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210 Hau Yan KWOK, Kenneth M.C. CHEUNG
spinal stenosis due to the change in the spinal
canal diameter.
Spinal stenosis
Spinal stenosis refers to narrowing of the spinal canal,
most commonly seen in the lumbar region. It results
in symptoms of neurogenic claudication, with or
without back pain, neurological deficit and disability.
It typically presents in patients in their mid-50s and
progresses in the next decade of life. Patients may
present at an earlier age if they have a congenitally
narrow spinal canal. e progressive stenosis is part
of a degenerative process, with compression by the
degenerative disc, the hypertrophic degenerated
facet, the infolded ligamentum flavum and crowding
of the neural foramen from loss of disc height.
e pathophysiological causes of claudication are
varied. ere is increase in intradural pressure [83],
reduction of blood flow with decreased nutrition
[73, 74] and compression of the spinal cord at
multiple levels [74, 91]. Inflammation also finds its
role in the symptoms, with various neuropeptides
being demonstrated in the compressed spinal tissue
[19].
e symptoms of spinal stenosis can mimic other
conditions. Vascular disease may present with
similar claudication symptoms. Myelopathy can
cause similar gait dysfunction and be associated
with bowel and bladder dysfunction, but may also
have symptoms and signs from a higher neurological
level. Degeneration of the other joints may mimic
or co-exist with stenosis symptoms. Peripheral
neuropathy can cause lower limb numbness, which
is typically “glove and stocking” in nature, and can
be differentiated by electromyography and nerve
conduction velocity studies.
Osteoporotic vertebral fracture
Collapse of the vertebral body related to osteoporosis
typically occurs at the thoracolumbar junction,
leading to acute onset of back pain with kyphotic
deformity. Postmenopausal women with a dual-
energy X-ray absorptiometry (DEXA) value of less
than - 2.5 are at high risk of developing such fractures.
Osteoporotic vertebral collapse usually runs a benign
course, with symptoms gradually subsiding within
6 to 8 weeks. Complications include recurrent and
multiple fractures, chronic pain and late neurological
complications [37], and patients should therefore be
carefully followed up after the fracture.
Failed back surgery syndrome
Failed back surgery syndrome is defined as
persistent, recurrent, or worsening back pain with
disability after previous spine surgery. It develops
in 10–20% of postoperative patients, and the rate
varies between the different preceding procedures
[18, 45, 61]. e causes can be broadly defined
as inappropriate or inadequate surgery of the
pre-existing pathology, recurrence of the pre-
existing pathology (e.g. recurrent of lumbar disc
herniation), new disease at a different level and
complications due to previous surgery (e.g. dural
adhesion, pseudoarthrosis, flat back syndrome,
etc.). e patients may present with back pain or
leg pain, and the cause should be diligently and
systematically assessed.
Facet joint dysfunction
Facet joint dysfunction has been described as a
cause of back pain. e diagnosis is based on the
clinical presentation of mechanical back pain worse
with extension and with radiological features of
facet joint arthritis. e specificity of diagnosis is
increased by the injection of a diagnostic anaesthetic
[84, 85]. However, modification of pain behaviour
can occur even with the injection of a distal site
[86], and thus the exact sensitivity and specificity
of facets blocks are still largely unknown. erapy
directed by these diagnostic findings has been tried,
but evidence of their efficacy is still lacking [71].
Other diagnoses
Spondylosis is a generally used term to describe the
degenerative process affecting the axial skeleton.
is is a natural ageing phenomenon, but our
on-going work suggests an association of severe
degeneration with pain. Diagnosis is enhanced by
functional injection studies, including discogram
and facet joint block, but often the clinical diagnosis
cannot be easily differentiated from non-specific
back pain. Full evaluation may need to include
psychosocial assessment to help to delineate the
underlying cause.
Non-specic Low Back Pain
Even taking into account the extensive list of back
pain with specific causes, overall, about three-
quarters of all back pain cases remain which have
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Back Pain 211
no exact identifiable pathological cause [24]. e
pain-generator, assumed to be the cause of painful
symptoms, may not account for all the back
complaints. It is certain that other biopsychosocial
issues can complicate the presentation of back pain
and affect the related disability.
e prognosis of this type of back pain is usually
favourable, with around 90% of patients recovering
within 12 weeks. Still, for a number of patients
the pain will become chronic, and therefore early
attention to the social and psychological factors is
important in the management of this type of pain.
is will be dealt with under clinical management
later in the chapter.
Clinical Presentation
Specific low back pain is usually caused by the
following factors:
Nerve compression
Often due to a prolapsed intervertebral disc, the
pathology may cause a direct irritation at the nerve
root or the dorsal horn. It is often described as a
sharp, shooting pain radiating from the back or
buttock into the leg, typically beyond the knee. e
referred pain in the distribution of the sciatic nerve
is termed “sciatica”. e distribution of the pain
pattern is confined to the dermatomal distribution
of the affected nerve root, and directs us towards
the disease level. e symptoms tend to increase
with coughing or the Valsalva manoeuvre and with
postures that increase intradiscal pressure, as in
spinal flexion and sitting.
e nerve root may also be affected in cases of
spinal stenosis when narrowing is in the lateral part
of the spinal canal, beneath the often hypertrophic
and degenerated facet joint, the so called lateral
recess. In which case, the pain is claudicating in
nature, and is usually a dull and deep ache, related
to walking and relieved by rest.
