Non-mechanical disorders of the lumbar spine: pathology

Transcription

Non-mechanical disorders of the lumbar spine: pathology
Non-mechanical disorders of the
lumbar spine: pathology CHAPTER CONTENTS
Disorders . . . . . . . . . . . . . . . . . . . . . . . . . e217
Spondylolisthesis . . . . . . . . . . . . . . . . . . e217
Osseous disorders . . . . . . . . . . . . . . . . . e219
Rheumatological disorders . . . . . . . . . . . . . e223
Infections . . . . . . . . . . . . . . . . . . . . . . e224
Intraspinal lesions . . . . . . . . . . . . . . . . . . e226
Pain referred to the back . . . . . . . . . . . . . . e228
to slip forwards. The condition occurs four times as
frequently in females than in males and nearly always at
the fourth lumbar level (Cyriax:3 p. 288; Rosenberg4). The
slip is never severe. This condition has been discussed in
Chapter 35 on the stenotic concept.
• Traumatic spondylolisthesis results from a fracture of a
posterior element other than the pars interarticularis.
• Pathological spondylolisthesis develops as the result of
weakness caused by a local or generalized bone disease.
In this chapter
spondylolistheses.
we
discuss
only
the
spondylolytic
Disorders
Aetiology
Spondylolisthesis
Isthmic spondylolisthesis has been defined as ‘a condition in
which fibrous defects are present in the pars interarticularis,
which permit forward displacement of the upper vertebrae and
separation of the anterior aspects of the vertebra from its
neural arch’ (Fig. 1).5 The aetiology of this bony defect (spondylolysis) has been discussed for decades but it is now widely
accepted to be the result of a congenital weakness. The defect
itself is not present at birth, however, but develops in childhood, probably as the result of repeated stress and trauma.6–8
Stress fractures form in the weakened pars interarticularis;
fibrous tissue fills the gap, and further tension enlarges the
defect.9 Forward slipping of the vertebral body therefore
occurs most frequently between the ages of 10 and 15 years,
and progression is unlikely after adolescence.10,11 The reported
incidence of spondylolisthesis is between 4 and 7%,12–14
although a higher incidence has been reported among Eskimos
(18–56%).15,16
In 1782, the Belgian gynaecologist Herbiniaux described a
severe case of lumbosacral luxation, which he considered as a
potential obstetrical problem.1
A precise definition of spondylolisthesis was first given by
Kilian in 18542 – a spinal condition in which all or a part of a
vertebra (spondylo) has slipped (olisthy) on another.
Wiltse et al9 described five major types:
• Dysplastic spondylolisthesis is secondary to a congenital
defect of the first sacral–fifth lumbar facet joints, with
gradual slipping of the fifth lumbar vertebra.
• Isthmic or spondylolisthetic spondylolisthesis is the most
common type of spondylolisthesis. The basic lesion is in
the pars interarticularis. The vertebra above can slip as the
result of a lytic process, an elongation without lysis or an
acute fracture (subtypes a, b and c). If a defect in the
pars interarticularis can be identified, but no slip has
occurred, the condition is called a ‘spondylolysis’.
• In degenerative spondylolisthesis an advanced degeneration
of the facet joints and a progressive change in the
direction of the articular processes allow the vertebra
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Grading
Spondylolysis is visualized by an oblique view of the lumbar
spine which shows the well-known ‘collar on the Scottie dog’s
neck’ (Fig. 2).
The Lumbar Spine
Superior articular facet
Transverse process
Inferior articular facet
Superior
facet
Defect
Transverse
process
Inferior facet
Fig 1 • Spondylolisthetic spondylolisthesis: fibrous defects in the
pars interarticularis permit forward displacement of the upper
vertebra and separation of the anterior part of the vertebra from its
neural arch.
Facet joint
Spinous process
Forward slipping is best visualized on a lateral radiograph
and the amount of listhesis is graded by the Meyerding’s
system (Fig. 3):17 the upper sacrum is divided into four parallel
quarters and the degree of slipping is calculated from the distance that the posterior edge of the fifth lumbar vertebra has
shifted on the posterior edge of the sacrum in relation to the
total width of the upper sacrum. Grade I is a shift of less than
25%, grade II between 25 and 50%, grade III between 50 and
75% and grade IV more than 75%.
Some authors emphasize that there is a significant difference in measurements when the radiographs are taken with
the patient in a recumbent rather than erect position.18
Clinical findings
It should be emphasized that most cases of spondylolisthesis
are asymptomatic. Even severe displacements may be present
in very active patients, without the slightest discomfort.
In a radiological study of 996 adult patients with low back
pain, MacNab found spondylolisthesis in only 7.6%, which is
not significantly higher than in the population as a whole
(4–6%).19 Therefore caution must be taken before ascribing
back pain or sciatica to spondylolisthesis and the radiological
demonstration of a defect in a patient with back pain does
not always indicate that the source of the symptoms has been
discovered.20,21
Spondylolisthesis can produce backache or sciatica in two
ways: spondylolisthesis as the basis of a secondary disc lesion
and the spondylolisthesis itself causing symptoms.
e218
Fig 2 • The defect in the pars interarticularis is best visualized in an
oblique view (‘Scottie dog with collar’). From Magee 2008 Orthopedic
Physical Assessment, 5th edn, Saunders, St Louis. Reproduced by kind
permission.
Spondylolisthesis with secondary disc lesion
As early as 1945, Key stated that symptoms in spondylolisthesis were far more often caused by a disc lesion than by slippage of the vertebra.22 The clinical features are exactly the
same as in patients without spondylolisthesis, and nothing in
the history or clinical examination arouses suspicion, except
some irregularity of the spinous processes on examination.
Radiographs carried out in the erect posture disclose the slip.
It is obvious that the management of disc lesions occurring
in spondylolisthetic spines is exactly the same as in those
without bony defects. The only difference is probably the
liability to recurrence of acute or chronic discodural conflicts.
As in other forms of lumbar instability, sclerosing injections
can have a good preventive outcome after reduction has taken
place.
Spondylolisthesis of itself causing symptoms
Spondylolisthesis can cause both backache and sciatica. The
former has postural ligamentous characteristics: the ache is
central, sometimes with vague and bilateral radiation over the
lower back. The discomfort is associated more with maintaining a particular position than with exertion. Dural symptoms
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology Normal
Grade 1
Grade 2
Grade 3
Grade 4
Fig 3 • Grades of spondylolisthesis (from Meyerding).17
are absent. There are no articular signs or symptoms; lumbar
mobility is full and painless. Root signs are also absent. The
only clinical finding is a bony irregularity palpated over the
spinous processes. Treatment is that for ligamentous backache
and consists of sclerosing injections (see p. 579).
Spondylolitic sciatica very much resembles a bilateral lateral
recess stenosis but the patient is much younger. Increasing pain
and paraesthesia appear in the standing position and may force
the patient to sit or lie down, which causes the symptoms to
disappear. Dural symptoms are absent. Clinical examination
reveals little: there is a normal range of movement without
pain. Root signs, such as positive straight leg raising, weakness
or sensory loss are not found (J. Cyriax, personal communication, 1983; Calliauw and Van23).
The cause of sciatic pain in spondylolisthesis is unknown.
The different hypotheses are:
• The forward movement of the listhetic vertebra drags on
the nerve roots, which engage painfully against the shelf
formed by the stable vertebra below (Cyriax:3 pp.
287–290).
• A fibrocartilaginous mass, with or without small ossicles,
may form at the defect in the pars interarticularis.
Adhesions around the nerve root and compression
result.24
• With the forwards and downwards drop of the vertebral
body, the pedicles descend on the nerve roots and kink
them as they emerge through the foramen.19
• A forwards slipping of the vertebral body moves the
transverse processes in a forwards and downwards
direction, allowing the L5 roots to be pinched
between the sacrum and transverse process
(the ‘far-out’ 25).
Treatment
Patients with an accidentally detected spondylolisthesis do not
need treatment. If the pain is caused by a secondary disc lesion,
the patient is treated by the normal procedures used in dis­
codural or discoradicular problems: manipulation, traction or
epidural anaesthesia. The liability to recurrences after successful treatment, however, is much increased and in patients with
© Copyright 2013 Elsevier, Ltd. All rights reserved.
both spondylolisthesis and a disc lesion the displacement will
reappear. In these instances, sclerosing injections are used as a
prophylactic measure.
Spondylolisthesis which of itself causes lumbar pain should
always be treated non-surgically. Sclerosing injections to the
ligaments often give good results.
If leg pain is a significant problem, nerve root infiltrations
can often abolish it. The patient can also be advised to wear a
corset during occasional strenuous activity. If root pain cannot
be abolished by these conservative measures, surgery should
be considered. Surgical intervention can also be considered if
the listhesis is progressive or the patient presents with a
Meyerding grade III or IV. The gold standard of surgical treatment is fusion in situ.26 The different techniques for fusion
have mixed and variable results27–29, and the possibility of complications.30 Recently, reduction of the listhesis and stabilization, whether by bilateral lateral fusion or interbody fusion, has
been recommended.31,32
It should be remembered, however, that even in grade III
and IV listhesis, good results have been described after nonsurgical treatment.33 Apel et al.34 reported on the long-term
results (40 years) after surgical and non-surgical treatment of
grade I and grade II spondylolisthesis. Of the conservatively
managed patients, all functioned well. Among those undergoing surgery, poor results were confined to those patients in
whom the fusion failed, and a pseudarthrosis developed (40%).
Frennered et al35 stated that operative treatment for low-grade
spondylolisthesis does not seem to give better results than
conservative treatment. More recent prospective studies,
however, conclude that surgical management of adult isthmic
spondylolisthesis improves function and relieves pain more
efficiently than an exercise programme.36,37
Osseous disorders
Osteoporosis
Osteoporosis is a metabolic disease, related to several different
disorders. It is characterized by a reduction of bone mass which
occurs predominantly in the axial skeleton, the femoral neck
e219
The Lumbar Spine
and the pelvis. By radiographic criteria, 18% of men and 29%
of women between the ages of 45 and 79 years of age have
evidence of osteoporosis and more sensitive methods for determining vertebral bone mineral density show that 50% of
women past the age of 65 have asymptomatic osteoporosis.38
The radiographic appearances are changes in bone porosity,
trabecular pattern and vertebral body shape (the so-called
biconcave fishmouth vertebrae).39 It is a common mistake to
believe that these changes account for patients’ backache. It
should be remembered that uncomplicated osteoporosis does
not cause any symptom except some loss of height of the spine.
Thus the major explanation for long-standing back pain in the
elderly does not appear to be related to spinal osteoporosis and,
if a radiograph shows uncomplicated osteoporosis in a symptomatic patient, other sources for the pain should be sought.40
Osteoporosis may, however, lead to a pathological fracture. If
this takes place, a sudden pain in a girdle distribution will
result.
