focus on understanding and treating spinal stenosis

1

©2010 British Editorial Society of Bone and Joint Surgery

Focus On

Understanding and treating spinal stenosis

IntroductionLumbar spinal stenosis is narrowing of the central spinal canal,lateral recess or the neural foramen. After initial recognition ofspinal stenosis in 1802, a gradual understanding evolved overthe next 150 years.1-4 Harris and Macnab described the impor-tance of disc degeneration in the pathogenesis of stenosis.5

Macnab highlighted the lateral recess beneath the posteriorfacet joint.6 Verbiest identified neurogenic claudication as aresult of spinal canal stenosis. 7

Anatomical considerationsThe shape of the lumbar spinal canal varies and may be an oval,rounded triangular or trefoil configuration.8 The trefoil configu-ration usually occurs at the fifth lumbar level, making L4-L5 thenarrowest level 9 (Fig. 1), and occurs in 25% of the population,only appearing in adulthood.10 The anteroposterior diameter ofthe lumbar spinal canal is critical in the pathogenesis and isaffected by the length of the pedicles.11

ClassificationLumbar spinal stenosis is classified according to its aetiology(Table I).11 Postacchini divided the stenosis into primary (con-genital), secondary (acquired) or combined forms.12

The congenital type is rare. There are anatomical abnormali-ties such as short pedicles in achondroplasia. Other causesinclude hypochondroplasia, diastrophic dwarfism, Morquio'ssyndrome, hereditary exostosis and cheirolumbar dysostosis.The majority of patients present with acquired stenosis becauseof degeneration in the fifth to seventh decades.

Anatomically, spinal stenosis can be central, within the lateralrecess, or in the foramen. Central canal stenosis occurs at thelevel of the intervertebral disc with midline sagittal narrowing.Lateral recess stenosis occurs when the traversing nerve root iscompressed beneath the superior articular process of the infe-rior vertebra, i.e. beneath the thickened facet joint.

Hansraj et al divided spinal stenosis into typical and complexlumbar spinal stenosis (Table II).13,14 Typical cases were treatedwith decompressive surgery, while complex stenosis requireddecompression and fusion.

PathogenesisKirkaldy-Willis et al described the sequence of degenerativechanges which result in central or lateral recess stenosis.15

Central canal stenosis (Fig. 2) is mainly created by hyper-trophy of the ligamentum flavum, facet joint osteophyte forma-tion and degenerative spondylolisthesis (Fig. 3).

Fig. 1

View of the L5 vertebra showing the trefoil configuration of the spinal canal.(Reprinted with permission from JBJS - Eisenstein S.M, The trefoil configuration ofthe lumbar vertebral canal; A study of South African skeletal material. J Bone JointSurg [Br];62-B(1):73-7).

Table I.

Aetiological classification of lumbar spinal stenosis

CongenitalIdiopathicAchondroplastic

AcquiredDegenerativeIatrogenic – post-surgicalMetabolic – Paget’s disease, fluorosisPost-traumaticStenosis due to spondylolisthesis

Combined Congenital with secondary degenerative changes

2 T. S. RAJAGOPAL, R. W. MARSHALL

THE JOURNAL OF BONE AND JOINT SURGERY

Lateral recess stenosis results from compression betweenthe medial aspect of a hypertrophic superior articular facet andposterior aspect of the vertebral body and disc (Fig. 4). Hyper-trophy of the ligamentum flavum and/or facet joint capsule, ver-tebral body osteophyte and disc protrusion exacerbate thestenosis. The traversing nerve root is compressed in the lateralrecess (i.e. the L5 nerve root in the L4-L5 lateral recess).

Foraminal stenosis is rare and mainly occurs in isthmicspondylolisthesis, where the exiting nerve root (i.e. the L5 nerveroot in L5-S1 isthmic spondylolisthesis) is compressed in the dis-torted foramen. It also occurs in far lateral disc herniation wherethe exiting nerve root is compressed in the foramen, or extra-foraminal zone (Fig. 5).

Lateral recess and foraminal stenosis are distinct entitieswith different clinical implications.16

Natural historyThe course of spinal stenosis is chronic and benign. Johnsson,Rosen and Uden reported on 32 patients followed up for a meanof 49 months (10 to 103) without any treatment.17 Of the32 patients, 15% improved, 70% stayed the same and only 15%became worse. The majority of patients followed up for fouryears thus remained unchanged.

Despite a benign natural history, the long term is character-ised by slow deterioration. A randomised study by Amundsen etal compared surgical and conservative treatment with a ten-yearfollow-up.18 The outcome was more favourable for surgical treat-

ment, but an initial conservative approach was recommendedas late treatment still achieved a good result.

