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ResearchGate See discussions, stats, and author profiles for this publication at: https:lJwww.researchgate.net/publication/26648260 Lumbar spinal stenosis: Syndrome, diagnostics and treatment Article in Nature Reviews Neurology • August 2009 0OI:10.lo3afnrneurol.3039.90• Source: Pubiled CITATIONS READS 64 434 6 authors, including: Vieri Failli Jan M Schwab quip Charite Universitatsmedizin Berlin The Ohio State University 20 PUBLICATIONS 700 CITATIONS 122 PUBLICATIONS 4,612 CITATIONS SEE PROFILE SEE PROFILE All content following this page was uploaded by Jan M Schwab on 28 February 2014. The user has requested enhancement of the downloaded file. EFTA00307993  REVIEWS Lumbar spinal stenosis: syndrome, diagnostics and treatment Eberhard Siebert, Harald Priiss, Randolf Klingeblel, Weal Fall!!, Karl M. Snitd' uel and Jan M. Schwab Abstract I Lumbar spinal stenosis (LSS) comprises narrowing of the spinal canal with subsequent neural compression, and is frequently associated with symptoms of neurogenic claudication. To establish a diagnosis of LSS, clinical history, physical examination results and radiological changes all need to be considered. Patients who exhibit mild to moderate symptoms of LSS should undergo multimodal conservative treatment, such as patient education, pain medication, delordosing physiotherapy and epidural injections. In patients with severe symptoms, surgery is indicated if conservative treatment proves ineffective atter 3-6 months. Clinically relevant motor deficits or symptoms of cauda equina syndrome remain absolute indications for surgery. The first randomized, prospective studies have provided class I—II evidence that supports a more rapid and profound decline of LSS symptoms after decompressive surgery than with conservative therapy. In the absence of a valid paraclinical diagnostic marker, however, more evidencebased data are needed to identify those patients for whom the benefit of surgery would outweigh the risk of developing complications. In this Review, we briefly survey the underlying pathophysiology and clinical appearance of LSS, and explore the available diagnostic and therapeutic options, with particular emphasis on neuroradiological findings and outcome predictors. Siebert. E. et al. Nat. Rev. Neared. 5.392-403 12009): dm.10.1038/nineurol.2009.90 Introduction M0dSCItpeCME Continuing Medical Education online The term lumbar spinal stenosis (LSS) refers to the ana- This activity has been planned and implemented in accordance tomical narrowing of the spinal canal and is associated with the Essential Areas and policies of the Accreditation Council with a plethora of clinical symptoms. The annual inci- for Continuing Medical Education through the joint sponsorship of MedscapeCME and Nature Publishing Group. dence of LSS is reported to be five cases per 100,000 individuals, which is fourfold higher than the inci- MedscapeCME is accredited by the Accreditation Council for Continuing Medical Education (ACCMEI to provide continuing dence of cervical spinal stenosis.' The characteristic Department of Neuroradidogy medical education for physicians. symptom of LSS is neurogenic claudication, which was (E. Siebert. MedscapeCME designates this educational activity for a maximum a term coined by Dejerine (1911)2 and defined by von R. laIngeblell. Department of of 1.25 AMA PRA Category 1 Credlte". Physicians should only Gelderen (1948)' and, later, Verbiest (1954).4 In his Neurologyand claim credit commensurate with the extent of their participation report, von Gelderen described neurogenic claudica- Everimental Neurcrogr in the activity. All other clinicians completing this activity will (H. Press. tion as localized, bony discoligamentous narrowing be issued a certificate of participation. To participate in this IL M. Journal CME activity: (1) review the learning objectives and author of the spinal canal that is associated with a complex of J. M. Schwab). Manta clinical signs and symptoms comprising back pain and School of Mecicine. disclosures: 12) study the education content: (31 take the posttest Humboldt University. and/or complete the evaluation at stress-related symptoms in the legs (claudication)'' This Berin.Gemnany. Wings publicinatuiereviews: and (4) New/print certificate. characterization is still in use today. LSS has become the for Ufe Spiral Cad Research Foundation. Learning objectives most common indication for lumbar spine surgery, in Satzburg.Austria Upon completion of this activity. participants should