radic stenosis cea_pmr clinics

Lumbar spinal stenosis, cauda equinasyndrome, and multiple lumbosacral

radiculopathies

Phillip B. Storm, MDa, Dean Chou, MDb,Rafael J. Tamargo, MDc,*

aDepartment of Neurological Surgery, Johns Hopkins University School of Medicine,

725 North Wolfe Street, 817 Hunterian Boulevard, Baltimore, MD 21205, USAbDepartment of Neurological Surgery, Johns Hopkins Hospital, Meyer 8-161,

600 North Wolfe Street, Baltimore, MD 21287, USAcDepartment of Neurosurgery, Johns Hopkins Hospital, Meyer 8-181,

600 North Wolfe Street, Baltimore, MD 21287-7713, USA

In 1954, Henk Verbiest, a Dutch neurosurgeon on the faculty at the Cityand University Hospital at Utrecht, published his classic paper entitledA radicular syndrome from developmental narrowing of the lumbar verte-bral canal [1]. Verbiest described a form of narrowing of the vertebral canalin middle-aged and older men with back pain, bilateral radicular pain, anddisturbances of sensation and strength in the lower extremities that was pre-cipitated by standing, walking, and hyperextension. This article is widelyaccepted as the rst description of the clinical syndrome of lumbar spinalstenosis. In fact, intermittent spinal claudication is called Verbiests syn-drome. Although Verbiest published his ndings on lumbar stenosis in the1950s, it is only within the past two decades that this condition has beendiagnosed and treated routinely.

Lumbar spinal stenosis is a progressive and dynamic process that causesnarrowing of the spinal canal, lateral recess, or the neural foramina and isdivided into two groups: congenital and acquired (Table 1). The narrowingresults from the compression of the lumbosacral roots by the bony canal orthe soft tissues, including the intervertebral discs, facet joints, and the liga-mentum avum. This narrowing causes axial lumbar pain, radicular pain,and cauda equina syndrome when the thecal sac and nerve roots are com-pressed.

* Corresponding author.

E-mail address: [email protected] (R.J. Tamargo).

1047-9651/02/$ see front matter 2002, Elsevier Science (USA). All rights reserved.PII: S 1 0 4 7 - 9 6 5 1 ( 0 2 ) 0 0 0 1 3 - X

Phys Med Rehabil Clin N Am

13 (2002) 713733

Approximately 90% of the population will report back pain, and the inci-dence of acquired lumbar stenosis is approximately 1 per 1000 in individualsolder than 65 years [2,3]. As life expectancy continues to increase, the pre-valence of symptomatic spinal stenosis will increase. Although lumbar steno-sis is not life threatening, it can cause chronic and substantial pain and canlimit activity severely [4]. Early and accurate diagnosis and treatment oflumbar stenosis is important in preserving activity in the elderly population.

Table 1

Etiology of spinal stenosis

Congenital

Idiopathic

Dwarsm

Achondroplasia

Morquios syndrome (mucopolysaccharidosis)

Hurlers syndrome (mucopolysaccharidosis)

Acquired

Degenerative

Spondylolisthesis

Scoliosis

Herniated/bulging intervertebral disc

Lateral recess stenosis

Facet hypertrophy

Neural foramen narrowing

Ligamentum avum hypertrophy

Synovial cysts

Degenerative superimposed on congenital

Spondylolytic (pars interarticularis defect)

Vertebral body compression fractures

Trauma

Metastatic disease

Spondylosis ankylopoetica (Bechterews disease)

Iatrogenic

Postlaminectomy

Postfusion

Tumors

Lymphoma

Meningioma

Schwannoma

Neurobroma

Conus medullaris tumors

Myxopapillary ependymoma

Pilocytic astrocytoma

Hemangioblastoma

Miscellaneous/metabolic

Pagets disease

Spinal epidural hematoma

Spinal epidural abscess

Diuse interstitial skeletal hypertrophy

714 P.B. Storm et al / Phys Med Rehabil Clin N Am 13 (2002) 713733

Proper evaluation and treatment of lumbar stenosis requires knowledge ofthe anatomy and pathophysiology of the lumbar spine.