Paget’s disease
Osteitis deformans or Paget’s disease of bone41 is a localized
disorder characterized by a remarkable hyperactivity of osteoclasts and subsequent increase of osteoblastic bone deposition.
As a result, the normal bone architecture is completely disturbed.42 In a vertebral body this can result in softening, broadening and collapse of the bone. The disease is reported to occur
in approximately 4% of individuals over the age of 40.43 In the
majority, the disease is restricted to a few bones.
It must be emphasized that most patients with Paget’s
disease are asymptomatic.44 The main problem for the clinician
therefore is not the discovery of the Paget’s disease but the
association of the back symptoms with the Pagetoid lesion.
Back pain and the associated angular kyphosis arise as the result
of collapse of the vertebral body. Sometimes new bone growth
in the vertebral arch may compress nerve roots, resulting in a
spinal stenosis or a lateral recess stenosis.45,46
Fractures
Crush fracture of the vertebral body
This causes a wedge deformity. It usually occurs at the upper
lumbar or at the thoracolumbar level and usually results from
axial trauma or from flexion injuries (see online chapter Disorders of the thoracic spine: non-disc lesions – disorders and
their treatment). Wedging of a vertebral body may also result
from a pathological fracture which is the consequence of senile
osteoporosis, tumour, Paget’s disease or tuberculous caries.
Immediate post-traumatic pain is referred bilaterally in the
appropriate dermatome. The diagnosis is not missed if backache follows a gross trauma. In a pathological fracture, however,
the patient probably does not recall an injury that can be
related to the onset of the symptoms. Nothing in the history
then warns the examiner of the possibility of a crushed vertebra. However, if the history is taken carefully, and compared
with the clinical findings, some unlikelihoods will immediately
become obvious. They are:
e220
• the pain is usually located in the upper lumbar area:
pathological fractures occur more often in the ‘forbidden
area’
• dural signs are absent: although the patient describes an
intense backache, coughing does not hurt
• inspection reveals an angular kyphosis
• examination shows a capsular pattern, with symmetric
limitation of lateral flexion
• there are no dural signs: straight leg raising is normal,
which is always suspicious in a case of acute lumbago.
The girdle pain lasts a week or two, whereafter a localized bone
pain remains. After 3 months the fracture will have united and
symptoms have ceased. Although a wedged vertebra results in
lasting malalignment of the related posterior joints, usually
little ligametous pain results. Any continuous pain after the
fracture has healed is from a coincident disc lesion. Indeed,
any force sufficient to break bone will also threaten disc tissue
and it is not hard to imagine that, after a crush fracture of
a vertebral body, the disc above or below the lesion may
also be damaged. The possibility of a coincident disc displacement should therefore be considered in a case with persistent
pain. Because of the permanent kyphosis and the possible
elongation of supra- and interspinous ligaments, the protrusion
may be very unstable and difficult to treat. Although manipulation usually affords excellent results, the improvement is
not lasting unless sclerosing injections are given to stabilize
the joint.
Spondylolysis
Isthmic spondylolysis is considered to represent a fatigue fracture of the pars interarticularis of the neural arch. There is a
relatively high incidence of radiographically identified spondylolysis in the general population, but the vast majority of these
lesions probably occur without associated symptoms.6,47,48 The
incidence of spondylolysis in the young athletic population
shows an almost fivefold increase compared to the general
population,49 with the highest rates in weight lifters,50 gymnasts51 and football players.52 Given this high incidence of
asymptomatic lesions, the relation between unilateral or bilateral back pain and a fatigue fracture of the pars interarticularis
remains unclear.53
However, recent histological studies could identify a welldeveloped ligamentous structure covering the defect (‘the
spondylolysis ligament’) and containing thin unmyelinated
nerves.54,55 Infiltration of bupivacaine hydrochloride (Marcain)
into the pars defect produced temporary symptom relief,
which proves the existence of symptomatic lesions.56
Symptomatic lesions appear to be particularly a clinical
problem in adolescents, especially adolescent athletes.
Although clinical features of active spondylolysis do not differentiate this condition from other causes of low back pain,57
suspicion may arise when an adolescent athlete presents with
unlilateral backache without dural signs nor symptoms, and
pain is provoked by full extension.58,59
On plain radiography, the defect in isthmic spondylolysis is
visualized as lucency in the region of the pars interarticularis.
The lesion is commonly described as having the appearance of
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology a collar on the ‘Scotty dog’ seen in lateral oblique radiographs
(see Fig. 2). Plain radiography has limited sensitivity, however,
and nowadays bone scintigraphy with single photon emission
computed tomography (SPECT) is considered as the gold
standard of investigation.60,61
Conservative treatment consists of relative rest and the
avoidance of activities associated with increased pain.62
Fractures of the transverse processes
These may occur after direct trauma to the back. Alternatively
they result from gross muscular effort, frequently a resisted
rotation strain; lumbar manipulation is a rare cause of
fracture.
The patient complains of post-traumatic and localized unilateral pain. Clinical examination reveals a partial articular
pattern, with pain during side flexion away from the affected
side. However, there is also pain during resisted movements:
resisted side flexion to the painful side and resisted extension
in the prone-lying position are both positive. The lesion may
appear insignificant on radiograph.
Pain usually ceases after a fortnight. If pain persists, a co­­
incident disc lesion should be suspected. Alternatively, an
emotionally unstable patient may capitalize on radiological
evidence of a ‘fractured spine’.
Stress fractures of the lumbar pedicle
Stress fractures of the contralateral pedicle in patients
with unilateral spondylolysis has recently been reported63,64
and termed ‘pediculolysis’.65 The development of a unilateral
spondylolysis probably leads to a redistribution of forces,
resulting in a stress fracture of the contralateral pedicle. Alternatively, not a fracture but a compensatory sclerosis and hypertrophy of the contralateral pedicle develop.66,67 To date, it is
not clear if the lesions are responsible for particular clinical
syndromes.68
Tumours
Classically, neoplastic lesions in the lumbar spine are classified
as benign or malignant lesions. The latter are subdivided into
primary malignancies and metastases. Benign and primary
malignant neoplasms are rare in the lumbar spine, whereas
secondary deposits are common. Although the diagnosis of
tumours of the lumbar spine is largely dependent on radiological examinations, it must be remembered that 30% of the
osseous mass of bone must be destroyed before a lesion is
radiologically evident.69 Therefore radiographs do not reveal
early disease and too much reliance on radiographic appearances can give both the patient and the physician a false feeling
of security. Therefore, in the diagnosis of neoplastic lesions,
the history and clinical examination remain vital. Special attention must be paid to warning signs. When routine radiographs
fail to support the clinical impression, a radioisotope scan must
be obtained, in order to demonstrate the presence of a malignant lesion and the extent of the spinal involvement.
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Benign tumours
Benign tumours of the vertebrae predominantly affect patients
under the age of 30 years and are mostly localized in the posterior wall. Chronic localized backache that is not dependent
on posture and movement and does not ease with recumbency
is the main characteristic of a benign tumour. Clinical examination may show a limited range of flexion due to a muscle
spasm. If the lesion compresses nerve roots, slowly progressing
sciatica will supervene. Early detection of the lesion on the
radiograph is not always easy.
Osteoid osteoma
This constitutes about 12% of all benign tumours (Dahlin and
Unni:70 pp. 88–101) and appears mostly in children and adults
below the age of 30 years. The pain is frequently exacerbated
at night and is often relieved by small doses of aspirin.71 Treatment consists of local excision of the tumour.
Osteoblastoma
This is a rare benign neoplasma of bone but has a predilection
for the spine: approximately 40% of all osteoblastomas are
found in the posterior elements of the spine and sacrum.72 The
tumour is seen most frequently in males under the age of 30
years.73 The back pain is localized, insidious in onset, with a
duration of months or years and not as severe as in osteoid
osteoma. Clinical examination may reveal muscle spasm
and localized tenderness. Because of the expansive nature of
the tumour, slowly progressive compression of nerve root(s),
with radicular pain and evidence of neurological deficit, may
occur.
Haemangiomas
These account for less than 1% of symptomatic primary bone
tumours (Mirra:74 pp. 492–497), although postmortem studies
have demonstrated that asymptomatic lesions exist in 12% of
all vertebral columns. This implies that most of these lesions
remain asymptomatic throughout life. The thoracic spine is
the location for 65%, the cervical spine 25% and the lumbar
for only 10%. Patients with symptomatic haemangiomas are
usually between 40 and 50 years of age.75 The main complaint
is localized pain. Clinical examination may show limitation of
movement from muscle spasm and localized tenderness.
Increased weakening may result in a pathological fracture,
which in turn may cause neurological symptoms.76 Since
vertebral haemangiomas are usually asymptomatic and have
a benign course, treatment is expectant. Radiation seems
to afford a good outcome in patients with constant,
disabling pain.77
Eosinophylic granuloma
This is a rare bone lesion characterized by the infiltration of
bone with histiocytes, mononuclear phagocytic cells and eosinophils. It was first described by Jaffe and Lichtenstein in
1944.78 It occurs most commonly in children and adolescents79
and only 10% of the lesions are localized in the spine. Local
and constant back pain is the first symptom. Clinical examination shows muscle spasm and local tenderness. If the lesion
e221
The Lumbar Spine
affects a vertebral body, a flattening – vertebra plana – will
result. This spontaneous collapse of the vertebral body in children was first described by Calvé in 192580 and was thought
to be a manifestation of osteochondritis juvenilis.79 It seems
that the collapse of the vertebra induces spontaneous healing
of the granuloma, in that symptoms usually cease after the
body has collapsed.81,82
Aneurysmal bone cyst
This is a benign, cystic vascular lesion of bone. The majority
of aneurysmal bone cysts occur in the long bones of the
extremities of young adults.83 The lumbar spine is affected in
only 10% of cases.84 The clinical presentation is lumbar pain
that usually has an acute onset and increases in severity over a
short period of time. Depending on the location and size of
the lesion, the other clinical manifestations vary. If the lesion
is at the spinous or transverse processes, the pain remains
local.85 If the vertebral body is affected, the lesion may expand,
which can result in weakening of the bone, pathological fractures and serious neurological deficits. Although aneurysmal
bone cysts are benign lesions, they may cause severe damage
because of their expansive characteristics. The lesion therefore
must be diagnosed early and treatment instituted without
delay in order to keep disability to a minimum. Treatment is
by surgery, radiotherapy or cryotherapy.
Malignant tumours
Malignant tumours of the spine predominantly affect patients
over the age of 50 and are mostly localized in the anterior spine
elements. Metastatic lesions of the axial skeleton are much
more common than primary malignant lesions (chordoma,
myeloma and chondrosarcoma), the overall ratio being 25 : 1
(Francis and Hutter;86 Mirra:74 pp. 448–454).
