The Spine Journal 7 (2007) 428–436

Review Article

Degenerative lumbar scoliosis associated with spinal stenosis

Avraam Ploumis, MD*, Ensor E. Transfledt, MD, Francis Denis, MDTwin Cities Spine Center, 913E 26th Street, Minneapolis, MN 55404 USA

Received 16 March 2006; accepted 29 July 2006

Abstract BACKGROUND CONTEXT: Degenerative de novo scoliosis is commonly present in older adultpatients with spinal pain. The degenerative process including disc bulging, facet arthritis, and lig-amentum flavum hypertrophy contributes to the appearance of symptoms of spinal stenosis in thesepatients.PURPOSE: The etiology, prevalence, biomechanics, classification, symptomatology, and treat-ment of degenerative lumbar scoliosis in association with spinal stenosis are reviewed.STUDY DESIGN: Review study.METHODS: Retrospective analysis of studies focused on all parameters concerning degenerativescoliosis associated with stenosis.RESULTS: There is a variety of treatment methods of degenerative scoliosis based on symptom-atology and radiologic measurements of scoliosis and stenosis. Satisfactory clinical results reportedin relevant retrospective studies after operative treatment range from 83% to 96% but with increasedpercentage of complications. An algorithm for operative treatment corresponding to a newly pro-posed classification system of degenerative lumbar scoliosis with associated canal stenosis ispresented.CONCLUSIONS: There is an increasing prevalence of degenerative scoliosis in the aged popula-tion. Even though the exact percentage of patients with symptomatology of spinal stenosis is notknown, the main goal is to provide pain relief and improved functional lifestyle with minimumintervention. � 2007 Elsevier Inc. All rights reserved.

Keywords: Degenerative scoliosis; Spinal stenosis; Decompression; Fusion

Introduction

Adult scoliosis is defined any curvature of the spinemore than 10� in a skeletally mature individual. The termdegenerative de novo scoliosis (DDS) refers to scolioticcurves developing after skeletal maturity without previoushistory of scoliosis. Scoliosis occurs de novo in later lifeand is associated not only with severe back or leg painbut also with complicated surgical outcomes [1].

Degenerative spondylolisthesis is very common in casesof degenerative scoliosis. In a study of patients with degen-erative scoliosis, 55% of them had additional degenerativespondylolisthesis [2]. Rotatory olisthesis coexists in 13% to34% of adult scoliosis cases [3,4]. It is a triaxial deformity

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manuscript.

* Corresponding author. Twin Cities Spine Center, 913 E 26th Street,

Minneapolis, MN 55404. Tel.: (612) 775-6200; fax: (612) 775-6222.

E-mail address: ploumis@med.auth.gr (A. Ploumis)

1529-9430/07/$ – see front matter � 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.spinee.2006.07.015

consisting of axial rotation on the vertical axis, lateraltranslation toward the convexity of the curve, and anteriortranslation in the sagittal axis. Trammell et al. [4] originallydescribed rotatory olisthesis as the apparent lateral sublux-ation of one vertebral body upon another seen in the ante-roposterior films. Other terms used in the past for the samepathology are lateral spondylolisthesis, translatory shift,lateral olisthesis, and lateral subluxation. It occurs most fre-quently at the L3–L4 level, in women, and increases withage and magnitude of the curve.

Lumbar spinal stenosis is a common problem in the olderadult population. It is defined as a pathologic conditionin which the neural elements are compressed by bone, softtissue, or both resulting in ischemia of nerve roots [5]. It isdistinguished in central stenosis, when there is abnormalnarrowing of the spinal canal, and lateral stenosis, whenthere is lateral recess (subarticular stenosis) or foraminal(foraminal stenosis) narrowing [6]. Symptoms of neuro-genic claudication and radiculopathy predominate. Fre-quently, it is accompanied by degenerative olisthesis and

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degenerative scoliosis. The adjuvant scoliosis complicatesneural compression and makes surgical treatment more dif-ficult [7].