Anatomy and pathophysiology of the lumbar spine

The mobile, lordotic lumbar spine consists of ve vertebrae and articu-lates with the rigid, kyphotic thoracic region superiorly and the rigid,kyphotic sacrococcygeal region inferiorly. Each lumbar vertebra (Fig. 1)consists of a body, pedicles, lamina, pars interarticularis, transverse pro-cesses, spinous process, superior and inferior articular processes, and a neuralforamen. Intervertebral discs separate the vertebral bodies superiorly andinferiorly, and the articular processes form the zygapophyseal facet joint.Anterior and posterior longitudinal ligaments unite the vertebral bodies.The ligamentum avum is a yellow, elastic tissue that forms the posterolat-eral wall of the vertebral canal. The ligamentum avum spans the inferioredge of the lamina above and the superior edge of the lamina below [5].As the spine degenerates, there is a loss of intervertebral disc height, theinterlaminar distance decreases, and the ligamentum avum becomes hyper-trophied, redundant, and occasionally, calcied. The redundancy worsenswhen the spine is in an erect position and particularly during extension[6]. These changes in the ligamentum avum can cause central stenosis byseverely narrowing the midsagittal diameter of the lumbar spinal canal.

The normal midsagittal diameter of the lumbar vertebral canal is denedas greater than 12 mm [7,8]. Relative stenosis occurs when the canal dia-meter is between 10 and 12 mm, and absolute stenosis is dened as less than10 mm [7,9,10]. These measurements, however, are only guidelines. Theextent of compression of the nerve roots and cauda equina and the patientssigns and symptoms are more important than canal diameter [11].

Lumbar stenosis results from changes in the three-joint complex [12,13].The three-joint complex denes the spine as a tripod, with the disc as one legand the facet joints as the other two legs, forming the posterior supports.Dysfunction in any of these joints leads to abnormal biomechanical stressesthat result in accelerated degeneration in the other joints and thereby createa cycle of degenerative changes. These degenerative changes cause centraland lateral stenosis secondary to remodeling and overgrowth of bone, withosteophyte formation, ligamentum avum hypertrophy, facet hypertrophy,and disc bulging [14].

Degeneration can begin at any of these sites, but disc degeneration seemsto be the initiating event, with the articular processes aected secondarily.[12,13,1519]. As the disc degenerates and collapses, it can compress the the-cal sac between a bulge in the annulus, encroaching on the vertebral canalanteriorly, and a hypertrophied ligamentum avum, encroaching on thecanal posteriorly [20]. In a normal-sized canal, degenerative discs usuallydo not cause symptoms of central stenosis; however, these degenerative

715P.B. Storm et al / Phys Med Rehabil Clin N Am 13 (2002) 713733

Fig. 1. Anatomy of the rst lumbar vertebra. (A) Axial, (B) lateral, and (C) posterior views are

shown. a vertebral body; bpedicle; c vertebral canal; d transverse process; e superiorarticular process; f lamina; g spinous process; hneural foramen; ipars interarticularis;j inferior articular process; kmamillary process; l accessory process.


changes superimposed on a congenitally narrowed canal can cause profoundsymptoms. A large disc herniation can compress the thecal sac suciently tocause symptoms, regardless of canal size. This compression of nerve rootsis especially true at higher lumbar levels, where the thecal sac has a similardiameter but a higher concentration of nerves. Weisz and Lee [21] used theterm container content dierence to describe this observation. Intervertebraldiscs contribute to lumbar stenosis not only by direct compression but alsoby increased mobility owing to loss of disc height, causing ligamentous lax-ity and accelerated degeneration of the facet joint.

The facet joint is a zygapophyseal joint composed of a descending infe-rior articular process from the vertebra above and the ascending superiorarticular process from the vertebra below. As the intervertebral disc losesheight, increased stresses are placed on the facet joints, and the orientationof the facets begins to change (facet arthritis precedes disc degeneration in20% of degenerative spines) [22,23]. The increased mechanical stresses causesynovitis and cartilage erosion in the facet joint [24]. As this process pro-gresses, the joint undergoes arthritic and degenerative changes, and the facetcapsule loosens, spinal motion increases, and further degeneration of theintervertebral disc and facet joint is accelerated. The increased spinal motioncauses bone remodeling and overgrowth that lead to osteophyte formationand facet hypertrophy. Although osteophytes and hypertrophied facetsreduce excessive joint motion by local physiologic arthrodesis (autofu-sion), they also can narrow the canal, lateral recess, and neural foramina[25]. Successful physiologic arthrodesis decreases segmental mobility at thatlevel; however, the loss of mobility in one segment creates abnormal forceson adjacent levels that accelerate degenerative changes [14].

