CHAPTER 82 An Algorithmic Methodology
Lumbosacral radiculopathy is defined as the neurophysiologic dysfunction of the nerve roots affecting both motor and sensory fibers in varying proportions. Signs and symptoms of motor fiber involvement include paresis and atrophy, hyporeflexia, fatigue, cramps, or fasciculations. Sensory abnormalities can range from mild distal paresthesias to anesthesia, dysesthesias, or severe pain. These painful symptoms may be the sole complaint of the patient, while in other instances motor deficits may predominate.1 Nerve root pain can appear in any anatomical area subserved by that nerve root. Hence, any region between the midline spinous processes and lower extremity digits, may be perceived as painful to the patient due to nerve root irritation. Although radicular pain can occur in the absence of overt weakness, it can be quite impairing for the patient, and can represent a challenge to the treating spine care specialist.
Lumbosacral (L/S) nerve root injury can occur anywhere along its long subarachnoid course through the cauda equina within the spinal canal. Clinical clues for segmental localization are less reliable than in the cervical spine.1 The L/S nerve roots exit from the intervertebral disc space below their respective vertebral body. Hence, in the lower limb, sensory deficits may be a more reliable discriminator of the involved level than motor impairments.1 Accurate localization allows for an accurate diagnosis, and both are necessary for successful treatment.
THE ETIOLOGIES AND IMITATORS OF LUMBOSACRAL RADICULOPATHY
The chief complaint of limb pain greater than axial pain typifies radicular symptomatology, but can also be present in other conditions. Sacroiliac joint dysfunction can present with gluteal and proximal lower limb pain.2–4 Piriformis syndrome, as described by Yeoman in 1928,5 represents a constellation of symptoms including limb pain and/or paresthesias with or without gluteal or lumbar pain.6–8 Intrinsic hip joint pathology, such as osteoarthritis, will present with gluteal, groin, or anteromedial thigh pain.9 Strain injuries to the hamstring musculature will cause complaints of soreness and pain in the posterior thigh. Pain in the region of the greater femoral trochanter, buttock, or lateral thigh depicts greater trochanteric pain syndrome, has a 20% prevalence in patients referred to surgical spine specialists,10 and can mimic symptoms of lumbar radiculopathy.11 Lumbosacral plexopathy or peripheral nerve entrapment, such as meralgia paresthetica, can also approximate radicular symptoms. Various spinal structures such as the intervertebral disc, dura, ligaments, or zygapophyseal joints may refer pain distally. However, the primary complaint in these instances is axial pain sometimes associated with less severe lower limb symptomatology.
Since Mixter and Barr’s seminal paper in 1934,12 the intervertebral disc has widely been recognized as a cause of L/S radiculopathy. However, several other etiologies of L/S radiculopathy have been annotated. Central or lateral canal stenosis13,14 can arise due to an array of causes: congenitally short pedicles, ligamentum flavum buckling, facet joint arthropathy, vertebral body hyperostosis, spondylolisthesis, spinal tumors, or spinal cysts. Intraspinal cysts may evolve as a consequence of the degeneration of the zygapophyseal joint,15 ligamentum flavum,16 posterior longitudinal ligament,17 dura mater,18 or chronic spondylolysis,19 and can arise from the root sheath itself.20 Diabetic patients are prone to thoracic radiculopathy,21 perhaps due to intraneural absorption of sorbitol while confined by a nonexpansile dural sheath. Extraforaminal compression by the L/S ligaments may also result in lumbar radiculopathy.22
PATHOPHYSIOLOGY OF LUMBOSACRAL RADICULOPATHY
Mixter and Barr’s landmark description in 193412 had led many spine care practitioners to suspect intervertebral disc (IVD) herniation to be causative in a variety of lumbar radicular pain syndromes. The implicit premise has been that biomechanical compression of neural elements was the sole etiologic factor leading to the manifestation of signs and symptoms.23 However, there is evidence that mechanical influence is not the sole etiologic factor.24–33 There is little correlation between the severity of radiculopathy and the size of the disc herniation.25,28,29 Resolution of symptoms after conservative treatment has been observed without a concurrent reduction in disc herniation volume.28,29 Mixter and Ayer, a year after Mixter and Barr’s hallmark paper, demonstrated that radicular pain could occur without significant disc herniation.30 However, it was not conclusive if this ‘radicular pain’ was nerve-root mediated or somatically referred from another spinal structure. It is probable that, in most instances, biomechanical injury is not the singular cause for the expression of lumbar radicular symptoms related to lumbar intervertebral disc herniation.