Chordoma
This is a slowly developing malignant tumour that originates
from the remnants of notochordal tissue and therefore occurs
exclusively in the midline of the axial skeleton. It has a predilection for either end of the spinal column: 50% of cases occur
in the sacrum and 38% in the skull base.87 The lesion is rarely
reported below the age of 30 years and most tumours become
evident between the ages of 40 and 70.88 Chordomas are slowgrowing tumours with a locally invasive and destructive
character.
The common sacral tumours may be difficult to detect. The
patient initially presents with localized pain in the sacral area
or with coccygodynia. The pain is dull, constant and not
relieved by recumbency. Often it is of long duration and only
moderate, so that it does not force the patient to seek treatment.89 Chordomas of the sacrum extend anteriorly into the
pelvis. Because the dural sleeve is not involved, presacral invasion of the nerve roots does not provoke radicular pain. Straight
leg raising is also not limited. However, gross muscular weakness of one or both legs, together with considerable sensory
deficit is detected. Sometimes the patient presents with
urinary or bowel incontinence as well.90 Such a gross paresis
in the absence of root pain always suggests a tumour. A
radiograph of the lumbar spine and sacrum discloses lytic
e222
bone destructions with calcified foci and a pre-sacral soft
tissue mass.91,92
Patients with chordomas of the lumbar spine may present
with localized central lumbar pain sometimes radiating bilaterally. Involvement of nerve roots may induce bilateral sciatica.
Clinical examination then shows muscle spasm and bilateral
weakness.93
Treatment consists of total resection of the tumour, which
usually presents a major problem. Often partial resection, followed by radiation therapy, is the only option.94 Chemotherapy
is ineffective.95
Chondrosarcoma
This is a malignant tumour that forms in cartilaginous tissue.
The tumour is frequently located in the pelvis and lumbar
spine and grows extremely slowly. The usual age of onset is
between 40 and 60 years (Dahlin and Unni:70 pp. 227–259).
The tumour may be symptomless over many years. Local pain
is very suggestive of actively growing tumour. When neural
elements are compressed by the tumour, abnormalities are
found on neurological examination. The treatment of choice is
total resection of the tumour.
Myeloma
This is a malignant tumour of plasma cells and is the most
common primary tumour of bone; the spine is almost always
involved. The disseminated form is multiple myeloma and
accounts for 45% of all malignant bone tumours (Dahlin and
Unni:70 pp. 193–207). The patients are usually in an older age
group, in that the disease is rare below the age of 50 years.
Plasmacytoma is the solitary form and affects the spine in
about 50% of patients.96
The most common complaint is of back pain, which does
not vary with exertion, although initially may be relieved somewhat by bed rest. Malignant disease is suggested by steady
worsening of the backache which eventually becomes continuous, irrespective of posture or movement. As the backache
becomes more severe, sciatica, which is often bilateral,
appears.97 The fact that the backache does not cease after the
root pain comes on and that the root pain is bilateral, immediately draws attention to the possibility of an expanding
lesion. Alternatively, the backache is sudden as the result of a
pathological fracture.
Findings on clinical examination depend on the extent
of the disease. In the early stage, there is usually only lumbar
muscle spasm and localized tenderness. In later stages, angular
kyphosis and signs of nerve root compression at different levels
can be seen. Finally, signs of generalized illness, such as fever,
weight loss and pallor, become prominent.
Radiographically, multiple myeloma is characterized by the
presence of round lytic defects in the bone without any surrounding reactive sclerosis. Occasionally, lytic defects may not
be obvious, and the radiograph shows nothing more than a
diffuse osteopenia.98 In such circumstances the differential
diagnosis must be made by laboratory examinations,99 which
consistently reveal an elevated erythrocyte sedimentation rate
– seldom less than 100 mm/h. Characteristically, abnormal
Bence-Jones proteins can be demonstrated in the urine.100 The
most important test is serum protein electrophoresis, which
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology identifies a monoclonal spike in more than 75% of patients and
hypogammaglobulinaemia in 9%.101
The usual course of multiple myeloma is one of gradual
progression. Systemic therapy with melphalan and cortisone
may improve clinical symptoms, but the average survival
seldom exceeds 5 years.102
Metastatic tumours
The most common malignant tumour in the spine is metastatic
cancer. The prevalence of metastases increases with increasing
age, and patients who are aged 50 years or older are the population at greatest risk. Neoplasms frequently associated with
spinal metastases are of prostate,103 breast, lung, thyroid and
colon.104 Up to 70% of patients with a primary neoplasm will
sooner or later develop metastases in the thoracolumbar
spine.105 The predilection of metastases for the lumbar spine
may be explained by the functioning of Batson’s plexus. This
is a venous network, located in the epidural space between the
bony spinal column and the dura mater. Because this plexus
has no valves to control blood flow, metastatic cells may easily
enter it and lodge in the connected sinusoidal systems of the
red bone marrow of the vertebral bodies.106
Some suspicion may arise when, for the first time, a patient
over the age of 50 presents with an attack of low back pain.
Especially if the pain has a gradual onset and increases in intensity over time, the patient should be suspected of suffering
from a malignant disease. The concern should be even greater
if there is a prior history of malignancy. In the beginning the
pain is localized but very soon it spreads down the leg in a
distribution not corresponding to a single root. Sometimes
there is bilateral sciatica and the lumbar pain does not ease but
becomes even worse when the sciatica appears. Because the
tumour often extends into the epidural space, dural symptoms
may be present. However, not all skeletal metastases cause
pain: symptoms may occur only when the lesion is complicated
by a pathological fracture.107
Results of the clinical examination depend on the stage; at
first, there will be muscle spasm, markedly limiting movements, especially side flexions. Localized tenderness, particularly at the ‘forbidden’ upper lumbar area causes more suspicion.
Later, distinctive neurological signs will immediately draw
attention to the possible existence of a spinal neoplasm:
Cure is seldom possible and treatment of metastatic deposits in the spine is palliative: it includes radiation therapy, corticosteroids and decompressive laminectomy.
Rheumatological disorders
Ankylosing spondylitis
This disease usually affects the sacroiliac joints initially, and
then appears in the thoracolumbar area. Thereafter, the lower
lumbar, the thoracic and the cervical spine also become
affected111 (see Ch. 43). Although the lesion invariably starts
at the sacroiliac joints, it is possible that this does not cause
any symptoms and the first complaint is then of backache.
Backache in ankylosing spondylitis is typically intermittent;
it comes and goes irrespective of exertion or rest. However,
the pain and the stiffness are greatest in the morning and
usually improve with movement. Several segments at the
upper lumbar and thoracolumbar level become involved at
about the same time.112 Because the pain is usually limited
to the central part of the spine and does not refer laterally,
the patient complains of vertical distribution (Fig. 4a).
This contrasts with the more or less horizontal, gluteal and
asymmetrical reference of dural pain in a lumbar disc disorder
(Fig. 4b).
(a)
(b)
• Bilateral weakness
• Weakness of the psoas muscle
• Signs of involvement of two or three consecutive roots, or
non-adjacent roots
• Discrepancy between pain and weakness
• A warm foot on the affected side.
It is important to stress that radiographs may be normal and
are not reliable early in the course of a metastatic lesion. Clinical symptoms and even signs of gross muscular weakness may
appear before the radiograph shows erosion or collapse of
bone.108 If the clinical features of metastasis are present but
the radiographic examination remains negative a bone scan may
be necessary to establish the diagnosis.109
MRI examination is a quite sensitive complementary technique and appears to be more specific for metastasis in certain
locations of the spine.110
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Fig 4 • Localization of pain affecting the upper lumbar level in
ankylosing spondylitis (a), dural reference of low back pain in a
lumbar disc disorder (b).
e223
The Lumbar Spine
Inspection usually shows a flat lumbar spine, together with
the beginning of an upper thoracic kyphosis. The motion of the
spine is impaired in a symmetrical way, which is best demonstrated by a gross limitation of side flexion in both directions.
There is also upper lumbar tenderness and the end-feel during
a downwards thrust on the prone spine is hard.
Sometimes an acute increase in pain caused by a sprain of
the stiffened lumbar joints can simulate an attack of lumbago.
The patient then states that lifting something heavy caused
immediate and agonizing pain at the upper lumbar level.
Although the history probably suggests a disc protrusion, there
is a complete absence of dural signs, which is rather unusual
in such an acute case. Furthermore, there is a symmetrical
limitation of side flexion and the pain on the palpation is upper
lumbar, in the ‘forbidden area’.
Diagnosis is confirmed by radiography of the sacroiliac
joints. Because lumbar manifestations occur some years after
sacroiliac manifestations, plain radiographs of the latter will
almost certainly reveal the typical narrowed joint spaces and
surrounding sclerosis. In later stages, radiographic abnormalities also appear in the lumbar and thoracolumbar spines. First
there are signs of osteitis of the anterior corners of the vertebral bodies. This results in the typical ‘squaring’ of the vertebrae. Healing of the inflammation leads to a reactive sclerosis
in the anterior portions of the vertebral bodies. Later on, thin,
vertically orientated calcifications of the annulus fibrosus and
anterior and posterior longitudinal ligaments appear. These
growing ‘syndesmophytes’ can enclose the whole axial skeleton, which is then called a ‘bamboo spine’.113
Rheumatoid arthritis
Rhematoid arthritis, a systemic chronic inflammatory disease
which involves synovial joints, may affect the facet joints of
the lumbar spine, although it is found more frequently in the
cervical articulations. The disease does not affect the sacroiliac
joints.114 Those who develop low back pain secondary to rheumatoid arthritis usually have a long-standing history of disease
in the joints usually affected by the illness.115
Pain stems from the facet joints and therefore its reference
does not spread beyond the hips.116 The symptoms are inflammatory in nature, with pain and stiffness increasing with rest,
greater in severity in the morning and improving during activity. Clinical examination reveals limitation of movement in a
capsular way and localized tenderness. The diagnosis is based
upon the typical history, the clinical appearances of the peripheral joints and the characteristic laboratory findings.
Reiter’s syndrome
This is a triad of urethritis, arthritis and conjunctivitis.117 It is
the most common cause of arthritis in young men and primarily affects the joints of the lower extremity. The disease
results from the interaction of a specific infection and a genetically predisposed host. Although back pain is a frequent
symptom of patients with Reiter’s syndrome, pain usually
stems from the sacroiliac joint and lesions of the lumbar spine
area118 (see Ch. 43).
e224
Ankylosing hyperostosis
This disease is also known as the vertebral hyperostosis of
Forestier.119 More recently ‘diffuse idiopathic skeletal hyperostosis’ (DISH) has been suggested, in recognition of the frequent combination of both spinal and extraspinal foci.120
According to autopsy findings, it seems to be a common entity
in the eldery.121
Despite the impressive anatomical abnormalities, most
patients rarely have significant disability from the illness, the
principal complaint being increasing stiffness. Some patients
develop a vague and local ache in the entire trunk.122 Clinical
examination shows marked limitation of movement at every
spinal joint. Dural and radicular signs are of course absent.