As the intervertebral discs narrow, the facets hypertrophy, and the liga-ments weaken; there is a realignment of forces that can lead to degenerativespondylolisthesis [26]. Spondylolisthesis is the anterior (anterolisthesis) orposterior (posterolisthesis) subluxation of the superior vertebral body rela-tive to the subjacent one. Degenerative spondylolisthesis can not only causenarrowing of the vertebral canal but also can produce symptoms of spinalstenosis [27]. Degenerative spondylolisthesis, however, should not be con-fused with isthmic spondylolisthesis.

In 1976, Wiltse et al [28] classied spondylolisthesis into the following vecategories: dysplastic (congenital), isthmic (spondololytic), degenerative,traumatic, and pathologic. The two most common types of spondylolisthesisare isthmic (51%) and degenerative (25%) [29]. Isthmic spondylolisthesisresults from a neural arch defect causing a lesion in the pars interarticularis,and it is the most common type of spondylolisthesis in patients younger than50. Anterior isthmic spondylolisthesis occurs most commonly at the L5-S1level; however, degenerative anterolisthesis occurs almost invariably at theL4-5 level [27]. The L5-S1 segment rarely has degenerative slips because thefacets have a coronal orientation (L4-5 has a sagittal orientation), andthe large transverse processes of L5 have strong ligamentous attachments


to the iliac crest [26,30]. Degenerative spondylolisthesis can cause, or worsen,symptoms of stenosis because the anterior slip of the vertebra narrows thecanal and compresses the thecal sac against the posterior body of the verte-bra below. This condition usually occurs in a canal that is already stenoticfrom disc bulging, facet hypertrophy, and ligamentum avum hypertrophy.Symptoms of stenosis, however, are fewer with isthmic spondylolisthesisbecause the degree of slip is less and the compression of the thecal sac is mini-mal because of the neural arch defect [27].

The chronic compression of the nerve roots of the cauda equina contributesto pain in lumbar stenosis. The mechanical deformation of the cauda equinacauses venous congestion, ischemia, and axonal injury [31,32]. Chronic com-pression can induce radicular ischemia [33], sensitize nerve roots and dorsalroot ganglia to inammation [34,35], lead to Wallerian degeneration [36],cause hyperalgesia, and release neurogenic pain mediators [37,38]. Non-neuronal tissues important in stenosis (eg, ligamentum avum, intervertebraldiscs, facet joints) release endogenous chemicals that can produce pain[3739]. These factors can combine to produce neurogenic claudication andmultiple lumbar radiculopathies. Understanding the anatomy and patho-physiology of the lumbar spine allows physicians to study and conse-quently to diagnose and treat the clinical syndrome of lumbar stenosis moreeectively.

Clinical syndrome

The syndrome of lumbar spinal stenosis is a clinical entity in which thereis a strong correlation between symptoms and narrowing of the midsagittaldiameter of the spinal canal, the lateral recess, and the neural foramina. Theonset of symptoms is related to whether the stenosis is congenital (second orthird decade) or acquired (sixth or seventh decade), but in either case, symp-toms coincide with the development of osteoarthritis in a stenotic vertebralcanal [40,41]. Degenerative spinal stenosis, the most common form of thedisease, typically becomes symptomatic when patients are in their middleto late 50s or early 60s [14,42].

Degenerative lumbar spinal stenosis is three to ve times more commonin women than men, most commonly aects the L4-5 segment (followed bythe L3-4 segment), and in approximately 5% of cases is associated with cer-vical stenosis [4345]. Degenerative spondylolisthesis is also ve times morecommon in women and probably is related to hormonal factors leading toligamentous laxity [26,28,46].