Neurological deficit may occur in cases of
significant compression, especially if acute.
It may not fully recover even after surgical
decompression. Bilateral leg symptoms should
raise the suspicion of cauda equina syndrome,
especially if there is saddle anaesthesia, bowel or
bladder disturbance.
Irritation at the disc
e diseased intervertebral disc may irritate the
surrounding nociceptor at the annulus and produce
pain. Sometimes the dorsal primary ramus can
also be affected. e nature of the pain is usually
a deep ache over the midline and will refer to the
sacroiliac area or the posterior thigh. e intensity
of pain may change with different disc loading and
therefore varies with posture.
Instability
Instability is defined as movement beyond the
normal constraints of the spine and can result in
symptoms. It may be due to the degeneration of
the disc or other supporting structures such as
facet joints, leading to spondylolisthesis (slippage
of one vertebral body on another). e pain is
precipitated by motion and is mechanical in nature.
It can be evident radiologically by demonstrating
excessive movement across the spinal segments on
flexion-extension radiographs, although the exact
correlation of it to patients’ surgical outcome is not
direct [66, 68].
Problem in alignment
A change in alignment, whether scoliosis or
kyphosis, would induce strain on the supporting
musculoskeletal structure, and causes fatigue and
pain. e symptoms are usually on the side under
tension, which requires more force in maintaining
a balanced posture. An example of that would
be the chronic back pain after an osteoporotic
vertebral collapse as a result of the kyphotic
deformity.
Management
Clinical history
A detailed history should be directed towards the
nature and characteristic of the pain. e behaviour
and the chronology of that may help to define the
pathology. Symptoms should be directed toward
the primary cause, including instability, nerve
root irritation and mal-alignment. If possible, the
anatomical region responsible for the pain should
be delineated. e “red flags” signs [54], which may
indicate a fracture, spinal tumour, inflammatory
process, or severely comprised nervous function,
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212 Hau Yan KWOK, Kenneth M.C. CHEUNG
e.g. cauda equina compression by a large central
disc, should be sought.
Sciatica pain should be differentiated from referred
pain from the spine. e latter usually will not
radiate beyond the knee and is characteristically
different from the sharp and localised pain of nerve
root irritation [53, 105].
Around 3% of patients with low back pain may
have an extra-spinal cause [12, 23]. Possible
pathologies include posterior penetrating gastric
ulcer, pancreatitis, renal disease, abdominal aorta
aneurysm, hip pathology and other vascular
causes.
Patients with prolonged symptoms without a
definitive pathological cause are referred to as
having chronic non-specific low back pain. Factors
other than the physical cause should be considered
when treating this group of patients. Screening
should be done to determine the presence of any
psychosocial factors that may complicate the course
and the recovery of the back pain.
Different risk factors, or “flags”, will indicate an
increased possibility of chronicity. ese include
the “yellow flags”, which indicate a belief of injury
to the back causing disability, pain avoidance,
poor coping mechanism, etc. [54]. Other social,
occupational and economical factors should be
explored; they are referred to as “occupational
blue flags” and “socio-occupational black flags”
[60]. Examples of these would be involvement in
litigation or workmen’s compensation, previous
work status, work satisfaction, the social policy
towards workmen’s injury, etc.
Physical examination
e examiner should relate the site of tenderness
to the various anatomical parts. Deep palpation
at different landmarks may help to identify the
painful anatomical structure. Bony tenderness
is more reliable than soft tissue tenderness [64].
Spinal motion in the flexion, extension, lateral
flexion and rotation should be tested. e Schober
technique, by marking the spinous process, allows
measurement of the movement at each spinal
segment. Limitation of spinal flexion may be a good
indication of significant spinal pathology [109].
e examiner should also look for signs of nerve
root irritation. e Laseque test or passive straight
leg raise should reproduce the usual symptoms of
the patient [22]. e test has a high sensitivity, but
only a fair specificity of around 20% for prolapsed
intervertebral disc. e test can be performed with
patients in the sitting position, which is in fact a
way to differentiate the inorganic symptoms in
some patients, as one of the Waddell Inorganic
Signs [108]. e bowstring test is another variation
of the test. e cross straight-leg raising test, where
pain is reproduced on the symptomatic leg by
raising the contralateral leg, is a more specific test
for prolapsed intervertebral disc [64]. e femoral
stretch test may signify nerve root irritation at a
higher spinal level and pathology should be sought
proximally.