Aging affects bony structures, discs, ligaments, facetjoints, and muscles. This causes wedging of both vertebralbodies and discs and may ultimately lead to a domino-likeeffect of rotation and translation into the upper lumbar andsometimes thoracolumbar spine. Degenerative scoliosis,reduced lumbar lordosis, and neural element compressionis the final end result. Also, the combination of ligamentumflavum hypertrophy, facet hypertrophy, disc collapse, andolisthesis cause neural compression.

The purpose of this article is the in-depth analysis ofdegenerative scoliosis associated with symptoms of canalstenosis. A comprehensive and simple classification systemwith corresponding algorithm for operative treatment fordegenerative lumbar scoliosis associated with spinal steno-sis is presented.

Etiology

Decreased bone density was initially considered to bethe cause of degenerative scoliosis [8,9], but this haschanged after finding that no significant difference existsin the bone density between patients with degenerative sco-liosis and patients with adolescent scoliosis of the adult[10]. Actually, degenerative changes, especially of the disc,vertebral body wedging, and facet joint arthrosis areresponsible for the appearance of ‘‘de novo’’ scoliosis anddegenerative rotatory scoliosis [11,12].

A cadaver study of 19 lumbar spines with degenerativeolisthesis without scoliosis showed it was mostly associatedto disc degeneration and osteophytosis of apophyseal jointsand less to fractured endplates. The joint capsules becomeattenuated as a new false articular surface is created on thelamina next to the inferior articular process. In the samestudy, canal constriction was not found because of olisthe-sis, but this was without acknowledging the possible steno-sis of soft tissues (ligamentum flavum, facet capsules, andso on) [13].

Kobayashi et al. [11] studied the prevalence of degener-ative de novo scoliosis in normal-aged people and con-cluded that more than 5 mm lateral osteophyte of anendplate or more than 3� asymmetric tilt of a disc spaceare risk factors for development of degenerative scoliosis.This confirms the notion that degenerative scoliosis startsas disc degeneration [11,12].

In addition, aging may induce ‘‘degenerative myopathy’’leading to rupture of the equilibrium and kyphotic deforma-tion of the spine. Repetitive torsional loads may progres-sively provoke rotational deformation of the posteriorvertebral elements and lead to degenerative rotatory scolio-sis [14].

Iatrogenic instability caused by iatrogenic facetectomiesis another cause of rotary olisthesis. The vertebrae without

facet joints lack the second most significant factor of inter-vertebral stability in the horizontal anteroposterior Z andlongitudinal vertical Y axis of the global reference system.Therefore, the vertebra above in the spinal unit progressgradually to forward olisthesis and rotation that leads torotatory scoliosis and stenotic symptoms caused by thekinking of the neural elements by the malrotated pedicles[13–15].

Prevalence and natural history

The prevalence of degenerative scoliosis is reported tobe from 6% to 68% [8,11,16,17] and increases with age[2]. Pritchett and Bortel [2] studied 200 patients more than50 years old (70% women) with late-onset scoliosis. Theyfound that most of the lumbar degenerative curves did notexceed 60� and progressed an average 3� per year. Factorsfor curve progression were Nash- Moe grade 3 apical rota-tion, a Cobb angle more than 30�, lateral vertebral transla-tion of 6 mm or more, and the prominence of the L5vertebra in relation to the intercrest line. On the contrary,Murata et al. [12] showed in the early phase of degenerativecurves they might also regress after consequential wedgingin the disc space or the vertebral bodies for compensatingimbalance.

The mean age of patients with degenerative scoliosiswas less than 60 years in 38% of Perennnu’s study and33% in Kostuik’s study, whereas 41% of scoliotic patientswere younger than 64 years old in Robin’s study. In Tram-mell’s study, the average age of patients with rotatory sco-liosis was 41 years. Right-sided degenerative scoliosesworsen with aging twice as much than left-sided scoliosis[3,17]. This is associated also with deterioration of rotaryolisthesis.

