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ix
Preface
Conditions causing spinal pain syndromes are many and thorough physical examination followed, as indicated, by
varied and patients can present with a wide variety of appropriate imaging and laboratory procedures.
symptoms. Therefore, each patient needs to be thoroughly During the last few years of a 37-year career
investigated before treatment commences i.e. diagnosis specializing in spinal pain syndromes, interesting challeng-
must be a prerequisite to treatment. ing spinal pain syndrome cases have been collected, 100 of
It behoves all clinicians dealing with spinal pain syn- which are presented in this text. In some of the cases pre-
dromes to note the following: sented, gross anatomy and pathology, as well as some his-
topathology specimens, obtained from postmortem
First, do no harm (Hippocrates, Epidemics, Bk. 1, Sect.
material, with changes similar to the clinical cases pre-
XI).
sented, are used to illustrate how such conditions in
”If you listen carefully to the patient they will tell you the
patients may cause spinal pain syndromes and provide a
diagnosis” (Quotation of Sir William Osler 1849–1919). This
basis upon which to recommend treatment options.
statement still holds true and emphasizes the great impor-
In some cases patients merely wanted reassurance,
tance of taking a good history.
based upon a thorough evaluation leading to a likely
Remember that patients may present with more than one
explanation for their chronic pain syndrome(s), rather than
condition, so consider all possibilities.
requesting treatment. The importance of providing ade-
Get back to the basic principles (Frymoyer JW 1997 Fore-
quate, albeit time consuming, psychological assurance
word. Clinical anatomy and management of low back
should not be underestimated. Obviously, it is important
pain. In: Giles LGF and Singer KP, Butterworth–Heine-
to consider a particular pain syndrome in great detail
mann, Edinburgh) e.g. be conversant with the principles
while not forgetting that psychology must be taken into
of anatomy, physiology, pathology, etc.
account for each patient, as symptoms and signs should
Knowledge is ever increasing on spinal anatomy and histo- not be isolated from the patient as a whole being.
pathology and the possible physiological mechanisms by The cases begin with the most frequently involved spi-
which pain may be generated and experienced. Therefore, nal level (lumbar spine) and conclude with the least fre-
in this text an introductory chapter summarizes possible quently involved spinal level (thoracic spine).
pain sources based on known anatomical principles. The cases represent what actually takes place in day-to-
Because spinal pain syndromes can be complex, there often day clinical practice and illustrate some of the various
is a tendency for clinicians to incorrectly label patients as shortcomings of health care providers.
being ‘neurotic’, or when patients are involved in litigation It should be noted that it is the responsibility of the
they may be considered to have litigation ‘neurosis’ as a treating clinician, relying on independent expertise and
motive. However, it should be remembered that it is not knowledge of the patient, to determine the best treatment
always possible to diagnose a patient’s spinal pain condi- and method of application for their individual patients.
tion because of many factors such as the limitations of Finally, all clinical professionals may make errors of
imaging procedures and the specificity and sensitivity of judgement in the diagnosis and management of patients.
laboratory tests. Therefore, patients should not be consid- Therefore, it is not the intention of this text to criticize
ered as malingerers unless there are very strong grounds any particular profession but rather to draw to the atten-
for doing so. Imaging frequently only provides shadows tion of health practitioners from various backgrounds what
of the truth and laboratory tests can be misleading, so it actually takes place in the health care domain in the hope
is imperative to take a careful history and to perform a that clinicians, and students embarking upon a health care
x PREFACE
career, will glean some insight into the possible difficulties of such syndromes – no one profession has all the answers
that may arise with respect to individual cases. to manage challenging acute and chronic spinal pain syn-
In my opinion, multidisciplinary cooperation is essential if drome patients.
clinicians from different backgrounds are to best serve indivi- L.G.F. Giles
duals with spinal pain syndromes and the possible sequelae
xi
General introduction
pain unit Giles et al (2003) found that, of the 949 male patients
INTRODUCTION
and 826 female patients (aged 10 to 91 years; average age 43
The diagnosis of spinal pain syndromes is often difficult, as years), all of whom had some form of spinal imaging, 1% of
the anatomy of the spine and its adjacent soft tissue struc- patients had radiologically identifiable life threatening path-
tures is complex. For details of spinal anatomy including his- ological processes. This percentage concurs with the serious
tology and histopathology see Rickenbacher et al (1982), pathology percentage of up to 1% as stated by Waddell
Giles (1989), Von Hagens et al (1991), Rauschning (1997), (2004).
Giles & Singer (1997, 1998, 2000), Cramer & Darby (2005), Pain in any structure requires the release of inflamma-
Moore & Dalley (2006). The purpose of this introduction is tory agents, including bradykinin, prostaglandins and leu-
to provide a synopsis of possible diagnoses based on a sound kotrienes, that stimulate pain receptors and generate a
anatomical foundation as well as on the clinical history, nociceptive response in the tissue; the spine is unique in
physical examination, imaging and laboratory findings. In that it has multiple structures that are innervated by pain
addition, it should be noted that the neurophysiology of pain fibres (Haldeman et al 2002).
is not fully understood at this time. For example, when Slip- Spinal pain syndromes must be viewed in the context of
man et al (1998) studied the mechanical stimulation of cervi- (i) clearly defined pathological conditions, and (ii) the less
cal nerve roots C4 to C8 in patients with cervical radicular well-defined, but much more prevalent, condition of non-
symptoms who were undergoing diagnostic selective nerve specific spinal pain of mechanical origin (Stoddard 1969,
block, to document the distribution of pain and paraesthesiae Kenna & Murtagh 1989). It is imperative to distinguish
that result from stimulation of specific cervical nerve roots, dysfunctional mechanical causes of spinal pain from other
and to compare that distribution to documented sensory der- causes, as patients with mechanical disorders of the spine
matomal maps, they demonstrated a distinct difference are likely to respond dramatically to manual treatment
between dynatomal and dermatomal maps. A dynatome is (Kenna & Murtagh 1989).