Early observations by Lindahl and Rexed32 in 1951 established the presence of pathologic changes including inflammatory cells in nerve roots of patients suffering from sciatica. Subsequent animal studies have demonstrated autoimmune and inflammatory reactions to autogenous nucleus pulposus.34,35 The human intervertebral disc has been shown to be a potent source of phospholipase A2,31 a regulator of the inflammatory cascade which causes perineural inflammation, conduction block, axonal injury,36 and dorsal root demyelination and mechanically induced ectopic discharges in the rat animal model.37 Herniated lumbar intervertebral discs have been observed to spontaneously produce increased amounts of other potentially neurotoxic inflammatory mediators.38 A rapid transport route may exist, bridging the epidural space and intraneural capillaries, providing quick access for this nuclear material to spinal nerve axons.39,40
In stark contrast to the peripheral nerve, the nerve root lacks a perineurium, which provides tensile strength and a diffusion barrier.41,42 Consequently, the nerve root possesses less resilience to tension forces and chemical irritants.42 Furthermore, the epineurium, which provides mechanical cushion to resist compression, is less abundant or developed in the nerve root.42 Within the nerve root itself the fasciculi do not branch to form a plexiform pattern; instead, they run in parallel, loosely held together by connective tissue.41,42 Hence, the nerve root is not as well suited to withstand either mechanical or chemical insult as compared to a peripheral nerve. Furthermore, once the inflammatory cascade is initiated, the nerve root lymphatic system is poorly equipped to adequately clear the inflammatory mediators.42 An inflamed nerve root is thus predisposed to a chronic inflammatory reaction with invasion by fibroblasts with eventual development of intraneural fibrosis.42
Cadaveric studies have discovered a functional tethering of the nerve root to the intervertebral foramen.42,43 When an intervertebral disc herniates in a posterior or posterolateral fashion, the exiting nerve root is placed under tension and not always compressed.42 The ensuing inflammatory response sensitizes the involved nerve root, decreasing its resilience to biomechanical influences. An inflamed nerve will fire repetitively with just minor perturbations; whereas a nonirritated nerve will tolerate more vigorous manipulation without prolonged firing patterns.41,44 The length to which a nerve root must be stretched for it to incur neurophysiologic dysfunction is believed to be 10–15% of resting length.45,46 Clinically, nerve root irritability can be appreciated by elevating the involved lower limb with the knee extended, straight leg raising (SLR). Goddard and Reid43 demonstrated stretch without displacement of the nerve root upon raising the affected limb 20–30° to 70°. Since no nerve root motion is occurring, the radicular pain elicited by this maneuver is a consequence of nerve root tension.43 In asymptomatic patients this movement is nonpainful despite the same amount of tension placed on the neural elements. However, intraforaminal disc herniation or herniation in the presence of spinal stenosis may inflict a biomechanical compromise to the nerve root that may have implications for successful treatment.
The ramification of this growing body of evidence supporting a biochemical paradigm is an evolution of minimally invasive therapeutic interventions. Less than 15% of L/S radiculopathies will eventually require surgical correction.47 Thus, a large proportion of cases can be successfully managed conservatively.25 Conservative care includes physical therapy, oral antiinflammatory medications, and precision intraspinal injections; yet, as interventional spine care continues to evolve, further minimally invasive interventions are being offered. Directing a successful plan of care hinges on accurately diagnosing the patient’s condition. Diagnosing L/S radiculopathy does not always create a mystery for the spine clinician. However, proficiently maneuvering through the list of differential diagnoses, utilizing evidence-based medicine, and accounting for the pharmacologic effects of injected medications requires an appropriate algorithmic approach. This systematic evaluation relies upon thorough history acquisition and physical examination, the accurate assessment of imaging studies, astute electrodiagnostic examinations, and the appropriate use of diagnostic block injections.