A full neurological examination should be carried
out. Neurological deficit is usually confined to
dermatomic or myotomic distribution if there is a
specific nerve root dysfunction. A non-anatomical
distribution of neurological symptoms would
suggest a pain of non-organic nature [108]. Other
non-organic symptoms include an inappropriate
level of pain, pain on stimulation of spinal motion,
a distraction sign and over-reactivity.
e abdomen should be examined to exclude intra-
abdominal pathology. e peripheral pulses of the
lower limb should be examined to exclude vascular
causes of claudication.
Investigation
Plain X-rays of the lumbar spine in different views
help to delineate the bony anatomical structures in
cases of specific low back pain. Radiographs with a
flexion and extension view can further demonstrate
motion across spinal segments. Computerised
tomography scanning and magnetic resonance
imaging (MRI) have largely replaced the myelogram
and can better show the three dimensional bony
and soft tissue structures. ey are especially useful
in assessing the spinal cord and its nerve roots
in cases of prolapsed intervertebral disc or spinal
stenosis to see if they are under compression.
However, there is little evidence to suggest
that radiological investigation is of help in the
management of non-specific acute low back pain
[11, 48, 55, 56] and the demonstrated structural
changes can only be poorly correlated with the
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Back Pain 213
physical symptoms. e false positive rate of
degenerative features is as high as 90% on plain X-
ray [93, 100]. Changes evident on MRI, including
dark discs, bulging discs, or disc herniation, can be
identified in 30–57% of asymptomatic individuals
[29, 36, 79].
Radiological investigation can help to provide
evidence if a serious spinal pathology is in doubt,
as indicated by the history and physical signs, or
“red flags”. If the back pain persists for more than 8
weeks, radiological investigation can be considered
for the same reasons [59]. Radiological examination
should not replace a careful history and examination,
which can provide additional information to guide
the subsequent management. An MRI examination
of the spine is indicated in cases with at-risk physical
signs and for those with a specific diagnosis when
operation is an option [47].
Other diagnostic tools, including discogram, nerve
root block or facet joint injection, aim to either
provoke or to block off the painful symptoms from
the pain generating structures. e results are not
unanimous, with some reports showing a high
correlation rate [81, 85, 115], while others suggest a
significantly high false-positive rate in non-specific
low back pain. e tests may also be unreliable in
patients with psychosocial variables that affect their
pain behaviour [16, 17, 27, 46]. ese injection
studies should be carefully interpreted and critically
correlated with the clinical findings and the other
investigation results.
Blood investigations including infective and
immunological markers are indicated if a serious
spinal pathology is suspected, especially if there is
the presence of “red flags”.
Treatment Options
e treatment approach for specific and non-
specific low back pain is different. Treatment
for specific low back pain can be operative
and conservative. Operative treatment aims at
removing the pain-generator. By various surgical
techniques the neural structure under pressure is
decompressed and stability achieved across spinal
segments to eliminate the painful motion. e
spinal column can be realigned to provide the
optimal biomechanics for spinal motion.
Treatment for non-specific low back pain should
aim to control painful symptoms, maximise
the patient’s function, prevent recurrence, and
minimise the development of chronicity and
disability [20].
Treatment of specic low back
pain
Prolapsed intervertebral disc
Symptoms of prolapsed intervertebral disc
may improve after conservative treatment.
Approximately 50% of patients find their pain
resolves in 6 weeks and 75% after 3 months [7,
112, 113]. Conservative treatment includes various
physical modalities for pain control. An exercise
programme is frequently started as pain improves,
although a meta-analysis of the present literature
failed to show that this is more effective than
other forms of treatment in acute pain, despite
its effectiveness in chronic low back pain [40, 89,
99, 102]. Centralisation with improving leg pain
signifies improvement of nerve irritation with
the exercise programme [1, 25]. As it progresses,
physical treatment should include dynamic trunk
stabilisation and strengthening exercises.
e indications for surgical intervention include
patients with neurological complications (e.g.
cauda equina syndrome), patients with symptoms
not responding to conservative treatment within
3 months, and patients with significant and
progressive neurological deficit. Relative indications
for surgery would be patients with recurrent and
significant relapse of symptoms.
Surgery aims to decompress the compressed
nerve root. is can be achieved by a discectomy
through open surgery, or by using a minimally
invasive technique. At the same time, consideration
should be given to any back pain symptoms that
may be related to the instability of the diseased
intervertebral disc. If these are significant, fusion
surgery, either through an anterior or posterior
approach, is indicated to remove the instability
factor causing the back pain.
e result of surgery is satisfactory in a carefully
selected group when compared with other forms
of treatment [35]. Good to excellent clinical results
can be expected after discectomy surgery [44]. Some
65–85% of patients report no sciatica 1 year after
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214 Hau Yan KWOK, Kenneth M.C. CHEUNG
the surgery. e complications of surgery include
persistent pain due to retained fragments, recurrent
disc, discitis, epidural abscess and epidural fibrosis.
Degenerative disc disease
e treatment of this group of problems remains
controversial. Studies have shown that the long-
term results in cases treated conservatively had
similar outcomes to those treated with surgery [31].
