretation serves only as initial assessment of treatment safety, not conclusive evidence of treatment effectiveness. Thus, it is the opinion of this author that muscle strength and endurance in individuals with SCS systems intended for analgesia offers opportunity for methodical study. Perhaps such proposed future studies could be modeled, in part, from experimental use of SCS therapy in physical medicine and rehabilitation applications to reduce muscle spasticity and gait training for spinal cord injured patients [88], as well as to promote recovery in post-stroke patients [89].


In current practice, an exercise program that facilitates general conditioning and challenges posture is reasonable once SCS leads are completely healed in placed by scar tissue after implant, as such regimens may help some patients overcome activity-avoidance behaviors (kinesiophobia) by promoting optimal psycho-physical domains. In this view, a seminal analysis by Feirabend et al. [90] on the morphology of the dorsal column and juxtaposed fibers of the spinal cord under influence by SCS suggests no negative (or positive) effect on kinesthesia as a result of the stimulation.

Sacroiliac (SI) Joint

Interventional treatment

A variety of pain referral patterns have been linked to sacroiliac joint dysfunction: buttock pain; lumbar pain; groin pain; lower extremity pain; distal knee pain; and foot pain [37]. Of these referral zones, only the groin-pain-referral-pattern was found to be associated with response to SI joint blockade [91]. However, age-related changes can have a statistical significance on pain referral locations, with younger patients more likely to describe pain distal to the knee [37]. Refer to Figure 10 to view the International Spine Intervention Society suggested algorithm to investigate suspected SI-related pain.

When diagnostic blockade successfully ameliorates SI joint pain symptoms (see Figure 11), then radiofrequency (RF) ablation/denervation may be the appropriate next step in pain control [92,93]. For example, in one study, pain scores as reported using the visual analog scale, were decreased [greater than or equal to] 50% for a period of at least 6 months, and notably certain pre-RF abnormal physical findings (such as SI joint pain provocative tests) reverted to normal [93]. However, according to an analysis of the literature by Rupert et al. [94], the hierarchy of evidence for the efficacy of interventional SI joint procedures is, for the most part, currently limited to less stringent study protocols. Therefore, opportunities exist for rigorous interventional/physical medicine and rehabilitation based study designs that improve the outcomes data on SI blockades and/or RF ablation.



From a clinical perspective, because the SI joint is complex both morphologically and biomechanically [37,41,42], it is important to note that further testing by imaging and/or rheumatology assays may be needed to evaluate for rheumatoid arthritis or spondyloarthropathies-particularly in middle-aged patients where sacroiliitis may be indicative of early ankylosing spondylitis. Such tests may be ordered either simultaneously with SI joint blockade consultation or upon reports of unresponsive SI joint pain relief from diagnostic blocks or therapeutic injections at follow-up. It is noted here that radiographic plain films may not be sensitive to sacroiliitis in the early stages of the disease [95,96], and rheumatologic screens may exhibit false negatives [97]. Thus, a structured physical examination may be more appropriate [9799], as well as MRI examination of the SI joint [96,97,100].



Physical rehabilitation considerations

When SI joint pain exists in the absence of rheumatological or other lumbosacral conditions, SI joint dysfunction is suspected. Cibulka et al. [101] investigated the potential for SI joint dysfunction to be a precursor for hamstring strain, which implies early kinematic based detection via the associated effects on the metrics of gait analysis (i.e., step length, stride length, velocity, and cadence). The control group received moist heat and passive stretching, while the experimental group received the same treatment followed by SI joint manipulation. Results suggested a positive correlation exists between SI joint dysfunction and hamstring muscle strain. The interested reader may refer to Cibulka et al. [101] for a summarized description of the applied techniques. It is noted here that for this patient population (without known IVD herniation), SI joint manipulation was performed with the patient in the supine position, as opposed to the prone technique employed by Galm et al. [79] for those patients with IVD herniation. However, instrumentally over the long term, it is again emphasized that exercise regimens which incorporate gentle stretching of the hamstring muscles and body mechanics training are vital to acquire satisfactory lumbopelvic rhythm to not only achieve an optimal neutral spine during activities [77,78], but to also help avoid hamstring muscle strain as well as altered gait.

Special note: it is recognized that joint manipulation may be a controversial topic; however, it is beyond the scope of this article to present an exhaustive list on the points/counterpoints of whether or not to include lumbosacral manipulation as a component of a therapy regimen for low back pain patients. Therefore, it is being explicitly stated by the author that precautions and/or contra-indications should be strictly followed in all cases of the lumbosacral conditions discussed here. The reader is directed to the February 2009 white paper issued by the American Physical Therapy Association on thrust joint manipulation for additional information [80].



Lumbar Facet/Zygapophysial Joints Interventional treatment

Free nerve endings transmit nociceptive impulses from each facet joint and their joint capsules via segmental innervation from the medial branch of the dorsal ramus [31,102], and thus low back pain generated from the lumbar facet joints/capsules (such as due to trauma or arthritis) is transmitted by the medial branch nerves [102]. However, the medial branches of the dorsal rami are mixed nerves that also independently and segmentally innervate the lumbar multifidus muscles [30]. Per attachments on the individual lumbar FSUs, the lumbar multifidi dynamically stabilize the lumbar spine throughout segmental motion [29,30]. Furthermore, as noted in the kinesiology section above, multifidi are also integrated with facet joint capsules. An associated action of healthy multifidus activity retracts the lumbar facet joint capsules during joint articulation [30]. While this action helps prevent entrapment of the capsule by the articular surfaces (and any resultant associated pain), this functionality may be impaired in the compromised multifidus muscle.