Laboratory parameters are normal and the diagnosis of
DISH is a radiographic one. The criteria are a flowing calcification along the anterolateral aspect of four contiguous vertebral
bodies, preservation of the normal intervertebral disc height
and absence of apophyseal arthrosis or sclerosis.123
Treatment is seldom necessary, in that the complaints are
rather minor.
Infections
Infections of the spine are rare. However, it is important to
remember them as a potential source of backache. An early
diagnosis is vital, because the prognosis of infections of the
vertebral column is excellent if the disease is recognized early.
Infections involving the lumbar spine include vertebral osteomyelitis, intervertebral discitis and herpes zoster, and viral
infection of the dorsal root ganglia.
Vertebral osteomyelitis
Pyogenic vertebral osteomyelitis
This occurs as the result of haematogenous spread through the
blood stream. Pelvic lesions, such as urinary tract or rectosigmoid infections, preferentially spread to the vertebral column
through the venous plexus of Batson.124 During recent decades
the clinical features of vertebral osteomyelitis have changed.125
Before the antibiotic era, it used to be a disease of children
and adolescents, with a rapid evolution and in most cases
caused by Staphylococcus aureus. Now, the mean age of patients
reported with osteomyelitis is 50 years, the onset is insidious
and the development is slow.126 The diagnosis of vertebral
osteomyelitis is frequently missed because the patient’s symptoms are ascribed to mechanical problems.
Onset of back pain is insidious and it becomes more and
more severe. The central ache is usually constant, although it
is sometimes increased by exertion. If the lesion becomes more
invasive, the patient will find it difficult to stand or sit upright.
In a later stage, the infection may extend beyond the bone and
can produce a psoas abscess: the patient may then present with
an abdominal syndrome or with hip pain.127 Should the infection drain into the spinal canal, an epidural abscess or meningitis will result.128
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology In the early stage, the signs may be insignificant, with only
slight limitation of movement. As a rule, side flexions are symmetrically limited. Local tenderness at the affected level can
be detected during passive forcing of extension in the pronelying position.129 Because the first and second lumbar vertebrae
are the levels in the axial skeleton most commonly affected,130
the discovery of pain at the ‘forbidden area’ during selective
examination will alert the examiner.
As the pain worsens, side flexions become more and more
limited and muscle spasm limits flexion. Because of severe
pain, the patient finds it more and more difficult to remain
upright. This could suggest an attack of lumbago but when it
comes to further clinical examination, straight leg raising is
found to be of full range and completely painless.
Patients with psoas muscle irritation also present with
decreased hip motion and a painful weakness of hip flexion. It
is important to notice that, in most cases, fever and signs of
general illness only appear if an abscess forms.131
Radiographic evidence of the disease follows the symptomatic onset by 1–2 months. Bone scintigraphy usually demonstrates abnormalities at an earlier stage of disease, although it
should be remembered that false positives and negatives do
occur. Computed tomography may also show bony changes
before their appearance on routine radiographs.132
Treatment includes antibiotics and bed rest. The choice of
antibiotic is dependent on the identification of the organism
causing the infection.133 Surgical interventions such as laminectomy, discectomy or vertebral fusion may be indicated in case
of neurological compromise or mechanical instability.134
Tuberculous vertebral osteomyelitis
This has a clinical course that can be distinguished from pyogenic infections. Before the antibiotic era, it was a disease of
children but nowadays patients with spinal tuberculosis have
an average age between 40 and 50 years.135 Alcoholics and drug
addicts are at greatest risk of developing the disease.136
Tuberculous spondylitis occurs as the result of haematogenous spread from foci in either the lungs or the genitourinary
tract. The lesion begins under the bony endplate and, although
initially only the vertebral body is affected, in a later stage the
infection can spread to disc, soft tissues and spinal cord.
Abscess formation is present in about 50% of the cases.137 The
disease is very insidious, and the time elapsing before a diagnosis is made may be as long as 3 years.138
Initially there is a vague and localized backache. Later the
pain can spread to the buttock. A careful history also reveals
the existence of constitutional problems such as anorexia,
weight loss, intermittent fever and night sweats.
Limitation of movement in a capsular way and muscle
spasm, together with localized tenderness over the involved
vertebra, are the main clinical findings in the early stage. Later
there is localized bony deformity, resulting from vertebral collapse or neurological abnormalities. Because of the insidious
nature of the disease and the insignificant and local symptoms,
the onset of paraplegia is sometimes the first manifestation of
tuberculous spondylitis.139
Because the disease has a slow development, patients
with tuberculous spondylitis usually present with identifiable
© Copyright 2013 Elsevier, Ltd. All rights reserved.
destruction of vertebral bodies. Investigation by CT seems to
be the best way of searching for abscess formation.140
Treatment consists of antituberculous drugs and immobilization. Surgery must be considered if, despite antituberculous
therapy, abscesses progress.
Intervertebral disc space infections
Infections of the intervertebral disc can develop secondary to
haematogenous invasion via the blood stream. The primary
lesion is usually an infectious endocarditis or a urinary tract
infection.140 The most common cause for spondylodiscitis,
however, is a direct complication of disc surgery.141–143
The clinical picture is that of an acute lumbago which
appears 1 week to 2 months after the discectomy. The pain
radiates in a dural manner to the gluteal region, groin and
limbs, is exacerbated by movement and is relieved by absolute
rest. Dural symptoms are present.
There are dural and articular signs. Fever is rarely present
but the erythrocyte sedimentation level is usually elevated.144
Since the condition closely resembles a discodural conflict,
nothing except the previous disc surgery will draw attention to
the possibility of an infection. It is therefore wise to consider
every case of ‘acute lumbago’ occurring in the first months after
discectomy as a discitis until the reverse is demonstrated.
Radiographs do not show abnormality during the first few
weeks. The earliest change is a decrease in the height of the
affected intervertebral disc space. Later, relative sclerosis and
irregularity at the vertebral endplates will be noted. If a disc
infection is suspected, a bone scintillation scan is indicated and
identifies an area of increased bone activity in the adjacent
vertebrae.145 During the last decade, MRI has become the
radiological method of choice for establishing the diagnosis of
spondylodiscitis, in particular with regard to differentiating
between cases with and without abscess formation.146,147
Treatment includes antibiotics and immobilization.
The childhood form of discitis develops in children between
2 and 6 years old. The patient presents with antalgic posture,
muscular defence, unexplained fever and increased erythrocyte sedimentation rate.148,149
Herpes zoster
This is a sequela of previous infection with chickenpox. After
the termination of the illness, the virus remains dormant in the
posterior spinal sensory ganglia. During a period of low host
resistance, the virus multiplies, which results in pain and skin
lesions.150 Herpes (shingles) occurs more frequently in the
elderly and in patients with impaired immune function.
The patient complains of segmental pain which is burning
or shooting in character. Since the pain antedates the appearance of the vesicles by 4–7 days, the early diagnosis can be
missed and the patient may be mistakenly regarded as suffering
from sciatic pain, although examination of the lumbar spine
and the neurological examination of the limbs are normal.149
Sometimes, however, dysaesthesia in the area of skin supplied
by the affected nerve root can be detected. Once the skin
lesions develop in a segmental distribution, the diagnosis will
e225
The Lumbar Spine
be obvious. Sometimes patients with herpes zoster may also
demonstrate a mild and temporary paresis in the motor nerve
that corresponds to the affected level.
Treatment is directed at controlling the pain.
Intraspinal lesions
Neurofibromas and meningomas
Pathological processes may affect tissues inside the spinal
column (Fig. 5). In the lumbar area they can be extradural or
intradural.
Extradural lesions
Extradural neoplasms
These are metastatic lesions that have invaded the intraspinal
space from contiguous structures. They usually remain extradural because the dura is resistant to invasion by the
neoplasm.
Epidural abscesses and epidural haematomas
These present as acute backache with severe dural signs and
symptoms. There is a rapid progression to bilateral sciatica and
neurological weakness.151–154
Intraspinal synovial cysts
Cysts arising from the synovium-lined facet joints can exert
pressure on the nerve root sleeve and cause unilateral sciatica.155 Cauda equina compression has also been reported.156
Diagnosis is made by CT or MRI and the treatment is
surgical.157
Intradural lesions
Arachnoiditis and arachnoid cysts
Inflammatory changes to the arachnoid space (arachnoiditis)
develop after myelography with iophendylate, in spinal injuries
1
2
2
2
1
3
2
1
Fig 5 • Intraspinal lesions: 1, extraspinal, osseous lesions;
2, intraspinal, extradural lesions; 3, intraspinal, intradural lesions.
e226
and as a complication of haemorrhages or meningitis.158 The
patient complains of diffuse and constant back pain, sometimes
radiating to both legs. Paraesthesia and dysaesthesia may be
present. The prognosis is poor and there is no effective
treatment.
Meningomas and neurofibromas are slowly growing benign
tumours, arising from meninges and spinal nerves. They are
rarer at the lumbar spine than at the cervical level. As intradural spinal tumours can compress the dura mater, the nerve
roots and the nerve root sleeves, dural and radicular symptoms
and signs will be present and the clinical picture usually mimics
a herniated disc – between 0.8 and 1.0% of patients presenting
with symptoms consistent with disc herniation have intraspinal
tumours.159,160 If the tumour involves the nerve roots of the
first or second level, diagnosis is not very difficult because first
and second lumbar disc lesions are extremely rare. At the lower
lumbar levels, however, neuromas are very difficult to detect,
which explains the considerable delay in diagnosis.161, 162
The patient presents with back pain and/or root pain. Sometimes the pain increases at night or in the supine position.
Dural symptoms, such as pain during coughing and sneezing,
are always present – a neuroma is unlikely if a cough does not
hurt. Unlike a disc lesion, coughing usually hurts in the limb
rather than in the back.
Clinical examination shows limitation of spinal movements
and straight leg raising. Motor and sensory deficit together with
reflex disturbances can be present. Differential diagnosis of
neuromas and lumbar disc lesions is almost impossible if only
the actual symptoms and signs are considered. However, when
the duration and evolution of the symptoms are analysed,
certain features should arouse suspicion. The evolution of
radicular pain in neuroma is that of a slowly progressive lesion.