Conservative treatment with physiotherapy should
be tried first, aiming for improvement in function
in the presence of the degenerated disc. When
conservative treatment is deemed to have failed,
surgery should be considered for a radiologically
diseased disc with concordant painful symptoms
with the aim of removing the painful pathology
and regaining stability over the spine. Various
techniques of fusion surgery can achieve this
purpose with satisfactory results in carefully selected
cases [33]. Recently, a motion-preserving surgical
option, e.g. artificial disc replacement, has been
widely discussed. e proponent of this has shown
good clinical outcome with improvement of painful
symptoms and function after the operation [87].
However, the long-term clinical outcome is as yet
unknown and it is impossible to scrutinise the exact
behaviour of the patients who respond to surgery
due to the complexity of spinal pathology [34].
Spinal stenosis
Conservative treatment with analgesics and a course
of physiotherapy should be tried first with the aim of
correcting posture and providing endurance training
for the spinal muscle. Around 15–30% of patients
will experience symptoms improvement with
conservative treatment, while most patients’ will
have stable symptoms over time [3, 4, 5, 50, 51].
Operation aims at decompression of the compressed
nervous structure at the area of stenosis. All
symptomatic levels should be decompressed. Fusion
surgery with or without instrumentation may have
to be considered if there is an element of segmental
instability, as in cases of spondylolisthesis, where
the stability may be further compromised by the
decompressive procedure.
Spondylolisthesis
Symptomatic patients should be started on physical
therapy and analgesics for control of symptoms.
Truncal and aerobic exercise will help develop
better balance and endurance.
An operation is indicated if conservative treatment
fails and there is persistent radicular or claudication
pain. e goal of surgery is to decompress the
nervous structure, as well as fusion and anterior
column augmentation (by reconstruction cage or
bone graft) to regain segmental stability.
Osteoporotic vertebral fracture
Prevention is important with management of
osteoporotic patients at high risk. e early
treatment of vertebral collapse includes adequate
pain relief and an early regain of mobility. Physical
exercise focusing on postural training is beneficial
to patients for long-term symptom control [88].
Minimally invasive vertebral augmentation
techniques, i.e. vertebroplasty or kyphoplasty,
provide alternatives for patients with persistent
pain and disability.
Failed back surgery syndrome
Treatment is dictated by the cause of symptoms.
Repeated surgical decompression can be considered
for recurrent or residual neural compression, and
fusion surgery considered if instability is evident.
Generally, the outcome is likely to be poorer
compared with the primary surgery [30]. It is
probable that some level of pain and disability
will remain and the treatment should emphasise a
restore of function. For recalcitrant cases which are
beyond surgical help, intrathecal opioid and spinal
cord stimulation have been reported to have some
success [13, 62, 92, 94].
Treatment of non-specic low
back pain
Stay active
International guidelines for the treatment of
chronic non-specific low back pain no longer
recommend prolonged bed rest, but suggest
that patients are advised to stay active [20, 54].
Systematic reviews of randomised controlled trials
showed a strong favour towards this approach in
providing quicker symptomatic relief, less chronic
disability, less time off work and a faster rate of
recovery [39, 106]. Prolonged bed rest is associated
with a negative effect in the outcome, compared
with other forms of treatment [9, 28, 39, 58, 101,
106]. Patients should be encouraged to stay active
and continue with their normal activities as much
as possible.
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Back Pain 215
Pharmacotherapy
Pharmacological pain control is important in
the management of acute back pain symptoms.
Paracetamol may be useful for mild symptoms,
whereas non-steroidal anti-inflammatory drugs
(NSAIDs) are indicated for mild to moderate pain.
Cyclo-oxygenase 2 (Cox 2) selective inhibitors are
a newer type of NSAID with less gastrointestinal
side effect [42], but may have an increased risk
of thrombotic and cardiovascular complications
after prolonged use. Both NSAIDs and Cox 2
inhibitors can provide good symptom control for
acute back pain, but may not be helpful with long-
term symptoms [57, 103]. Morphine or morphine-
like drugs may be indicated for stronger pain, but
there is a risk of psychological dependence and
therefore the dose has to be carefully monitored.
Tramadol is a newer centrally acting analgesic
with fewer side effects compared with traditional
opioids and is useful in the control of moderate
and severe pain [52, 82]. Muscle relaxants can be
considered for control of acute symptoms [8, 9, 96,
101]. Anticonvulsants and antidepressant drugs
(e.g. amitriptyline, gabapentin) may not be useful
in acute back pain, but recent evidence has shown
that these groups of drugs are useful in controlling
chronic symptoms, especially for patients with
mood disturbance related to chronic pain [80, 90].
Physical modality
Physiotherapy can be of value in controlling of
acute symptoms. Various physical modalities are
recommended for pain control. Although they
are frequently prescribed, traction, electrotherapy,
ultrasound, interferential therapy, laser treatment
and transcutaneous electrical nerve stimulation
(TENS) were not showed to be more effective than
placebo treatment in recent systematic reviews of
randomised controlled trials [78, 101].