be able to: part because of the increasing quality and availability of tv. raid). radiological imaging.' The increasing frequency of LSS 1 Diagnose lumbar spinal stenosis effectively. Correspondence: 2 Distinguish recommended conservative treatment strategies surgery also reflects the elevated demand for mobility J. M. Schwab. for patients with lumbar spinal stenos's. and flexibility in the aging population. Propagated by Depanmem of 3 Analyze the relative benefits of conservative therapy Neurology and vs surgery for patients with lumbar spinal stenosis. the increasing prevalence of this condition, controlled, Experimental 4 Describe outcomes related to surgery for lumbar spinal evidence-based advice for individual treatment decisions Neurology. Spinal Cad is stating to emerge.'-' stenosis. Injury Research. Manta School or Medicine. LSS can be classified according to etiology (primary Humbo!dt University. and secondary stenoses) and to anatomy (central, lateral Campus Mine. Chenteplatz I. or foraminal stenosis), as summarized in Box 1. Primary 01.0117 stenosis is caused by congenital narrowing of the spinal Germany Competing interests jartschwabei, The authors. the Journal Editor H. Wood and the CME canalrwhereas secondary stenosis can result from a wide chmite.de questions author C. P. Vega declare no competing interests. range of conditions, most often chronic degeneration, 392 I JULY 2009 I VOLUME 2009 Macmillan Publishers Limited. All rights reserved EFTA00307994  REVIEWS which leads to a destabilized vertebral body. Other causes Key paints ofsecondary stenosis include rheumatoid diseases, osteo- • A patient's medical history and clinical symptoms are more-decisive factors myelitis. trauma, tumors, and, in rare cases, Cushing than radiological observations in confirming a diagnosis of lumbar spinal disease or iatrogenic cortisone application.1' stenosis (LSS) In this Review, we explore the underlying patho- • Patients with mild to moderate symptoms of LSS should be treated with physiology of LSS, focusing on degenerative LSS, and conservative therapies. including delordosing measures. and epidural injections discuss the characteristic hallmarks of the resulting clini- and other pharmacological measures cal syndrome. paraclinical determinants of the condition • In cases of severe symptomatic LSS, surgery is indicated if conservative and the results of interventional trials. therapy proves ineffective after 3-6 months • Class I evidence-based recommendations cannot be made for any conservative Pathophyslology or surgical therapy in relation to mid-term and longterm patient outcomes Stenosis development • Future mid-term and long-term studies should identify subgroups of patients LSS can be monosegmental or multisegmental, and uni- who are more likely to benefit from surgery than from conservative treatment lateral or bilateral. Anatomically, the stenosis can be clas- sified as central, lateral or foraminal. Depending on the extent of the degeneration, central, lateral and foraminal Box 1 I Classification and differential diagnoses of lumbar spinal stenosis stenosis can occur alone or in combination. The L4-5 spinal discs are most frequently affected by LSS, followed Classification according to etiology by L3-4, LS-S1. and LI-2. Primary stenosis Multiple factors can contribute to the development • Idiopathic stenosis of spinal stenosis, and these can act synergistically to • Achondrodysplasia exacerbate the condition. Degeneration of the vertebral disc often causes a protrusion, which leads to ventral Secondary stenosis narrowingof the spinal canal (central stenosis; Figure la). • Degenerative (for example. spondylosis. spondyfolisthesis. scoliosis) As a consequence ofdisc degeneration, the height of the • Ossification of the ligamentum longitudinale posterius and ligamentum fiavum intervertebral space is further reduced, which causes • Metabolic or endocrine causes (for example. epidural lipomatosis. acromegaly) the recess and the intervertebral foramina to narrow • Infections (discitis. osteomyelitis. Potts disease [tuberculous spondylitisj) (foraminal stenosis), exerting strain on the facet joints (Figure 1). Such an increase in load can lead to facet • Neoplastic joint arthrosis, hypertrophy of the joint capsules and the • Rheumatological conditions (for example. Paget disease. spondylosis development of expanding joint cysts (lateral stenosis), ankylopoetica. rheumatoid arthritis) which in combination propagate spinal instability." The • Posttraumatic or postoperative stenosis (for