Refer to Figure 12 to view the International Spine Intervention Society suggested algorithm to investigate suspected lumbar facet/zygapophysial joint-related pain. A positive response (pain relief achieved) to fluoroscopically guided diagnostic intra-articular (Figure 13) or medial branch blockade can provide evidence that a facet joint/capsule is the generator of low back pain (e.g., facetogenic in nature related to trauma or arthritis) (3). Subsequent to such confirmatory-diagnostic procedures, medial branch neurotomy by means of RF ablation (see Figure 14) is an option for treatment [103,104]. While a depiction of accurate placement of the RF probe is shown in Figure 14, the following neuro-anatomical review [10,30,31,102,103] is presented with respect to the L4 medial branch nerve:

1) The medial branch of the dorsal ramus associated with the L4 spinal nerve (i.e., the L4 medial branch nerve) lies within the junction of the transverse process and SAP associated with the L5 vertebral body.

2) At the transverse process/SAP junction, an ascending articular sensory branch supplies the caudal end of the L4-L5 facet joint, and a descending articular sensory branch supplies the cranial end of the L5-S1 facet joint.

3) Accordingly, the L4 medial branch nerve innervates the multifidus muscle acting on the L4 vertebral body.

The role of EMG as a tool to determine the outcome of RF ablation has been explored [103,104]. EMG studies performed one week pre- and one week post- neurotomy have shown that myoelectric silence associated with denervation of the multifidus is correlated with successful medial branch neurotomy [103]. However, Windsor [104] has argued that successful medial branch neurotomy is experimentally-achieved by doubling the sensory threshold obtained intraoperatively (i.e., acquired only by repeat intraoperative lesioning), and that denervation of the multifidus may be associated with suboptimal pain relief obtained by the patient. The latter is due to placement of the RF probe in relation to the mixed fibers (both sensory and motor neurons) within the medial branch nerve [104].

It is noteworthy to mention that a promising interventional treatment option for facetogenic pain is percutaneous placement of facet dowels (allographic bone) to pin the joints and thus limit motion/stabilize the spine. Advocates of this technique view this option as an early treatment step (less invasive) to lumbar fusion surgery. However, long-term outcomes (e.g., biomechanical effects or functional improvement measures) of the use of facet dowels are not yet available.

Physical rehabilitation considerations

Since the deeper fibers of multifidi are contiguous with facet joint capsules, therapeutic exercise is pivotal in the management of low back pain that is facetogenic in origin [105]. Further, MRI has been used to characterize activity levels and recruitment patterns of lumbar extensor muscles by looking at transverse relaxation times (T2-weighted images) following trunk extension exercise [106], and numerous MRI studies have investigated morphology and CSA of the lumbar paraspinal muscles in patients with low back pain [107-109]. Alternatively, Hides et al. [110] were among the first investigators to use diagnostic ultrasound to show ipsilateral multifidus muscle wasting in acute/subacute low back pain, and to subsequently compare MRI and sonography of the lumbar multifidus [111]. Currently, ultrasound imaging techniques are described to measure the lumbar multifidus CSA and reference ranges for the CSA are available [112], and good between-day repeatability has been demonstrated among a physical therapist (upon receiving a short-course in ultrasound imaging techniques) and skilled sonographers [113].

While ultrasound imaging reveals asymmetrical lumbar multifidus CSA (specifically, multifidus muscle wasting/atrophy) in acute unilateral back pain [32,109,113], CSA ultrasonographic images also show that spontaneous muscle recovery of the affected multifidus does not occur after resolution of acute or chronic low back pain without physical rehabilitation [29,105,114,115]. Further, it is reasonable to suggest, that therapeutic exercise in combination with interventional management of intra-articular generated and/or medial branch nerve transmitted facetogenic pain, such as due to arthritis or trauma, may offer the best treatment outcomes for long-term improvement to physical functioning. Currently, the author is exploring research opportunities for mapping the recovery of multifidus muscle function following medial branch neurotomy.


The scope of this article provided a brief analysis of the psycho-physical factors that contribute to functional outcomes associated with nonsurgical treatment of lumbosacral-related pain. To accomplish this, the article was heavily weighted on lumbosacral spine kinesiology--as related to pathomechanics and, when applicable, the study of biomechanics using imaging modalities--relative to select interventional pain medicine procedures. Pain interventionalists are those medical professionals who, by means of each physician's background, bring an extensive range of expertise for a united purpose, to treat patients who seek pain relief. It is imperative that such practitioners not only keep their expertise at close hand, but also work closely with physical rehabilitation specialists to provide continuity of care for their patients. Interventional-based pain control for lumbosacral pain may be optimized when practitioners combine therapeutic exercise regimens, as appropriate, into treatment plans to address both physical functioning and quality of life, as a typical spine pain patient often exhibits some degree of impaired spinal mobility that may impose functional limitations. It is equally important for spinal interventionalists to remain aware of the effects of pain-catastrophizing and kinesiophobia, which may, in part or in whole, contribute to any functional limitations noted.

Apart from the clinical questions with respect to surgical and nonsurgical approaches to treat low back pain that SPORT attempted to answer, the impetus behind SPORT was related to the insufficient evidence for many of the surgical approaches currently employed to treat such spinal-related pain [11]. Similarly, it is argued that there is insufficient data for many of the interventional pain medicine procedures (including those procedures discussed here) [116-118]. In practice, however, anecdotal evidence suggests spinal interventionalists and neurosurgeons/orthopaedic surgeons routinely work together for the benefit of the patient.