There are no studies estimating what percentage of pa-tients with degenerative scoliosis will need evaluation andtreatment for their symptoms, axial back pain, or symptom-atology of spinal stenosis. It is also unknown what is thenatural history of these symptoms without treatment. How-ever, the symptoms of spinal stenosis irrespective of scoli-osis have been found to be improving over time in 15% ofcases, deteriorating during the initial 2 to 3 yeas of follow-up requiring surgical intervention in 40% of the patientsand maintaining their status over long-term in the rest45% of the cases [6,18].

Biomechanics

It is known that the kinematics and the coupling patternare different from one spinal region to another. The cou-pling pattern of lateral bending and axial rotation is con-verging in the lumbosacral junction meaning that rightlateral bending coincides with right axial rotation of L5vertebra on the sacrum. However, in the lumbar spine, thecoupling pattern of lateral flexion and axial rotation is

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diverging; that means right axial rotation results in left lat-eral bending [19,20].

In scoliosis, thoracic spine motion is balanced but thecoupling mechanism is abnormal. Instead of axial rotationto be toward the concavity, it is occurs into the convexityof the curve [21]. It is unknown what the etiology is of thisabnormal coupling motion pattern.

On the contrary, Veldhuizen and Scholten [15] foundthat the coupling mechanism of axial rotation and lateralbending does not differ in normal and scoliotic spines.However, they supported that there exists a special couplingmechanism between sagittal plane motion and axial rota-tion in the scoliotic spine.

Disc and facet degeneration leads to increased axialrotation of the functional spinal unit. The increase in axialrotation caused by spinal degeneration was more pro-nounced than the increase of motion in flexion-extension[20]. Degenerative scoliosis is also followed by decreasedlumbar lordosis and, subsequently, low back pain [2,12].

There have been described various methods for determi-nation of vertebral rotation [22–24]. The most widely usedmethod of radiographic determination of vertebral rotationis the pedicle method (grade 0–IV) introduced by Nash andMoe [22]. Grade 0 defines the neutral vertebra when thereis no asymmetry between the anteroposterior pedicle pro-jection in the convex and the concave side. Grade IV isthe total disappearance of the pedicle in the concave side,whereas the pedicle on the convex side migrates pastmidline.

Clinical presentation

The incidence of low back pain in patients with degener-ative scoliosis is not significantly more common than in thegeneral population. Paraspinal muscle electrodiagnostic ex-amination has helped to define the association between radio-logical spinal stenosis and back pain [25]. Lumbar scoliosiswith degenerative changes most prominent at the scolioticapex can produce lumbar stenosis resulting in disablinglow back pain and leg pain in a neurogenic claudication mode[26]. However, sometimes leg symptoms appear from thecontralateral side because of the lumbosacral curve [27,28].Liu et al. [29], in their study of patients with degenerativelumbar scoliosis and stenosis, concluded that L3 and L4nerve roots are compressed in the foramen or extraforami-nally on the concave side of the main curve, whereas theL5 and S1 roots are affected more by lateral recess stenosisat the convex of the lumbosacral fractional curve.

However, rotatory olisthesis does correlate with backpain associated with idiopathic scoliosis. It is significantlyassociated with increasing age and magnitude of the curve[4]. Smaller Cobb angles and lateral and rotatory olisthesisare more frequently seen in degenerative scoliosis than inadult idiopathic scoliosis.

On the contrary, Perennou et al. [3] showed that there isdefinitely correlation between anterior femoral radicular

pain and degenerative rotatory olisthesis especially at L3–L4 and L4–L5 levels. However, the mean age of patientswas 62 years in Perennou’s study and 23 years in Tram-mel’s study.