example. fracture of vertebrae. reduced height of the segment leads the ligamenta flava laminectomy. fusion. fibrosis) to form creases, which exert pressure on the spinal dun Classification according to anatomy from the dorsal side (central stenosis). Concomitant • Central stenosis (with or without lateral stenosis) instability due to loosened tendons (for example, the • Isolated lateral stenosis ligamenta !lava) further propagates pre-existing hyper- trophic changes in the soft tissue and osteophytes, creat- • Foraminal stenosis ing the characteristic trefoil-shaped narrowing of the Differential diagnoses central canal.m". • Intermittent claudication or vascular claudication LSS can also be subdivided into relative and absolute • Radiculopathies or polyneuropathies LSS—a classification that has not yet been clinically validated—according to the anterior-posterior diameter • Intraspinal synovial cyst of the spinal canal (Figure la). Relative LSS (spinal canal • Disc prolapse 10-12 mm in diameter; physiological value is 22-25mm) • Tethered cord or spina bifida is usually asymptomatic, whereas absolute LSS (spinal • Coxarthrosis or arthrosis of the iliosacral joint canal <10 mm in diameter) is often symptomatic and is • Abdominal aortic aneurysm associated with absence of free subarachnoid space (as • Neoplasia (for example. tumor of myelon. spinal roots. meninges. bones or filiae) observed on lateral plain X-ray films). The lateral recess • Inflammatory conditions (for example. spondylodiscitis. meningeosis. can be considered stenotic if it has a diameter of <2mm arachnoiditis) (physiological diameter is 3-5 mm). • Dissociative syndromes From stenosis to claudication Derived from Haam',eler and steike.ls Each of the various degenerative processes that partici- pate in the development of LSS can independently cause clinical symptoms that frequently make diagnosis and the comprises limping or cramping lumbar pain that radi- choice of therapy difficult. The most common symptom ates into the legs primarily during walking. Degenerative associated with LSS is neurogenic claudication, which LSS can ultimately lead to the compression of individual NATURE REVIEWS] NEUROLOGY VOLUMES I JULY 2009 1 393 2009 Macmillan Publishers Limited. All nets reserved EFTA00307995  REVIEWS a nerve roots, the meninges, the intraspinal vessels, and, in exceptional cases the cauda equina (Figure 2)." Nerve root compression triggers localized inflammation, Vertebral body which affects the nerve root's excitatory state." In addi- Lateral recess Bulging or tion, at least two interdependent vascular mechanisms (entry zone) protrusion of Foramina' - - invertebral disc are hypothesized to contribute to the development of narrowing neurogenic claudication in LSS: reduced arterial blood aserdiiri Peclicle b flow resulting in ischemia, and venous congestion with Forame iis C ----F-2cet Joint: compression of the nerves and secondary perfusion deli- (ext zone) superior rophy of Lamina articular facet ciente Conversely, compressive radiculopathy can 'ter/Let Joint Anterior-posterior diameter cause autonomic dysregulation and impaired circula- Ugamenturn flavum (thickening) Spinous process tion in the legs." The extent of compression is increased by hyperextension or hyperlordosis of the lumbar spine, because these postures cause additional narrowing of the b Nerve fibers (cauda &pima) spinal canal. By contrast, hyperflexion abrogates lordosis, cr cr :j i i Trransw ssfsle4 resulting in a widening of the spinal canal. A functional LSS can be diagnosed only if a clinically relevant LSS develops in certain spinal postures (for example, when Facet pint: Spinous standing as opposed to sitting). Such stenoses are fre- L4 Inferior process I.4 articular facet quently exacerbated further by vertical load.22 Indeed, (hypertrophy) Transverse process LS epidural pressure is elevated while standing or walking, and lowered when sitting and in flexion."'" CZ Facet pint: Experimental animal models have been developed to investigate the underlying pathophysiology of LSS in LS superior more detail" and to test pharmacological interventional articular facet : (hypertrophy) Nerve root strategies," but the validity of these models for the multi- faceted. etiologically diverse human condition remains Degenerative disc signs: height loss and protrusion limited. In one such experimental model for spinal canal (e.g. into foramen) Spinous process LS stenosis, a piece of silicon is placed under the lamina at lumbar level 4 in young adult rats. This model might