Clinical featuresHistory. The symptoms are insidious, presenting in the sixth orseventh decade. There may be a long history of low back painbut the leg symptoms lead to presentation.

The patient with central canal stenosis has bilateral leg symp-toms which are vague and often described as heaviness, sore-ness or weakness. The cardinal symptom is neurogenicclaudication which presents as numbness, weakness or discom-fort in the legs; this may come on with walking or prolonged

Table II.13,14

Typical lumbar spinal stenosis•No previous lumbar spine operation•No radiographic evidence of instability•Degenerative spondylolisthesis < grade I, with no instability•Degenerative scoliosis with < 20° curve

Complex Lumbar Spinal Stenosis•Previous lumbar spine operation•Radiographic evidence of instability•Radiographic evidence of post operative junctional stenosis•Degenerative spondylolisthesis > grade I, with instability•Degenerative scoliosis with > 20° curve

Fig. 2

Sagittal and axial T2-weighted MRI scans showing central canal stenosis.

Fig. 3

Sagittal, axial and coronal T2-weighted MRI scans in an 80-year-old patient show-ing a degenerative spondylolisthesis at L4-L5. There is lateral recess stenosis butthere is no compression of the exiting nerve root on the coronal images (arrowed).

Fig. 4

Sagittal and axial T2-weighted MRI scans in a 74-year-old patient showing lateralrecess stenosis at L4-L5

UNDERSTANDING AND TREATING SPINAL STENOSIS 3

standing and is relieved by sitting or rest. The patients are ableto walk further when leaning on a shopping trolley or walkinguphill because spinal flexion increases the space available forthe cauda equina and unfolds the ligamentum flavum. The pain-free walking distance may vary.

Patients with lateral recess stenosis present with unilateralradicular symptoms of leg pain along with numbness, paraesthe-siae or burning in a dermatomal distribution. Pain radiates fromthe buttock to the posterior thigh and lateral calf because mostcompression occurs at L4-L5. If there is a higher lumbar lesionthen anterior thigh pain will be present. The symptoms may alsobe provoked by walking.

Cauda equina syndrome or major neurological deficits arevery rare in the presence of canal stenosis.Examination. Physical findings are limited. The diagnosis ismade from the history and confirmed with imaging. There maybe limitation of lumbar spinal extension, sensory deficit, muscleweakness, limited straight leg raise, absent knee reflexes andabsent ankle reflexes.19 Neurological abnormalities are uncom-mon at rest. The “Shuttle walking test” has been suggested as areliable objective assessment of walking distance.20 Loss ofdistal vibration sense may be present but is common in olderpatients anyway. Signs of cervical myelopathy may be detected,as lumbar spinal stenosis is associated with cervical canal nar-rowing in 5% of the patients (Tandem stenosis).21

Differential diagnosisPeripheral Vascular Disease. Table III shows the differencesbetween neurogenic and vascular claudicationHip Osteoarthritis. Anterior thigh pain can be present in hiparthritis as well as in spinal stenosis with involvement of the L3or L4 nerve roots. However, pain on passive rotation of the hipshould alert the clinician to the possibility of hip disease. The twoconditions can coexist, so nerve root blocks and/or hip jointinjections with local anaesthetic and steroid may be necessaryto differentiate between them.Peripheral Neuropathy. This diagnosis is determined more byneurological symptoms than pain, and produces a stocking pat-tern of numbness. Electrophysiological testing confirms thediagnosis.Trochanteric Bursitis. Sometimes spinal stenosis patients arediagnosed as having trochanteric bursitis. Some have suggesteda predisposition to this condition because of an “altered pelvicbalance”.22

InvestigationRadiographs. Plain radiographs of the lumbosacral spine mayshow narrowing of the disc space, facet joint osteoarthritis,degenerative spondylolisthesis or degenerative scoliosis. Radio-graphs are also useful to exclude conditions such as tumour orinfection. Dynamic instability can be demonstrated by lateralradiographs taken in the standing position with spinal flexionand extension.Computed Tomography (CT) Myelography. CT or CT myelo-graphy is useful in patients who have a contraindication to mag-netic resonance imaging (MRI) scan (pacemaker, metallicimplants, etc.). On CT, midsagittal lumbar canal diameters ofless than 10 mm are regarded as an absolute stenosis while lessthan 13 mm represents relative stenosis.23

MRI. MRI is the investigation of choice in confirming the diagno-sis of spinal canal stenosis. Standard MRI examination includesT1- and T2-weighted sagittal and axial sequences. The typicalfindings in central or lateral recess stenosis include thickeningof the ligamentum flavum, facet joint hypertrophy and synovialcysts, a trefoil appearance of the thecal sac, vertebral endplateosteophytes and obliteration of perineural fat in the neuralforamina.