While the subjectivity of pain creates challenges to implementing randomized, placebo-controlled interventional pain medicine trials, such study designs are the goal and are being conducted (e.g., the EVIDENCE trial [86]). To this end, it is important to also encourage biomedical research initiatives to further develop conclusions and statements about diagnosis and treatment of lumbosacral pain [12]. For example, in the nearly two-decades since Drs. Aprill and Bogduk [64] first introduced the high-intensity-zone MRI sign (a simplistic and accurate marker for internal disc derangement available to any physician viewing T2-weight images), advances in MRI sequencing have produced more elaborate techniques, such as T1p{rho}-weighted images (Figure 15), which remain under-utilized because they are not widely available [119,120]. Finally, professional organizations such as the International Spine Intervention Society, the American Society of Interventional Pain Physicians, and the International Neuromodulation Society methodologically prepare guidelines based upon literature searches, literature synthesis, systematic review, open forum presentation, and blinded peer review to provide spinal interventionalists and others with up to date consensus on interventional techniques [2,121-123].


In summary, best practices in interventional spine care are aimed at restorative treatment goals that converge on improving quality of life. Interventional pain medicine is the medical practice by which the diagnosis of pain generators (such as discogenic or facetogenic pain) can subsequently allow treatment independently or in conjunction with other therapeutic activities. With a better understanding of the anatomy and kinesiology of the lumbar spine, spinal interventionalists and physical rehabilitation specialists can improve patient care for the nonsurgical treatment of lumbar spine and sacral etiologies. Finally, opportunities exist for physical rehabilitation specialists to contribute in a meaningful way to the collection of evidence for all procedures (surgical or nonsurgical) mentioned here.


[1.] The National Uniform Claims Committee. Specialty Designation for Interventional Pain Management--09.

[2.] Standards Committee of the International Spine Intervention Society. Spinal Diagnostic & Treatment Procedures. San Francisco, Ca: International Spine Intervention Society; 2004.

[3.] Raj, P.P. Practical Management of Pain. 3rd ed. St. Louis, Mo: Mosby Inc; 2000.

[4.] Medicare Payment Advisory Commission Report to Congress. Paying for Interventional Pain Services in Ambulatory Settings. December 2001.

[5.] Weinstein, J.N., Tosteson. T.D., and J.D. Lurie, et al. Surgical versus nonsurgical treatment for lumbar disk herniation: the spine patient outcomes research trial (SPORT) a randomized trial. JAMA 296:2441-2450, 2006.

[6.] Weinstein, J.N., Lurie, J.D., and T.D. Tosteson, et al. Surgical versus nonsurgical treatment for lumbar disk herniation: the spine patient outcomes research trial (SPORT) observational cohort. JAMA 296:2451-2459, 2006.

[7.] Weinstein, J.N., Lurie, J.D., and T.D. Tosteson, et al. Surgical versus nonsurgical treatment for degenerative lumbar spondylolisthesis. N Engl J Med 356:2257-2270, 2007.

[8.] Weinstein, J.N., Tosteson, T.D., and J.D. Lurie, et al. Surgical versus nonsurgical treatment for lumbar spinal stenosis. N Engl J Med 358:794810, 2008.

[9.] Birkmeyer, N.J.O., Weinstein, J.N., and A.N.A. Tosteson, et al. Design of the spine patient outcomes research trial (SPORT). Spine 27:1361-1372, 2002.

[10.] Bogduk, N. Low back pain. In: Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 187-214.

[11.] Truumees E. Surgical versus nonsurgical treatment: analyzing the SPORT data. SpineLine July/August 2007. pp 11-13.

[12.] Schaefer, G.O., Emanuel, E.J., and A. Wertheimer. The obligation to participate in biomedical research. JAMA 302:67-72, 2009.

[13.] Beattie, P.F. Structure and function of the bones and joints of the lumbar spine. In: Oatis, C.A. Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Pa: Lippincott Williams & Wilkins; 2004.

[14.] Bogduk, N. The inter-body joints and the intervertebral discs. In: Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 13-32.

[15.] Nachemson, A.L., and G. Elfstrom. Intravital dynamic pressure measurements in lumbar discs. A common study of movements, maneuvers and exercises. Scand J Rehabil Med 1(suppl):1-40, 1970.

[16.] Wilke, H.J., Neef, P., Caimi, M., Hoogland, T., and L.E. Claes. New in vivo measurements of pressures in the intervertebral disc in daily life. Spine 24:755-762, 1999.

[17.] Westbrook, C., Kaut-Roth, C., and J. Talbot. Image weighting and contrast. In: MRI in Practice. 3rd ed. Malden, Ma: Blackwell Publishing Inc; 2005. pp. 21-60.

[18.] Schnebel, B.E., Watkins, R.G., and W. Dillin. A digitizing technique for the study of movement of intradiscal dye in response to flexion and extension of the lumbar spine. Spine 13:309-312, 1988.

[19.] Beattie, P.F., Brooks, W.M., Rothstein, J.M., et al. Effect of lordosis on the position of the nucleus pulposus in supine subjects. A study using magnetic resonance imaging. Spine 19:2096-2102, 1994.

[20.] Alexander, L.A., Hancock, E., Agouris, I., Smith, F.W., and A. MacSween. The response of the nucleus pulposus of the lumbar intervertebral discs to functionally loaded positions. Spine 32:1508-1512, 2007.