Patients typically present with insidious onset of chronic low back painthat progresses to coccygeal, gluteal, thigh, and leg pain [44]. The qualityof the axial back pain in lumbar stenosis is the ache and stiness of osteo-arthritis; activity exacerbates the pain, and rest relieves it [47]. Patients oftenreport limitations during spinal extension but not during exion. Extensionfrequently causes severe and lancinating pain into the buttocks and lower


extremities. Patients often report that they are able to relieve their pain bysitting down and exing their low back.

The lower extremity pain associated with lumbar spinal stenosis is depen-dent on the area of stenosis and is characterized by the syndrome of neuro-genic claudication. This syndrome is characterized by poorly localizedpain, numbness, paresthesias, weakness, and cramping or burning in the lowback, buttocks, and lower extremities [19,48]. The pain typically radiates fromthe lowback or buttocks into the thigh andknee in a radicular pattern.As acti-vity increases or the condition progresses, the leg and foot may becomeinvolved [48,49]. Walking or standing exacerbates symptoms, whereas sit-ting or lying with the hips and spine exed substantially alleviates the pain[50]. Because exion relieves discomfort, many patients with stenosis ambu-late with a stooped posture [14]. Patients often can increase walking toler-ance when leaning forward over a shopping cart (shopping-cart sign),lawn mower, or while walking uphill. This posture exes the lumbar spineand widens the interlaminar distance, thereby decreasing the redundancyof the hypertrophied ligamentum avum and reducing the compression onthe cauda equina. The opposite is true of postures that increase lumbar lor-dosis, such as sleeping, which explains why many patients report worseningof symptoms in the middle of the night or early in the morning. As thestenosis progresses, rest pain may develop, postural changes may no longerrelieve pain, and a neurogenic bladder may develop; however, patients withlumbar stenosis rarely present with a cauda equina syndrome [14,48,51].

The diagnosis most often confused with neurogenic claudication is vascu-lar claudication from peripheral vascular disease (Table 2) [52]. The maindierence is the absence of low back pain in vascular claudication. Claudi-cation caused by peripheral vascular disease is characterized by crampingpain or tightness that begins in the calves and progresses proximally (neuro-genic claudication begins proximally and progresses distally) and reprodu-cibly occurs at a constant distance. The pain of vascular claudicationimproves with standing and is exacerbated by lying. Having the patient ridea stationary bicycle is an excellent way to dene the type of claudication;patients with vascular claudication should become symptomatic, but pa-tients with neurogenic claudication should tolerate the exercise because theirlumbar spine is exed. Patients with vascular claudication more commonlyhave diabetes mellitus, smoke cigarettes, have decreased dorsalis pedis andposterior tibialis pulses, have cutaneous changes over the distal lower ex-tremities, and have an ankle/brachial pressure index of 0.7 [14,48]. Thesetwo conditions, however, can exist simultaneously, making the correct diag-nosis dicult and possibly requiring consultation with a vascular surgeon todetermine the best treatment.

Other conditions in the dierential diagnosis include herniated discsand peripheral neuropathy. Herniated discs typically occur in a youngerpopulation, and the onset of symptoms is usually sudden. For example, sud-den onset of a cauda equina syndrome (discussed in a following section)


resulting from a large herniated disc is dierent from the insidious onsetof a cauda equina syndrome from spinal stenosis. Peripheral neuropathy canbe confused with lumbar spinal stenosis in an elderly person. Patientswith peripheral neuropathy, however, typically have diabetes and report aburning sensation in their feet that progresses proximally. These symptomsare unrelated to activity and occur in a stocking distribution [53]. It is impor-tant to rule out osteoarthritis of the hips, tumors at the conus medullaris,metastatic disease to the spine, infections, and fractures. A careful historyallows the physician to make the diagnosis of lumbar stenosis in most cases;however, physical examination is extremely important to conrm the diag-nosis of stenosis and rule out other conditions in the dierential diagnosis.