Parasagittal images can overdiagnose the incidence of foram-inal stenosis. We recommend additional T2-weighted coronaland Short T1 Inverted Recovery (STIR) sequences which demon-strate the nerve roots very well and confirm that the incidence offoraminal stenosis is low in degenerative spondylolisthesis orspinal stenosis, but exists mainly in isthmic spondylolisthesis orextraforaminal disc protrusion.24 Neurophysiology. Peripheral neuropathy is a frequent concomi-tant finding or differential diagnosis in elderly patients withspinal stenosis. Neurophysiological assessments including elec-tromyography and nerve conduction studies are useful in identi-fying peripheral neuropathy and in differentiating betweenradiculopathy and mononeuropathy (e.g. femoral neuropathy indiabetics).

Fig. 5

Sagittal, coronal and axial T2-weighted MRI scans in a 62-year-old patient showing foraminal stenosis (arrow) caused by a farlateral disc prolapse at L4-L5



ManagementConservative treatment. Analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), weight loss and physiotherapy areused in the management of patients with spinal stenosis. Porterand Hibbert25 reported that nasal calcitonin improved the symp-toms of neurogenic claudication but a further randomised con-trolled study in 2004 showed no benefit.26

There is conflicting evidence in the literature about the use ofepidural steroids.27-29 However, they can provide temporaryrelief of symptoms. Nerve root blocks are useful in treating rad-icular pain due to lateral recess stenosis.30

Surgical treatment. Surgery is indicated when conservativemeasures fail and if moderate to severe leg symptoms interferewith the patient's lifestyle. While these indications remain rela-tive, progressive neurological deficit or cauda equina syndromerepresent absolute indications for surgery.

The greater the degree of compression, the better the out-come of surgery. While the primary objective of surgery is torelieve the patient's leg symptoms, it is important to consider themechanical back pain and/or instability before deciding on thetype of surgical procedure.

The surgical options include:• Decompressive laminotomy and partial facetectomy• Decompressive laminectomy and partial facetectomy• Micro-decompression• Decompression and non-instrumented fusion• Decompression and instrumented fusion• Decompression and flexible stabilisation• Inter-spinous spacer devices.Decompressive Laminotomy and Laminectomy. The aim ofdecompression is to remove the pressure on the cauda equinaand the individual nerve roots. The standard wide midlinedecompressive laminectomy involves the removal of the spinousprocesses, laminae, ligamentum flavum, medial part of the facetjoints and the facet capsule at all involved vertebral levels. How-ever, the potential for segmental instability has led to more con-servative operations.

The popular technique of multiple laminotomies may pre-serve segmental spinal stability, but Postacchini et al found thatpatients who had laminotomies had less back pain but a slightlyhigher incidence of nerve damage.31 Laminectomy was found tobe better for tight stenosis, as it allowed safer neural decompres-

sion. Multiple laminotomies are recommended in developmen-tal stenosis since the patients are younger, the stenosis is rarelysevere and additional disc excision is often necessary.16

The results of surgical decompression for lumbar spinal steno-sis vary from 57% to 81% excellent and good.32 The results foropen31,33 or microsurgical laminotomy34,35 are similar. No differ-ence between clinical outcome and spondylolisthesis progressionwas found when comparing laminectomy with laminotomy.36

While the initial results of decompressive laminectomy arefavourable, they can deteriorate in the longer term. Jonsson et alreported on a prospective study of 108 patients who had laminec-tomy without fusion; 67% had excellent results at two years, butdeteriorated to 50% at five years; 18% required re-operation.37

It has been suggested16,37 that the ideal surgical patientwould have: • Severe osteoligamentous compression of the neural struc-

tures• Severe leg symptoms• Moderate or no neurological deficit• Little or no back pain• Symptoms for less than four years• No associated condition to impair mobility

Old age does not compromise the results of decompressivesurgery.38

Microdecompression. “Microdecompression” minimises opera-tive trauma by approaching and entering the canal from one sideonly. After decompressing the ipsilateral open side, the dissec-tion crosses the midline beneath the overhanging spinous proc-esses and contralateral laminae, allowing trimming of the facetjoints and other compressive structures on the contralateralside from within the canal39 (Fig. 6). Mayer et al. reported suc-cess in 275 patients at a mean of two years, with an improve-ment in back pain in 48% of patients and of leg pain in 51%.40

In another study, with a longer follow-up of 100 patients, sci-atica improved in 90% and back pain in 84%. For 82% of thepatients their results were graded as good or excellent accordingto the Macnab criteria.39