only deliver incomplete information, since acute narrow- Spinous ing of the spinal canal per se does not fully recapitulate / process the features of chronic degenerative LSS in humans, Facet Joint: and the young adult animals used in those experiments I.4 inferior articular facet lack comorbidities. In addition, the spine biomechanics IrlyPertreohyl of quadripedal rats differ substantially from those of Degenerative ) bipedal patients. disc signs: Freet Joint heigm loss L5 supenot and protrusion articular facet Signs and symptoms IllyPertrol") In contrast to the well-defined pathoanatomical hall- Foramina' marks of LSS, the clinical features of the condition narrowing are heterogeneous, and often, but not always, include Nerve root neurological symptoms." Typically. patient symptoms comprise unilateral or bilateral (exertional) back and leg pain, which slowly develops and persists over several months, or even years (Box 2). The back pain is localized Figure 1 i Pathoanatomical illustration of LSS. to the lumbar spine and can radiate towards the gluteal Osteolisthesis and disc prolapse are distinct entities from LSS. although these conditions will frequently exacerbate region, groin and legs, frequently displaying a pseudo- the pre-existing lumbar stenosis. a I Corona', b I dorsal radicular pattern. In cases of lateral recess stenosis or and e I lateral views of LSS. In a I distinct stenosis areas foraminal stenosis, isolated radiculopathy can occur. are depicted in red. Ventral compression can be caused Neurogenic claudication is the most specific symptom of by medially bulging or protrusion of intervertebral discs. LSS,° although it is nearly always accompanied by further Lateral stenosis can be caused by lateral prolapse, symptoms. Taking into account all the symptoms, LSS stenosis of the neuroforamen or hypertrophy of the facet can be clinically classified into grades Grade I joints. b I Dorsal view of lateral stenosis (red dots) caused by hypertrophic facet joints and narrowing of the (neurogenic intermittent claudication) is characterized neuroforamen. e I Corresponding lateral perspective of by a reduced walking distance (caused by pain) and short narrowed neuroforamen causing a lateral stenosis. intermittent sensomotoric deficits that at rest might Abbreviation: LSS, lumbar spinal stenosis. be unremarkable, but can deteriorate while walking. 394 1 JULY 3009 I VOLUMES 2009 Macmillan Publishers Limited. All rights reserved EFTA00307996  REVIEWS However, not all patients with LSS exhibit symptoms consistent with neurogenic intermittent claudication, which is why other classifications of LSS exist. Grade II r illICsure: tension: cbronic inflammation Etisevnental stenosis Segmental stenosis (intermittent paresis) refers to already persistent sensi- t tivity deficits, loss of reflexes and intermittent paresis. intraneural fibrosis venous s asls and low perfusion pressure Grade III is reached if persistent, progressing paresis is present, accompanied by partial regression of pain? Neurogenic claudication can be clinically distinguished Ectopic neural excitation Neural ischemla High epidural pressure from vascular intermittent claudication by the presence in the former of pain regression following flexion (delor- dosis) of the spine (for example, while cycling). In con- Neurogenic claudication trast to vascular claudication, pain sensation in patients with LSS does not ease while standing. The relative pro- Figure 2 I Processes involved in neurogenic claudication development in lumbar portions of the low back pain component (an indicator spinal stenosis. of pathology such as concomitant vertebral instability or facet joint arthrosis) and the leg pain component have proved helpful for dinical orientation." Laskgue testing (a Box 21 Symptoms and features of lumbar spinal stenosis passive leg flexing test) often remains negative in patients with LSS and is frequently accompanied by a feeling of Classic symptoms 'heavy legs, a characteristic sign of LSS. Straightforward • Lumbago detection of LSS is hampered by a number of frequent • Neurogenic claudication comorbiditiessuch as peripheral neuropathies, which can • Hypesthesia and paresthesia of the legs themselves be relevant differential diagnoses (Box 1). • Ataxia Approximately 20% of patients with LSS exhibit symp- • Weakness and feeling of heavy legs toms of depression and 25% are dissatisfied with their life before surgery—a similar pattern to that seen in patients Features with other chronic disorders?" Evaluation of mood and • Improvement