Velis and Thorne [30] and Kostuik et al. [31] describedlateral olisthesis as an important prognostic factor for thedevelopment of back pain and curve deterioration afterskeletal maturity. Scwab et al. [32] comparing radiographicparameters with VAS scores in adult scoliotic patientsfound that pain correlates with L3 and/or L4 obliquity, lat-eral rotatory olisthesis, lumbar lordosis, and thoracolumbarkyphosis. Curve magnitude and number of levels involvedin the curvature were unrelated to pain. Degenerative insta-bility is the cause of pain and a common pathway in theprogression of all types of adult scolioses.

The etiology of the pain might be mechanical or neuro-genic [33]. Commonly, mechanical back pain presents incases with longstanding idiopathic scoliosis. It appears withmuscle pain because of fatigue of spinal muscles (along thewhole length of the spine and specifically in the convexside of the curve) and is attributed to the loss of lumbar lor-dosis. The pain in the concavity of the scoliosis is causedby facet arthritis and degenerative changes of the discspaces (disc changes, ligament tension and tears, spurs,and so on).

The sagittal gravity line passes in front of the S1 verte-bral body and back musculature is over functioning forkeeping an upright position. The notion that clinical symp-toms of back pain increase linearly with the degree ofpositive sagittal imbalance is supported by the findings ofGlassman et al. [34] in a retrospective review of 752patients with adult scoliosis.

Neurogenic pain is mainly a feature of patients with denovo scoliosis. It is possible, although, to be present incases of adult idiopathic scoliosis. Neurogenic pain iscaused by either foraminal nerve root or dorsal root gaglioncompression (concave side of the curve) or central spinalstenosis leading to neurogenic claudication.

It is imperative to distinguish the neurogenic claudica-tion symptoms from the pain caused from vascular claudi-cation. The pain in neurgenic claudication is reduced if thepatient acquires a forward flexed (like bicycling) or sittingposition. The pain in vascular claudication is relieved bystanding still and accompanied with peripheral vascularloss and skin changes.

The accompanying medical comorbidities in these el-derly patients should not be overlooked. It should be keptin mind that the patient is being operated on is a whole per-son, not just a spine. Keeping the surgical intervention asminimal as possible should be the ideal goal.

Lumbar spinal stenosis

Spinal stenosis is the narrowing of the spinal canal and canbe local, segmental, or generalized. It is divided into the con-strictive stenosis caused by bony or ligamentous reduction in

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the size of the canal and the restrictive stenosis, which is at-tributed to intracanal fibrosis (i.e., arachnoiditis) restrictingthe mobility of neural elements [35]. Usually, it is acquiredas in degenerative diseases or spondylolisthesis and less com-monly is congenital. The degenerative disease of the spineleads to constrictive-compressive type stenosis. It reducessubstantially the spinal reserve capacity; this is the ratiobetween the horizontal distance of posterior middle of thelamina from the posterior end of the vertebral body and theanteroposterior diameter of neural canal measured in CTtransverse sections. Spinal reserve capacity is actually a func-tional factor of spinal canal and is better than other staticmeasurements like the AP canal diameter [35]. It is com-monly admitted that absolute stenosis exist when AP canaldiameter is less than 11 mm [36]. However, the use of subjec-tive criteria to characterize spinal stenosis by radiologists andrelevant clinical physicians (spine surgeons, neurologists,and physiatrists) led to high variability of results for the samepatients [37]. Radiologists specialized in spine imaging sub-jectively grade the stenosis as mild, moderate, and severe,according to the degree.

