Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 18 ppt

ceptive stimuli before transmission to the somato-
sensory cortex (perception).
Neuroplasticity. Alterations in the physiological
function of pain pathways as a result of tissue dam-
age or neural injury are referred to as neuroplasti-
city. Injured tissue can release inflammatory media-
tors which activate and sensitize receptor channels
in the peripheral terminal of the nociceptor. High-
threshold and silent nociceptors are activated by a
decrease in their threshold and show an increase in
the responsiveness (peripheral sensitization). Tis-
sue damage may also result in transcriptional
changes in the dorsal root ganglion. Similarly, pain
transmission is facilitated and inhibitory influences
are attenuated by distinct neurobiological alter-
ations of the receptor channels in the dorsal horn
(central sensitization). Afferent nociceptive signals
from the periphery to the brain are modulated by a
well balanced interplay of excitatory and inhibitory
neurons which can be disturbed as a result of an
injury. Disinhibition is the disturbance of this bal-
ance with relief from inhibitory neuronal mecha-
nisms. Genetic predisposition and biopsychoso-
cial factors have a significant influence on the mod-
ulation of the afferent sensory input.
Clinical assessment. The clinical assessment of pain
encompasses a detailed medical history, sophisti-
cated quantitative sensory testing, neurophysio-
logical studies, imaging studies, and pharmacologi-
cal tests. The clinical differentiation of persistent
inflammatory pain and neuropathic pain remains

difficult because of the lack of an objective test for
neuropathic pain (the missing gold standard). It is
important to note that not all persistent pain is neu-
ropathic. The diagnosis of neuropathic pain should
be based on the presence of negative and positive
sensory symptoms and signs.
General treatment concepts. The pharmacological
treatment of acute pain must be aggressive, multi-
modal and preemptive to reduce the likelihood of
pain persistence. The WHO three-step pain relief
ladder indicates one should start with a weak anal-
gesic and stepwise increase the potency of the med-
ication until pain relief is felt. Analgesics can be dif-
ferentiated into non-opioid analgesics (e.g. parace-
tamol, tramadol, ketamine), NSAIDs,andopioids.
Opioids include all the endogenous and exogenous
compounds that possess morphine-like analgesic
properties. Adjuvant drugs (e.g. antidepressants,
anticonvulsants, anxiolytics) are useful adjunct med-
ications because they enhance the central effect of
analgesics and target associated depression, fear
or anxiety. Non-pharmacological treatments of
chronic back pain such as back school, exercise ther-
apy, or spinal manipulation have not passed the test
of mid- and long-term clinical effectiveness. Cogni-
tive-behavioral treatment is effective in chronic LBP
only in the short term. Surgical treatment of chronic
pain syndromes particularly chronic LBP has not
been proven to be effective in the long term.
Key Articles

Melzack R, Wall PD (1965) Pain mechanism: A new theory. Science 150:971 –979
This paper introduced the gate control theory and substantially contributed to our
increasing understanding of the pain signal.
Engel GL (1977) The need for a new medical model: a challenge for biomedicine. Science
196:129 – 36
The previous dominant model of disease in the late 1970s was biomedical, and it left no
room within its framework for the social, psychological, and behavioral dimensions of
illness. Therefore, Engel proposed a biopsychosocial model that closed the gap between
the mind and the body.
Wo olf C J ( 1983) Evidence for a central component of post-injury pain hypersensitivity.
Nature 306:686 – 8
This landmark paper introduces the phenomenon of central sensitization demonstrating
that the long-term consequences of noxious stimuli result from central as well as from
peripheral changes.
Review Articles (recommended for fur ther reading)
Besson JM (1999) The neurobiology of pain. Lancet 353:1610–5
Pathways of Spinal Pain Chapter 5 145
Furst S (1999) Transmitters involved in antinociception in the spinal cord. Brain Res Bull
48:129–41
Julius D, Basbaum AI (2001) Molecular mechanisms of nociception. Nature 413:203–10
Scholz J, Woolf CJ (2002) Can we conquer pain? Nat Neurosci 5 Suppl:1062–7
JensenTS,BaronR(2003)Translationofsymptomsandsignsintomechanismsinneuro-
pathic pain. Pain 102:1–8
Woolf CJ (2004) Pain: moving from symptom control toward mechanism-specific phar-
macologic management. Ann Intern Med 140:441–51
Almeida TF, Roizenblatt S, Tufik S (2004) Afferent pain pathways: a neuroanatomical
review. Brain Res 1000:40–56
Kehlet H, Jensen TS, Woolf CJ (2006) Persistent postsurgical pain: risk factors and pre-
vention. Lancet 367:1618–25
Appendix: IASP Pain Terminology (www.iasp-pain.org)