during lumbar delordosing contentment in patients is important, as both can mark- • Deterioration during lumbar lordosing edly differ between patients with LSS and healthy controls, • Weakness of the legs and can influence diagnostic and therapeutic decisions. Patient-reported symptoms—even those that are transient • Attenuated reflexes (pseudoradicular) in nature—should be considered seriously in the diagnostic Derived from Heeimeier end Stolke.m work-up, especially during initial consultations. Diagnosis occasionally mimics LSS, with low back pain radiating to The frequency of degenerative LSS diagnosis has risen the buttocks and the thighs when standing and walking. over time, as a result of increasing lifespan and demand Unlike LSS, however, iliosacral joint pain is characterized for a better quality of life, awareness of the disease, and by tenderness of the joint. The development of cauda the availability of advanced imaging techniques. ISS can equine syndrome, which comprises sacral hypesthesia, be difficult to diagnose, however, because the symptoms loss of tendon reflexes in the lower limbs and incon- can mimic other diseases. On the other hand, various tinence, as a result of 1SS is only found in exceptional comorbidities, which are prevalent in the aging popula- cases. Sphincter involvement is very rare in LSS, as the tion, can result in secondary stenosis or imitate symptoms sacral nerves are relatively protected from compression of it. Thus, the differentiation of LSS from numerous owing to their central position within the cauda equina.'' other pathologies is vital (Box 1). Clinical symptoms of In patients exhibiting vesicorectal voiding and upper BS are often absent at rest. In addition, it can be difficult motor neuron signs (for example, Babinski's reflex and to establish whether pain (and other patient-reported hyperreflexia), cervical or thoracic myelopathy needs to symptoms) relates to ISS or to other factors (for example, be ruled out. instability, facet joint arthrosis, osteoporosis, arthritis, or diabetic polyneuropathy). Hence, a diagnosis of LSS Neuroradiological assessment can only be established through a combination of clinical When performing radiological assessment of MS, some history, physical examination and radiological changes. inherent problems with imaging of the lumbar spinal canal need to be considered. First, imaging of sympto- Differential diagnoses matic patients is confounded by the fact that degenerative In contrast to the situation in LSS, hyposensibility result- changes in the lumbar spine are highly prevalent in the ing from peripheral neuropathies usually exhibits a asymptomatic population: among patients over 60 years bilateral distal stocking-shaped pattern, irrespective of of age, 20% will reveal signs of LSS." Second, imaging posture, rest or physical stress. Iliosacral joint disorder tends to exaggerate pronounced degenerative changes NATURE REVIEWSI NEUROLOGY VOLUMES I JULY 2009 1 395 X', 2009 Macmillan Publishers Limited. All rights reserved EFTA00307997  REVIEWS reactive end-plate and bone marrow changes, and spondylophytes, can be visualized to differing degrees by the various imaging techniques applied. Increased stress on the facet joints leads to hypertrophic facet degenera- tion, as well as inwardly buckled and hypertrophied liga- menta flava. These changes can lead to central, lateral or foraminal stenoses (Figure I). MR1 MRI is the preferred imaging modality for the radio- logical assessment of LSS.J6 This technique provides superior soft-tissue contrast compared with other imaging modalities, has multiplanar imaging capabili- ties and does not produce ionizing radiation. In patients with pacemakers, certain other types of metal implants or claustrophobia, however, MRI is contraindicated or impossible to perform. MRI ofpatients with LSS usually comprises orthogonal TI-weighted and T2-weighted images (sagittal and axial). A fat-suppressed T2-weighted sequence can be added, as such images seem to allow more accurate detection of associated degenerative bone marrow changes. With T2-weighted images and the inherent signal intensity of cerebrospinal fluid, 'myelography-like' images that illus- trate the thecal sac, the intrathecal and intraforaminal nerve roots, and the spinal cord can be obtained non- invasively. LSS can be monosegmental (Figure 3) or Figure 3 I Spinal alterations in a patient with occur on multiple levels (Figures 4 and 5). Like CT monosegmental LSS at L4-5. Sagittal and axial images imaging, MRI can define the contribution of osseous and were obtained using T2-weighted turbo spin-echo MRI. discoligamentous structures to LSS. a I A sagittal image reveals reductions in the disc signal Despite detailed depiction of the spinal anatomy, and the disc space height, which are attributable to studies have produced conflicting results concerning the dehydration. Disc bulging and slight ventral listhesis of L4 clinical usefulness of the information gained by MRI."