Exercise therapy
Systemic reviews have shown the beneficial effect of
exercise in chronic, but not in acute low back pain
[40, 98]. Back extensor strengthening, isometric
flexion exercise and stretching are frequently
prescribed when the patient becomes more active
after the initial painful period.
Interventional treatment
Interventional treatment with the injection of
corticosteroid and local anaesthetics uses a different
approach to treat low back pain. By injecting
into the painful area, the treating physician can
sometimes make a target-specific diagnosis and plan
for a specific intervention as judged by the injection
findings [104]. Discogenic pain has a prevalence
of 40% in cases referred for intervention therapy,
while sacroiliac joint pain and zygapophysial (facet)
joint pain constitute around 20% and 15% in this
group of patients respectively [84, 85].
e commonly injected structures include the
sacroiliac joint, the zygapophysial (facet) joint,
the exiting nerve root, the epidural space and the
intervertebral disc. Injection can be both diagnostic
and therapeutic. ere is no convincing evidence
that these different interventional procedures are
more effective in controlling chronic low back pain,
but success is reported in well-selected patients [71].
Once the diagnosis is confirmed with injection
study, radiofrequency neurotomy or intradiscal
electrothermal annuloplasty (IDET) can be
considered. ese radiofrequency or electrothermal
interventions target the dorsal rami of the spinal
nerve or the nociceptors of the intervertebral disc.
Again, success has been reported in well-selected
cases [10, 21, 26, 32, 75, 95].
Surgery
Results of surgery for chronic back pain have
been variable. Even if an operative procedure is
indicated in a case with a radiologically identified
degenerative disc and concordant symptoms, the
results are often complicated by other psychosocial
variables and a successful outcome is not always
guaranteed [107, 108]. Surgery may still have a
role in cases where symptoms cannot be adequately
controlled by conservative measures. In carefully
selected patients, operation, very often fusion
surgery, may help to decrease the level of pain and
disability [33].
Multidisciplinary approach to
non-specic low back pain
e multimodal rehabilitation programme adopts
the principle of functional rehabilitation in the
treatment of low back problems. It addresses the
physical, as well as psychosocial and functional
deconditioning of the chronic low back pain
patient, guided by objective measurement of
the patient’s function. is treatment approach
emphasises the active elements, such as restoration
of joint mobility, muscular strengthening, exercise
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216 Hau Yan KWOK, Kenneth M.C. CHEUNG
endurance, as well as cardiovascular function.
Integrated multidisciplinary pain management also
includes psychological and social evaluation, to
help patients cope with and manage their pain as
effectively as possible. e results are satisfactory in
reducing patients’ disability and improving physical
function [6, 15, 38, 41, 63, 77].
Conclusion
Back pain is a common health problem and
its effect on the behaviour of the patient poses
additional diagnostic and therapeutic difficulties in
its management. A careful plan should be followed
which guides the treating physician to appropriate
investigation and intervention. It is important to
identify and correctly diagnose back pain with
specific pathology and to then focus treatment on
the cause of the disease.
For patients with non-specific low back pain,
treatment should aim at control of symptoms,
and appropriate biopsychosocial intervention
should be used to encourage patients to stay
active. Clinical management should be directed at
modifying the disability associated with the back
pain problem and maximise patients’ function in
various activities.
Summary
• Different pathologies can cause low back
pain
• It is important in management to differentiate
specific from non-specific low back pain
• Patients should be assessed with consideration
to the different facets of their problem
• Specific intervention should be offered if
a definite pain-causing pathology can be
identified
• Management of chronic non-specific low
back pain should involve a multidisciplinary
approach to address the different
biopsychosocial issues.
Table13.01 Evidence-based practice of non-specific low back pain [2, 20, 38, 78, 97, 99, 101]
Acute pain Subacute pain Chronic pain
Rest
-ve -ve -ve
Stay active
+ve ID ID
Traction
-ve -ve -ve
NSAID
+ve ID ID
Lumbar support
ND ND -ve
Therapeutic ultrasound
-veND-ve
TENS
-ve ND +ve
Massage
ND +ve ID
Spinal manipulation
+ve ID
+ve
(moderate)
Exercise
ID +ve +ve
Multidisciplinary treatment
ID ND +ve
ID = Insufficient data; ND = no data; +ve = benefit demonstrated; -ve = no benefit demonstrated.
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Back Pain 217
References
Aina A, May S, Clare H. e centralisation phenomenon of spinal symptoms: A systematic review. Maner
2004;9:134–43.
Airaksinen O, Brox JI, Cedraschi C, et al. Chapter 4. European guidelines for the management of chronic non-specific
low back pain. Eur Spine J 2006;15(Suppl 2):S192–S300.
Amundsen T, Weber H, Nordal HJ, et al. Lumbar spinal stenosis: Conservative or surgical management?: A prospective
10-year study. Spine 2000;25:1424–35.
Atlas SJ, Deyo RA, Keller RB, et al. e Maine Lumbar Spine Study, Part III. one-year outcomes of surgical and
nonsurgical management of lumbar spinal stenosis. Spine 1996;21:1787–94.