allodynia pain due to a stimulus that does not normally provoke pain
analgesia
absence of pain in response to stimulation that would normally be painful
anesthesia dolorosa
pain in an area or region that is anesthetic
causalgia
a syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion,
often combined with vasomotor and sudomotor dysfunction and later trophic changes
dysesthesia
an unpleasant abnormal sensation, whether spontaneous or evoked
hyperalgesia
an increased response to a stimulus that is normally painful
hyperesthesia
increased sensitivity to stimulation, excluding special senses
hyperpathia
a painful syndrome, characterized by increased reaction to a stimulus, especially a repetitive
stimulus, as well as an increased threshold
hypoalgesia
diminished sensitivity to noxious stimulation
hypoesthesia
diminished sensitivity to stimulation, excluding special senses
neuralgia
pain in distribution of nerve or nerves
neuritis
inflammation of a nerve or nerves
neurogenic pain
pain initiated by a primary lesion, dysfunction, or transitory perturbation in the peripheral or
central nervous system
neuropathic pain
any pain syndrome in which the predominating mechanism is a site of aberrant somatosensory

processing in the peripheral or central nervous system
neuropathy
a disturbance of function or pathologic change in a nerve; in one nerve, mononeuropathy; in
several nerves, mononeuropathy multiplex; if symmetrical and bilateral, polyneuropathy
nociceptor
a receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become
noxious if prolonged
noxious stimulus
a noxious stimulus is one that is potentially or actually damaging to body tissue
pain
an unpleasant sensory and emotional experience associated with actual or potential tissue dam-
age, or described in terms of such damage
pain threshold
the least experience of pain that a subject can recognize
pain tolerance level
the greatest level of pain that a subject is prepared to tolerate
paresthesia
an abnormal sensation, whether spontaneous or evoked
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Pathways of Spinal Pain Chapter 5 151
6
Epidemiology and Risk Fac tors
of Spinal Disorders
Achim Elfering, Anne F. Mannion
Core Messages
✔
In 85% of patients with a spinal disorder the
etiology is unclear
✔
In non-specific spinal disorders, axial pain (i.e.

cervical, thoracic, lumbar pain without radia-
tion into the extremities) is the main symptom
✔
Back pain in non-specific spinal disorders is a
symptom, not a disease
✔
With a 12-month prevalence of 15 – 45 %, a
12-month incidence of up to 20 %, and a yearly
recurrence rate of up to 60%, low back pain
(LBP) is a major health problem.
✔
Theprevalenceandincidenceratesforneck
pain are only slightly lower
✔
For the majority of people with an acute epi-
sode of LBP (80–90%), the prognosis is good:
within 1 month, marked improvements in pain
and disability occur, and work can be resumed
✔
Work-related disability from non-specific spinal
disorders has become epidemic in industrial-
ized countries
✔
Only a minority of patients are chronically dis-
abled, but such cases cause most of the costs
✔
Over 50% of the costs of spinal disorders are
related to indirect societal costs
✔
The best predictor of future episodes of back

pain is previous back pain
✔
Models of back pain are multifactorial, and
include genetic, biological, physical, psycholog-
ical, sociological, and health policy factors
✔
Occupational psychosocial variables are clearly
linked to the transition from acute to chronic
neck and back pain, work disability, recovery,
and return to work
General Scope
Epidemiology estimates
the association between
risk factors and diseases
in statistical terms
Epidemiology is research on t he frequency and causes of diseases or s yndromes
in different populations. The baseline idea of epidemiology is that disease and
causal factors are not distributed at random in human populations. Individuals
who develop a disease are expected to be exposed to antecedent risk factors to a
greater degree or for a longer time than are individuals who stay healthy. It is
important to bear in mind that epidemiology estimates the association between
risk factors and diseases in statistical terms.
A second significant goal of epidemiology therefore is to rule out alternative
sources of association, e.g. confounding factors, study bias, and chance. Epidemi-
ological knowledge contributes to the planning and evaluation of primary pre-
vention. Epidemiological data also serve as a guide to the management of
patients in whom disease has already developed. The number of individuals that
suffer from a disease or a syndrome is expressed in terms of prevalence rates, and
the number of new cases is expressed in incidence rates.
Prevalence. Prevalence refers to the percentage of a population that is affected