the distribution of referred symptoms from root irritation A major difficulty involved in evaluating a patient with
and this is different to the sensory deficit outlined by derma- non-specific spinal pain of mechanical origin, with or with-
tomal maps. Slipman et al (1998) suggest that cervical derma- out root symptoms, is that many causes of pain are possible.
tomal mapping is inaccurate, as the distribution of referred Because the painful structure, or structures, are not amenable
symptoms from cervical root irritation is different than the to direct scrutiny, a tentative diagnosis is usually arrived at
sensory deficit outlined by dermatomal maps. Therefore, it for an individual case by taking a careful case history and
is reasonable to suggest that a similar neurophysiological employing a thorough physical examination, with imaging
finding may occur at other spinal nerve root levels. Thus, and laboratory procedures as indicated. There are several
when considering neurological tests such as pinprick or light main approaches to patient evaluation: (i) history taking;
touch, summarized later in this text, it would be prudent to (ii) assessment of pain (using subjective self-report measures
remember the work of Slipman et al (1998). estimating pain severity, quality and location); (iii) investiga-
Low back pain is experienced by 80–90% of the population tion of personality structure, including the use of appropriate
(Deen 1996), while 34–40% of the population experience neck subjective questionnaires; (iv) clinical identification of signs
and arm pain (Hardin & Halla 1995) compared to 7–14% of and symptoms; (v) the use of appropriate imaging; and
the population that experience thoracic spine pain (Pedersen (v) the use of appropriate laboratory investigations. Evidence
1994, Hinkley & Drysdale 1995). Therefore, musculoskeletal of signs and symptoms deemed excessively, or inappropri-
spinal pain can be a significant health problem. On analysing ately, abnormal (Main & Waddell 1982) should be recorded.
1775 new patients presenting to a multidisciplinary spinal However, caution has to be exercised when making
xii GENERAL INTRODUCTION
judgements on an individual’s behavioural responses to of nuclear anatomy and not for symptomatology, and Schell-
examination as serious misuse and misinterpretation of has et al (1996) showed that significant cervical disc annular
behavioural signs has occurred in medicolegal contexts using tears often escape MRI detection. In addition, Osti & Fraser
such signs (Main & Waddell 1998). These behavioural signs (1992) concluded that lumbar discography is more accurate
have been questioned by Giles (2005). than MRI for the detection of annular pathology. However,
There is still little consensus, either within or among spe- according to Shalen (1989), lumbar discography is a contro-
cialties, on the use of diagnostic tests for patients with spinal versial examination that is regarded by some radiologists
pain syndromes, and the underlying pathology responsible and spine surgeons as barbaric and non-efficacious (Wiley
for various spinal pain problems remains elusive (Videman et al 1968, Clifford 1986, Shapiro 1986). For lumbar spine
et al 1998). Furthermore, in spite of following a thorough CT and MR imaging, Willen et al (1997) showed that the
examination procedure, one often merely eliminates overt diagnostic specificity of spinal stenosis will increase consid-
pathologies and the precise cause of non-specific spinal pain erably when the patient is subjected to an axial load, and
syndromes of mechanical origin often remains obscure Danielson et al (1998) concluded that, for an adequate evalu-
(Turner et al 1998). ation of the cross-sectional area, CT or MR imaging studies
Specifically, diagnostic problems relate to: (a) the limita- should be performed with axial loading in patients who
tions of many diagnostic procedures, including plain film have symptoms of lumbar spinal stenosis. The advantage
radiography, computerized tomography (CT), positron of MRI, which is considered to be the major medical imag-
emission tomography (PET) scan, magnetic resonance imag- ing development of the century (Wong & Transfeldt 2007),
ing (MRI), myelography, discography and bone scans; (b) is that it is a non-invasive procedure, without any recognized
some diagnostic and therapeutic chemical agents being biological hazard, that combines a strong magnetic field
harmful, as can be the case when such chemicals injected and radiofrequency energy to study the distribution and
into intervertebral discs extravasate into the epidural space behaviour of hydrogen protons in fat and water (Weir &
(Weitz 1984, Adams et al 1986, MacMillan et al 1991) caus- Abrahams 2003). More recently, exciting new developments
ing complications due to contact between them and neural have occurred with, for example, upright, dynamic-kinetic
structures (Dyck 1985, Merz 1986, Watts & Dickhaus 1986); i.e. ‘functional’ MRI and its ability to detect load- and
(c) inadequacies in the precise anatomical knowledge of motion-dependent disc herniations, stenosis, instabilities,
the spine including its nociceptive tissues; (d) anatomical and combinations of these pathologies not seen during
complexity of the spine often making roentgenographic recumbent imaging (Jinkins et al 2003, Elsig & Kaech 2006,
interpretation difficult (Le-Breton et al 1993); and (e) there Jinkins JR personal communication 2007). In addition,
sometimes being multifactorial causes of pain at a given 3 Teslar (T) MRI units are becoming available that can pro-
level of the spine (Haldeman 1977, Gross 1979), e.g. injury vide higher-quality images than those obtained at 1.5 T
to the intervertebral disc, the zygapophysial facet joints (Tanenbaum 2006).