Atlas SJ, Keller RB, Wu YA, et al. Long-term outcomes of surgical and nonsurgical management of lumbar spinal
stenosis: 8- to 10-year results from the Maine lumbar spine study. Spine 2005;30:936–43.
Bendix AF, BendixT, Lund C, et al. Comparison of three intensive programs for chronic low back pain patients: A
prospective, randomized, observer-blinded study with one-year follow-up. Scand J Rehabil Med 1997;29:81–9.
Benoist M. e natural history of lumbar disc herniation and radiculopathy. Joint Bone Spine 2002;69:155–60.
Bernstein E, Carey TS, Garrett JM. e use of muscle relaxant medications in acute low back pain. Spine 2004;29:1346–
51.
Bigos S, Bowyer O, Braen G, et al. Acute Lower Back Problems in Adults. Clinical Practice Guideline No. 14. AHCPR
Publication No. 95-0642, 1994.
Biyani A, Andersson GB, Chaudhary H, et al. Intradiscal electrothermal therapy: A treatment option in patients with
internal disc disruption. Spine 2003;28:S8–14.
Boden SD. e use of radiographic imaging studies in the evaluation of patients who have degenerative disorders of the
lumbar spine. J Bone Joint Surg Am 1996;78:114–24.
Borenstein DG. A clinician’s approach to acute low back pain. Am J Med 1997;102:S16–22.
Boswell MV, Shah RV, Everett CR, et al. Interventional techniques in the management of chronic spinal pain: Evidence-
based practice guidelines. Pain Physician 2005;8:1–47.
Buckwalter JA. Aging and degeneration of the human intervertebral disc. Spine 1995;20:1307–14.
Burke SA, Harms-Constas CK, Aden PS. Return to work/work retention outcomes of a functional restoration program.
A multi-center, prospective study with a comparison group. Spine 1994;19:1880–5.
Carragee EJ, Alamin TF, Miller JL, et al. Discographic, MRI and psychosocial determinants of low back pain disability
and remission: A prospective study in subjects with benign persistent back pain. Spine J 2005;5:24–35.
Carrage EJ, Hannibal M. Diagnostic evaluation of low back pain. Orthop Clin North Am 2004;35:7–16.
Cinotti G, Roysam GS, Eisenstein SM, et al. Ipsilateral recurrent lumbar disc herniation: A prospective, controlled
study. J Bone Joint Surg Br 1998;80:825–32.
Corneord M, Olmarker K, Farley DB, et al. Neuropeptide changes in compressed spinal nerve roots. Spine
1995;20:670–3.
COST, European Cooperation in the field of Scientific and Technical Research: European Guidelines for the
Management of Acute Non-specific Low Back Pain in Primary Care. Europe. 2004.
Davis TT, Delamarter RB, Sra P, et al. e IDET procedure for chronic discogenic low back pain. Spine 2004;29:752–
6.
Deville WL, van der Windt DA, Dzaferagic A, et al. e test of Lasegue: Systematic review of the accuracy in diagnosing
herniated discs. Spine 2000;25:1140–7.
Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA
1992;268:760–5.
Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363–70.
Donelson R, Silva G, Murphy K. Centralization phenomenon. Its usefulness in evaluating and treating referred pain.
Spine 1990;15:211–3.
Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar
zygapophysial joint pain. Spine 2000;25:1270–7.
Esses SI, Moro JK. e value of facet joint blocks in patient selection for lumbar fusion. Spine 1993;18:185–90.
Evans G, Richards S. Low Back Pain: An Evaluation of erapeutic Interventions. Bristol: Health Care Evaluation Unit,
1996.
Evans W, Jobe W, Seibert C. A cross-sectional prevalence study of lumbar disc degeneration in a working population.
Spine 1989;14:60–4.
Fager CA, Freidberg SR. Analysis of failures and poor results of lumbar spine surgery. Spine 1980;5:87–94.
Fairbank J, Frost H, Wilson-MacDonald J, et al. Randomised controlled trial to compare surgical stabilisation of the
lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: e MRC spine
stabilisation trial (LINKED). BMJ 2005;330:1233–9.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
https://t.me/medicina_free
218 Hau Yan KWOK, Kenneth M.C. CHEUNG
Freeman BJ, Walters RM, Moore RJ, et al. Does intradiscal electrothermal therapy denervate and repair experimentally
induced posterolateral annular tears in an animal model? Spine 2003;28:2602–8.
Fritzell P, Hagg O, Wessberg P, et al. 2001 Volvo Award Winner in Clinical Studies: Lumbar fusion versus nonsurgical
treatment for chronic low back pain: A multicenter randomized controlled trial from the Swedish Lumbar Spine Study
Group. Spine 2001;26:2521–32.
Frymoyer JW. Least invasive spine procedures and artificial disc replacement — past, present, and future. In Frymoyer
JW, Wiesel SW, An HS, eds. e Adult and Pediatric Spine. Philadelphia: Lippincott Williams and Wilkins, 2004:
xxvii–xl.