[21.] McKenzie, R. The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikanae, New Zealand: Spinal Publications; 1981.

[22.] Bashir, W., Torio, T., Smith, F., Takahashi, K., and M. Pope. Alteration of water content in lumbar intervertebral discs related to variable sitting postures using whole-body positional MR imaging [abstract]. 2006; Radiologic Society of North America.

http: // nce/event display.cfm?em id=4441036. Accessed March 14, 2008.

[23.] Bashir, W., Torio, T., Smith, F., Takahashi, K., and M. Pope. The way you sit will never be the same! Alterations of lumbosacral curvature and intervertebral disc morphology in normal subjects in variable sitting positions using whole body positional MRI [abstract]. 2006; Radiologic Society of North America.

http: // nce/event display.cfm?em id=4435870. Accessed March 14, 2008.

[24.] McGill, S.M. Analysis of the forces on the lumbar spine during activity. In: Oatis, C.A. Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Pa: Lippincott Williams & Wilkins; 2004.

[25.] Willen, J., Schonstrom, N., and B. Danielson. Kinematic MRI of the lumbar spine: assessment in the axial-loaded, supine position. In: Shellock, F.G., and C.M. Powers. editors. Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, Fl: CRC Press; 2001. pp. 23-26.

[26.] Weishaupt, D., Wildermuth, S., Schmid, M.R., and J. Hodler. Kinematic MRI of the lumbar spine: assessment in the upright, seated position. In: Shellock, F.G., and C.M. Powers. editors. Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, Fl: CRC Press; 2001. p. 50.

[27.] Panjabi, M., Takata, K., and V.K. Goel. Kinematics of the lumbar intervertebral foramen. Spine 8:348-357, 1983.

[28.] Kostelic, J.K., Haughton, V.M., and L.A. Sether. Lumbar spinal nerves in the neural foramen: MR appearance. Radiology 178:837-839, 1991.

[29.] McGill, S.M., Mechanics and pathomechanics of muscles acting on the lumbar spine. In: Oatis CA. Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Pa: Lippincott Williams & Wilkins; 2004.

[30.] Bogduk, N. The lumbar muscles and their fascia. In: Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 101-126.

[31.] Bogduk, N. Nerves of the lumbar spine. In: Bogduk N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 127-144.

[32.] Lee, S.W., Chan, C.K., and T.S. Lam, et al. Relationship between low back pain and lumbar multifidus size at different postures. Spine 31:2258-2262, 2006.

[33.] Descarreaux, M., Lafond, D., Jeffrey-Gauthier, R., Centomo, H., and V. Cantin. Changes in the flexion relaxation response induced by lumbar muscle fatigue. BMC Musculoskelet Disord 9:10, 2008.

[34.] Bogduk, N. The zygapophysial joints. In: Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 33-42.

[35.] Nachemson, A. The load on lumbar disc in different positions of the body. Clin Orthop 45:107-122, 1966.

[36.] Christian, E. Structure and function of the bones and joints of the pelvis. In: Oatis, C.A. Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Pa: Lippincott Williams & Wilkins; 2004.

[37.] Slipman, C.W., Jackson, H.B., Lipetz, J.S., Chan, K.T., Lenrow, D., and J. Vresilovic. Sacroiliac join pain referral zones. Arch Phys Med Rehabil 81:334-338, 2000.

[38.] Forst, S.L., Wheeler, M.T., Fortin, J.D., and J.A. Vilensky. The sacroiliac joint: anatomy, physiology and clinical significance. Pain Physician 9:61-68, 2006.

[39.] Bogduk, N. The sacroiliac joint. In: Bogduk, N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. New York: Churchill Livingstone; 1997. pp. 177-186.

[40.] International Anatomical Nomenclature Committee: Nomina Anatomica. Baltimore, Md: Williams & Wilkins; 1983.

[41.] Irwin, R.W., Watson, T., Minick, R.P., and W.T. Ambrosius. Age, body mass index, and gender differences in sacroiliac joint pathology. Am J Phys Med Rehabil 86:37-44, 2007.

[42.] Walker, J.M. The sacroiliac joint: a critical review. Phys Ther 72:903-916, 1992.

[43.] Picavet, H.S.J., Vlaeyen, J.W.S., and J.S.A.G. Schouten. Pain catastrophizing and kinesiophobia: predictors of chronic low back pain. Am J Epidemiol 156:1028-1034, 2002.

[44.] French, D.J., France, C.R., Vigneau, F., French, J.A., and R.T. Evans. Fear of movement/(re)injury in chronic pain: a psychometric assessment of the original English version of the Tampa scale for kinesiophobia (TSK). Pain 127:42-51, 2007.

[45.] Dworkin, R.H., Turk, D.C., and J.T. Farrar, et al. Core outcome measures for chronic pain clinical trials: IMMPACT recommendations. Pain 113:9-19, 2005.

[46.] Fishbain, D.A., Abdel-Moty, E., and R. Cutler, et al. Measuring residual functional capacity in chronic low back pain patients based on the dictionary of occupational titles. Spine 19:872880, 1994.

[47.] Fishbain, D.A., Cutler, R.B., Rosomoff, H., Khalil, T., Abdel-Moty, E., and R. Steele Rosomoff. Validity of the dictionary of occupational titles residual functional capacity battery. Clin J Pain 15:102-110, 1999.

[48.] Fishbain, D.A. Functional capacity evaluation [letter]. Phys Ther 80:110-112, 2000.

