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Chronic pain is a very common problem, impacting on many patients. Assessment and management can be challenging. The ABC of Pain focuses on the pain management issues often encountered in primary care.
Covering major chronic pain presentations, such as musculoskeletal pain, low back pain and neuropathic pain, the ABC of Pain also provides guidance on the management of pain in pregnancy, children, older adults, drug dependency and the terminally ill. Beginning with an overview of the epidemiology of chronic pain, pain mechanisms and the assessment of pain, it then provides practical guidance on interventional procedures and methods of effective pain management.
The ABC of Pain is a comprehensive, evidence-based reference. It is ideal for GPs, junior doctors, nurse specialists in primary care, palliative care specialists, and also hospital and hospice staff managing chronically and terminally ill patients.
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Seitenzahl: 291
Veröffentlichungsjahr: 2012
Table of Contents
Series Page
Title Page
Copyright
Contributors
Preface
Chapter 1: Epidemiology of Chronic Pain
Introduction
What is Chronic Pain?
Why is Epidemiology Important?
How Common is Chronic Pain?
The Impact of Chronic Pain
Factors Associated with Chronic Pain
What is the Cost of Chronic Pain?
Summary
Further reading
Chapter 2: Pain Mechanisms
Introduction
Basic Pain Pathway
Chronic Pain
Acute Peripheral Sensitisation
Chronic Changes in Peripheral Sensitisation
Peripheral Sensitisation can Trigger Spontaneous Pain
Central Sensitisation
Summary
Further reading
Chapter 3: Evaluation of the Patient in Pain
The Nature of Chronic Pain
Medical and Physical Evaluations
Psychological Assessment
Conclusions
Acknowledgement
Further reading
Chapter 4: Chronic Musculoskeletal Pain
Introduction
The Anatomy and Physiology of Musculoskeletal Pain
The Experience of Musculoskeletal Pain
A Classification of Musculoskeletal Disease and Pain
Regional Pain and the ‘Soft-tissue’ Periarticular Disorders
Arthritis
Fibromyalgia
Further reading
Chapter 5: Management of Low Back Pain
Introduction
Mechanical Dysfunction
Guidelines
Investigations – How Valuable is Magnetic Resonance Imaging (MRI)?
Acute, Chronic and Recurrent Pain
Treatment Options
Central Sensitivity Syndrome (CSS)
Conclusion
Further reading
Chapter 6: Neuropathic Pain
Introduction
Epidemiology
Mechanisms of Neuropathic Pain
Aetiology
Diagnosis
Management of Neuropathic Pain
Summary
Further reading
Chapter 7: Visceral Pain
Introduction
Pathophysiology of Visceral Pain
Visceral Pain Assessment
Management of Visceral Pain
Summary
Further reading
Chapter 8: Post-surgical Pain
Introduction
Assessment
Aetiology of Prolonged Pain Following Surgery
Risk Factors for the Development of Chronic Pain Following Surgery
Can Post-operative Neuropathic Pain be Prevented or Reduced?
How is Post-operative Neuropathic Pain Managed?
Possible Treatment Options
Summary
Further reading
Chapter 9: Headache and Orofacial Pain
Introduction
History
Examination
Investigations
Management Issues
Primary Headaches
Temporomandibular Disorders (TMD)
Trigeminal Neuralgia
Persistent Idiopathic Facial Pain
Further reading
Further resources
Chapter 10: Cancer Pain
Introduction
Cancer Pain Versus Non-malignant Pain
Assessment
Management of Cancer Pain
Strategies to Improve Opioid Responsiveness
Special Considerations
Newer Treatments
Summary
Further reading
Chapter 11: Treating Pain in Patients with Drug-dependence Problems
Introduction
Defining Addiction
Treating Acute Pain
Palliative Care
Treating Chronic Pain
Conclusion
Further reading
Chapter 12: Pain in Children
Pain Assessment
Analgesia
Procedural Pain
Post-operative Pain
Chronic Pain
Further reading
Chapter 13: Pain in Older Adults
Introduction
Evaluation
Further reading
Chapter 14: Pain in Pregnancy
Introduction
Musculoskeletal Problems
Gestational Problems
Reproductive Organs
Renal Tract
Other Abdominal Viscera
Chronic Pain and Pregnancy
Further Reading
Chapter 15: Psychological Aspects of Chronic Pain
Introduction
Early Involvement of Psychology in Pain Management
Cognitive Behavioural Therapy in Pain Management
The Fear–Avoidance Model of Chronic Pain
Pain Catastrophising
Appraisal-based Models
Efficacy of Psychological Therapies for Chronic Pain
The Influence of Other Healthcare Providers
Summary
References
Further reading
Chapter 16: Interventional Procedures in Pain Management
Introduction
Patient assessment and selection
General complications
Pharmacological intervention
Non-pharmacological intervention
Myofascial trigger point injections
Facet joint injection
Epidural steroid injections
Selective nerve root injection
Lumbar sympathetic block
Intrathecal drug delivery
Spinal cord stimulation (neuromodulation)
Summary
Further Reading
Chapter 17: The Role of Physiotherapy in Pain Management
Introduction
Physiotherapy in Acute Injury
Electrotherapies
Manual Therapies
Exercise Therapy
Behaviour Modification
Conclusion
Further reading
Chapter 18: The Role of Transcutaneous Electrical Nerve Stimulation (TENS) in Pain Management
Introduction
Techniques and Mechanism of Action
Practicalities
Contraindications, Precautions and Adverse Events
Clinical Research Evidence
References
Further reading
Chapter 19: Complementary and Alternative Strategies
Introduction
Who Should Deliver the Treatment?