Decompression and fusion. Fusion is generally recommendedin addition to decompression in the following circumstances:• Degenerative spondylolisthesis• Degenerative scoliosis• Concomitant moderate to severe back pain

Table III.22,32 Differences between neurogenic and vascular claudication

Symptom/sign Neurogenic Claudication Vascular Claudication

Pain Proximal to distal Distal to proximalRelief of symptoms Relieved by sitting/forward bending Relieved by standingWalking up hill Better WorseWalking down hill Worse BetterCycling No symptoms Symptoms presentWalking distance Variable FixedNeurological symptoms Commonly present Not presentNeurological signs May be positive especially after walking NegativePulse Present AbsentSkin No changes Atrophic changes


• Necessity for wide decompression with facet joint removal• Recurrent spinal stenosis

Herkowitz and Kurz prospectively compared decompressionalone with decompression and fusion in 50 patients with spinalstenosis and degenerative spondylolisthesis with a follow-up ofthree years.41 The results were satisfactory (excellent or good) in44% of the unfused and 96% in the fused group. Fischgrund et alprospectively randomised 76 patients and compared intertrans-verse non-instrumented fusion with pedicle screw fusion.42

Excellent or good results were obtained in 82% of the intertrans-verse group (45% fusion rate) and 76% of the pedicle screwgroup (82% fusion rate). The authors concluded that the use ofinstrumentation leads to a higher rate of fusion but there was nostatistically significant clinical difference.

Kornblum et al later showed that the patients with a solidfusion had improved long-term clinical results after five to14 years.43

We can thus conclude that an instrumented fusion should beperformed in addition to decompression in the management ofdegenerative spondylolisthesis.Decompression and flexible stabilisation. In patients with spinalstenosis who have segmental instability or degenerative spond-ylolisthesis, spinal decompression and stabilisation with a flexi-ble or dynamic stabilisation system (e.g. Dynesys (Zimmer Ltd,Swindon, Wilts)), is a controversial option, but Schnake,Schaeren and Jeanneret found clinical results similar to decom-pression and fusion with pedicle screws.44 Interspinous spacer devices. Interspinous spacer devices areinserted between the spinous processes to prevent extension of

the symptomatic levels, but allow flexion, axial rotation and lat-eral bending.

Biomechanical studies have shown that in extension theimplants increase the dimensions of the spinal canal.45 There aresome favourable reports of outcome with interspinous devices;46-48

however, others report high failure rates for these implants and theneed for further surgery.49 The evidence is thus still inconclusive.Interspinous spacer devices may have a place in elderly patientswho are unfit for anaesthesia and more major surgery.

Degenerative scoliosisSpinal stenosis associated with degenerative scoliosis is a com-plex problem and its treatment is controversial. These patientshave multilevel disease with varying combinations of central, lat-eral recess or foraminal stenosis. They have a mixed pattern ofsymptoms, which include stenotic, radicular and arthritic pain(Fig. 7). Nerve root compression is present more often on theconcave side of the curve.50 True foraminal compression canoccur due to lateral disc herniation, collapse of the disc and sco-liosis. The incidence of complications is high after surgery51 asthese are patients of advanced age who may have multiple med-ical comorbidities. Two types of deformity have beendescribed.52 Type I is a lumbar scoliosis with no or minimal rota-

Fig. 6

Post-operative axial CT scan showing the spinal canal to be opened up after micro-decompression.

Fig. 7

Sagittal, coronal and axial T2-weighted MRI Scans in an 89-year-old patient show-ing degenerative scoliosis and multilevel spinal stenosis



tional deformity. Type II curves have degeneration superimposedon a pre-existing scoliosis with greater rotational deformity andloss of lordosis. Shorter segmental instrumentation is usuallypossible for type I deformities while longer instrumentation withsagittal plane reconstitution is necessary for type II curves(Fig. 8).52 The choice of surgical technique remains controversialbut most would agree that decompression and instrumentedfusion is necessary for a successful outcome.13

Trichy S Rajagopal FRCS, Robert W Marshall FRCS

Department of Orthopaedic Surgery, Royal Berkshire Hospital, ReadingRG1 5AN, UK.

Corresponding author: R. W. Marshall,e-mail: [email protected]

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Fig. 8b

Anteroposterior and lateral radiographs of a 79-year-old patient with degenerative scoliosis, loss of lumbar lordosis and rotational deformity. The patient had persistentback pain after a single-level fusion that had been performed many years earlier. a) pre-operative views, b) post-operative views showing correction of the degenerativescoliosis and restoration of sagittal alignment.

Fig. 8a


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focus on understanding and treating spinal stenosis

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