withaparticulardiseaseatagiventimeorforagivenperiod.Frequentlyused
time periods are the whole adult lifetime until the establishing diagnosis (life-
Basic Science Section 153
time prevalence), or 1, 6, or 12 months before the interview-establishing diagno-
sis (1-, 6-, or 12-month prevalence rates; also called current prevalence rates).
Point prevalence indicates the percentage of those reporting pain on the day of
the interview.
Incidence. Incidence refers to the number or rate of new cases of the disorder per
persons at risk (usually 100 or 1000) during a specified period of time (usually
one year). To determine the incidence rate, individuals who were healthy at the
beginning of the observation period and who become affected during the obser-
vation period are counted. From this definition it follows that incidence rates are
hard to estimate when conditions are widespread or often reoccur and therefore
lack clear information on first onset. Incidence rates tend to be higher when com-
parably weak criteria are used to define health at the beginning (“no symptoms
during 2months before”), andare lowerwhencriteria arestricter (“never experi-
enced symptoms before”).
Persistence and Recurrence. Because of the high prevalence and incidence rates,
theburdenofbackpaininadultpopulationsisbetterestimatedwithmeasuresof
the persistence (“duration of p ain episodes”) and recurrence (“number o f recur-
rent episodes”). Persistence and recurrence are also captured by measuring the
totalnumberofdayswithpaininthelastyear.Forinstance,workdisabilityis
longer in recurrent compared with first episodes to low back pain [107].
Severity. The intensity of pain and functional disability represent the main focus
in attempts to devise a grading system indicating the severity of disorders [78,
97].
Objectives in Spinal Disorders
The specific objectives of epidemiology in the management of spinal disorders
are to [77]:
pinpoint the problem

estimate the societal and economic burden of spinal disorders
forecast the problem in future
describe and differentiate spinal disorders
classify and grade symptoms within spinal disorders
describe the natural history (assisting decision making)
identify preceding risk factors and estimate their impact (alone or com-
bined)
identify protective resource factors preventing disease or promoting healing
evaluate primary and secondary prevention efforts
provide guidance for health care planning
Epidemiology helps
to classify spinal disorders,
identify risk factors,
predict natural history
and estimate costs
Epidemiology contributes to the standardization of terminology, a matter that is
still unsatisfactory in spinal disorders. For instance it was shown recently that
different definitions of back pain are systematically related to differences in prev-
alence rates [68].
Risk and resource factors comprise demographic, genetic, and other individ-
ual factors, and occupational, societal and even non-identified cultural charac-
teristics [52]. Epidemiology is often a source for methodological development
that helps to crystallize evidence from a data pool. Finally, epidemiology helps to
evaluate primary and secondary prevention efforts and offers important guid-
ance for planning health policy [77].
154 Section Basic Science
Classification of Spinal Disorders
Spinal disorders are a wide and heterogeneous variety of diseases affecting the
vertebrae, intervertebral discs, facet joints, tendons and ligaments, muscles, spi-
nal cord and nerve roots of the spine (

Table 1).
Etiology
Spinal disorders comprise
a variety of disorders that all
involve the spinal column
We can differentiate spinal disorders according to their etiology. We differentiate
on the basis of whether a specific cause can be found which conclusively explains
the patient’s symptoms:
Specific spinal disorders have an unambiguous etiology and can be diagnosed
on the basis of specific structural pathologies that are consistent with the clinical
picture.
Non-specific spinal disorders are not diseases per se but more of a syndrome.
In the vast majority of patients (85–90%) presenting with a spinal disorder it is
not possible to identify a pathomorphological source of the problem despite a
thorough diagnostic work-up [66]. There are many potential causative and
aggravating factors associated with non-specific spinal disorders but no struc-
turalpathologycan,withcertainty,beheldresponsibleforthesymptoms.Itis
not easy to differentiate between specific and non-specific spinal disorders by
early symptoms, because the primary manifestation of most spinal disorders is
pain involving the neck and back.
For pain which isnot radiating into the extremities the term axial pain is often
used. We can differentiate between:
axial neck pain
axial dorsal pain
axial back pain
Time Course
Spinal disorders can be further classified according to the time course of symp-
toms:
acute–durationlessthan1month
subacute – duration up to 3 months

chronic – duration more than 3 months
Neck and back pain are the
most common symptoms in
non-specific spinal disorders
Spinal disorders are labeled as acute if persisting for a short time period (less
than 1 month) with a sudden onset. Symptoms are classified as subacute if they
occur after a prolonged period (6 months) without pain and with a retrospective
duration of less than 3 months. A chronic stage is reached if symptoms occur epi-
Table 1. Classification of spinal disorders
Specific spinal disorders Non-specific spinal disorders
With clearly identifiable pathomorphological
correlate (10 –15%) such as:
Without clearly identifiable pathomor-
phological correlate (85–90%):
congenital non-specific axial neck pain
developmental non-specific axial dorsal pain
traumatic non-specific axial back pain
infectious
tumorous
metabolic
degenerative (depending on the disorder)
Epidemiology and Risk Factors of Spinal Disorders Chapter 6 155