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Focus On Understanding and treating spinal stenosis Introduction Classification Lumbar spinal stenosis is narrowing of the central spinal canal, Lumbar spinal stenosis is classified according to its aetiology lateral recess or the neural foramen. After initial recognition of (Table I).11
  1 ©2010 British Editorial Society of Bone and Joint Surgery Focus On Understanding and treating spinal stenosis Introduction Lumbar spinal stenosis is narrowing of the central spinal canal,lateral recess or the neural foramen. After initial recognition of spinal 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 considerations The 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 of the lumbar spinal canal is critical in the pathogenesis and isaffected by the length of the pedicles. 11 Classification Lumbar 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. Pathogenesis Kirkaldy-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. 1View of the L5 vertebra showing the trefoil configuration of the spinal canal.(Reprinted with permission from JBJS - Eisenstein S.M, The trefoil configuration of the 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 CongenitalIdiopathicAchondroplasticAcquiredDegenerativeIatrogenic – post-surgicalMetabolic – Paget’s disease, fluorosisPost-traumaticStenosis due to spondylolisthesisCombined Congenital with secondary degenerative changes  2T. 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 history The 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 the32patients, 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 features History. 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 ãNo previous lumbar spine operationãNo radiographic evidence of instabilityãDegenerative spondylolisthesis < grade I, with no instabilityãDegenerative scoliosis with < 20° curve Complex Lumbar Spinal Stenosis ãPrevious lumbar spine operationãRadiographic evidence of instabilityãRadiographic evidence of post operative junctional stenosisãDegenerative spondylolisthesis > grade I, with instabilityãDegenerative scoliosis with > 20° curveFig. 2Sagittal and axial T2-weighted MRI scans showing central canal stenosis.Fig. 3Sagittal, 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. 4Sagittal and axial T2-weighted MRI scans in a 74-year-old patient showing lateralrecess stenosis at L4-L5  UNDERSTANDING AND TREATING SPINAL STENOSIS3 standing and is relieved by sitting or rest. The patients are ableto walk further when leaning on a shopping trolley or walking uphill 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 of distal 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 diagnosis Peripheral Vascular Disease. Table III shows the differencesbetween neurogenic and vascular claudication Hip 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 Investigation Radiographs. 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 of less 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 thickening of 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 of foraminal 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. 5Sagittal, 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  4T. S. RAJAGOPAL, R. W. MARSHALL THE JOURNAL OF BONE AND JOINT SURGERY  Management Conservative treatment. Analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), weight loss and physiotherapy areused in the management of patients with spinal stenosis. Porterand Hibbert 25  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 of epidural 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:ãDecompressive laminotomy and partial facetectomyãDecompressive laminectomy and partial facetectomyãMicro-decompressionãDecompression and non-instrumented fusionãDecompression and instrumented fusionãDecompression and flexible stabilisationãInter-spinous spacer devices. Decompressive Laminotomy and Laminectomy. The aim of decompression 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 facet joints 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 foropen 31,33  or microsurgical laminotomy 34,35  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 suggested 16,37  that the ideal surgical patientwould have: ãSevere osteoligamentous compression of the neural struc-turesãSevere leg symptomsãModerate or no neurological deficitãLittle or no back painãSymptoms for less than four yearsãNo associated condition to impair mobilityOld 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 facet joints and other compressive structures on the contralateralside from within the canal 39  (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 according to the Macnab criteria. 39 Decompression and fusion. Fusion is generally recommendedin addition to decompression in the following circumstances:ãDegenerative spondylolisthesisãDegenerative scoliosisãConcomitant moderate to severe back pain Table III. 22,32 Differences between neurogenic and vascular claudication Symptom/signNeurogenic ClaudicationVascular Claudication PainProximal to distalDistal to proximalRelief of symptomsRelieved by sitting/forward bendingRelieved by standing Walking up hillBetterWorseWalking down hillWorseBetterCyclingNo symptomsSymptoms presentWalking distanceVariableFixedNeurological symptomsCommonly presentNot presentNeurological signsMay be positive especially after walkingNegativePulsePresentAbsentSkinNo changesAtrophic changes
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