This is completely different from the evolution in discoradicular interactions, in which the sciatica becomes rapidly worse
and reaches a peak within 1–2 months; severe symptoms may
then persist for a certain length of time, which seldom exceeds
2 months. Although primary posterolateral protrusion in young
patients can have a slower and more gradual onset, the evolution usually does not take more than 6 months. Hence any case
of root pain that is getting worse at the end of 18 months is
suspect (Cyriax:3 p. 293). Also, increasing backache after root
pain has set in must alert the examiner. The range of straight
leg raising is not much help in the differential diagnosis: if the
lesion lies upwards in the canal, straight leg raising may be
normal, but if the neuroma lies near the intervertebral foramen
it will be markedly and often bilaterally restricted.163 Palsies
affecting two non-adjacent roots may suggest a neuroma, and
bilateral sciatica should also alert the clinician to the possibility
of a cauda equina tumour (Fig. 6).165,166 Late manifestations are
marked motor deficit, with drop foot or widespread weakness
and muscle atrophy. Bladder dysfunction also tends to be a late
manifestation, although urinary and rectal incontinence sometimes appear early in the evolution.167,168
Sometimes the diagnosis of a neuroma is suggested by the
unusual response to a sacral, epidural anaesthesia. Although the
introduction of the fluid creates considerable and sometimes
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology Discoradicular interaction
Symptoms
Backache ceases when root pain comes on
Root stabilizes after 2–4 months
Recovery of root pain after 1 year
A cough sometimes hurts in the back
Backache increases
Root pain continues to worsen after 8 months
Persisting or increasing root pain after 1 year
A cough always hurts, mostly in the limb
3
6
Months
9
12
Root signs evolve in the course of 1–4 weeks
They continue unchanged for 6–8 months
Recovery may be expected within 1 year after onset
Palsy is uniradicular or involves two adjacent roots
(L4–L5 or L5–S1)
Backache
Root pain
Pain
Pain
Backache
Root pain
0
Signs
Neuroma
0
3
6
Months
9
12
Root signs appear insidiously
Progression is very slow, month by month
No spontaneous recovery, but steadily
increasing weakness
Triple palsies, a palsy affecting two non-adjacent
roots or a bilateral palsy are all possible
Straight leg raising may be positive or negative in both cases and is therefore no help in differential diagnosis
Fig 6 • Differential diagnosis of discoradicular conflict and neuroma in the lower lumbar area.164
unbearable root pain, it has no immediate effect on the symptoms or on the range of straight leg raising because the fluid
cannot touch the neuroma, which is intradural. Had the root
pain been caused by an inflammation of the dural sheath, the
injection would have created some anaesthesia immediately
afterwards. No improvement of straight leg raising after the
epidural injection thus strongly suggests the possibility of a
neuroma and the patient should be referred for further
investigation.
MRI is the most useful method for the differentiation of
spinal tumour from lumbar disc herniation.167 In MRI imaging,
schwannomas commonly appear isointense on T1-weighted
images and markedly hyperintense on T2-weighted images.169
Computed tomography is not the technique of choice because
a lesion higher up in the spinal canal will always be missed. In
addition, as disc protrusions are often asymptomatic,170 the
clinical picture may be wrongly ascribed to such a cause, surgical opinion sought and an exploration of the disc undertaken.171
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Craig et al172 summarized this in 1952 when they stated: ‘It is
not unusual at this clinic to remove a spinal cord tumor from
a patient who has had a previous operation for protruding disc
without relief of symptoms’.
Treatment consists of laminectomy and total excision of the
tumour, which gives excellent results, provided there is not too
much neurological dysfunction.
Differential diagnosis
The following conditions may resemble a neuroma.
Adherent nerve root
There are rare cases of root adherence to the posterior aspect
of the intervertebral joint, which occur after the herniation has
shrivelled away as the result of the natural course of the disc
lesion. The patient’s sciatica slowly subsides and after 2 years
the pain may have gone. However, the patient continues to
find that they cannot bend forwards, and examination shows
about 45° limitation of straight leg raising on the affected side.
e227
The Lumbar Spine
Attempted trunk flexion causes pain in the back and the leg.
Apart from that, there are no other complaints and the sciatic
pain is slight. The pain also does not increase; there is no
appreciable neurological deficit and certainly not an increasing
one. The condition thus presents as sciatica, usually in a young
man in whom the symptoms have abated but the signs continue. As in neuroma epidural local anaesthesia does not alter
the range of straight leg raising.
Increasing protrusion on an atrophied root
The patient has suffered from severe sciatica some years ago.
There is sudden loss of pain, together with considerable weakness of one or two roots, which indicates that root atrophy has
taken place. There is no recovery from the palsy; however, one
day, without pain, the patient notices increased weakness and
numbness. This can be explained by a further protrusion of
disc substance at the original level. Because it impinges against
the atrophied nerve root there is no pain, but there is further
loss of sensory and motor conduction.
Lesions of the aorta
An arterial aneurysm is a localized or diffuse enlargement of
an artery. In the abdominal aorta it occurs most commonly in
men over the age of 50 years.173 The majority of patients with
a stable abdominal aneurysm are asymptomatic, and pain is
only associated with enlargement or rupture. Most frequently
the pain is abdominal, dull and steady. Sometimes the main
symptom is severe and increasing backache, accompanied by
L3 pain in the left leg.174 Increasing back pain and L3 pain in
an elderly patient with a negative functional examination
should therefore always arouse suspicion. The patient should
be referred immediately for ultrasonography and CT of the
abdomen. These methods are non-invasive and very reliable in
identifying the location of the lesion.175
Acute occlusion of the abdominal aorta presents as acute
and severe low back pain and abdominal pain together with
acute claudication of the lower extremities.176
A second disc protrusion
The patient is suffering from sciatica, which is improving (as
expected) after some months. After a while, a new disc lesion
develops at an adjacent level, impinging against an adjacent or
a contralateral root. Of course, weakness extending to another
level after some months’ sciatica is suspect, but the differential
diagnosis will easily be made on a myelogram.
3
Neuralgic amyotrophy (Cyriax: p. 300)
This uncommon parenchymatous disorder of the peripheral
nerves usually afffects three to four consecutive roots at the
same side. The origin is unknown but the disease has a spontaneous and complete recovery within a year.
The patient, usually a man aged between 50 and 70 years,
experiences a sudden and severe ache in one leg. The pain is
considerable and not altered by position or motion. There is
no pain on coughing or sneezing. After about 3 months the
symptoms slowly ease, and 6 months after the onset they have
disappeared.
Examination shows a full range of movement and full
and painless straight leg raising. Considerable muscle weakness
is detected where the muscles are innervated by two to
three different roots. An important differential diagnostic
finding is that the palsy is maximal from the first onset and
does not increase or spread to the other limb. There is no
sensory loss.
There is no treatment for this condition. As the pain ceases,
so the muscles gradually recover. The disorder completely
resolves 1 year after its onset.
Pain referred to the back
It should be remembered that back pain occurs not only due
to lesions of bones, discs and ligaments, but also as referred
from intra-abdominal or pelvic lesions. The prominent feature
will then be the complete absence of articular, dural and radicular signs during routine clinical examination. Lesions of the
aorta and genitourinary or gastrointestinal diseases should be
suspected in such circumstances.
e228
Genitourinary diseases
The colic and excruciating pain caused by a kidney or ureteral
stone is well known. The pain is sudden, sharp and has a spasmodic character. It is upper lumbar and radiates to the lateral
flank and along the course of the ureter into the ipsilateral flank
and along the course of the ureter into the ispilateral testicle
(men) or labium (women).
Renal infarction causes a sudden and sharp pain in the costovertebral angle. Renal cancers may present as increasing
upper lumbar and flank pain, which is constant and dull.177
Clinical examination reveals a limitation of the side flexion
away from the painful side as the only finding. This warning
sign should always prompt the physician to refer the patient
for further internal examination.
Diseases of the bladder and the prostate rarely cause lumbosacral pain. Lesions of the testis, however, often cause backache and back pain may be a presenting symptom in 10–21%
of patients with testicular carcinoma.178 Patients may even
present with back pain in the absence of any testicular
symptoms.179 In testicular carcinoma, the pain is dull and persistent, localized over the lumbosacral and paravertebral region.
Functional lumbar examination is completely negative, but
examination of the testicles reveals a testicular mass together
with diffuse induration.
In women, referred pain from the genital organs (uterus,
fallopian tubes or ovaries) is possible, although backache from
gynaecological causes should not be overestimated. For instance
malposition of the uterus in times past was regarded as a main
source of backache in women, but this certainly does not cause
any back trouble.180 In contrast, endometriosis, a disease associated with the presence of endometrial tissue outside the
uterine cavity, is often associated with intermittent back pain.
The pain is lower lumbar and often irradiates to the buttocks
or thighs. The symptoms characteristically increase at the time
of menstruation and persist throughout the entire period of
bleeding. Other symptoms associated with the disease are dyspareunia, infertility and menorrhagia.181
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology It is a well-known fact that women complain more often
of low back pain during pregnancy. The incidence reported
varies between 24 and 49%.182–185 The increase in backache
during pregnancy is not very well understood. Hormonally
induced laxity probably allows increased biomechanical stress
on the pelvis and spine, which results in more postural
ligamentous pain.181,186 But there are several studies indicating that pregnancy is also a risk factor for lumbar disc
herniations.182,183
Pelvic inflammatory disease, an acute or chronic infection
of the fallopian tubes, is also associated with pain at the lower
back, radiating into the buttocks. The chief clinical symptoms,
however, will be lower abdominal and pelvic pain, with a
feeling of pelvic pressure.183
Gastrointestinal diseases
Diseases of the pancreas, stomach, duodenum and colon may
be associated with low back pain. The gallbladder has a T5–T9
origin and pain is therefore felt in the thoracic region.
Cyriax described cases of gastric ulcer adherent to the
lumbar spine. The back symptoms are connected both with
eating and with posture. The pain is upper lumbar, with radiation into one or other iliac fossa. It is not brought on by
exertion but appears during eating. The only finding during
clinical examination is central discomfort during extension.
The combination of pain influenced by posture and abdominal
visceral function brings the diagnosis to mind, and the diagnosis
is confirmed by gastroscopy.
A peptic ulceration of the posterior duodenal wall can also
cause low back pain. Again the pain is localized to the L2–L3
lumbar level, but appears 1–3 hours after the meal, and is
relieved by further intake of food. The pain has no relation to
physical activity.187 Sometimes there is tenderness at the upper
lumbar (‘forbidden’) area.
Pain from chronic pancreatitis or carcinoma of the pancreas
is felt in the epigastrium and is referred to the upper lumbar
area.188 Disease processes that affect the head of the pancreas
cause pain to the right of the spine, while lesions of the tail
are felt at the left side.