THE CLINICAL APPROACH TO LUMBOSACRAL RADICULOPATHY
Although radicular pain is categorically defined as limb pain greater than axial pain, occasionally, a patient might report paramedian lumbar pain that could be perceived as back pain. However, this region of discomfort may very well represent the sole region exhibiting painful nerve root symptoms. Yet, the spine clinician must recognize the overlap of referral patterns of pain emanating from nerve root, zygapophyseal joint, intraspinal ligament, intervertebral disc, sacroiliac joint, trochanteric bursa, or the piriformis muscle, and then perform a probability analysis of which structure, or segmental level, is likely generating the symptomatology. Lumbosacral radicular symptoms commonly arise in conjunction with focal intervertebral disc pathology12 or spinal stenosis.13 Disc herniations can lead to functional stenosis and a clinical picture of neurogenic claudication. However, symptom onset associated with disc herniation commonly occurs explosively after a short stint of axial pain or symptoms, and are exacerbated by prolonged sitting or Valsalva maneuvers. Neurogenic claudication due to spinal stenosis progresses more insidiously and its symptoms are exacerbated by prolonged standing and walking. Typically, patients will report bilateral or unilateral lower limb paresthesias, weakness, fatigue, or heaviness that is absent at rest and precipitated by walking that eventually persuades them to stop and rest.48 The patient’s walking tolerance, the point at which pain forces the patient to stop and rest, is usually twice the distance at which discomfort is first felt.48 Assuming a forward stooping posture may dissipate some of the symptoms, and the capability to walk further while traveling uphill, in contrast to downhill, can discriminate between neurogenic and vascular claudication.
No clinical features characteristically identify sacroiliac joint-mediated pain.49 However, a history of a direct fall onto the buttock, rear-end motor vehicle accident (with the ipsilateral foot on the brake), and a fall into a hole (with one foot in the hole and the other extended outside) provides a potential mechanism of injury.49 Patients suffering from greater trochanteric pain syndrome have difficulty sleeping on the affected side,10 and may experience worsening symptoms during ambulation or squatting. Piriformis syndrome is most commonly due to overuse or trauma.8 Magnetic resonance imaging studies have suggested the presence of effacement of the fatty sciatic foramen in elite athletes diagnosed with piriformis syndrome.8 Lumbosacral plexopathy can be due to pelvic trauma, hip arthroplasty, pelvic or gastrointestinal neoplasms, and autoimmune or vascular disorders.1 Meralgia paresthetica, lateral femoral cutaneous neuropathy, can be due to compression by tight belts, corsets, seatbelts, psoas muscle tumor, or prolonged hip flexion.1
Physical examination findings can be helpful in formulating a differential diagnosis, and help guide the diagnostic work-up. Yet, the distribution of radicular pain in radiculopathy appears to be the only sensitive, thus useful, sign indicating the segmental level of disc herniation.50 In the authors’ experience at the Penn Spine Center, upper buttock radicular pain has proven to be a manifestation of L4 nerve root-mediated pain, midgluteal pain a representation of L5 root pain, and lower gluteal pain an expression of S1 root pain. Limb pain referred from the L4 nerve root may trigger painful symptoms solely in the anterior knee and/or medial ankle, while L5 nerve root pain may masquerade as isolated lateral knee and/or dorsal foot symptomatology (Fig. 82.1). Although lateral thigh and lateral calf pain characterizes L5 nerve root involvement, posterolateral thigh and posterolateral calf pain implicates S1, or L5 and S1 fiber alterations. Meticulously differentiating between lumbar pain and buttock pain is imperative as patients may refer to both synonymously, but to the interventional spine clinician each indicates different potential pain generators. Employing various dural tension maneuvers will help illuminate the pattern of pain referral into the lower limb. Straight leg raising (SLR), reproducing radicular pain between 20–30° and 70°,43 seems to be sensitive, while crossed SLR is more specific for the level of disc herniation.50 Reverse SLR with the patient prone, will assess upper lumbar nerve root fibers. Sensory impairments are less reliable and the diagnostic value of historical findings remains unclear.50 Vibratory sensation abnormalities in dermatomal distributions may be the most reliable measure of sensory disturbances.51