[49.] Richardson, J., and G.J. Groen. Applied epidural anatomy. Continuing Education in Anaesthesia, Critical Care & Pain 5:98-100, 2005.

[50.] Raoul, S., Faure, A., and R. Robert, et al. Role of the sinu-vertebral nerve in low back pain and anatomical basis of therapeutic implications. Surg Radiol Anat 24:366-371, 2003.

[51.] Martin, M.D., Boxell, C., and D.G. Malone. Pathophysiology of lumbar disc degeneration: a review of the literature. Neurosurg Focus 13:E1, 2002.

[52.] Lawrence, J.P., Greene, H.S., and J.N. Grauer. Back pain in athletes. J Am Acad Orthop Surg 14:726-735, 2006.

[53.] Eisenberg, R.L., and N.M. Johnson. Skeletal System: Herniation of Intervertebral Disks. In: Comprehensive Radiographic Pathology. 3rd ed. St. Louis, Mo: Mosby Inc; 2003: pp. 146-150.

[54.] Ward, P., Backus, A., and C. Murphy. Lumbar Spine, Sacrum, and Coccyx. In: Bontrager K.L., and J.P. Lampignano. (eds). Textbook of Radiographic Positioning and Related Anatomy. 6th ed. St. Louis, Mo: Mosby Inc.; 2005. p. 331.

[55.] Sato, K., and S. Kikuchi. Critical analysis of two-level compression of the cauda equina and the nerve roots in lumbar spinal canal stenosis. Spine 22:1989-1903, 1997.

[56.] Chen, A.L., and J.M Spivak. Degenerative lumbar spinal stenosis: options for aging backs. Phys Sportsmed 31:25-34, 2003.

[57.] Westbrook, C., Kaut-Roth, C., and J. Talbot. Contrast agents in MRI. In: MRI in Practice. 3rd ed. Malden, Ma: Blackwell Publishing Inc; 2005. pp. 352-371.

[58.] Rajasekaran, S., Babu, J.N., Arun, R., Armstong, B.R.W., Shetty, A.P., and S. Murugan. A study on diffusion in human lumbar discs: a serial magnetic resonance imaging study documenting the influence of the endplate on diffusion in normal and degenerative discs. Spine 29:26542667, 2004.

[59.] Savolaine, E.R., Pandya ,J.B., Greenblatt, S.H., and S.R. Conover. Anatomy of the human lumbar epidural space: new insights using CT-epidurography. Anesthesiology 68:217-220, 1988.

[60.] Fukushige, T., Kano, T., and T. Sano. Radiographic investigation of unilateral epidural block after single injection. Anesthesiology 87:1574-1575, 1997.

[61.] Seeling, W., Tomczak, R., Merk, J., and I.N. Mrakov. Die CT-epidurographie. [CT-epidurography. Comparison of conventional and computed tomographic eipdurography with contrast medium injection using thoracic epidural catheters.] Anaesthetist 44:24-36, 1995.

[62.] Stevens, D.S., and A.D. Balkany. Appearance of the plica mediana dorsalis during epidurography. Pain Physician 9:268-270, 2006.

[63.] Wininger, K.L., Deshpande, K.K., and K.K. Deshpande. Radiation exposure in percutaneous spinal cord stimulation mapping: a preliminary report: Pain Physician 13:7-18, 2010.

[64.] Aprill C., and N. Bogduk. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 65:361-369, 1992.

[65.] Hwang, G.J., Suh, J.S., Na, J.B., Lee, H.M., and N.H. Kim. Contrast enhancement pattern and frequency of previously unoperated lumbar discs on MRI. J Magn Reson Imaging 7:575-578, 1997.

[66.] Kapural, L., and A. Goyle. Imaging for provocative discography and minimally invasive percutaneous procedures for treatment of discogenic lower back pain. Tech Reg Anesth Pain Manag 11:73-80, 2007.

[67.] Carragee, E.J., Don, A.S., Hurwitz, E.L., Cuellar, J.M., Carrino, J.A., and R. Herzog. Does discography cause accelerated progression of degeneration changes in the lumbar disc: a ten-year matched cohort study. Spine 34:2338-2345, 2009.

[68.] Kapoor, V., Rothfus, W.E., Grahovac, S.Z., and R.E. Latchaw. Radicular pain avoidance during needle placement in lumbar discography. AJR Am J Roentgen 181:1149-1154, 2003.

[69.] Goodman, B.S., Lincoln, C.E., Deshpande, K.K., Poczatek, R.B., Lander, P.H., and M.J. DeVivo. Incidence of intravascular uptake during fluoroscopically guided lumbar disc injections: a prospective observational study. Pain Physician 8:263-266, 2005.

[70.] Chang, G., Kim, H.J., Kaplan, D., Vunjak-Novakovic, G., and R.A. Kandel. Porous silk scaffolds can be used for tissue engineering annulus fibrosus. Eur Spine J 16:1848-1857, 2007.

[71.] Mizuno, H., Roy, A.K., Zaporojan, V., Vacanti, C.A., Ueda, M., and L.J. Bonassar. Biomechanical and biochemical characterization of composite tissue-engineered intervertebral discs. Biomaterials 27:362-370, 2006.

[72.] Gokorsch, S., Nehring, D., Grottke, C., and P. Czermak. Hydrodynamic stimulation and long term cultivation of nucleus pulposus cells: a new bioreactor system to induce extracellular matrix synthesis by nucleus pulposus cells dependent on intermittent hydrostatic pressure. Int J Artif Organs 27:962-970, 2004.