The criteria for central and lateral stenosis are difficult todefine. Verbiest [38] was the first to introduce the terms ofabsolute and relative value of spinal stenosis. The shape ofthe spinal canal, the facet joints, and the measured spinaldimensions (interpedicular distance, sagittal diameter ofthe dural sac, and pedicle length) are some of the measure-ments evaluating spinal stenosis [39]. Hypertrophy of theascending facet is the main cause of lateral stenosis [7].Biomechanical studies of the foramen of the lumbar spineproved that during flexion and contralateral lateral bendingof the spine the foraminal cross sectional area increases,whereas in extension or ipsilateral lateral bending theforaminal area decreases. Distraction may increase the fo-raminal height, but the osteophytic changes continue to ap-ply pressure to the nerves in the stenotic foramen [40]. Inhistologic studies of the neural foramen, it was found thatthe nerve root and ganglion are within the upper pole ofthe foramen above the disc and never occupy more than35% of the cross-sectional area. In foraminal morphometricstudies of cadaveric spines, it was found that the foramenhave variable size between 40 and 160 mm2 and definedthe normal limits of foraminal cross-sectional area in thesagittal plane [41]. Measurement of vertebral foraminausing calipers is superior to that with CT scan [42].

Often, the radiological findings are more severe than thepatients’ symptoms. Studies of patients with lumbar spinalstenosis have shown that there is no statistically significantcorrelation between the intensity of pain and the degree ofstenosis. Most commonly, the radiologic image of stenosiswas more extensive than expected from the clinical picture[39]. Therefore, spinal stenosis can be either radiographic-only spinal stenosis or symptomatic spinal stenosis witha combination of clinical and radiographic characteristics.

It is mentioned earlier in the etiology of rotatory scolio-sis that there is compression of the dura and traction of the

nerve roots because of vertebral rotation and subluxation.Additionally, hypertrophy of ligamentum flavum, discdegeneration and protrusion, facet joint osteophytosis, andcysts of the facet joints are significantly decreasing thefunctional capacity of the spinal canal.

Classification

The only classification system that exists for degenera-tive lumbar scoliosis addresses only the existence of rota-tion or/and lumbar lordosis loss. It does not includerotatory olisthesis or stenosis. Simmons characterized astype I the degenerative scoliosis with no or minimal rota-tion, whereas type II was defined as the degenerative scoli-osis with rotational deformity and reduced lumbar lordosis[1,43,44].

Schwab et al. [32] recently published a classification ofadult scoliosis based on radiographic measurements inanteroposterior and lateral standing radiographs. Theymeasured the lordosis L1–S1 and the obliquity of L3 verte-bral body and divided the population in three types ofseverity with decreasing lordosis and increasing L3obliquity [32].

There is need for a classification system that it will ad-dress the segmental type of deformity, the sagittal spinalcontour, and the symptomatology. The proposed classifica-tion system is shown in the Table 1. However, the validityand reliability of this system are still under investigation,and this is a best-guess approach based on our experience.

Radiographic evaluation

Plain full-spine standing AP and lateral radiographs arenecessary to evaluate case of degenerative scoliosis associ-ated with rotary olisthesis. In the coronal plane, useful pa-rameters are the following: 1) C7PL (plumbline from thecenter of C7 vertebral body) horizontal distance fromCSVL (central sacral line), 2) scoliosis Cobb angle (major,hemicurve, and proximal thoracic), 3) proximal stable anddistal stable vertebra of the major curve, 4) L3 endplateobliquity, 5) L4 endplate obliquity, 6) maximal lateral olis-thesis (mm), and 7) maximal vertebral rotation (Nash-Moegrades).

In the sagittal plane, parameters to be measured are thefollowing: 1) sagittal Cobb angle (thoracic [T1–T12], thor-acolumbar [T10–L2],and lumbar [T12–S1], 2) PLC7-S

Table 1

Type I: minimal or no rotation

Type II: rotatory olisthesis (intersegmental rotation and translation)

Type III: rotatory olisthesis and structural coronal (O4cm distance from C7

plumbline) or positive sagittal imbalance (O2cm from anterior sacral

corner)

A: back pain without radicular sx

B: sciatic pain (from the lumbosacral hemicurve) 6back pain

C: femoral pain (from the major curve) 6back pain

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horizontal distance of the C7 plumb line starting in the cen-ter of C7 body and the anterosuperior corner of S1, 3) max-imal anteroposterior olisthesis (mm), and 4) sagittal pelvictilt index [32].