Repetitive motor examination maneuvers such as repetitive calf raises, will elicit subtle motor weakness not detected on static manual muscle testing. When assessing strength statically, the examiner should place the muscle at a biomechanical disadvantage to completely reveal a deficit. Typically, L2 myotomal strength is assessed by hip flexion, L3 by knee extension, L4 by ankle dorsiflexion, L5 by great toe extension, and S1 by ankle plantar flexion. Yet, an astute spine clinician must be aware of anomalous innervation patterns in transitional spinal segments. In instances of sacralization of L5, myotomal innervation patterns overlap so that an L5 radiculopathy may present clinically as L5, S1, or both. Conversely, in lumbarization of S1, innervation patterns are more discrete and clinical findings correlate more closely with the expected compromised nerve root.52
DIAGNOSTIC EVALUATION
Treatment failure may reflect an inaccurate diagnosis, ineffective treatment, or misguided intervention. Lumbosacral radicular symptoms that have not responded to conservative care or are incapacitating for the patient warrant further diagnostic studies to clarify the diagnosis and redirect treatment strategies. Accurately diagnosing the etiology of lower limb pain requires astute and thorough history gathering and physical examination, and the appropriate prescription of imaging studies, electrodiagnostic evaluation, and precision diagnostic injections. These diagnostic evaluations are appropriately divided into visual anatomic, neurophysiologic, and functional diagnostic assessments.53 Plain radiography, radionuclide imaging, myelography, computed tomography, and magnetic resonance imaging constitute the visual anatomic studies. Neurophysiologic tests include electromyography (EMG) and nerve conduction studies (EDX). Anesthetizing injections have been termed functional tests because patient participation is essential to identify the abolition of their typical pain complaints (see Chs 16, 17, 18, 19).53 Although these diagnostic tools have been thoroughly discussed, the following will highlight their clinical utility in evaluating L/S radiculopathy.
Visual anatomic tests
Plain radiography
Plain films of the L/S spine detail the osseous structures of the vertebral column. However, radiographs have a limited capacity to identify soft tissue abnormalities within the spinal canal. Lumbar flexion–extension views can identify gross segmental instability, which may cause L/S radiculopathy due to central or foraminal stenosis. The identification of anomalous segmentation, spondylolysis, or spondyl-olisthesis on plain films may increase one’s suspicion of these entities as the etiology of the spinal pain. However, further diagnostic testing is required to confirm this suspicion because these conditions are commonly encountered in the asymptomatic population. Yet, the presence of anomalous segmentation should alert the spine clinician to the possibility of atypical nerve root pain due to altered innervation patterns.52 Except for these entities or when the presence of fracture, malignancy, or infection are suggested by history, plain films are of little value in the investigation of L/S radiculopathy. At the Penn Spine Center, for the most part, the authors utilize plain films to assess for gross segmental instability (excessive sagittal translation, rotation, or sagittal angulation), segmentation anamolies, spondylolysis, spondylolisthesis, compression fracture, and disc height when considering percutaneous discectomy.
Myelography
Myelography’s utility in diagnosing clinically significant spinal abnormalities was first investigated in 1967. Hitselberger and Witten24 observed a lumbar myelographic abnormality in 24% of 71 examinations in adults 18–76 years of age (mean, 51) without complaints of lumbar or L/S radicular pain. Although myelography has been highly sensitive in detecting a posterolateral disc protrusion in the nonoperated lumbar spine,54 its ability to reveal a central protrusion at the L5–S1 level is impaired due to this segment’s large epidural space.55 In addition, myelography is incapable of detecting a lateral disc herniation, beyond the spread of the contrast column ending at the neural foramen (termination of the dura),56 and relatively incapable of demonstrating foraminal stenosis. Myelography cannot differentiate epidural fibrosis from recurrent disc herniation or other extradural lesions in the postoperative patient, and its accuracy in this patient population has been demonstrated to be as low as 24%.57 Currently, myelography is rarely used as the sole imaging study in the work-up of L/S radiculopathy, due its limitations, except in extenuating circumstances such as severe scoliosis or metallic implants that would cause artifact on both magnetic resonance imaging (MRI) and computed tomography (CT).