and to the segmental soft tissue structures. In addition, there In the thoracic spine, with its particular combination of
may be several types of spinal pain that closely mimic each intervertebral and various synovial joints, the most common
other (Haldeman 1977). A further important point to cause of thoracic spine pain syndromes is dysfunction and
remember is that a central disc herniation may cause spinal degeneration of spinal intervertebral joints and the asso-
pain alone without radiculopathy (Postacchini & Gumina ciated rib articulations (Kenna & Murtagh 1989). Further-
1999) whereas a posterolateral or far lateral disc herniation more, Erwin et al (2000) showed that costo-vertebral joint
will, in all likelihood, cause radicular pain (Keim & anterior capsule and synovial tissues are innervated,
Kirkaldy-Willis 1987). demonstrating that these joints have the requisite innerva-
The nerve root compression that occurs in lumbar disc tion for pain production. Root compression due to postero-
herniation and lumbar canal stenosis often results in a range lateral disc protrusion, with resulting signs and symptoms
of symptoms, including low back pain, sciatic pain, and sen- of intercostal radiculopathy, such as pain, paraesthesiae
sory disturbances and muscle weakness in the legs (Kobaya- and sensory disturbances, has to be differentiated from
shi et al 2005). Summers et al (2005) consider that the degree overt pathological conditions such as neoplasms. Thoracic
of back or leg pain caused by an acute disc prolapse depends, disc protrusion has long been a difficult clinical entity to
in part, on the position, size, and level of the disc prolapse. diagnose (Brown et al 1992) as symptoms can vary dramati-
There often is disagreement on which imaging procedures cally from none at all to motor and sensory deficits resulting
have diagnostic validity for non-specific spinal pain of from spinal cord compression (myelopathy) – pain, muscle
mechanical origin, although it is generally agreed that, for weakness, and spinal cord dysfunction are the most com-
plain film X-ray examinations, two views of the same anato- mon clinical symptoms (Cramer 2005). On the other hand,
mical region at right angles is the minimum requirement thoracic disc protrusion can produce spinal cord compres-
(Henderson et al 1994), and that erect posture radiography sion with bladder incontinence and signs of an upper motor
(Giles & Taylor 1981) and functional views ( Jackson 1977) neuron lesion (Kenna & Murtagh 1989) and occasionally
are more useful. Furthermore, Buirski & Silberstein (1993) paraplegia. As the thoracic cord is immobilized by the
correctly noted that MRI can only be used as an assessment dentate ligaments, the anterior spinal artery may be
GENERAL INTRODUCTION xiii
significantly compressed by a relatively small central disc for anatomically normal spines and which needs to be con-
protrusion (Pate & Jaeger 1996) and, because there is little sidered during the examination is that the distribution of
extradural space in the thoracic spinal canal, a compara- cutaneous areas supplied with afferent nerve fibres by sin-
tively small disc protrusion may have pronounced effects gle posterior spinal nerve roots, i.e. dermatomes of the
on the neurology (Hoppenfeld 1977). Thoracic cord com- human body (Dorland’s Illustrated Medical Dictionary 1974,
pression can also be caused by ossified ligamenta flava in Barr & Kiernan 1983), has been fairly well established
Caucasians (van Oostenbrugge et al 1999) as well as in Jap- (Fig. i). Myotomes, a group of muscles innervated from a
anese people (Otan et al 1986, Yonenobu et al 1987, Kojima single spinal segment (Dorland’s Illustrated Medical Dictio-
et al 1992). nary 1974), likewise, have been fairly well established.
As it is still only rarely possible to validate a diagnosis According to Keim & Kirkaldy-Willis (1987), dermatomes
in cases where pain arises from the spine (White & Gordon enable deficits of a specific nerve root to be accurately loca-
1982) and, because it is not possible to establish the patho- lized during sensory examination. However, it is important
logical basis of spinal pain in 80–90% of cases (Chila et al to note that Jinkins (1993) and Slipman et al (1998) question
1990, Spratt et al 1990, Pope & Novotny 1993), this leads this concept and suggest that there is, in fact, some overlap
to diagnostic uncertainty and suspicion that some patients of sensation.
have a ‘compensation neurosis’ or other psychological
problem. It is also appropriate at this time to recognize the
role of psychosocial factors in spinal pain. Although the
complex interaction of psyche and soma in the aetiology of
spinal pain is not well understood, a psychogenic compo-
nent may be primary (conversion disorder), secondary
(depression caused by chronic pain), contributory (myofas-
cial dysfunction), or absent (Keim & Kirkaldy-Willis 1987).
Nonetheless, clinicians must have a good understanding of
possible causes of symptoms and a high suspicion of possi-
ble underlying pathology, e.g. patients presenting with
symptoms of tethered cord syndrome (Yamada 1996, Giles
2003, Yamada et al 2004), or patients presenting with symp-
toms of arteriovenous malformations (Criscuolo & Rothbart
1992), i.e. an abnormal communication between an artery
and a vein (Beers et al 2006), should not be overlooked.
It is reasonable to broadly classify acute spinal pain as
being of 7–28 days or less duration, which may be followed
by a sub-acute stage of up to 12 weeks; after this the pain
can be considered chronic (Skoven et al 2002).
Figure v A schematic diagram of a typical cervical vertebra showing basic cervical vertebral anatomy and part of the neuroanatomy within
the spinal and intervertebral foramen canals. The long arrow points to the origin of the recurrent spinal meningeal nerve and the insert shows
this nerve in detail. The short arrow points to the anterior spinal artery. The diagram does not show the peripheral innervation of the
intervertebral disc or of the zygapophysial (facet) joints. 1 ¼ intervertebral disc; 2 ¼ posterior longitudinal ligament; 3 ¼ uncovertebral joint;
4 ¼ deep sympathetic chain; 5 ¼ vertebral artery and spinal branch; 6 ¼ anterior nerve root; 7 ¼ anterior primary ramus; 8 ¼ posterior
primary ramus; 9 ¼ posterior nerve root and ganglion of C5; 10 ¼ posterior spinal arteries; 11 ¼ spinal canal; 12 ¼ subdural space;
13 ¼ dura; 14 ¼ arachnoid; 15 ¼ dentate ligament; 16 ¼ epidural space; CN ¼ cervical nerve; RSMN ¼ recurrent spinal meningeal nerve;
SG ¼ sympathetic ganglion; PGF ¼ post ganglionic fibres. (Modified and reproduced with permission from: Jackson R 1977 The cervical
syndrome, 4th edn. Charles C Thomas, Springfield.)