Lesions of the colon – both diverticulitis and carcinoma –
can be associated with low back and flank pain.189 Patients with
a rectal carcinoma often complain of sacral pain. Invasion of
the nerve roots at the front of the sacrum gives rise to gross
weakness of the muscles in both legs. As the dural sleeve is not
affected here, the lesion does not provoke pain and the weakness often remains silent. Similar back pain may be the first
sign of recurrence after apparently successful excision of a
rectal cancer.
References
1. Herbiniaux G. Traite sur Divers
Accouchements Laborieux, et sur les
polypes de la Matrice. Bruxelles: Be
Boubers; 1782.
2. Kilian HF. Schilderunden neuer
Beckenformen und ihres Verhaten im
Leben. Monnheim: Bassermen und Mathy;
1854.
3. Cyriax JH. Textbook of Orthopaedic
Medicine, vol I, Diagnosis of Soft Tissue
Lesions. 8th ed. London: Baillière Tindall;
1982. p. 263.
4. Rosenberg N. Degenerative
spondylolisthesis predisposing factors.
J Bone Joint Surg 1975;57A:467.
5. American Academy of Orthopaedic
Surgeons, Committee on the Spine. A
Glossary on Spinal Terminology. Chicago:
American Academy of Orthopaedic
Surgeons; 1987.
6. Wiltse LL, Widell EH, Jackson DW.
Fatigue fracture: the basic lesion in isthmic
spondylolisthesis. J Bone Joint Surg
1975;57A:17.
7. Lonstein JE. Spondylolisthesis in children.
Cause, natural history, and management.
Spine 1999;24(24):2640–8.
8. Hutchinson MR. Low back pain in elite
rhythmic gymnasts. Med Sci Sports Exer
1999;31(11):1686–8.
9. Sairyo K, Goel VK, Grobler LJ, Ikata T,
Katoh S. The pathomechanism of isthmic
lumbar spondylolisthesis. A biomechanical
study in immature calf spines. Spine
1998;23(13):1442–6.
10. Fredrickson BE, Baker D, McHollick W,
et al. The natural history of spondylolysis
© Copyright 2013 Elsevier, Ltd. All rights reserved.
and spondylolisthesis. J Bone Joint Surg
1984;66A:699–707.
11. Turner RH, Bianco AJ Jr. Spondylolysis
and spondylolisthesis in children and
teenagers. J Bone Joint Surg
1971;53A:1298–306.
12. Moreton RD. Spondylolysis. J Am Med
Assoc 1966;195:671–4.
13. Neugebauer FL. The classic: a new
contribution to the history and etiology of
spondylolisthesis. Clin Orthop
1976;117:4–22.
14. Sakai T, Sairyo K, Takao S, Nishitani H,
Yasui N. Incidence of lumbar spondylolysis
in the general population in Japan based
on multidetector computed tomography
scans from two thousand subjects. Spine
2009;34(21):2346–50.
15. Stewart TD. Incidence of separate neural
arch in the lumbar vertebrae of Eskimos.
Am J Phys Anthropol 1931;16:51–62.
16. Kettelkamp DB, Wright DG.
Spondylolysis in the Alaskan Eskimo. J
Bone Joint Surg 1971;53A:563–6.
17. Meyerding HW. Low backache and sciatic
pain associated with spondylolisthesis and
protruded intervertebral disc. J Bone Joint
Surg 1941;23:461.
18. Lowe RW, Hayes TD, Kaye J, Bagg JR,
Leukens CA Jr. Standing roentgenograms
in spondylolisthesis. Clin Orthop
1976;117:80–4.
19. MacNab I. Backache. Baltimore/London:
Williams & Wilkins; 1977. p. 50.
20. Virta L, Roonemaa T. The association of
mild–moderate isthmic lumbar
spondylolisthesis and low back pain in
middle-aged patients is weak and it only
occurs in women. Spine 1993;18:1496–
503.
21. Kalichman L, Kim DH, Li L, Guermazi A,
Berkin V, Hunter DJ. Spondylolysis and
spondylolisthesis: prevalence and
association with low back pain in the adult
community-based population. Spine
2009;34(2):199–205.
22. Key JA. Intervertebral disc lesions are the
commonest cause of low back pain, with
or without sciatica. Ann Surg
1945;121:534.
23. Calliauw L, Van Velthoven V. Ervaringen
bij de behandeling van spondylolisthesis.
Ned Tijdschr Geneeskd
1987;43(13):849–58.
24. Gill GC, Manning JC, White HL. Surgical
treatment of spondylolisthesis without
spine fusion. Excision of the loose laminar
with decompression of the nerve roots. J
Bone Joint Surg 1955;37A:493–520.
25. Wiltse LL, Guyer RD, Spencer CW,
Glenn WV, Porter IS. Alar transverse
process impingement of the L5 spinal
nerve: the far-out syndrome. Spine
1984;9:31–41.
26. Poussa M, Remes V, Lamberg T,
Tervahartiala P, et al. Treatment of severe
spondylolisthesis in adolescence with
reduction or fusion in situ: long-term
clinical, radiologic, and functional
outcome. Spine (Phila Pa 1976)
2006;31(5):583–90;
27. Laurent LE, Österman K. Operative
treatment of spondylolisthesis in young
patients. Clin Orthop 1976;117:85–91.
e229
The Lumbar Spine
28. Johnson JR, Kirwan EO. The long-term
results of fusion ‘in situ’ for severe
spondylolisthesis. J Bone Joint Surg
1983;65B(1):43–6.
29. Seitsalo S, Österman K, Schlenzka D,
Poussa M. Severe spondylolisthesis in
children and adolescents. J Bone Joint Surg
1990;77B:259–65.
30. Esses SI, Sachs BI, Drezyn V.
Complications associated with the
technique of pedicle screw fixation. A
selected survey of ABS member. Spine
1993;18:2231–9.
31. DeWald CJ, Vartabedian JE, Rodts MF,
Hammerberg KW. Evaluation and
management of high-grade
spondylolisthesis in adults. Spine
2005;30(6 Suppl):S49–59.
32. Zagra A, Giudici F, Minoia L, Corriero
AS, Zagra L. Long-term results of
pediculo-body fixation and posterolateral
fusion for lumbar spondylolisthesis. Eur
Spine J 2009;18(Suppl 1):151–5.
33. Harris IE, Weinstein SL. Long-term
follow-up of patients with grade III and
IV spondylolisthesis. Treatment with and
without posterior fusion. J Bone Joint Surg
1987;69A:960–9.
34. Apel DM, Lorenz MA, Zindrick MR.
Symptomatic spondylolisthesis in adults:
four decades later. Spine 1989;14:
345–8.
35. Frennered AK, Danielson BI, Nachemson
AL, Nordwall AB. Midterm follow-up of
young patients fused in situ for
spondylolisthesis. Spine 1991;16:
409–16.
36. Moller H, Hedlund R. Surgery versus
conservative management in adult isthmic
spondylolisthesis: a prospective
randomized study: Part I. Spine
2000;25(13):1711–1715.
37. Ekman P, Möller H, Hedlund R. The
long-term effect of posterolateral fusion in
adult isthmic spondylolisthesis: a
randomized controlled study. Spine J
2005;5(1):36–44.
38. Riggs BL, Wahner HW, Dunn WL, Mazes
RB, Offord KP, Melton LJ III. Differential
changes in bone mineral density of
appendicular and axial skeleton with aging.
J Clin Invest 1981;67:328.
39. Parfitt AM, Duncan H. Metabolic bone
disease affecting the spine. In: Rothman
RH, Simeone FA, editors. The Spine. 2nd
ed. Philadelphia: Saunders; 1982. p.
775–905.
40. Zetterberg C, Mannius S, Mellstrom D.
Osteoporosis and back pain in the elderly:
a controlled epidemiologic and
radiographic study. Spine 1990;15:783–8.
41. Paget J. On a form of chronic
inflammation of bone (osteitis deformans).
Trans R Chir Soc Lond 1877;60:37.
42. Barry HC. Paget’s Disease of Bone.
Edinburgh: E & S Livingstone; 1969.
43. Altman RD. Musculoskeletal
manifestations of Paget’s disease of bone.
Arthritis Rheum 1980;23:1121.
44. Altman RD, Brown M, Gargano GA. Low
back pain in Paget’s disease of bone. Clin
Orthop 1987;217:152.
e230
45. Hartman JT, Dohn DF. Paget’s disease of
the spine with cord and nerve root
compression. J Bone Joint Surg
1966;48A:1079–84.
46. Weisz GMM. Lumbar canal stenosis in
Paget’s diseases: the staging of the clinical
syndrome, its diagnosis and treatment.
Clin Orthop 1986;206:233.
47. Hambly MF, Wiltse LL, Peek RD.
Spondylolisthesis. In: Williams L, Lin P,
Elrod B, editors. The spine in sports. St
Louis: Mosby; 1996. p. 157–63.
48. Fredrickson BE, Baker D, McHolick WJ,
et al. The natural history of spondylolysis
and spondylolisthesis. J Bone Joint Surg
[Am] 1984;66:699–707.
49. Soler T, Calderon C. The prevalence of
spondylolysis in the Spanish elite athlete.
Am J Sports Med 2000;28:57–62.
50. Micheli LJ, Wood R. Back pain in young
athletes: significant differences from adults
in causes and patterns. Arch Pediatr
Adolesc Med 1995;149:15–8.
51. Goldstein JD, Berger PE, Windler GE, et
al. Spine injuries ingymnasts and
swimmers: an epidemiologic investigation.
Am J Sports Med 1991;19:463–8.
52. Semon RL, Spengler D. Significance of
lumbar spondylolysis in college football
players. Spine 1981;6:172–4.
53. Buck JE. Further thoughts on the direct
repair of the defect in spondylolysis. J
Bone Joint Surg 1979;61B:123.
54. Schneidermann GA, McLain RF, Hambly
MF, Nielsen SL. The pars defect as a pain
source – a histologic study. Spine
1995;20:1761–4.
55. Eisenstein SM, Ashton IK, Roberts S,
Darby AJ. Innervation of the spondylolysis
‘ligaments’. Spine 1994;19:912–6.
56. Wu SS, Lee CH, Chen PQ. Operative
repair of symptomatic spondylolysis
following a positive response to diagnostic
pars injection. J Spinal Disord
1999;12(1):10–6.
57. Micheli LJ, Wood R. Back pain in young
athletes: significant differences from adults
in causes and patterns. Arch Pediatr
Adolesc Med 1995;149:15–8.
58. Logroscino G, Mazza O, Aulisa AG, Pitta
L, Pola E, Aulisa L. Spondylolysis and
spondylolisthesis in the pediatric and
adolescent population. Child’s Nerv Syst
2001;17:644–655.
59. Masci L, Pike J, Malara F, Phillips B,
Bennell K, Brukner P. Use of the
one-legged hyperextension test and
magnetic resonance imaging in the
diagnosis of active spondylolysis. Br J
Sports Med 2006;40(11):940–6.