Computed tomography
Computed tomography is useful to delineate bony detail, which can be helpful in preoperative planning. Wiesel et al.26 found a false-positive rate of 35.4% in 52 asymptomatic individuals undergoing computed axial tomography. In subjects less than 40 years of age, disc herniation was identified in 19.5%. In subjects over 40 years of age, 26.9% demonstrated herniated discs, 10.4% facet joint disease, and 3.4% stenosis.26 The sensitivity of CT images in identifying neurocompressive lesions has been reported to be 91%.58 In patients with L/S radiculopathy who have not undergone surgery, CT images adequately resolve disc abnormalities such as lateral and far lateral herniations, bulging annuli, ligamentum flavum hypertrophy, vacuum disc phenomenon, facet arthrosis, endplate sclerosis, and foraminal or central canal stenosis. Sagittal and coronal reconstructed sequences improve the diagnostic accuracy and should be utilized in all instances. However, the sensitivity of CT in evaluating the postoperative patient decreases to 71%.59 Hence, CT is a useful assessment tool in the evaluation of the spine patient, without previous history of spine surgery, with signs and symptoms of L/S radiculopathy, and its sensitivity approaches that of MRI, especially when performed after myelography. Contrast enhanced MRI remains the anatomic test of choice in the postoperative spine. The authors rely on CT to evaluate for etiologies of L/S radiculopathy in two circumstances. When MRI is contraindicated, such as with pacemakers, or to assess boney stenosis, multiplanar reformatted CT scan is used. In patients who have hardware in place, image artifact often impairs the ability to visualize the discs that are of concern with MRI.
Magnetic resonance imaging
The sensitivity of MRI for the detection of lumbar spinal abnormalities approaches 100% and has been reported to be as high as 96% in the postoperative patient.60 Although MRI is highly sensitive, its clinical, not radiologic, specificity is lacking. Boden et al.27 found abnormalities on MRI scans of lumbar spines in 28% of asymptomatic subjects, 24% demonstrated herniated nucleus pulposus (HNP), and 4% stenosis. In subjects less than 60 years old, 20% had HNP, while 57% of those over 60 years of age demonstrated HNP and stenosis, and the proportion of degenerative discs increased with advancing age.27 However, no study attempted to differentiate disc protrusions from disc extrusions until the 1994 publication by Jensen et al.33 Their work showed that 64% of 98 asymptomatic subjects had an intervertebral disc abnormality, 52% of which had a bulge at one level, 27% a protrusion, and 1% an extrusion.33 The presence of intervertebral disc extrusion may be significant and causally related to nerve root injury.25,29,61 Determining the clinical significance of abnormalities discovered on MR imaging has led to the increased use of diagnostic injection procedures in this patient population.53,62–68 The authors’ algorithmic approach to L/S radiculopathy involves the judicious use of precision, fluoroscopically guided diagnostic spinal injections when necessary to better elucidate the level of clinically relevant pathology.