Gibson JN, Grant IC, Waddell G. Surgery for lumbar disc prolapse. Cochrane Database Syst Rev 2007;(1):CD001350.
Gibson MJ, Buckley J, Mawhinney R, et al. Magnetic resonance imaging and discography in the diagnosis of disc
degeneration. A comparative study of 50 discs. J Bone Joint Surg Br 1986;68:369–73.
Glassman SD and Alegre GM. Adult spinal deformity in the osteoporotic spine: Options and pitfalls. Instr Course Lect
2003;52:579–88.
Guzman J, Esmail R, Karjalainen K, et al. Multidisciplinary bio-psycho-social rehabilitation for chronic low back pain.
Cochrane Database Syst Rev 2002;(1):CD000963.
Hagen KB, Hilde G, Jamtvedt G, et al. Bed rest for acute low-back pain and sciatica. Cochrane Database Syst Rev
2004;(4):CD001254.
Hayden JA, van Tulder MW, Malmivaara A, et al. Exercise therapy for treatment of non-specific low back pain. Cochrane
Database Syst Rev 2005;(3):CD000335.
Hazard RG, Fenwick JW, Kalisch SM, et al. Functional restoration with behavioral support. A one-year prospective
study of patients with chronic low-back pain. Spine 1989;14:157–61.
Henry D, Lim LL, Garcia Rodriguez LA, et al. Variability in risk of gastrointestinal complications with individual non-
steroidal anti-inflammatory drugs: Results of a collaborative meta-analysis. BMJ 1996;312:1563–6.
Hestbaek L, Leboeuf-Yde C, Manniche C. Low back pain: What is the long-term course? A review of studies of general
patient populations. Eur Spine J 2003;12:149–65.
Hoffman RM, Wheeler KJ, Deyo RA. Surgery for herniated lumbar discs: A literature synthesis. J Gen Intern Med
1993;8:487–96.
Hu RW, Jaglal S, Axcell T, et al. A population-based study of reoperations after back surgery. Spine 1997;22:2265–70.
Ito M, Incorvaia KM, Yu SF, et al. Predictive signs of discogenic lumbar pain on magnetic resonance imaging with
discography correlation. Spine 1998;23:1252–8.
Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586–
97.
Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low
back pain: A randomized controlled trial. JAMA 2003;289:2810–8.
Jensen S. Back pain — clinical assessment. Aust Fam Physician 2004;33:393–401.
Johnsson KE, Rosen I, Uden A. e natural course of lumbar spinal stenosis. Clin Orthop Relat Res 1992;(279):82–6.
Johnsson KE, Uden A, Rosen I. e effect of decompression on the natural course of spinal stenosis. A comparison of
surgically treated and untreated patients. Spine 1991;16:615–9.
Keating GM. Tramadol sustained-release capsules. Drugs 2006;66:223–30.
Kellgren JH. e anatomical source of back pain. Rheumatol Rehabil 1977;16:3–12.
Kendall NAS, Linton SJ, Main C. New Zealand Acute Low Back Pain Guide, Incorporating the Guide to Assessing
Psychosocial Yellow Flags in Acute Low Back Pain, Wellington, NZ: Accident & Compensation Corporation and the New
Zealand Guidelines Group, 2003.
Kendrick D, Fielding K, Bentley E, et al. Radiography of the lumbar spine in primary care patients with low back pain:
Randomised controlled trial. BMJ 2001;322:400–5.
Kerry S, Hilton S, Dundas D, et al. Radiography for low back pain: A randomised controlled trial and observational
study in primary care. Br J Gen Pract 2002;52:469–74.
Koes BW, Scholten RJ, Mens JM, et al. Efficacy of non-steroidal anti-inflammatory drugs for low back pain: A systematic
review of randomised clinical trials. Ann Rheum Dis 1997;56:214–23.
Koes BW, van den Hoogen HMM. Efficacy of bed rest and orthoses of low back pain. A review of randomized clinical
trials. Eur J Phys Med Rehabil 1994;4:86–93.
Liang M, Komaroff AL. Roentgenograms in primary care patients with acute low back pain: A cost-effectiveness analysis.
Arch Intern Med 1982;142:1108–12.
Main CJ, Williams AC. Musculoskeletal pain. BMJ 2002;325:534–7.
Malter AD, McNeney B, Loeser JD, et al. 5-year reoperation rates after different types of lumbar spine surgery. Spine
1998;23:814–20.
Mavrocordatos P, Cahana A. Minimally invasive procedures for the treatment of failed back surgery syndrome. Adv Tech
Stand Neurosurg 2006;31:221–52.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
https://t.me/medicina_free
Back Pain 219
Mayer T, Tabor J, Bovasso E, et al. Physical progress and residual impairment quantification after functional restoration.
Part I: Lumbar mobility. Spine 1994;19:389–94.
McCombe PF, Fairbank JC, Cockersole BC, et al. 1989 Volvo Award in clinical sciences. Reproducibility of physical
signs in low back pain. Spine 1989;14:908–18.