(TFLs) (Amonoo-Kuofi et al 1988, Giles 1992a, Cramer et al paresis; pain may be present in various forms and may take
2002) that reduce the space available for the spinal nerve the form of low back pain or neurogenic claudication or, if
root within the intervertebral foramen (Min et al 2005) subarachnoid haemorrhage occurs, then severe headaches,
and thus may play a role in giving rise to severe pain photophobia, and meningism may be present (Rothbart et al
and paraesthesiae along the distribution of a nerve due 1997). A spinal dural arteriovenous fistula, where a direct
to direct mechanical pressure on the neural complex connection between the radicular branch of a radicular artery
(Amonoo-Kuofi & El-Badawi 1997). TFLs can successfully and the corresponding radicular vein at the dorsal root sleeve,
be imaged with low-field-strength MRI; if a trained radiol- results in signs of a progressive myelopathy (van der Meulen
ogist identifies a TFL, there is an 87% chance that one is et al 1999, Jellema et al 2007).
present and, if a trained radiologist does not identify a MRI of the spinal cord plays a very important role in the
TFL in an intervertebral foramen, there remains a 51% diagnosis of AVMs. For example, high T2 signal MRI of the
chance that one is present (Cramer et al 2002). spinal cord is the most sensitive imaging finding in spinal
Another structure to be considered, and alluded to above, dural arteriovenous fistula (Gilbertson et al 1995).
is that of spinal arteriovenous malformations (AVMs) i.e. Because of the lack of pathognomonic symptoms and signs
dural arteriovenous fistulas, intradural arteriovenous mal- associated with spinal arteriovenous malformations, the dif-
formations, and extradural venous varices (Criscuolo & ferential diagnosis is extremely important because the asso-
Rothbart 1992, Mascalchi et al 2001) that, although rare, ciated progressive myelopathy may be confused with other,
may occur in any region of the spine (Royston 2007) includ- more common, neurological conditions (Rothbart et al 1997).
ing the sacrum (Schaat et al 2002). The spinal level of the arte- For a full appreciation of the various types of AVMs, their
riovenous malformation will determine the symptoms in a symptoms, signs and a differential diagnosis work-up, see
particular patient. Symptoms associated with AVMs include Rothbart et al (1997). Essentially, neuroradiological studies
pain, sensory abnormalities, sphincter disturbances and should demonstrate the presence and precise location of the
GENERAL INTRODUCTION xvii
IMAGING
Routine radiographs of the spine, and when indicated by
the history and symptoms, the chest, should be taken to
establish a baseline and to rule out metabolic, inflamma-
tory, and malignant conditions (Keim & Kirkaldy-Willis
1987), bearing in mind the limitations of plain X-ray exam-
inations. As long as proper coning of the X-ray beam is
used in conjunction with high speed screens and films,
and appropriate filtration of the X-ray beam, there is mini-
mal X-radiation to the patient while obtaining maximum
quality X-ray films. These radiographs should be taken in
the erect posture, whenever possible, using carefully stan-
dardized procedures; for example, to accurately determine
whether possibly significant leg length inequality is pres-
ent with corresponding pelvic obliquity causing postural
(compensatory) scoliosis in the spine (Giles & Taylor 1981,
Giles 1984, 1989). In the cervical spine, functional flexion
and extension views may show instability; sagittal plane dis-
placement between two adjacent cervical vertebrae of more
than 3.5 mm, or relative sagittal plane angulation greater
than 11 , is considered to represent cervical segmental insta-
bility (White et al 1975) – that is, horizontal or angular
instability (Dai 1998).
Bogduk’s (1999) ‘modified criteria for the use of plain
Figure vi A schematic diagram showing basic thoracic vertebral films in low back pain’ which are based on the work of
anatomy and the nerve supply of the thoracic ventral compartment Deyo & Diehl (1986) are of concern when viewed in the
at the level of the vertebral body (c) and at the level of the light of some of the following cases from over 37 years
intervertebral disc (d). The ventral and dorsal roots of the spinal experience in the diagnosis of spinal pain syndromes. Bog-
nerve are retracted dorsally (arrow). Bundles of nerve fibres duk (1999) states ‘plain films may be used as a screening
originating from rami communicantes (3) pass cranial and caudal to test for "red flag" conditions if a patient presents with
the spinal nerve and the dorsal root ganglion (G) towards the dorsal
any of the following features’: history of cancer, significant
ramus of the spinal nerve (5). Large and small sinuvertebral nerves
(6) derive from the rami communicantes. 1 ¼ anterior longitudinal trauma, weight loss, temperature >37.6 C, risk factors for
ligament nerve plexus; 2 ¼ paraspinal sympathetic ganglion; infection, neurological deficit, minor trauma in patients
3 ¼ rami communicantes; 4 ¼ ventral ramus of the spinal nerve; (over 50 years of age, known to be osteoporotic or taking
5 ¼ dorsal ramus of the spinal nerve; 6 ¼ sinuvertebral nerves; corticosteroids), and no improvement over a 1 month
7 ¼ posterior longitudinal ligament nerve plexus. The diagram does period. Clearly, it is better for a patient to undergo plain
not show the innervation of the intervertebral disc or the film radiography when indicated by the history (unless
zygapophysial (facet) joints and other structures. (Reproduced with there is a contraindication such as pregnancy) at the onset
permission from Groen G J et al 1990 Nerves and nerve plexuses of of symptoms, rather than to risk misdiagnosis and mis-
the human vertebral column. Am J Anatomy 188(3): 282–296, management, both of which would be disadvantageous to
Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.) patients. This is particularly important when treatment by
spinal manipulation is considered, as the application of
mechanical forces to a spine that may have degenerative
vascular nidus of the AVM, define the angioarchitecture, changes, or overt pathological changes, could be dangerous.