The most predictive radiologic parameters for the asso-ciate clinical presentation of the patients with adult scolio-sis are the upper endplate obliquities L3 and L4, lateralolisthesis, lumbar lordosis, and thoracolumbar kyphosis[32]. The positive sagittal balance has been shown to corre-late statistically significantly with the clinical presentation,preoperatively and postoperatively [34].

In order to assess the degree of spinal stenosis it is im-perative to review a CT scan or MRI of the lumbar spine.Especially the T2 sequense of the MRI shows the size ofthe spinal canal and the existence or intrathecal fluid inthe transverse sections, whereas the patency of the foramenis better shown in the sagittal views. The myelography isnot used so often nowadays because of its side effects; how-ever, the CT myelogram gives a profound demonstration ofthose levels with spinal stenosis (Figs. 1–3).

Nonoperative treatment

Requirement for surgical treatment of degenerative sco-liosis is the application and failure of nonoperative treat-ment. The first step of pain management is the use ofnonsteroidal antiinflammatory drugs and nonnarcotic anal-gesics as well as the avoidance strenuous spinal motions. Asession of oral administration of methylprednizolone is pre-scribed in cases of acute onset severe pain. Tricyclic antide-pressants (amitriptylin) and anticonvulsion (carbapentin)drugs are preserved for cases of chronic pain. In case ofsymptoms persistence, the use of custom-made spine im-mobilization and vertebral joints’ injections follow. Epidu-ral steroid injections may provide short- or long-term reliefof symptoms. They are performed mainly for radiculopathybut also for back pain with radiographic spinal stenosis.Translaminar injections should be done always under fluo-roscopy in order to avoid missing the target. Transforaminalepidural injections are indicated for one-level stenosis withunilateral symptoms and are certainly more selective to thelocation of spinal stenosis than translaminar injections. The

Fig. 1. (A) Anteroposterior and (B) lateral view full spine of a patient with degenerative rotary scoliosis with the apex to the left. Note the lateral olisthesis at

L2–L3 and L3–L4 and the positive sagittal imbalance.

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time delay between epidural injections should be at least 3weeks, and the total number of injections allowed is no morethan three to four within 6- to 12-month interval. In a recentrandomized prospective study to assess the efficacy of epidu-ral steroids injections versus intramuscular steroid and anes-thetic for patients with lumbar stenosis, it was found that eventhough there was a significant reduction of pain in the short-term the long term results did not show any difference in thenumber of patients that needed surgery [45]. Abdominal andback muscle strengthening together with swimming areconsidered other methods of pain management [1,8,46,47].

The efficacy of nonoperative treatment (analgesics, exer-cises, and steroid injections) was studied in 49 patients withradiographic and clinical spinal stenosis. Thirty-three (67%)patients showed mild or significant clinical improvement at

Fig. 2. Computed tomography myelogram transverse cuts at the (A) L3–

L4 and (B) L4–L5 level showing the central and subarticular stenosis.

the 3-year follow-up [46]. Furthermore, the systematic sideeffects (gastrointestinal, circulatory, haematological, and re-nal) from the prolonged use of nonsteroidal anti-inflamma-tory drugs should be kept in mind and their prescription belimited only for short-term use.

Operative treatment

All nonoperative ways of treatment should be exhaustedbefore considering surgical treatment. The aim of the sur-gery is to decompress the comprised neural elements, incase of symptomatic spinal stenosis and to end with a bal-anced and stable spine in the coronal and sagittal plane,when there is imbalance. However, these patients are el-derly patients with other comorbidities, and surgical treat-ment should be performed in a safe and effective way.The ideal is to proceed with only the least aggressive pro-cedure, usually posterior only, that would involve bothdecompression and stabilization, if needed, of the spine.