Physical examination of the back may show a loss of lordosis of the lum-bar spine, but palpation usually does not produce tenderness. The mostcommon nding in lumbar stenosis is absence of the ankle (gastrocne-mius/soleus) deep tendon reexes. Range-of-motion maneuvers demonstratethat forward exion is decreased but painless, and that extension is re-stricted severely and may cause pain into the buttocks and lower extremities.Straight legraise testing results are usually negative but may be positive,depending on the extent of lateral recess stenosis [48]. Straight legraisingresults are much more likely to be positive in younger patients with adisc herniation. Motor testing is usually normal or reveals, at worst,only a minimal loss of function [26,48]. If weakness is present, it is usuallymild and involves the extensor hallucis longus or tibialis anterior because theL4-5 level and L5 root are aected most frequently. Atrophy in the thigh orleg is uncommon but can exist in the presence of long-standing compression.

Table 2

Neurogenic vs. vascular claudication

Signs and symptoms Neurogenic claudication Vascular claudication

Pain on lifting or bending Common Uncommon

Claudicating distance Variable Constant

Pain distribution Distribution of a nerve

(dermatomal)

Distribution of a muscle group

(sclerotomal)

Pain relief Sitting or exed posture Not dependent on posture

Standing and resting

usually insucient

Relief while standing

Pain relief is often slow

(>510 min)

Pain relief is almost immediate

Bicycle ride No pain Pain

Quality of pain sensation Aching and numb Cramping and tight

Peripheral pulses Present Absent or diminished

Femoral or aortic bruits

Ankle/brachial

pressure index

0.95

Ciric et al [54] found a higher correlation between weakness and atrophy inpatients with lateral recess stenosis compared with patients with centralstenosis only.

Cauda equina syndrome

The distal spinal cord terminates at the L1-2 level in a diamond-shapedenlargement called the conus medullaris. The lower motor and sensory nerveroots exit the conus medullaris and form the cauda equina (horses tail) inthe thecal sac [55,56]. Compression of the lumbosacral nerve roots located inthe thecal sac may produce multiple unilateral or bilateral radicular signsand symptoms diagnosed as cauda equina syndrome (CES) [57]. There aremultiple compressive causes of CES, including herniated lumbar interver-tebral discs, spinal stenosis, trauma, chiropractic manipulation, and spinalneoplasms [57,58]. Noncompressive causes also must be considered in thedierential diagnosis and include ischemic injury, inammatory conditions,spinal arachnoiditis, and infections [57]. The classic clinical presentation ofCES is characterized by low back pain, bilateral sciatica, saddle anesthesia,weakness of the lower extremities that may progress to paraplegia, boweland bladder dysfunction, and impairment of the bulbocavernous, medio-plantar, and Achilles tendon reexes [57,59,60]. These signs and symptomsare typically bilateral but may be asymmetric [59].

Although evaluating a patient with back pain who presents with classicCES typically does not represent a diagnostic challenge, evaluating a patientwith back pain who has early and incomplete signs and symptoms of CES isa dicult problem. Back pain is a common complaint that aects up to 90%of the general population at some time in life, and most have complete res-olution of symptoms by 4 weeks [3,61]. Because most back pain is benign,early CES often goes undiagnosed. In 1999, Kennedy et al [58] publisheda retrospective review of 19 patients with CES. They found that all patientshad saddle hypoaesthesia and bladder dysfunction. The group with a satis-factory outcome had a mean time from onset of symptoms to decompres-sion of 14 hours (range, 624 hours), but the group with a poor outcomehad a mean time of 30 hours (range, 2072 hours).

There is much confusion among physicians about urinary incontinenceassociated with spinal cord compression and CES. Patients with spinal cordcompression and CES develop urinary retention initially, and only later dothey develop overow incontinence. Many patients deny urinary inconti-nence but may have large urine volumes in their bladder on post-voidresidual testing. Therefore, it is imperative to check a post-void residual testif there is the slightest suspicion of CES. Deyo et al [62] report that the nd-ing of urinary retention has a sensitivity of 90% and a specicity of 95% inCES. They also report that the absence of a large post-void residual essen-tially rules out CES, with a negative predictive value of 99.9%. We do notrecommend, however, relying solely on the post-void residual test to make


the diagnosis of CES when evaluating back pain. Instead, we recommendcareful history taking and physical examination, with an emphasis on peri-neal sensation, rectal tone, and measurement of post-void residual forproper and early diagnosis of CES as well as early and prompt surgicaldecompression.