determine the operability of the malformation, and aid in In my opinion, not looking at the spine and pelvis in all cases
the safe obliteration of the lesion by defining the vascular prior to using mechanical treatment may well explain the
anatomy of the malformation and the normal spinal cord occurrence of some adverse events, even though most
(Rothbart et al 1997). According to Xia et al (2007), intraopera- authors have reported a low rate of adverse events asso-
tive angiography for AVMs has been found to result in ciated with spinal manipulation.
favourable clinical results by ensuring safe and accurate Further imaging procedures may be necessary. These
occlusion of the fistula. include (i) magnetic resonance imaging, which can provide
From the above, it is clear that clinicians need to be very good detail of soft tissue structures in and about the
familiar with both normal and abnormal anatomy in order spinal column without the need of radiation or of contrast,
for them to think laterally when confronted with challeng- (ii) CT scans, which are particularly good at showing bony
ing spinal pain syndromes. structures and are useful for some neural problems,
xviii GENERAL INTRODUCTION
(iii) myelography or post-myelography CT scans for agree, stating that even the most severe degenerative changes
demonstrating lesions of the spinal cord and canal such can occur in the absence of symptomatology, but back pain is
as neoplasm and other space occupying lesions, for exam- more common in individuals who demonstrate these degen-
ple disc herniation, (iv) bone scans when tumour, infection erative changes. The specificity difficulties encountered with
or small fracture(s) are suspected, and (v) discography MRI studies to date may relate to the fact that recumbent
when indicated, to show tears in the intervertebral disc MRI technology was used; new technology allowing for com-
with internal disc disruption. The usefulness of a positron parisons between upright, weight-bearing, dynamic, posi-
emission tomography (PET) scan, used heavily in clinical tional MRI and traditional supine MRI has shown that there
oncology, should not be underestimated. When invasive is a very significant difference between the pathology visua-
imaging is being considered, the possible complications lized between the two MRI procedures; therefore, the diag-
of such a procedure should always be considered. nostic information that can be derived from routine supine
Unfortunately, all the preceding procedures have some MRI studies is extremely limited (Jinkins JR, personal com-
limitations, for example plain film radiographs will not munication, 2007).
show an osseous erosion until approximately 40% decrease It should be noted that another limitation of MR imag-
in bone density has occurred (Michel et al 1990, Perry ing is the resolving power (i.e. ability to distinguish small
1995), and Schellhas et al (1996) and Osti & Fraser (1992) or closely adjacent structures) of the MRI machine; this
found that discography is more accurate than MRI for the has to be taken into account when considering what cannot
detection of annular pathology in the cervical and lumbar be seen. I am advised that the latest MRI scanners have a
spines respectively. Therefore, these limitations show, as resolving power of 100 to 250 microns i.e. 1/10th to 1/4
stated above, that imaging procedures may only give a of a millimetre, so any lesion smaller than this would not
‘shadow of the truth’; this important fact should be remem- be seen. For this reason, it is not uncommon for imaging
bered. This is particularly true when a patient’s physical reports to fail to indicate injuries that may be the cause of
examination and imaging studies are not remarkable and pain.
do not pinpoint the cause of symptoms, as imaging cannot It is of interest to note that cervical spine investigations
show all tissue changes (Giles & Crawford 1997a). The lim- with plain radiography, myelography, and computed
itations of present diagnostic imaging procedures (Finch tomography have shown that degenerative disease fre-
2006) in not being able to show all soft tissues are an unfor- quently occurs in the absence of clinical symptoms (Boden
tunate but obvious fact. The following comments are of et al 1990b) while Gore (1999) stated that degenerative
interest with respect to some limitations of imaging changes of the cervical spine, as seen on plain roentgen-
procedures. ograms and more sophisticated studies, are common in
With respect to the lumbar spine, and with the same both symptomatic and asymptomatic patients.
principle applying to the cervical and thoracic regions, Nonetheless, various studies have shown a significant
Vernon-Roberts (1980) wrote: ‘It may be a minor consola- association between some structural abnormalities and
tion to clinicians and others who have to deal with the the presence (Parkkola et al 1993, van Tulder et al 1997,
problem of low back pain to know that even clinically Paajanen et al 1997, Luoma et al 2000), frequency (Vide-
and radiologically ‘normal’ spines can have pathological man et al 2003, Videman & Nurminen 2004) or severity
changes which, until proved otherwise, could be a cause (Videman et al 2003, Peterson et al 2000) of low back pain.
of much stress to both doctor and patient’. Using flexible fibrescopes (external diameter of 0.6–1.5 mm)
According to Osti & Fraser (1992), a normal MRI does not Tobita et al (2003) stated, with respect to the entire spine:
exclude significant changes in the peripheral structure of the ‘Although the diagnosis of spinal disease has been greatly
intervertebral disc that can produce spinal pain. Further- improved by computed tomography (CT) and magnetic
more, Schellhas et al (1996) demonstrated that ‘significant resonance imaging (MRI), there are still many conditions
cervical disc annular tears often escape magnetic resonance that are difficult to diagnose by these means as patho-
imaging detection, and magnetic resonance imaging cannot logical changes were seen by fibrescopic examinations in
reliably identify the source(s) of cervical discogenic pain’. patients in whom no abnormal changes were found by
The same principle is likely to apply to all spinal disc levels. MRI or CT’.