The most frequent indication of surgical treatment ispain [31,48,49]. However, the degree of any individual pa-tient is very objective and cannot be measured indepen-dently. Usually, the most important question that a patienthas to answer is how much his/her symptoms affect his/her life. The patients who present with back pain onlyshould be warned that they would not be completely painfree, especially after a fusion surgery.

Progressive neurologic deficit is another indication forsurgery. Increasing leg weakness and paresthesias that arenot caused by vascular pathology should make the surgeonto suspect spinal stenosis. Symptoms originating from spinalstenosis typically appear between the 5th and 7th decade oflife (40–60 years) [50]. Blood loss should be controlled tominimum amounts. Finally, bone quality should be exam-ined before undertaking a surgical procedure, especially inaged patients, in case of instrumented fusion.

Patients who present with symptoms of spinal stenosisand have degenerative scoliosis less than 20� and withoutinstability could be treated with spinal decompression only[51]. Especially, male patients with large vertebral struc-tures and stabilizing osteophytes can tolerate more than2-level laminectomy without fusion [52].

Otherwise, patients with degenerative scoliosis morethan 15� to 20�, lateral subluxation, or dynamic instabilityshould be treated with decompression and fusion. Simmonsselects different fusion strategies according to his classifica-tion’s types of degenerative scoliosis. For type I, he prefersthe short instrumented fusions with distraction forces ap-plied to the concavity of the curve in order to decompressthe nerve roots. For type II, he prefers the long instrumen-tation and fusion with a derotation maneuver for scoliosisreduction. In situ rod contouring into lordosis and properpatient bed positioning are methods for restoring better me-chanical alignment and lordosis. A less extensive fusionsurgery can be preferable even though the upper and lowerend of the fusion are not parallel to the sacrum [53,54].

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Fig. 3. (A) Anteroposterior and (B) lateral view full spine after anterior interbody fusion L1–L4, posterior decompression L3–L5, and posterior instrumented

fusion T9–S2.

Pedicle screws are considered the most appropriate fixationmethod for the aged osteoporotic bone with absent posteriorelements after decompression [55]. In case of significantdecompensation in the sagittal and coronal plane, it is oftenimperative to extend the fusion to the sacrum. Additional fix-ation points in the sacrum and the pelvis reduce the increasedstrains to the implants and help the healing of the fusion.

In Table 2, an algorithm of treatment of patients with de-generative scoliosis and stenosis is presented based on theclassification system presented in Table 1. An extensivestudy of our patients treated using the aforementioned algo-rithm is under publication and showed statistically signifi-cantly improved outcomes (measured by SF-36, Oswestry,and VAS scores) postoperatively.

Results of surgical treatment

The degree of pain relief after adult scoliosis surgery isdebatable. There are not many studies assessing the resultsof surgical treatment for adult patients with scoliosis andstenosis. Simmons and Simmons [43] studied 40 patients

with 44 months average follow-up treated with decompres-sion and fusion. Eighty-three percent of the patients reportedsevere pain before surgery, and 93% reported mild or no painpostoperatively. Scoliosis was reduced from 37� to 18� at thelatest follow-up. Shapiro et al. [56] reported 94% satisfactionrate at 2 years postoperatively in 16 patients treated with an-terior and posterior surgical reconstruction for adult idio-pathic scoliosis and stenosis. The Oswestry Disability Indeximproved from 44.3 and preoperatively to 26.4 at the most re-cent follow-up, and the curve correction reached 50.4%.Hansraj et al. [51] in a study involving 47 patients with com-plex lumbar stenosis only (without scoliosis) and decompres-sion surgery reported 89% to 98% satisfaction rates indifferent functional outcomes (ability to walk, pain, musclestrength and balance) with 92% to 94% chance of not needingrevision surgery average 39 months postoperatively.

Frazier et al. [57] reported 15 patients with scoliosis andstenosis treated with lumbar decompression only. All thepatients had postoperatively increased VAS score comparedwith preoperatively, even though the improvement of thescoliotic curve did not correlate with the outcomes.