[73.] Sakai, D., Mochida, J., and Y. Yamamoto, et al. Transplantation of mesenchymal stem cells embedded in Atelocollagen[R] gel to the intervertebral disc: a potential therapeutic model for disc degeneration. Biomaterials 24:35313541, 2003.

[74.] Risbud, M.V., Albert, T.J., and A. Guttapalli, et al. Differentiation of mesenchymal stem cells towards a nucleous pulpuosus-like phenotype in vitro: implications for cell-based transplantation therapy. Spine 29:2627-2632, 2004.

[75.] Gruber, H.E., Hoelscher, G.L., Leslie, K., Ingram, J.A., and E.N. Hanley Jr. Three-dimensional culture of human disc cells within agarose or a collagen sponge: assessment of proteoglycan production. Biomaterials 27:371-376, 2006.

[76.] Richardson, C.A., Snijders, C.J., Hides, J.A., Damen, L., Pas, M.S., and J. Storm. The relationship between the transversus abdominis muscles, sacroiliac joint mechanics, and low back pain. Spine 27:399-405, 2002.

[77.] Saal, J.A., and J.S. Saal. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy: an outcome study. Spine 14:431-437, 1989.

[78.] Bridger, R.S., Orkin, D. and M. Henneberg. A quantitative investigation of lumbar and pelvic postures in standing and sitting. Interrelationship with body position and hip muscle length. Int J Ind Ergonomics 9:235-244, 1992.

[79.] Galm, R., Frohling, M., Rittmeister, M., and E. Schmitt. Sacroiliac joint dysfunction in patients with imaging-proven lumbar disc herniation. Eur Spine J 7:450-453, 1998.

[80.] American Physical Therapy Association. Position on Thrust Joint Manipulation Provided by Physical Therapists. American Physical Therapy Association. February, 2009. Available at: http: //www. apta. org/AM/Template. cfm?Section =State Gov t Affairs&Template=/CM/Content Display.cfm&ContentID=54885. Accessed August 9, 2010.

[81.] North R.B., Lanning, A., Hessels, R., and P.N. Cutches. Spinal cord stimulation with percutaneous and plate electrodes: side effects and quantitative comparisons. Neurosurg Focus 2:E3, 1997.

[82.] North, R.B., Campbell, J.N., and C.S. James, et al. Failed back surgery syndrome: a five-year follow-up in 102 patients undergoing repeated operation. Neurosurgery 28:685-691, 1991.

[83.] Bel, S., and B. Bauer. Dorsal column stimulation: cost-to-benefit analysis. Acta Neurochir Suppl 52:121-123, 1991.

[84.] Probst, C. Spinal cord stimulation in 112 patients with epi-/intradural fibrosis following operation for lumbar disc herniation. Acta Neurochi 107:147-151, 1990.

[85.] Melzack, R., and P.D. Wall. Pain mechanisms: a new theory. Science 150:971-978, 1965.

[86.] U.S. National Institutes of Health. Spinal cord stimulation with Precision(r) SCS System versus reoperation for failed back surgery syndrome (Evidence). Identifier: NCT01036529. Clinical Trials website. Accessed May 5, 2010.

[87.] Buonocore, M., Demartini, L., and C. Bonezzi. Improvement of muscle strength independently of analgesic effect following spinal cord stimulation. A case report. Eura Medicophys 40:273-275, 2004.

[88.] Herman, R., He, J., D'Luzansky, S., Willis, W., and S. Dilli. Spinal cord stimulation facilitates functional walking in a chronic, incomplete spinal cord injured. Spinal Cord 40:65-68, 2002.

[89.] Robaina, F., and B. Clavo. Spinal cord stimulation in the treatment of post-stroke patients: current state and future directions. Acta Neurochir Suppl 97:277-282, 2007.

[90.] Feirabend, H.K.P., Choufoer, H., Ploeger, S., Holsheimer, J., and J.D. van Gool. Morphometric of human superficial dorsal and dorsolateral column fibres: significance to spinal cord stimulation. Brain 125:1137-1149, 2002.

[91.] Schwarzer, A.C., Aprill, C.N., and N. Bogduk. The sacroiliac joint in chronic low back pain. Spine 20:31-37, 1995.

[92.] Hansen, H.C., McKenzie-Brown, A.M., Cohen, S.P., Swicegood, J.R., Colson, J.D., and L. Manchikanti. Sacroiliac joint interventions: a systematic review. Pain Physician 10:165-184, 2007.

[93.] Ferrante, M.F., King, L.F., and E.A. Roche, et al. Radiofrequency sacroiliac joint denervation for sacroiliac syndrome. Reg Anesth Pain Med 26:137-142, 2001.

[94.] Rupert, M.P., Lee, M., Manchikanti, L., Datta, S., and S.P. Cohen. Evaluation of sacroiliac joint interventions: a systematic appraisal of the literature. Pain Physician 12:399-418, 2009.

[95.] Rothchild, B.M., Poteat, G.B., Williams, E., and W.L. Crawford. Inflammatory sacroiliac joint pathology: evaluation of radiologic assessment techniques. Clin Exp Rheumatol 12:267-274, 1994.

[96.] Oostveen, J., Prevo, R., den Boer, J., and M. van de Laar. Early detection of sacroiliitis on magnetic resonance imaging and subsequent development of sacroiliitis on plain radiography. A prosective, longitudinal study. J Rheumatol 26:1953-1958, 1999.

[97.] Deshpande, K.K., and K.L. Wininger. Spinal cord stimulation for pain management in ankylosing spondylitis: a case report. Neuromodulation 12:54-59, 2009.