Several MRI studies have shown that 20–76% of asymp- The abovementioned findings raise questions about the
tomatic adults exhibit abnormalities of lumbar discs morphology-based understanding of pain pathogenesis in
(Boden et al 1990a; Buirski & Silberstein 1993, Jensen et al patients with disc abnormalities (Boos et al 2000). Further-
1994, Deyo 1994, Boos et al 1995, Jarvik et al 2001) in other more, Karppinen et al (2001) found that MRI scans from
words, 24–80% of symptomatic adults exhibit abnormalities 180 patients with unilateral sciatic pain suggested that a
of lumbar discs on MRI. Kleinstuk et al’s (2006) lumbar discogenic pain mechanism other than nerve root entrap-
spine MRI study showed that symptomatic adults with ment generates the subjective symptoms among sciatic
chronic, non-specific low back pain appear to have an overall patients.
higher prevalence of structural abnormalities than previously A further difficulty is that the nomenclature and classifi-
reported for asymptomatic individuals. Haldeman et al (2002) cation of lumbar disc pathology is not standardized
GENERAL INTRODUCTION xix
(Fardon & Milette 2001), although Pfirrmann et al (2001) intestine, and placenta (Brabson 2001). Evaluation of
have suggested a method for grading disc degeneration enzymes more specific to the liver, 50 -nucleotidase or g-glu-
on T2-weighted MRI. tamyltranspeptidase (GGT), can differentiate hepatic from
When nerve root dysfunction is suspected, electromyog- extra-hepatic sources of alkaline phosphatase (Beers et al
raphy (EMG) and nerve root conduction studies can be 2006). Early inflammatory changes may be detected by an
helpful (Hoppenfeld 1977). increase in C-reactive protein (CRP) and/or an increase in
It is important to note the following comments regard- the erythrocyte sedimentation rate (ESR). A full blood count
ing imaging shown in this text: can be helpful, for example, in cases where there is suspi-
cion of primary haematological disorders and for some
Most plain film anteroposterior radiographic images of the infections (Henderson et al 1994). Immunoelectrophoresis
spine and or pelvis are printed as if the clinician were look- of serum and urinary proteins may also be useful diagnostic
ing at the patient’s back; i.e. a marker showing ‘R’ indicates procedures in the diagnosis of multiple myeloma (Brown
the patient’s right side. 1975, Beers et al 2006). Examples of other tests that should
Spinal axial CT scans are viewed, as usual, from ‘below’; be considered, when indicated, are: (i) latex flocculation
i.e. remember that the clinician ‘looks up’ the patient’s for rheumatoid spondylitis; (ii) serum and urine amylase
spinal canal with the patient supine, so the patient’s right and lipase for chronic pancreatitis (Collins 1968, Schroeder
side is marked ‘R’ on the left side of the axial CT scan fig- et al 1992); and (iii) blood culture and sensitivity, and for
ure(s). genitourinary tract infections urine culture and sensitivity.
For spinal axial MRI scans, the same principle as for CT In addition, it may be necessary to assess bone density using
axial scans is applied; i.e. the patient’s right side is on a dual energy X-ray absorption (DEXA) bone densitometer
the left side of the figure(s). in osteoporotic patients. In males, prostate-specific antigen
MRI T1-weighted images produce essentially a fat image in (PSA) should be considered if there is any suspicion of pros-
which structures containing fat (bone marrow, subcutaneous tate malignancy (Kingswood & Packham 1996).
fat) appear bright, while structures containing water In this book it is not necessary to list every spine-related
(oedema, neoplasm, inflammation, cerebrospinal fluid, scle- condition with its possible abnormalities in serology, haema-
rosis, large amounts of iron) appear dark (Yochum & Barry tology, urinalysis and other laboratory tests, as these have
1996). been well documented in numerous clinical diagnosis texts.
MRI T2-weighted images produce essentially a water In some publications, particular reference to spinal patholog-
image in which structures containing predominantly free ical conditions and related pathology tests have been sum-
or loosely bound water molecules (neoplasm, oedema, marised (Haldeman et al 1993, Henderson et al 1994).
inflammation, healthy nucleus pulposus, cerebrospinal A large range of laboratory evaluations are important
fluid) appear bright, while substances with tightly bound when the clinician suspects metabolic disturbance, malig-
water (ligaments, menisci, tendons, calcification, sclerosis nancy, infection or one of the arthritides such as ankylosing
or large amounts of iron) appear dark (hypointense) spondylitis or rheumatoid arthritis. Nonetheless, it should
(Yochum & Barry 1996). be noted that various tests have different levels of accuracy,
Patient identification details have been blacked out to as calculated from their sensitivity (proportion of individuals
maintain patient confidentiality. with the condition whose tests are positive) and specificity
(proportion of individuals without the condition whose tests
are negative (Bloch 1987, Nachemson 1992, Henderson et al
LABORATORY TESTS 1994)).
When bony pathology is suspected, useful laboratory tests
that may be helpful in detecting bone disease include serum
CONDITIONS ASSOCIATED WITH SPINAL PAIN
calcium, phosphorus, acid phosphatase, and alkaline phos-
SYNDROMES
phatase (particularly alkaline phosphatase isoenzyme deter-
mination by electrophoresis, which differentiates alkaline A summary of the chief conditions causing spinal tender-
phosphatase of osteoblastic origin from alkaline phosphatase ness is shown in Table i. In addition, it is necessary to list
from other sources) (Brown 1975). On electrophoresis, liver some possible causes of non-specific spinal pain of
isoenzyme levels usually range from 20 to 130 U/L; bone iso- mechanical origin, with or without radicular pain, as
enzyme levels from 20 to 120 U/L; and intestinal isoenzyme briefly summarized in Table ii, which provides a summary
levels (which occur almost exclusively in individuals with of some literature references over the years in order to give
blood group B or O and are markedly elevated 8 hours after a historical background to the complex issue of non-spe-
a fatty meal) from undetectable to 18 U/L (Brabson 2001). cific spinal pain of mechanical origin. As Waddell (2004)
The five alkaline phosphatase isoenzymes of greatest clini- stated, most back pain is ‘ordinary backache’. This often
cal significance originate in the liver (includes kidney and is referred to as ‘mechanical’, ‘non-specific’ or ‘idiopathic’
bile fractions), bone (may also include bile fraction), spinal pain. In a large number of these cases, it may not
xx GENERAL INTRODUCTION
Table i Summary of chief conditions causing spinal tenderness Table ii Some possible causes of non-specific spinal pain
of mechanical origin with or without radicular pain
1. Diseases of the overlying skin and subcutaneous tissue.
These are usually clinically obvious and include poten- Nerve root conditions
tially serious conditions such as melanoma Adhesions between dural sleeves and (a) the joint cap-
2. Diseases of the vertebral column sule with nerve root fibrosis (Sunderland 1968, Jackson
Inflammatory 1977, Wilkinson 1986) and (b) intervertebral disc hernia-
Pott’s disease tion (Wilkinson 1986).