Diagnostic workup

After a careful history is taken and a physical examination is performed,the diagnosis of lumbar stenosis is conrmed by radiographic studies. Elec-trodiagnostic studies of the lower extremity are rarely necessary because thediagnosis is established clearly by the history, examination, and most impor-tantly, the radiographic studies.

Imaging

The most important radiographic studies (Figs. 2 and 3) for evaluatinglumbar stenosis are MRI, CT, and rarely, CT myelography. Plain lumbosac-ral radiographs, including exion/extension views, always are obtained. Inmost instances of lumbar stenosis, these techniques not only have similaraccuracy rates but also are often complementary; however, they all haveadvantages and disadvantages, depending on the source of the stenosis[63,64]. Because all of these treatment modalities can diagnose lumbarstenosis adequately, MRI is the initial study of choice because it does notuse ionizing radiation or require contrast injection [65].

Plain lumbosacral radiographs that include exion/extension views arealso an integral component of the radiographic workup. These radiographsprovide an estimation of the degree of mechanical instability, which maynecessitate supplementing the surgical decompression with a fusion.

MRI is a noninvasive study that is outstanding for delineating hypertro-phied ligamenta ava, bulging discs, compressed nerve roots, dural sacimpingement, lateral recess stenosis, and narrowed neural foramina. It pro-vides both sagittal and axial images of the spine. MRI, however, tends tounder-represent bony abnormalities such as hypertrophied facets and spon-dylolisthesis, and it is not as reliable as CT for this purpose. Two other dis-advantages of MRI are that patients with ferromagnetic implants cannot be

Fig. 2. A 67-year-old man with neurogenic claudication and a left L4 radiculopathy. (A)

Midline sagittal T2-weighted image showing a bulging degenerative disc (arrow) at L4-5 and

thickening of the ligamentum avum (arrowhead ). (B) Sagittal T2-weighted image of the left

neural foramina. The hypointensity of the L4-5 neural foramen, which is traversed by the L4

nerve root, represents soft tissue in the foramen (arrow). The neural foramina at the other levels

are normal. (C) Axial T2-weighted image showing the bulging disc (arrow) and thickened

ligamentum avum (arrowhead ). (D) Axial CT scan showing lateral recess stenosis (arrows) and

extensive facet hypertrophy (arrowheads).

c


Fig. 2 (continued )


scanned and that even MRI-compatible metallic implants generate signi-cant scatter artifact.

CT is a noninvasive study that is better than MRI at dening bonyabnormalities and also is less expensive. Unfortunately, CT scans do notprovide the soft tissue information seen on MRI and use ionizing radiationto generate images. CT myelography is an invasive study that gives excellentsoft tissue and bony denition, but it is used less frequently because itrequires the injection of dye and uses ionizing radiation. The soft tissue res-olution of MRI is superior. CT myelography is the study of choice, however,when the patient has had prior surgery either with or without instrumenta-tion [65].

Even though the resolution of CT and MRI provides invaluable detail, itis important not to underestimate the importance of plain radiographs.Plain lms provide excellent bony detail, illustrating fractures, osteophytes,hypertrophied facets, spondylolisthesis, pars interarticularis fractures, discdegeneration, spinous process settling (kissing spines), narrowing of theinterpediculate distance, scoliosis, and metastatic disease. As already men-tioned, exion/extension lateral views are useful in determining the extentto which translational or angular mobility occurs at a potentially unstablesegment. In the authors practice, it is routine for all patients who are beingoperated on to have plain lms in addition to MRI or CT scans.

Electrodiagnosis

Electrodiagnostic testing consists of electromyography (EMG), nerve con-duction velocities, and somatosensory-evoked potentials. As imaging tech-niques have improved, electrodiagnostic testing is no longer used routinelyin the workup of spinal stenosis, but there are instances when it may helpthe physician make the diagnosis of neurodegenerative or neuromuscularconditions resembling spinal stenosis. For example, a patient whose historyand physical examination ndings are suggestive of lumbar spinal stenosisbut also are accompanied by an MRI that does not show narrowing shouldundergo electrodiagnostic testing. The three major electrodiagnostic tests arediscussed briey.

ElectromyographyElectromyography evaluates the physiology of lower motor neurons. It

does not evaluate sensory abnormalities or upper motor neuron disturban-ces. If the nerve supply to a muscle is damaged by disease of the ventral horncell, nerve root, or peripheral nerve, the muscle is denervated and has atypical pattern on EMG [66].