60. Raby N, Mathews S. Symptomatic
spondylolysis: correlation of CT and
SPECT with clinical outcome. Clin Radiol
1993;48:97–9.
61. Lusins JO, Elting JJ, Cicoria AD, et al.
SPECT evaluation of lumbar spondylolysis
and spondylolisthesis. Spine 1994;19:608–
12.
62. Lim MR, Yoon SC, Green DW.
Symptomatic spondylolysis: diagnosis and
treatment. Curr Opin Pediatr
2004;16(1):37–46
63. Aland C, Rineberg BA, Malberg M, Fried
SH. Fracture of the pedicle of the fourth
lumbar vertebra associated with
contralateral spondylolysis. J Bone Joint
Surg 1986;68A:1454–5.
64. Garber JE, Wright AM. Unilateral
spondylolysis and contralateral pedicle
fracture. Spine 1986;11:63–6.
65. Gunsburg R, Fraser R. Stress fractures of
the lumbar pedicle: case reports of
‘Pediculolysis’ and review of the literature.
Spine 1991;16:185–9.
66. Maldague BE, Malghem JJ. Unilateral arch
hypertrophy with spinous process tilt: a
sign of arch deficiency. Radiology
1976;121:567–74.
67. Wilkinson RH, Hall JE. The sclerotic
pedicle: tumour or pseudotumour?
Radiology 1974;111:683–8.
68. Sherman FC, Wilkinson RH, Hall JE.
Reactive sclerosis of a pedicle and
spondylolysis in the lumbar spine. J Bone
Joint Surg 1977;59A:49–54.
69. Edelstyn GA, Gillespie PG, Grebbel FS.
The radiological demonstration of skeletal
metastases: experimental observations.
Clin Radiol 1967;18:158.
70. Dahlin DC, Unni K. Bone Tumors. General
Aspect and Data on 8542 Cases. 4th ed.
Thomas Springfield, 1986.
71. Saville DP. A medical option for the
treatment of osteoid osteoma. Arthritis
Rheum 1981;23:1409.
72. Marsh BW, Bonfiglio M, Brady LP,
Enneking WF. Benign osteoblastoma: range
of manifestations. J Bone Joint Surg
1975;57A:1.
73. Nemoto O, Moser R, Van Dam B.
Osteoblastoma of the spine. A review of
75 cases. Spine 1990;15:1272–80.
74. Mirra J. Bone Tumors: Diagnosis and
Treatment. Philadelphia: Lippincott; 1980.
75. Schmorl G, Junghanns H. The Human
Spine in Health and Disease. 2nd ed. New
York: Grune & Stratton; 1971. p. 325.
76. Mohan V, Gupta SK, Tuli SM, Sanyal B.
Symptomatic vertebral hemangiomas. Clin
Radiol 1980;31:575.
77. Manning JH. Symptomatic hemangioma of
the spine. Radiology 1951;56:58.
78. Jaffe HL, Lichtenstein L. Eosinophilic
granuloma of bone. Arch Pathol
1944;37:99.
79. Cheyne C. Histiocytosis X. J Bone Joint
Surg 1971;53B:366.
80. Calvé JA. Localized affection of spine
suggesting osteochondritis of vertebral
body, with clinical aspects of Pott’s
disease. J Bone Joint Surg 1925;7:41.
81. Weston WJ, Goodson GM. Vertebra
plana. J Bone Joint Surg 1959;41B:
477.
82. Ippolito E, Farsetti P, Tudisoc C. Vertebra
plana. J Bone Joint Surg 1984;66A:
1364.
83. Biesecker JL, Marcove RC, Huvos AG,
Mike V. Aneurysmal bone cyst: a
clinicopathologic study of 66 cases.
Cancer 1970;26:615.
84. Hay MC, Patterson D, Taylor TKF.
Aneurysmal bone cysts of the spine. J
Bone Joint Surg 1978;60B:406.
© Copyright 2013 Elsevier, Ltd. All rights reserved.
Non-mechanical disorders of the lumbar spine: pathology 85. Dabska M, Buraczewski J. Aneurysmal
bone cyst: pathology, clinical course and
radiologic appearance. Cancer
1969;23:371.
86. Francis KC, Hutter RVP. Neoplasms of the
spine in the aged. Clin Orthop
1963;26:54.
87. Huvos AG, Bone Tumors. Diagnosis,
Treatment and Prognosis. Philadelphia:
Saunders; 1979. p. 373–91.
88. Mindell ER. Chordoma. J Bone Joint Surg
1981;63A:501.
89. Hudson TM, Galceran M. Radiology of
sacrococcygeal chordoma: difficulties in
detecting soft tissue extension. Clin
Orthop 1983;175:237.
90. Congdon CC. Benign and malignant
chordomas: a clinico-anatomical study of
twenty-two cases. Am J Pathol
1952;28:793.
91. Sundaresan N, Galicich JH, Chu FCH,
Huvas AG. Spinal chordomas. J Neurosurg
1979;50:312.
92. Cheng EY, Ozerdemoglu RA, Transfeldt
EE, Thompson RC Jr. Lumbosacral
chordoma. Prognostic factors and
treatment. Spine 1999;24(16):
1639–45.
93. Bjornsson J, Wold LE, Ebersold MJ, Laws
ER. Chordoma of the mobile spine. A
clinicopathologic analysis of 40 patients.
Cancer 1993;71(3):735–40.
94. Boriani S, Chevalley F, Weinstain JN, et
al. Chordoma of the spine above the
sacrum. Spine 1996;21:1569–77.
95. Kamrin RP, Potatos JN, Pool JL. An
evaluation of the diagnosis and treatment
of chordoma. J Neurol Neurosurg
Psychiatry 1964; 27:157.
96. Valderrama JAF, Bullough PG. Solitary
myeloma of the spine. J Bone Joint Surg
1968;50B:82.
97. Paredes JM, Mitchell BS. Multiple
myeloma: current concepts in diagnosis
and management. Med Clin North Am
1980;64:729.
98. Wooltenden JM, Pitt MJ, Durie MGM,
Moon TE. Comparison of bone
scintigraphy and radiography in multiple
myeloma. Radiology 1980;134:723.
99. Gompels BM, Votaw ML, Martel W.
Correlation of radiological manifestations
of multiple myeloma with immunoglobulin
abnormalities and prognosis. Radiology
1972;104:509.
100. Bence-Jones H. On a new substance
occuring in the urine of a patient with
mollities ossium. Phil Trans R Soc Lond
(Biol) 1984;1:55.
101. Kyle RA. Multiple myeloma: review of
869 cases. Mayo Clin Proc 1975;50:
29.
102. Costa G, Engle RL Jr, Schilling A, et al.
Melphalan and prednisone – an effective
combination for the treatment of multiple
myeloma. Am J Med 1973;54:589.
103. Johnson TL Jr. Diagnosis of low back pain,
secondary to prostate metastasis to the
lumbar spine, by digital rectal examination
and serum prostate-specific antigen.
J Manip Physiol Ther 1994;17(2):
107–12.
© Copyright 2013 Elsevier, Ltd. All rights reserved.
104. Galasko CSB. Skeletal Metastases. Boston:
Butterworths; 1986.
105. Fornasier VL, Horne JG. Metastases to
the vertebral column. Cancer
1975;36:590.
106. Batson OV. The function of the vertebral
veins and their role in the spread of
metastasis. Ann Surg 1940;112:138.
107. Constans JP, De Divitis E, Donzelli R, et
al. Spinal metastases with neurological
manifestations: review of 600 cases. J
Neurosurg 1983;59:111.
108. Emsellem HA. Metastatic disease of the
spine: diagnosis and management. South
Med J 1986;76:1405.
109. Shaberg J, Gainor BJ. A profile of
metastatic carcinoma of the spine. Spine
1985;10:19.
110. Gosfield E 3rd, Alavi A, Kneeland B.
Comparison of radionuclide bone scans
and magnetic resonance imaging in
detecting spinal metastases. J Nucl Med
1993;34(12):2191–8.
111. Hard FD, MacLagen NF. Ankylosing
spondylitis: a review of 184 cases. Ann
Rheum Dis 1975;34:87.
112. Kinsella TD, MacDonald FR, Johnson LG.
Ankylosing spondylitis: a late re-evaluation
of 92 cases. Can Med Assoc J 1966;
95:1.
113. Dale K. Radiographic changes of the spine
in Bechterew’s syndrome and allied
disorders. Scand J Rheumatol
1979;32(suppl):103.
114. Graudal H, de Carvalho A, Lassen L. The
course of sacroiliac involvement in
rheumatoid arthritis. Scand J Rheumatol
1979;32(suppl):34.
115. Resnick D. Thoracolumbar spine
abnormalities in rheumatoid arthritis. Ann
Rheum Dis 1978;37:389.
116. Sims-Williams H, Jayson MIV, Baddeley
H. Rheumatoid involvement of the
lumbar spine. Ann Rheum Dis 1977;36:
524.
117. Bauer W, Engleman EP. A syndrome of
unknown etiology characterized by
urethritis, conjunctivitis, and arthritis
(so-called Reiter’s disease). Trans Assoc
Am Phys 1942;57:307.
118. Russell AS, Davis P, Percy JS, Lentle GC.
The sacroiliitis of acute Reiter’s syndrome.
J Rheumatol 1977;4:293.
119. Forestier J, Rotes-Querol J. Senile
ankylosing hyperostosis of the spine. Ann
Rheum Dis 1950;9:321.
120. Resnick D, Shaul SR, Robins JM. Diffuse
idiopathic skeletal hyperostosis (DISH):
Forestier’s disease with extraspinal
manifestations. Radiology 1975;115:
513.
121. Boachie-Adjei O, Bullough PG. Incidence
of ankylosing hyperostosis of the spine
(Forestier’s disease) at autopsy. Spine
1987;12:739–41.
122. Forestier J, Lagier R. Ankylosing
hyperostosis of the spine. Clin Orthop
1971;74:65.
123. Harris J, Carter AR, Glick EN, Storey
GO. Ankylosing hyperostosis. I. Clinical
and radiological features. Ann Rheum Dis
1974;33:210.
124. Wiley AM, Trueta J. The vascular anatomy
of the spine and its relationship to
pyogenic vertebral osteomyelitis. J Bone
Joint Surg 1959;41B:796.
125. Lifeso R. Pyogenic spinal sepsis in adults.
Spine 1990;15:1265–71.
126. Sapico FL, Montgomerie JZ. Pyogenic
vertebral osteomyelitis: report of nine
cases and review of the literature. Rev
Infect Dis 1979;1:754.
127. Ross PM, Fleming JL. Vertebral body
osteomyelitis: spectrum and natural
history: a retrospective analysis of 37
cases. Clin Orthop 1976;118:190.