-" (arrow) can also be observed. b I Narrowing of the neuroforamen (arrow). which affects the right L4 radix.Is Results from a study conducted by Modic and colleagues, caused by e consecutive hypertrophic facet joint in patients with radiculopathy, low back pain and scia- degeneration with intra-articular effusions (arrowheads) tica, implied that changes observed by means of MRI and hypertrophy of the ligamentum flawm (arrow), as add little or no clinically useful information to clinical observed on an axial image. assessment alone in relation to prognosis and predicting the outcome of surgery."" and effects on the spinal canal." Thus, radiologically Gadolinium-based contrast media are not routinely diagnosed LSS usually identifies involvement of more required for imaging of LSS unless previous surgery was segments than is suspected clinically. In the majority of performed and fibroid scar tissue might have to be identi- cases, a presumptive diagnosis of LSS can be made on the fied by its contrast enhancement" Some studies,however, basis of the clinical appearance of the condition and indicate a possible superior role for contrast-enhanced MRI the patient's medical history. Imaging tends, therefore, to in LSS patients with neurogenic claudication, as enhance- be selectively employed when any type of interventional ment of compressed nerve roots can be visualized in a or surgical therapy is contemplated. Notably, imaging subset of these patients.'[-"' This enhancement is thought tends to be used most frequently in patients with medium to reflect either obstructed periradicular veins, indicating to severe symptoms ofI-SS." venous stasis, or breakdown of the blood-nerve barrier, a In presurgical patients with symptoms of LSS, the sign ofchronic compressive radiculitis (Figure 2). purpose of imaging is to confirm the presence or Through the use of heavily T2-weighted fat-suppressed absence of LSS, to exclude differential diagnoses, to relate sequences, magnetic resonance (MR) myelography congesting symptoms to osseous and discoligamentous can be performed noninvasively and without contrast structures, and to identify the exact location of LSS for administration. Despite the capacity of this technique to accurate presurgical planning." As described previously. accurately depict the thecal sac, however, studies have LSS mostly results—at least initially—from degenerative yielded contradictory results regarding the usefulness disc disease. Morphological alterations, such as loss of of this sequences.* The use of MR myelography is, disc height, disc signal, bulging discs, disc herniations. therefore, only advocated as an additional sequence to 396 I JULY 2009 I VOLUME *32009 Macmillan Publishers Limited. All nein reserved EFTA00307998  REVIEWS conventional MRI. Currently, open MRI is the only tech- nique that enables a functional investigation of spinal flexion and extension during the application of axial loading, or even in the supine position!' CT scanning CT can be performed rapidly and allows precise evalua- tion of the spinal canal and differentiation between spinal canal compression caused by discs, ligaments and bony structures. In the latter respect, this approach is supe- rior to MRI. At present, CT is usually performed using a spiral multislice technique, acquiring isotropic data that enables multiplanar reformattingin any desired plane and three-dimensional reconstructions. Even in pronounced torsion scoliosis, therefore, multisegmental imaging in one plane can be achieved, which is not possible with Flgure 4 I Spinal alterations in a patient with MRI. A limitation of CT is that intrathecal nerve roots multisegmental LSS. Sagittal and axial images were and the spinal cord cannot be visualized, because these obtained using 12-weighted turbo spin-echo MRI. structures have similar densities to the cerebrospinal a I A sagjttal image reveals multisegmental LSS with signs fluid. This problem might be circumvented by using CT of spondylosteochondrosis. such as disc height and signal myelography (Figure 5). CT myelography entails spiral reduction. disc