[98.] Poley, R.E., and J.R. Borchers. Sacroiliac joint dysfunction: evaluation and treatment. Phys Sportsmed 36:42-49, 2008.

[99.] Chen, Y.C., Fredericson, M., and M. Smuck. Sacroiliac joint pain syndrome in active patients: a look behind the pain. Phys Sportsmed 30:3037, 2002.

[100.] Blum, U., Buitrago-Tellez, C., and A. Mundinger, et al. Magnetic resonance imaging (MRI) for detection of active sacroiliitis-a prospective study comparing conventional radiography, scintigraphy, and contrast enhanced MRI. J Rheumatol 23:2107-2115, 1996.

[101.] Cibulka, M.T., Rose, S.J., DeLitto, A., and D.R. Sinacore. Hamstring muscle strain treated by mobilizing the sacroiliac joint. Phys Ther 66:1220-1223, 1986.

[102.] Bogduk, N., and D.M. Long. The anatomy of the so-called "articular nerves" and their relationship to facet denervation in the treatment of low-back pain. J Neurosurg 51:172-177, 1979.

[103.] Dreyfuss, P., Halbrook, B., Pauza, K., Anand, J., McLarty, J., and N. Bogduk. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine 25:12701277, 2000.

[104.] Windsor, R.E. Radiofrequency lumbar zygapophysial (facet) joint denervation: a preliminary report of a new concept. Pain Physician 6:119-123, 2003.

[105.] Koumantakis, G.A., Watson, P.J., and J.A. Oldham. Trunk muscle stabilization training plus general exercise versus general exercise only: randomized controlled trial of patients with recurrent low back pain. Phys Ther 85:209-225, 2005.

[106.] Mayer, J.M., Graves, J.E., Clark, B.C., Formikell, M., and L.L. Ploutz-Snyder. The use of magnetic resonance imaging to evaluate lumbar muscle activity during trunk extension exercise at varying intensities. Spine 30:25562563, 2005.

[107.] Flicker, P.L., Fleckenstein, J.L., and K. Ferry, et al. Lumbar muscle usage in chronic low back pain. Magnetic resonance image evaluation. Spine 18:582-586, 1993.

[108.] Ranson, C.A., Burnett, A.F., Kerslake, R., Batt, M.E., and P.B. O'Sullivan. An investigation into the use of MR imaging to determine the functional cross sectional area of lumbar paraspinal muscles. Eur Spine J 15:764-773, 2006.

[109.] Kjaer, P., Bendix, T., Sorensen, J.S., Korsholm, L., and C. Leboeuf-Yde. Are MRI-defined fat infiltrations in the multifidus muscles associated with low back pain? BMC Med 5:2, 2007.

[110.] Hides, J.A., Stokes, M.J., Saide, M., Jull, G.A., and D.H. Cooper. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 19:165-172, 1994.

[111.] Hides, J.A., Richardson, C.A., and G.A. Jull. Magnetic resonance imaging and ultrasonography of the lumbar multifidus muscle. Comparison of two different modalities. Spine 20:54-58, 1995.

[112.] Stokes, M., Rankin, G., and D.J. Newham. Ultrasound imaging of lumbar multifidus muscle: normal reference ranges for measurements and practical guidance on technique. Man Ther 10:116-126, 2005.

[113.] Pressler, J.F., Heiss, D.G., Buford, J.A., and J.V. Chidley. Between day repeatability and symmetry of multifidus cross-sectional area measured using ultrasound. J Orthop Sports Phys Ther 36:10-18, 2006.

[114.] Hides, J.A., Richardson, C.A., and G.A. Jull. Multifidus muscle recovery is not automatic after resolution of acute, first episode low back pain. Spine 21:2763-2769, 1996.

[115.] Hides, J.A., Jull, G.A., and C.A. Richardson CA. Long-term effects of specific stabilizing exercises for first-episode low back pain. Spine 26:E243-E248, 2001.

[116.] Chou, R., Atlas, S.J., Stanos, S.P., and R.W. Rosenquist. Nonsurgical interventional therapies for low back pain: a review of the evidence for an American Pain Society clinical practice guideline. Spine 34:1078-1093, 2009.

[117.] Staal, J.B., de Bie, R.A., de Vet, H.C., Hildebrandt, J., and P. Nelemans. Injection therapy for subacute and chronic low back pain: an updated Cochrane review. Spine 34:49-59, 2009.

[118.] Manchikanti, L., Datta, S., Derby, R., Wolfer, L.R., Benyamin, R.M., and J.A. Hirsch. A critical review of the American Pain Society clinical practice guidelines for interventional techniques: Part 1. Diagnostic interventions. Pain Physician 13:E141-E174, 2010.

[119.] Nguyen, A.M., Johannessen, W., and J.H. Yoder, et al. Noninvasive quantification of human nucleus pulposus pressure with use of T1{rho}weighted magnetic resonance imaging. J Bone Joint Surg Am 90:796-802, 2008.

[120.] Witschey, W.R.T., Borthakur, A., and M.A. Elliott, et al. T1 p-prepared balanced gradient echo for rapid 3D T1 p MRI. J Magn Reson Imaging 28:744-754, 2008.

[121.] Manchikanti, L., Boswell, M.V., and V. Singh, et al. Comprehensive evidenced-based guidelines for interventional techniques in the management of chronic spinal pain. Pain Physician 12:699802, 2009.

[122.] International Neuromodulation Society. Ethical and legal aspects of neuromodulation: on the road to guidelines. Neuromodulation 10:177186, 2007.

