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 References 1. 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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 . 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. 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. 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