Blyth FM, Macfarlane GJ, Nicholas MK 2007 The contribution of psychosocial factors to the development of chronic pain: the key to better outcomes for patients?. Carter ML 2004 Spinal cor
Trang 1sensory 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 clinipharmacologi-cal differentiation of persistent
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, and opioids.
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
Woolf CJ ( 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 further reading)
Besson JM (1999) The neurobiology of pain Lancet 353:1610 – 5
Trang 2Furst 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
Jensen TS, Baron R (2003) Translation of symptoms and signs into mechanisms in neuro-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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Trang 8Epidemiology and Risk Factors
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.
✔ The prevalence and incidence rates for neck
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, sociologpsycholog-ical, 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 the frequency and causes of diseases or syndromes
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
with a particular disease at a given time or for a given period Frequently used
time periods are the whole adult lifetime until the establishing diagnosis
Trang 9(life-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 1 000) 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 2 months before”), and are lower when criteria are stricter (“never experi-enced symptoms before”).
Persistence and Recurrence. Because of the high prevalence and incidence rates, the burden of back pain in adult populations is better estimated with measures of
the persistence (“duration of pain episodes”) and recurrence (“number of
recur-rent episodes”) Persistence and recurrence are also captured by measuring the
total number of days with pain in the last year For instance, work disability is 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].
Trang 10Classification 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-tural pathology can, with certainty, be held responsible for the symptoms It is
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 is not 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 – duration less than 1 month
) 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 %):
) infectious
) tumorous
) metabolic
) degenerative (depending on the disorder)