Electromyographs of patients with spinal stenosis often show bilateralmultiradicular abnormalities, even if the patients symptoms are not bilat-eral [67]. In patients with a complete myelographic block, 87.5% had bilat-eral EMG changes, whereas 29% of patients had bilateral EMG changes


when their myelogram was normal [68]. Because symptoms of spinal steno-sis are predominantly sensory and EMG evaluates motor neurons, it is notuncommon to have a normal EMG. Electromyographic ndings do not pre-dict surgical outcome [69], and EMG alone should not be used to determinethe levels of decompression.

Nerve conduction velocitiesElectromyography measures the eect of a nerve on a muscle, but it does

not provide information on the speed at which the nerve impulse travels.Nerve conduction velocity is a test that accurately determines the time takenfor an impulse to traverse a measured length of nerve and reports the valuesin meters per second. It is a useful test for dierentiating peripheral neuro-pathy from radiculopathy [70].

Somatosensory-evoked potentialsSomatosensory-evoked potentials are transmitted through the dorsal col-

umns and measure the sensory component of the nerve. Lesions of periph-eral nerves prolong the latency response. Although somatosensory-evokedpotentials have been used to evaluate stenosis [18] because they measure thesensory component of the nerve, their greatest use has been for intraopera-tive monitoring [71].

Natural history

The natural history of degenerative lumbar spinal stenosis is not wellunderstood. Soon after Verbiest made lumbar stenosis a recognizable clini-cal entity, neurologic and orthopedic surgeons believed that spinal stenosiswas a degenerative and progressive disease that narrowed the canal, causedsymptoms, and required surgical decompression to break the cycle of insta-bility leading to more stenosis [7275]. As a result, most literature concen-trated on the surgical outcome, and little is known about nonoperativetreatments.

Clinical data and experience, however, now suggest that even thoughmost lumbar spinal stenosis is degenerative, it is not necessarily progressive,and surgical treatment can be avoided [6,7678]. Several studies report thatmany patients with mild to moderate stenosis do well without surgery[76,7981]. These studies emphasize that patients with radiographic and clin-ical lumbar spinal stenosis can have improvement by properly tailoring non-operative treatment. For example, strength training, weight loss, stretching,

Fig. 3. A 70-year-old woman with a pacemaker and neurogenic claudication. (A) Antero-

posterior view of a myelogram showing a complete block at L3-4 (arrow). (B) Axial CT myelo-

gram showing facet hypertrophy (arrowheads), a thickened ligamentum avum (double

arrow), a bulging disc (arrow), and compression of the thecal sac.

b


and cardiovascular training may improve circulation to the cauda equinaand decrease the severity of neurogenic claudication. Treatment with anti-inammatory medications can decrease the radicular pain associated withlumbar stenosis [82]. These therapies may ameliorate symptoms long enoughfor the spine to undergo physiologic arthrodesis or for pain bers to adaptto compression and no longer cause pain. These changes could result inlong-term symptomatic relief.

As a result of reports of patients who do well without surgery, investiga-tors began comparing surgical and nonsurgical outcomes. Johnsson et al [77]found that 60% of the patients treated surgically improved and 25% deterio-rated. Of the conservatively treated patients, 30% improved and 60% wereunchanged. In a separate study in 1992, Johnsson et al [76] examined thenatural course of spinal stenosis. The study reported on 32 patients followedup nonoperatively for an average of 49 months and found that 15% hadimprovement in their symptoms, 70% were the same, and 15% were worse.The authors could nd no evidence of deterioration at 4 years, and they con-cluded that expectant observation could be an alternative to surgical treat-ment because of the slow progression of degenerative lumbar stenosis.