128. Baker AS, Ojemann RG, Swartz MN,
Richardson EP Jr. Spinal epidural abscess.
N Engl J Med 1975;293:463.
129. Ergun T, Lakadamyali H, Gokay E. A
posterior epidural mass causing paraparesis
in a 20-year-old healthy individual. Int J
Emerg Med. 2009;2(3):195–8.
130. Garcia A Jr, Grantham SA. Hematogenous
pyogenic vertebral osteomyelitis. J Bone
Joint Surg 1960;42A:429.
131. Digby JM, Kersley JB. Pyogenic nontuberculous spinal infection: an analysis of
thirty cases. J Bone Joint Surg
1979;61B:47.
132. Kattapuram SV, Philips WC, Boyd R. CT
in pyogenic osteomyelitis of the spine.
AJR 1983;140:1199.
133. Livorsi DJ, Daver NG, Atmar RL,
Shelburne SA, White AC Jr, Musher DM.
Outcomes of treatment for hematogenous
Staphylococcus aureus vertebral
osteomyelitis in the MRSA era. J Infect
2008;57:128–31.
134. Hadjipavlou AG, Mader JT, Necessary JT,
Muffoletto AJ. Hematogenous pyogenic
spinal infections and their surgical
management. Spine 2000;25:1668–79.
135. Lifeso RM, Weaver P, Harder O.
Tuberculous spondylitis in adults. J Bone
Joint Surg 1985;67A:1405–13.
136. Forlenza SW, Axelrod JL, Grieco MH.
Pott’s disease in heroin addicts. JAMA
1979;241:379.
137. Janssens JP, De Haller R. Spinal
tuberculosis in a developed country. A
review of 26 cases with special emphasis
on abscesses and neurological
complications. Clin Orthop 1990;257:67–
75.
138. Gorse GJ, Pais MJ, Kusske JA, Cesario
TC. Tuberculous spondylitis: a report of
six cases and a review of the literature.
Medicine 1983;62:178.
139. Eismont FJ, Montero C. Infections of the
spine. In: Davidoff RA, editor. Handbook
of the Spinal Cord. New York: Marcel
Dekker; 1987. p. 411–49.
140. Rivero MG, Salvatore AJ, de Wouters L.
Spontaneous infectious spondylodiscitis in
adults. Analysis of 30 cases. Medicina
(Buenos Aires) 1999;59(2):143–50.
141. Pilgaard S. Discitis (closed space
infection) following removal of lumbar
intervertebral disc. J Bone Joint Surg
1969;51A:713.
142. Kylanpaa-Back ML, Suominen RA, Salo
SA, et al. Postoperative discitis: outcome
and late magnetic resonance image
e231
The Lumbar Spine
evaluation of ten patients. Ann Chir
Gynaecol 1999;88(1):61–4.
143. Hansen SE, Gutschik E, Karle A, Rieneck
K, Vinicoff PG. Spontaneous and
postoperative spondylodiscitis. A material
concerning 23 patients. Ugeskr Laeger
1998;160(41):5935–8.
144. Onofrio BM. Intervertebral discitis:
incidence, diagnosis and management. Clin
Neurosurg 1980;27:481.
145. Norris S, Ehrlich MG, Keim DE,
Guiterman H, McKusick KA. Early
diagnosis of disc-space infection using
gallium-67. J Nucl Med 1978;19:384.
146. Maiuri F, Iaconetta G, Gallicchio B,
Manto A, Briganti F. Spondylodiscitis
– clinical and magnetic resonance
diagnosis. Spine 1997;22:1741–6.
147. Wirtz DC, Genius I, Wildberger JE, et al.
Diagnostic and therapeutic management of
lumbar and thoracic spondylodiscitis – an
evaluation of 59 cases. Arch Orthop
Trauma Surg 2000;120(5–6):245–51.
148. Crawford AH, Kucharzyk DW, Ruda R, et
al. Discitis in children. Clin Orthop
1991;266:70–9.
149. Engelbert RH, Van der Net J,
Schoenmakers MA. Twee kinderen met
discitis. Casuistische mededelingen. Ned
Tijdschr Geneeskd 1993;137:1614–6.
150. Straus SE. Varicella-zoster virus infections:
biology, natural history, treatment and
prevention. Ann Intern Med
1988;108:221.
151. Helfgott SM, Picard DA, Cook JS. Herpes
zoster radiculopathy. Spine 1993;18:2523–
4.
152. Thomas JE, Howard FM Jr. Segmental
zoster paresis – a disease profile.
Neurology 1972;22:459.
153. Markham JW, Lynge HN, Stahlman GEB.
The syndrome of spontaneous spinal
epidural hematoma. Report of three cases.
J Neurosurg 1967;26:334.
154. Hancock DO. A study of 49 patients with
acute spinal extradural abscess. Paraplegia
1973;10:285–8.
155. Abdullah AF, Chambers RW, Daut DP.
Lumbar nerve root compression by
synovial cysts of the ligamentum flavum. J
Neurosurg 1984;60:617–20.
156. Baum JA, Hanley EN. Intraspinal synovial
cyst simulating spinal stenosis. Spine
1986;11:487–9.
157. Lemish W, Apsimon T, Chakera T. Lumbar
intraspinal synovial cysts. Recognition and
CT diagnosis. Spine 1989;14:1378–83.
158. Shaw MDM, Russel JA, Grossart KW. The
changing pattern of spinal arachnoiditis. J
e232
Neurol Neurosurg Psychiatry 1978;41:
97.
159. Epstein JA. Common errors in the
diagnosis of herniation of the
intervertebral disk. Industrial Medicine
1970;39:488.
160. Waddell G. An approach to backache. Br J
Hosp Med 1982;28:187–91.
161. Norstrom CW, Kernohan JW, Love JG.
One hundred primary caudal tumors.
JAMA 1969;178:1071–7.
162. Ker NB, Jones CB. Tumors of the cauda
equina: the problem of differential
diagnosis. J Bone Joint Surg
1985;67B:358–62.
163. Guyer RD, Collier RR, Ohnmeiss DD, et
al. Extraosseous spinal lesions mimicking
disc disease. Spine 1988;13:228–31.
164. Ombregt L. Tumoren van de cauda equina:
het belang van vroege diagnostieke. Ned
Tijdschr Geneeskdr 1986;130(8):
371–2.
165. Fearnside MR, Adams CBT. Tumours of
the cauda equina. J Neurolog Neurosurg
Psychiatry 1978;41:24–31.
166. Cervoni L, Celli P, Cantore G, Fortuna A.
Intradural tumors of the cauda equina: A
single institution review of clinical
characteristics. Clin Neurol Neurosurg
1995;97(1):8–12.
167. Garfield J, Lytle SN. Urinary presentation
of cauda equina lesions without
neurological symptoms. Br J Urol
1970;42:551–4.
168. Jeon JH, Hwang HS, Jeong JH, Park SH,
Moon JG, Kim CH. Spinal schwannoma;
analysis of 40 cases. J Korean Neurosurg
Soc 2008;43(3):135–8.
169. Colosimo C, Cerase A, Denaro L, Maira
G, Greco R. Magnetic resonance imaging
of intramedullary spinal cord
schwannomas. Report of two cases and
review of the literature. J Neurosurg
2003;99(1 Suppl):114–7.
170. Wiesel SW, Tsourmas N, Feffer HL, Citrin
CM, Patronas N. A study of computerassisted tomography. I. The incidence of
positive CAT scans in an asymptomatic
group of patients. Spine 1984;9:
549–51.
171. Palma L, Mariottini A, Muzii VF, Bolognini
A, Scarfò GB: Neurinoma of the cauda
equina misdiagnosed as prolapsed lumbar
disk. Report of three cases. J Neurosurg
Sci 1994;38(3):181–5,
172. Craig WM, Svien HJ, Dodge HW Jr,
Camp WM. Intraspinal lesions
masquerading as protruded lumbar
intervertebral discs. JAMA 1952;149:250–
3.
173. Gore I, Hirst AE Jr. Arteriosclerotic
aneurysm of the abdominal aorta: a review.
Prog Cardiovasc Dis 1973;16:113.
174. Barratt-Boyes BG. Symptomatology and
prognosis of abdominal aortic aneurysm.
Lancet 1957;ii:716.
175. Amparo EG, Hoddick WK, Hricak H,
Sollitto R, Justich E, Filly RA, Higgins CB.
Comparison of magnetic resonance
imaging and ultrasonography in the
evaluation of abdominal aortic aneurysm.
Radiology 1985;154:451.
176. Filtzer DL, Bahnson HT. Low back pain
due to arterial obstruction. J Bone Joint
Surg 1959;41B:244.
177. Gibbons RP, Montie JE, Correa RJ Jr,
Mason JT. Manifestations of renal cell
carcinoma. Urology 1976;8:201.
178. Paulson DF, Einhorn L, Peckham M,
William SC. Cancer of the testis. In: De
Vita VT, Hellman S, Rosenberg SA,
editors. Cancer: Principles and Practice of
Oncology. Philadelphia: Lippincott; 1982.
p. 786–822.
179. Cantwell BMJ, Mann KA, Harris AL. Back
pain – a presentation of metastic testicular
germ cell tumours. Lancet 1987;6(i):262.
180. Jeffcoate TNA. Pelvic pain. BMJ
1969;ii:431.
181. O’Connor DT. Endometriosis. New York:
Churchill Livingstone; 1987.
182. Mantle MJ, Greenwood RM, Currey HLF.
Backache in pregnancy. Rheum Rehabil
1977;16:95–101.
183. Svensson H-O, Andersson GB, Hagstad A,
Jansson P-O. The relationship of low-back
pain to pregnancy and gynecologic factors.
Spine 1990;15:371–5.
184. Ostgaard HC, Andersson GBJ, Karlsson K.
Prevalence of back pain in pregnancy.
Spine 1991;16:549–52.
185. Kristiansson P, Svärdudd K, von Schoultz
B. Back pain during pregnancy. A
prospective study. Spine 1996;21:
702–9.
186. Mens JMA, Vleeming A, Stoeckaert R,
Stam HJ, Snijders CJ. Understanding
peripartum pelvic pain. Implications of a
patient survey. Spine 1996;21:1363–70.
187. Ross JR, Reave LE III. Syndrome of
posterior penetrating peptic ulcer. Med
Clin North Am 1966;50:461.
188. Bank S. Chronic pancreatitis: clinical
features and medical management. Am J
Gastroenterol 1986;81:153.
189. Falterman KW, Hill CB, Markey JC, Fox
JW, Cohn I Jr. Cancer of the colon,
rectum and anus: a review of 2313 cases.
Cancer 1974;34:951.
© Copyright 2013 Elsevier, Ltd. All rights reserved.