Neurophysiologic evaluation
Electrodiagnostic medicine allows the physician to assess the neurophysiologic correlate of anatomical findings, and is an extension of the physical examination.69 If imaging studies corroborate the physician’s clinical impression, accurate treatment can be instituted. If imaging studies are equivocal, or the clinical findings are nondiagnostic, electrodiagnostic evaluations are pursued. Motor nerve conduction studies provide prognostic information regarding the recovery of motor function. The differential diagnosis for foot drop includes L5 radiculopathy, peroneal neuropathy at the fibular head, sciatic neuropathy involving the peroneal division, and alpha motor neuron disease. Although a thorough physical examination will typically detect a myotomal pattern rather than peripheral nerve pattern of weakness, the needle electrode examination can verify the diagnosis. For example, a physiatrist was consulted to evaluate an inpatient psychiatric patient with a chief complaint of isolated lateral ankle pain seemingly confined to the lateral malleolus. Plain radiography and a subsequent MRI of the foot and ankle were negative for osseous or soft tissue injury. Physical examination revealed subtle ankle inversion and great toe dorsiflexion weakness. Nerve conduction studies were normal, but electromyography revealed mild muscle membrane irritability in the lower lumbar paraspinals, and increased recruitment frequencies in the tibialis anterior, extensor hallicus longus, and tensor fascia lata of normal-appearing motor unit potentials. A follow-up lumbar spine MRI demonstrated a focal disc protrusion at L4–5 dorsally displacing the traversing L5 nerve root. The patient responded to conservative treatment, comprised of L/S stabilization, core conditioning, and oral antiinflammatory medications, once it was correctly directed at the accurate diagnosis. Similarly, in diabetic patients with preexisting peripheral neuropathy and a new complaint of anterior thigh pain, an electrodiagnostic study can detect a superimposed radiculopathy versus diabetic amyotrophy or mononeuropathy1 Needle electrode examination will characteristically detect acute membrane irritability in proximal limb muscles of a myotomal distribution or in the muscles innervated by the femoral nerve, respectively, in addition to the more chronic membrane irritability and motor unit potential changes in the distally sampled muscles due to the underlying metabolic peripheral neuropathy. Information gathered during the electrodiagnostic evaluation is indispensable in shaping an effective treatment plan. In a diabetic patient, a femoral mononeuropathy will respond to tighter glycemic control,1 which differs from the treatment protocol already mentioned, directed at an L5 radiculopathy.
Many clinicians do not appreciate the value of electrodiagnostic medicine in evaluating and treating L/S radiculopathy. A variety of subtle abnormalities can be detected by the astute electrodiagnostician from the onset of nerve root pain. If weakness is clinically apparent, an increased recruitment frequency will be noticed in the affected muscles upon minimal contraction.70 Within 1–3 weeks, early polyphasic motor unit potentials can be present and may represent ephaptic activation of neighboring axons adjacent to volitionally activated axons.71 Seven to eight days after the onset of radicular symptoms, positive sharp waves can be evoked in the corresponding deep paraspinal musculature,72,73 and these may be the only observed abnormal findings in 30% L/S radiculopathy cases.72 If so, the H-reflex measurement, the electrical correlate of the Achilles muscle stretch reflex, can differentiate between an L5 and an S1 radiculopathy.74 An asymmetry of 1 msec or greater is significant for sideto-side difference,75 and can be present from the onset of symptoms. By 2 weeks after symptom onset, fibrillation potentials may be present in the paraspinal muscles and positive sharp waves in the affected proximal limb muscles.72 Closer to 3 weeks after symptom onset, proximal and distal muscles of the affected myotome will show abnormalities to varying degrees.72 The value of electrodiagnostic medicine in diagnosing L/S radiculopathy has been well established in the literature since 1950.72,76 More recently, its prognostic value has been well validated.72,73
In 1971, Johnson and Melvin’s work was published addressing the clinical management of L/S radiculopathy.72 In a review of 314 cases, 170 electrodiagnostic studies were normal and 111 abnormal in patients presenting with L/S radicular signs and symptoms. After 3 days, only neurapraxic fibers will conduct distal to the affected nerve root. In contrast, wallerian degeneration due to axonotmesis will result in a decrement of the evoked compound muscle action potential (CMAP) amplitude.72,73 The area of this CMAP amplitude can be compared to that of the identical contralateral muscle. If the affected CMAP amplitude of the evoked potential is greater than 50% of the contralateral muscle, motor function recovers with conservative care.72,73 After 14 days, if little spontaneous activity is noticed compared to the amount of clinical weakness and there is less than 10–15% decrement in the CMAP amplitude, an accurate conclusion is that the motor fibers are neurapraxic and recoverable rather than irreversibly damaged.72,73