In 2000, Amundsen et al [83] performed a prospective, randomized studyof 100 patients, with a 10-year follow-up period, to identify the short- andlong-term results after conservative and surgical management. They foundthat after 3 months, pain relief had occurred in most patients. After 4 years,excellent or fair results were found in 50% of the patients selected for con-servative treatment and in 80% of the patients selected for surgery. Theyalso found that patients who had unsatisfactory results from conservativetreatment and then underwent delayed surgery had the same results aspatients initially randomly assigned into the surgery group. Taken together,the study of Amundsen et al and other studies [76,77,8284] suggest thatconservative treatment is advocated in patients with mild to moderate symp-toms of lumbar stenosis and that surgical treatment is indicated in patientswith severe symptoms. Of note, however, is that important variables such aspsychosocial factors, depression, anxiety, litigation, workmens compensa-tion, and general patient health and tness often are not assessed and canhave a signicant eect on outcomes.

Patients who fail to improve with conservative therapy and have clinicaland radiographic evidence of lumbar stenosis are candidates for surgicaldecompression. One of the risks associated with a decompressive laminec-tomy is the development of secondary spinal instabilityinstability thatoccurs after lumbar surgery (primary spinal instability occurs de novo andresults from trauma, infection, or neoplasm and degenerative disorders ofthe spine) [85]. An overzealous bony decompression that removes one facetjoint or more than 50% of both facet joints or that sacrices the pars inter-articularis is likely to lead to instability [86].

Lumbar instability is a common diagnosis of severe back pain and dis-ability and is treated with a fusion procedure; however, there is no clear


consensus of what constitutes instability [86]. The lack of consensusamong physicians regarding the denition of instability makes collectingdata dicult and developing evidence-based indications for fusion evenmore dicult. In 1995, Sonntag et al [86] published three dierent gradesof pathology (recommended, relative, and rare) warranting spinal fusion.Stable spinal stenosis and grade I spondylolisthesis are listed in the rarecategory. Obviously, several medical and psychologic factors must beconsidered, regardless of the pathology, before a patient is considered for afusion. This consideration is especially necessary for elderly patients.

It is of concern that the rates of lumbar fusion procedures are increasingrapidly, especially for lumbar stenosis in the elderly [87]. In 1995, Katz [87]reviewed the spinal fusion literature and found that fusion rates variedmarkedly among individual surgeons and geographic regions. He also foundthat fusion for spinal stenosis was associated with higher costs and compli-cation rates than decompressive surgery without fusion. The spines of theelderly have often physiologically autofused and tolerate a generous decom-pression without causing or exacerbating a spondylolisthesis [14,88]. Be-cause of the increased morbidity associated with lumbar fusion in theelderly and the fact that the rigid elderly spine has decreased mobility, theauthors rarely perform a fusion in patients more than 60 years old duringthe initial decompression for spinal stenosis. Younger patients are more dif-cult to manage because they still have mobile spinal segments that cancause or exacerbate a spondylolisthesis and cause pain, they have fewercomorbidities, and they do not tolerate an extensive decompression as wellas elderly patients. The authors still prefer, however, to avoid a fusion, butthe threshold to fuse at the initial decompression is lower in patients youn-ger than 50. When a fusion is necessary, the authors generally favor an insitu fusion of the facet joints over one with instrumentation.

A prospective study by Katz et al [89] to identify outcome predictorsof surgery for degenerative lumbar stenosis found that the patients as-sessments of his or her own health and comorbidity are the most cogentoutcome predictors. The study also found that low cardiovascular com-orbidity predicted a favorable outcome. Although outcome predictors forconservative management were not examined, it is likely that low cardio-vascular comorbidity similarly would predict a favorable outcome on non-operative management. An important component of nonoperative therapyconsists of therapeutic exercise [6,82]. A healthy cardiovascular systemwould allow patients to tolerate the stretching and strengthening programsof conservative therapy.

More prospective, randomized studies with valid and reliable outcomemeasures are required for better understanding of the natural history oflumbar stenosis and indications for conservative and surgical treatment.Indeed, additional clinical and experimental work is needed to elucidate themyriad causes of pain in the stenotic lumbar spine. This knowledge willprovide new and improved treatment options for patients with low back pain.


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Lumbar spinal stenosis, cauda equina syndrome, and multiple lumbosacral radiculopathiesAnatomy and pathophysiology of the lumbar spineClinical syndromeCauda equina syndromeDiagnostic workupImagingElectrodiagnosisElectromyographyNerve conduction velocitiesSomatosensory-evoked potentials

Natural historyReferences

radic stenosis cea_pmr clinics

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