Meyerding HW. Spondylolisthesis. Surg Gynecol Obstet 1932;54:371–7.
Nachemson AL. Instability of the lumbar spine. Pathology, treatment, and clinical evaluation. Neurosurg Clin N Am
1991;2:785–90.
Nachemson AL. Newest knowledge of low back pain. A critical look. Clin Orthop Relat Res 1992;(279):8–20.
Nachemson AL. Lumbar spine instability: Outcome and randomized controlled trials. Bull Hosp Jt Dis 1996;55:166.
Nachemson A. Epidemiology and the economics of low back pain. In Herkowitz HN, Dvorak J, Bell GR, Nordin M,
Grob D, eds. e Lumbar Spine, 3
rd
edn. Philadelphia: Lippincott, Williams & Wilkins, 2004:3–10.
Nachemson A, Waddell G, Norlund A. I: Epidemiology of neck and low back pain. In Jonsson E, Nachemson A, eds.
Neck and Back Pain: e Scientific Evidence of Causes, Diagnosis, and Treatment. Philadelphia: Lippincott Williams &
Wilkins, 2000:165–88.
Nelemans PJ, deBie RA, deVet HC, et al. Injection therapy for subacute and chronic benign low back pain. Spine
2001;26:501–15.
Ng KF, Tsui SL, Chan WS. Prevalence of common chronic pain in Hong Kong adults. Clin J Pain 2002;18:275–81.
Olmarker K, Rydevik B. Single- versus double-level nerve root compression. An experimental study on the porcine
cauda equina with analyses of nerve impulse conduction properties. Clin Orthop Relat Res 1992;(279):35–9.
Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by experimental, graded compression.
An experimental study on the pig cauda equina with special reference to differences in effects between rapid and slow
onset of compression. Spine 1989;14:569–73.
Pauza KJ, Howell S, Dreyfuss P, et al. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for
the treatment of discogenic low back pain. Spine J 2004;4:27–35.
Pengel LH, Herbert RD, Maher CG, et al. Acute low back pain: Systematic review of its prognosis. BMJ
2003;327:323.
Pfingsten M, Hildebrandt J, Leibing E, et al. Effectiveness of a multimodal treatment program for chronic low back
pain. Pain 1997;73:77–85.
Philadelphia Panel: Philadelphia Panel evidence-based clinical practice guidelines on selected rehabilitation interventions
for low back pain. Phys er 2001;81:1641–74.
Powell MC, Wilson M, Szypryt P, et al. Prevalence of lumbar disc degeneration observed by magnetic resonance in
symptomless women. Lancet 1986;2:1366–7.
Salerno SM, Browning R, Jackson JL. e effect of antidepressant treatment on chronic back pain: A meta-analysis.
Arch Intern Med 2002;162:19–24.
Schneiderman G, Flannigan B, Kingston S, et al. Magnetic resonance imaging in the diagnosis of disc degeneration:
Correlation with discography. Spine 1987;12:276–81.
Schnitzer TJ, Gray WL, Paster RZ, et al. Efficacy of tramadol in treatment of chronic low back pain. J Rheumatol
2000;27:772–8.
Schonstrom N, Hansson T. Pressure changes following constriction of the cauda equina. An experimental study in situ.
Spine 1988;13:385–8.
Schwarzer AC, Aprill CN, Derby R, et al. e prevalence and clinical features of internal disc disruption in patients with
chronic low back pain. Spine 1995;20:1878–83.
Schwarzer AC, Wang SC, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophysial joint pain: A study
in an Australian population with chronic low back pain. Ann Rheum Dis 1995;54:100–6.
Siddall PJ, Cousins MJ. Spinal pain mechanisms. Spine 1997;22:98–104.
Siepe CJ, Mayer HM, Wiechert K, et al.: Clinical results of total lumbar disc replacement with ProDisc II. ree-year
results for different indications. Spine 2006;31:1923–32.
Sinaki M. Critical appraisal of physical rehabilitation measures after osteoporotic vertebral fracture. Osteoporos Int
2003;14:773–9.
Slade SC, Keating JL. Trunk-strengthening exercises for chronic low back pain: A systematic review. J Manipulative
Physiol er 2006;29:163–73.
Staiger TO, Gaster B, Sullivan MD, et al. Systematic review of antidepressants in the treatment of chronic low back
pain. Spine 2003;28:2540–5.
Takahashi K, Olmarker K, Holm S, et al. Double-level cauda equina compression: An experimental study with
continuous monitoring of intraneural blood flow in the porcine cauda equina. J Orthop Res 1993;11:104–9.
Taylor RS, Van Buyten JP, Buchser E. Spinal cord stimulation for chronic back and leg pain and failed back surgery
syndrome: A systematic review and analysis of prognostic factors. Spine 2005;30:152–60.
Torgerson WR, Dotter WE. Comparative roentgenographic study of the asymptomatic and symptomatic lumbar spine.
J Bone Joint Surg Am 1976;58:850–3.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
https://t.me/medicina_free
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