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The procedure can involve posterior only or combinedanterior and posterior approach. Marchesi and Aebi [55]treated 27 patients with an average age of 60 and curvesfrom 22� to 82� with decompression and posterior segmen-tal instrumented fusion. In 4.5 years of average follow-up,86% of the patients were satisfied with pain relief and in-creased walking ability. The average curve correction was50%, and lumbar lordosis increased from 45� to 54� [55].Grubb et al. [58] reported 40% pseudoarthrosis rate in pa-tients with degenerative scoliosis treated with posterior-on-ly fusions to the sacrum, whereas all the cases treated withanteroposterior approach fused uneventfully. A comprehen-sive and long follow-up study of the outcomes (includingVAS, Oswestry Disability Index, or functional scores) ofoperative treatment in a large cohort of patients with degen-erative scoliosis and stenosis is lacking.

Complications of surgical treatment

The complications of the surgical treatment of degener-ative scoliosis with stenosis can be multiple and risky[44,48,59–61]. With reference to age of patients who hadanterior fusion for scoliosis, McDonnell and associates[62] noted a 41% (14% major and 27% minor) incidencefor ages 41 to 60 years and 64% (24% major and 40% mi-nor) for ages 61 to 85 years. The most common category ofmajor complication was the pulmonary and the most com-mon minor the genitourinary. Age more than 60 year wasa risk factor for perioperative complication [62].

Patient positioning and procedure length should be takeninto serious consideration for complication’s prevention.Surgeons should not hesitate to terminate an operationwhen some goals have been achieved and there is risk forthe patient if the operation continues [60]. Surgery can beresumed later as a second stage.

Table 2

UNSTABLESEGMENT

>2mm motion indynamic x-rays

Type I

Grade 1 (<5mm)LATERAL

ROTATORYOLISTHESIS

Type II Type III

Grade 2 (6-10mm) or 3(>11mm) LATERAL

ROTATORYOLISTHESIS

NOLATERAL

ROTATORYOLISTHESIS

STABLE SEGMENT<2mm motion in dynamic x-rays

IATROGENICINSTABILITY

SELECTIVE FUSION OF THEMAJOR CURVE OR THE

UNSTABLE SEGMENTS +DECOMPRESSION

LONGFUSION TO TL AREA +

DECOMPRESSION

DECOMPRESSION

CORONAL ORSAGITTAL

IMBALANCE

NON FUSION

YESNO

In the literature, there is a controversy in the question ifcomorbidities increase the risk for postoperative complica-tions [60,61]. Elderly patients could safely have spine sur-gery with an outcome similar to younger patients, if wedeemed that they do not have increased comorbidities [61].

The most important complications that can happen areserious blood loss, blindness, cerebral infraction, myocar-dial infarction, paralysis, neurological deficit, infection-sepsis, failure or breakage of the implants, pseudoarthrosis,pneumonia, deep vein thrombosis, and death [59]. A specialreport should be performed regarding lumbar lordosis lossor flat-back syndrome [63]. It is caused by distraction ofthe lower lumbar spine during fusion or translational ky-phosis of thoracolumbar spine cranially to the upper endof fusion. It leads to sagittal plane imbalance of the spine,chronic low back pain, and inability of keeping erect pos-ture. Possible iatrogenic aetiology of flat back syndromeshould be avoided during thoracolumbar scoliosis surgery.

Conclusions

Degenerative scoliosis is appearing more frequently be-cause of increased life duration or iatrogenic instability.Nonoperative treatment should be exhausted before pro-ceeding with surgical treatment, especially in cases needingmajor reconstructive procedures. The optimal is to managethe whole pathology with only one operation. Lumbar de-compression, fusion, and instrumentation are appropriatefor most of the patients with degenerative lumbar scoliosisand stenosis. The main goal is to provide pain relief andimproved functional lifestyle with minimum intervention.

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