Staphylococcal spondylitis Intervertebral disc degeneration and fragmentation
Typhoid spine (Schiotz & Cyriax 1975), or nucleus pulposus extru-
Spondylitis ankylopoietica (Spondylitis Ossificans sion (Mixter & Ayer 1935) causing nerve root com-
Ligamentosa/ankylosing spondylitis) pression (Kobayashi et al 2005), or nerve root
Actinomycosis ‘chemical radiculitis’ (Marshall & Trethewie 1973).
Hydatid cyst Zygapophysial joint conditions
Paget’s disease Joint derangement (subluxation) due to ligamentous
Degenerative and capsular instability (Hadley 1964, Cailliet 1968,
Spondylosis Jackson 1977, Macnab 1977, van Norel & Verhagen
Osteochondritis (rare) 1996).
Nucleus pulposus herniation and other soft tissue Joint capsule tension with encroachment upon the inter-
injuries vertebral foramen lumen (Jackson 1977).
Neoplastic Joint degenerative changes, e.g. ‘meniscal’ incarceration
Primary tumour (Schmorl & Junghanns 1971), traumatic synovitis due to
Secondary deposit ‘pinching’ of synovial folds (Giles 1986, Giles 1987, Giles
Myelomatosis & Harvey 1987, Giles & Taylor 1987a & b), synovial fold
Leukaemic deposits tractioning against the pain-sensitive joint capsule
Traumatic (Hadley 1964), and osteoarthrosis (Jackson 1977).
Fracture Joint effusion with capsular distension which may
Dislocation (a) exert pressure on a nerve root (Jackson 1977),
Nucleus pulposus herniation (b) cause capsular pain (Jackson 1966), or (c) cause
Erosion by aortic aneurysm nerve root pain by direct diffusion (Haldeman 1977).
3. Diseases of the spinal cord and meninges Joint capsule adhesions (Jackson 1977, Farfan 1980,
Metastatic epidural abscess or tumour Giles 1989).
Meningioma Intervertebral disc conditions
Neurofibroma Disc protrusion into the spinal and intervertebral
Herpes zoster canals.
Meningitis serosa circumscripta Disc/dural adhesions (Parke & Watanabe 1990)
Tumour of the spinal cord Spondylosis (Young 1967, Jackson 1977).
Syringomyelia Miscellaneous conditions
Arachnoid calcifications (Wijdicks and Williams 2007) Spinal and intervertebral canal (foramen) stenosis
4. Hysteria and malingering: compensation neurosis (Young 1967, Jackson 1977, Epstein & Epstein 1987,
5. Metabolic disorders: osteoporosis, osteomalacia, Rauschning 1992).
hyperparathyroidism Intervertebral canal (foramen) venous stasis (Giles
1973, Sunderland 1975).
Modified from Mackenzie I 1985 Spine, tenderness of. In: Hart FD (ed) French’s Myofascial genesis of pain (trigger areas) (Travell &
index of differential diagnosis, 12th edn. Butterworth & Co. Ltd, p 788. Rinzler 1952, Bonica 1957, Simons & Travell 1983).
Baastrup’s syndrome (Reinhardt 1951, Bland 1987)
Osseous spinal anomalies, e.g. bilateral cervical ribs,
be possible to identify the precise pain generator. How- block vertebra (Jackson 1977).
ever, an orthopaedic surgeon well versed in spinal pain Idiopathic scoliosis (Ramirez al 1997)
syndromes, Emeritus Professor Ruth Jackson, stated that
the word idiopathic is used by defeatists to signify ‘I don’t
know the cause’ and that, if one searches diligently for the provided from human postmortem material to illustrate
cause of any painful or abnormal condition, the answer can some possible causes of such pain (Figures vii.1–32). Most
usually be found (Jackson 1977). examples are from the lumbosacral spine as low back pain
As there are many putative causes of such spinal pain, is experienced by the majority of spinal pain syndrome
some gross anatomical and histopathology examples are patients.
Another Random Document on
Scribd Without Any Related Topics
ate. No, it can’t be little Miss Elizabeth,—it’s more likely some one
that has hired or bought the place and goin’ to upset and change it
all.”
“I didn’t say the lady was old, grandma; she has lots of soft,
silvery, wavy hair with big gray eyes to match, and such a pretty
colour in her cheeks, and her dress was soft and fluffy too and the
colour as if purple and white violets and silver popple leaves were all
mixed together,” said Sarah, moving her hands before her, a little
way she had when talking, as if in describing what she had seen she
was touching the real object, for Sarah, though only a little girl from
a bare hillside farm and taught at the school below at Foxes Corners,
had a keen eye for colour and loved beautiful things, so that ugliness
or unkindness of any sort really hurt her if she could have explained
her feelings.
“My Gray Lady’s first name is Elizabeth, though, and she knows
you and your molasses cakes,” continued Sarah, after a moment’s
pause, “for she said, ‘When you go home say to your grandmother
that Elizabeth who rode the black pony sends her love, and that she
will go to see her soon, and that she hopes that she will give the
little Elizabeth some of the cookies of which she has often heard.’