[123.] Deer, T., Krames, E., and S. Hassenbusch, et al. Future directions for intrathecal pain management: a review and update from the Interdisciplinary Polyanalgesic Consensus Conference 2007. Neuromodulation 11:92-97, 2008.

Kevin L. Wininger, BS RTR, RTK Orthopaedic & Spine Center, Columbus, Ohio


Kevin L. Wininger, BS, RTR, RKT

Orthopaedic & Spine Center

1080 Polaris Parkway, suite 200

Columbus, Ohio 43240

Business phone: (614) 468-0300

Business fax: (614) 468-0212

Table 1. Summary of the effects of posture on the structures of
the lumbar spine.

                                               Supine      Axial-
                                  Prone          No       load 50%
                                  Lying         Load        body
  L3-L4 disc [15]            --                250 N     --
  L4-L5 disc [16]            --                25/20     --

Migration of
nucleus                      --                --        --

content (22,23)
  L4-L5 disc                                   41.9%
  L5-S1 disc                 --                39.6%     --

Thecal Sac                                               ** varies
  CSA (25,26)                --                --        by 10-50

Foramina (27)

L4& L5
CSA ([dagger]) and
EMG (24,32)
  --Healthy population       7.42 [cm.sup.2]   --        --

  --LBP patient population   7.03 [cm.sup.2]   --        --

                                Standing        40 * Forward

  L3-L4 disc [15]            500 N             1000 N
  L4-L5 disc [16]            100/100           150/225

Migration of
nucleus                      --                posterior

content (22,23)
  L4-L5 disc
  L5-S1 disc                 --                --

Thecal Sac
  CSA (25,26)                --                --

Intervertebral                                 20%
Foramina (27)                                  [up arrow]

L4& L5
Multifidus                                     Flexion-
CSA ([dagger]) and                             relaxation
EMG (24,32)                                    phenomenon
  --Healthy population       8.53 [cm.sup.2]
                                               silence (33)
  --LBP patient population   7.58 [cm.sup.2]
                                               occurs earlier

                                            Sitting, 90 *
                              Extension          No

  L3-L4 disc [15]            --             700 N
  L4-L5 disc [16]            --             135/90

Migration of
nucleus                      anterior       --

content (22,23)
  L4-L5 disc
  L5-S1 disc                 --             --

Thecal Sac
  CSA (25,26)                --             --

Intervertebral               24-30%
Foramina (27)                [down arrow]

L4& L5
CSA ([dagger]) and
EMG (24,32)
  --Healthy population       --             --

  --LBP patient population   --             --

                             Sitting, 90 *       Sitting
                               Supported         Flexion

  L3-L4 disc [15]            400 N            --
  L4-L5 disc [16]            --               185/175

Migration of
nucleus                      --               posterior

content (22,23)
  L4-L5 disc                 34.7%            32.7%
  L5-S1 disc                 31.8%            29.2%

Thecal Sac
  CSA (25,26)                150 [mm.sup.2]   170 [mm.sup.2]

Foramina (27)

L4& L5
CSA ([dagger]) and
EMG (24,32)
  --Healthy population       --               --

  --LBP patient population   --               --

                                Sitting          25 * & 45 *
                                 135 *             Forward
                               Extension          Stooping

  L3-L4 disc [15]                             --
  L4-L5 disc [16]            --/55            --

Migration of
nucleus                      anterior

content (22,23)
  L4-L5 disc                 37.6%
  L5-S1 disc                 36.1%            --

Thecal Sac
  CSA (25,26)                110 [mm.sup.2]   --

Foramina (27)

L4& L5
Multifidus                                    25 *
CSA ([dagger]) and                              7.75 [cm.sup.2]
EMG (24,32)                                   45 *
  --Healthy population       --                 7.12 [cm.sup.2]

  --LBP patient population   --               25 *
                                                7.89 [cm.sup.2]
                                              45 *
                                                7.10 [cm.sup.2]

* Percentages above or below a standardized measure (100% for
standing) [15,16], with representative notation presented as
Nachemson / Wilke.

** Variance of thecal sac cross sectional area (CSA) under-load
from a range in supine no-load, psoas muscle relaxed, position of
250 to 50 [mm.sup.2].

([dagger]) Multifidus CSA represents the mean value calculated
from the average CSAs for the left L4, left L5, right L4, and
right L5 multifidi per posture.

Key: N = Newton, the International System of Units derived unit
of force; [up arrow] = increase; [down arrow] = decrease.

Table 2. Muscles and ligaments important to the lumbar spine. (29-31)

Fasciaand       Muscles:        Ligaments:      Ligaments:
muscles:        movement        posterior       vertebral bodies &
dynamic         (29,30)         lumbar spine    IVD (29,30)
stabilization                   (29,30)

Thoracolumbar   Longissimus-    Supraspinous    Anterior longitudinal
fascia          thoracis        ligament        ligament

Quadratus       Iliocostalis-   Interspinous    Posterior longitudinal
lumborum        lumborum        ligament        ligament

Transverse      Rectus          Ligamentum
abdominis       abdominis       flavurn

Internal                        Iliolumbar
oblique                         ligament


([dagger])  Innervated by the medial branch of the dorsal ramus,
independently and segmentally. (31)
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Author:Wininger, Kevin L.
Publication:Clinical Kinesiology: Journal of the American Kinesiotherapy Association
Article Type:Report
Geographic Code:1USA
Date:Sep 22, 2010
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