herniation. irregularity of end plates and CT imaging acquired after inthecal administration of bone marrow degeneration (arrows). and spondylarthrosis (hypertrophy and sclerosis of the facet joints: arrowheads). iodine, which is commonly performed under fluoro- The axial images depict b I a moderate (arrow) and scopic guidance. In some cases of extensive degenera- e 1 a severe (arrow) central LSS with different degrees of tive or postsurgical changes, lumbar puncture can also disc pathology, hypertrophy of ligaments flava and facet be performed under CT guidance. Such CT-guided joints. Abbreviation: LSS. lumbar spinal stenosis. puncture of the thecal sac is a robust technique, even in patients who cannot be assessed by other means. CT and CT myelography might be indicated in patients where in flexion and extension positions (so-called functional MRI is contraindicated, the MRI results are inconclusive radiographs) to rule out segmental instability is not rou- or where clinical symptoms correlate poorly with MRI tinely required, as signs of segmental instability can be findings.4' Furthermore, CT techniques might be used detected on conventional lateral radiographs in a suffi- for presurgical planning in cases where bony anatomy ciently accurate manner." Furthermore, no additional needs to be accurately depicted. benefits were gained from these additional views in a recently conducted study.50 Even in patients for whom Conventional )(gays and myelography segmental instability was expected, the diagnostic value The usefulness ofroutinely acquired plain radiographs in of lateral radiographs in flexion and extension could not the initial evaluation of patients with LSS has been ques- be definitively determined." tioned'"'" Indeed, the acquisition ofsuch radiographs is Conventional functional myelography has long been no longer part of the Agency for Health Care Policy and the method of choice for diagnosing LSS and is still an Research guidelines." Many patients, however, undergo important method for investigating the influence of conventional radiography as part of their initial evalu- hyperextension and hyperflexion on the extent of the ation, as this procedure is inexpensive and uncomplicated stenosis. This technique might still be the only routine to perform. Conventional radiographs might be of use, method that is suitable for detecting the morphological albeit in a limited fashion, in assessing the contribution correlates of a functional, posture-dependent, sympto- of bony degeneration to LSS and the alignment of the matic LSS (Figure 6).0 Furthermore, it is the only accu- vertebral bodies in lateral and coronal planes. This tech- rate imaging technique for patients with spinal metallic nique can also potentially be used to rule out traumatic implants, which can cause artifacts on MRI and CT. changes or other unanticipated findings (for example, Moreover, conventional functional myelography allows Paget disease, spondylodiscitis or scoliosis) as possibledif- the lumber spine to be examined in a standing posi- ferential diagnoses:. After surgery, plain radiographs are tion, and, hence, under the normal stress of the body useful in determining the integrity and the correct posi- weight. Conventional myelography is an invasive pro- tion of fusion material, and to visualize signs ofloosening cedure that requires intrathecal administration of iodi- of implanted fixating plates and/or screws. The sensitivity nated contrast agent, and is consequently associated and specificity of plain radiographs concerning the con- with adverse effects such as postpunctional headaches, tribution of bony changes to central spinal stenosis were and rare life-threatening complications such as anaphy- reported to amount to 66% and 98% respectively of those lactic reactions and spinal infections. Like other imaging of CT. The acquisition of additional lateral radiographs techniques, conventional myelography frequently reveals NATURE REVIEWS' NEUROLOGY VOLUMES JULY 2009 1 397 al 2009 Macmillan Publishers Limited. All rights reserved EFTA00307999  REVIEWS Additional diagnostics Selective diagnostic injections can be useful in some patients to estimate the contribution of different pain components to the patient's overall health, especially against the background of pain psychology in chronic pain. If vascular genesis of the symptoms is suspected, noninvasive diagnostic techniques include determina- tion of the ratio of the systolic blood pressure of the ankles to that of the arms (ankle-brachial index), which can