Elizabeth is the little girl, but I’m going to call her Goldilocks,
because the name matches her hair and she looks as if she was
meant to—
Only think, if all those robins’ eggs of yours, Bobby, and all your little
eggs, Dave, should suddenly turn into birds and fly about the room,
how many there would be! But now they will never have wings and
swell their throats to sing to us and use their beaks to eat up insects
that make the apples wormy and curl up the leaves of the great
shade trees.”
“Robins don’t do any good; they just spoil our berries and
grapes; dad says so, and he shoots ’em whenever he can, and he
likes me to take the eggs,” said Dave, stubbornly, while Sarah Barnes
exclaimed, “Yes, an’ my father says he ought to be ashamed of
himself!” almost out loud.
“I know that Robins sometimes eat fruit,” said Gray Lady, firmly,
“but they do so much more good by destroying bugs that the Wise
Men say that neither they nor their eggs shall be taken or destroyed,
and what they say is now a law. So that it is not for any one to do as
he pleases in the matter. To kill song-birds or destroy their eggs is as
much breaking the law as if you stole a man’s horse or cow, for
these birds are not yours; they belong to the state in which you live.”
Bobby and Dave looked surprised, but Tommy and Sarah nodded
to one another, as much as to say, “We knew that, didn’t we?”
“Some day, if you are clever with your lessons so that Miss Wilde
can spare the time for it, I will tell you all about the reasons for
these laws, and what the wild birds do for us, and what we should
do for them. But first you must learn to know the names of some of
the birds that live and visit hereabout, as I am now learning yours,
and make friends of some of them as I hope to make friends of
you.”
“Yes, yes, oh, yes!”
“You can’t make friends of birds; they won’t let you,” said Dave
Drake, who was a sickly, lanky boy of fourteen with a whining voice;
“they always fly away. That is, I mean tree birds, not chickens nor
pigeons.”
“Chickens aren’t birds, they’re only young hens,” put in Eliza
Clausen, with an expression of withering contempt. She was one of
the big fourteen-year-old girls, and not being a good scholar was apt
to use opposition in the place of information.
“We can make friends of at least some birds,” said Gray Lady, “if
we are kind to them. When we have human visitors come to stay
with us, what do we do for them?”
“We let them sleep in the best bedroom, and we get out the best
china and have awful good things to eat, and give ’em a good time,”
said Ruth Barnes, all in one breath.
“Yes, and we should do much the same with our bird friends.
They do not need to have a bedroom prepared; they can generally
find that for themselves, though even this is sometimes necessary in
bad weather; but they often need food, and in order that they
should have what Ruth calls ‘a good time,’ we must let them alone
and not interfere with their comings and goings.
“Go softly to the west window and look out,” continued Gray
Lady, raising a finger to caution silence, for from her seat on the
little platform she could see over the children’s heads and out both
door and windows, “and see the hungry visitors that a little food has
brought to the very door.”
The children tiptoed to one side of the room, and there, lo and
behold, was a great Blue Jay, a Robin, a Downy Woodpecker with his
clean black-and-white-striped coat and red neck bow, and a saucy
Chickadee, with his jaunty black cap and white tie, all feasting on
the broken bits of Miss Wilde’s ham sandwich, while a pair of Robins
were industriously picking the fruit from a remnant of huckleberry
pie. Unfortunately, before the children had taken more than a good
look, the door banged to and the birds flew away, the Woodpecker
giving his wild sort of laugh, the Robins crying, “Quick! quick!” in
great alarm, while the Jay and Chickadee told their own names
plainly as they flew.
“As we have agreed to talk and ask questions, I will ask the first
one,” said Gray Lady, as they all settled down, feeling very good-
natured and eager to listen.
“Eliza said a few minutes ago that a chicken isn’t a bird. Now a
chicken is a bird, though of course all birds are not chickens.
The Bird
“Who can tell me exactly what a bird is? You all may think you
know, but can you put it in words?”
“A bird isn’t a plant; it is an animal,” said Tommy Todd.
“Yes, but a cat is an animal, and a snake, and a horse; and we
are animals ourselves.”
“A bird is a flying animal,” returned Sarah.
“Very true, but so is a bat, and, as you know, a bat has fur and
looks very like a mouse, and a bird does not.
“Ah, you give it up. Very well, listen and remember. A bird is the
only animal which has feathers! With his hollow bones filled with
buoyant, warm air, and covered with these strong pinions, he rows
through the air, as we row a boat through the water with the oars,
balancing himself with these wings, also steering himself with them
and with his tail made of stiff feathers and shaped to his particular
need, while with small feathers laid close, overlapping each other
like shingles, and bedded on an under-coat of down, he is clothed
and protected from heat, cold, and wet.
“The eye of the bird is different from ours, for it magnifies and
makes objects appear much larger to it than they do to us. Also,
while with other animals each group has practically the same kind of
feet or beaks, birds have these two features built on widely different
plans, so that when you have learned to know the common birds by
name and are really studying bird-life, you will find that you must be
guided to the orders in which they belong often by their beaks and
feet.
“Barnyard Ducks, as you know, have webbed toes for swimming,
and flat bills to aid them in shovelling their natural food from the
mud.
“Birds of prey, like the Hawks and Owls, have strong hooked
beaks and powerful talons or claws, for seizing and tearing the small
animals upon which they feed.
“The Woodpeckers (all but one) have two front and two hind
toes; these help them grasp the tree bark firmly as they rest, while
they have strong-cutting, chisel-like beaks, which they also use for
tapping or drumming their rolling love-songs.
CHICKADEE
A LITTLE MINISTER
I know a little minister who has a big degree;
Just like a long-tailed kite he flies his D.D.D.D.D.
His pulpit is old-fashioned, though made out of growing pine;
His great-grandfather preached in it, in days of Auld lang syne.
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