Acupuncture
Hypnosis
Aromatherapy Massage
Evidence-based Summary
Further reading
Chapter 20: Opioids in Chronic Non-malignant Pain
Background
The Endogenous Opioid System
Opioids for Chronic Non-cancer Pain: What is the Evidence for Efficacy?
Risks and Benefits of Opioid Therapy
Basic Pharmacology of Opioids: Relevance for Clinical Use
Pharmacokinetic Aspects and Potential for Drug Interactions
Treatment of Opioid-induced Adverse Effects
Conclusions
Further reading
Index
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Library of Congress Cataloging-in-Publication Data
ABC of pain / edited by Lesley Colvin, Marie Fallon.
p. ; cm.—(ABC series)
Includes bibliographical references and index.
ISBN 978-1-4051-7621-7 (pbk. : alk. paper)
I. Colvin, Lesley, Dr. II. Fallon, Marie. III. Series: ABC series (Malden, Mass.)
[DNLM: 1. Pain Management. WL 704]
616′.0472—dc23
2011049095
Cover image: © iStockphoto.com/peepo
Cover design: Meaden Creative
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Contributors
Preface
The aim of the wise is not to secure pleasure, but to avoid pain.
Aristotle
Regardless of the area of healthcare we work in, we will meet patients suffering from chronic pain. Pain can cause significant distress and suffering, with a major impact on patients' quality of life and on their families. Careful assessment and management of pain is an integral part of good clinical care, not something that should only be available through specialist teams. The field of pain management is expanding rapidly, with novel approaches to assessment techniques, improved understanding of the pathophysiology and developments in both pharmacological and non-pharmacological management strategies. While there are many excellent textbooks for specialists, there is however a need for a clear and concise evidence-based text, that provides an accessible introduction to this important area. This new title in the ABC series has gathered together a range of internationally recognised experts and practising clinicians to produce a book that we hope will prove of real practical value to primary care staff, trainee doctors, students and allied health professionals.
We have not set out to write a comprehensive text of all aspects of pain management but have attempted to include commonly seen chronic pain conditions, or in areas that may provide particular challenges. The first part of the book explores the epidemiology of pain, where it is clear just how common chronic pain is – something that has not been well-recognised until relatively recently. A clear outline of the basic science of pain mechanisms helps to provide a framework for understanding how chronic pain develops and how treatment may work. This section should also be helpful for students and junior doctors preparing for exams. As with any medical problem, a comprehensive but focused approach to pain assessment underpins any successful management plan, as outlined in the chapter from Prof Dennis Turk.
Subsequent chapters examine very common pain conditions, including musculoskeletal pain, neuropathic pain and also visceral pain, In these chapters we have suggested various approaches to assessment and management that we hope you will find useful. We then focus on pain in patient populations with particular needs, such as children, the elderly, those with drug dependency issues, cancer pain and also pain in pregnancy.
The final part of the book examines the wide range of therapies that can be used in the management of chronic pain. While this includes pharmacological management, including opioids, we have tried to consider the multidisciplinary strategies that are used successfully in the specialist setting and how these can be used in the non-specialist setting. Thus we have addressed psychological therapies, physiotherapy, and complementary therapies.
Each chapter has used illustrations and text boxes to highlight important points, aiding ease of reading and making it more accessible. For those interested in more details on a particular topic we have provided a further reading list, including useful web-based resources. Each chapter can be read in isolation, although you hope you will find the style persuades you to read chapters that might otherwise not appeal to you.
The specialist nature of complex pain management has been increasingly recognised over recent years, both by professional bodies such as the Royal College of Anaesthetists (London) with the establishment of a Faculty of Pain Medicine in April 2007, and also by politicians. The fact remains however, that the vast majority of pain problems are dealt with by non-specialists: it is essential that all healthcare professionals have the basic training and education required to enable them to confidently address pain problems and thus reduce suffering in our patients. We would like to thank all our contributors for their expert chapters and also their patience, as this book has taken some considerable time to reach fruition. Despite this, we hope that the end result is enjoyed by our readership, and that their patients reap the benefits of this.
Lesley A Colvin Marie T Fallon
Chapter 1
Epidemiology of Chronic Pain
Blair H Smith and Nicola Torrance
Medical Research Institute, University of Dundee, Dundee, UK
Overview
Chronic pain persists beyond normal wound healing, with around one in four adults suffering from chronic pain
The majority of patients with chronic pain will be managed in the primary care setting, but complex cases will require specialist input
Chronic pain, especially neuropathic pain, has a major impact on all aspects of general health
Factors predisposing to chronic pain include those not amenable to intervention, such as increasing age and female gender, and also those that can be targeted, such as deprivation, or poor acute pain control
Early identification and management of chronic pain are essential in order to minimise long term suffering and disability
Pain is an individual experience, whose subjective nature makes it difficult to define, describe or measure, yet which is common to all human beings. As description and measurement are nonetheless essential, so, therefore, is a definition that suits both patients and professionals. Pain is helpfully, therefore, defined by the International Association for the Study of Pain (IASP) as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described by the patient in terms of such damage’.
Chronic pain is defined by the IASP as ‘pain that persists beyond normal tissue healing time’. A range of factors may be involved, including physical and biological factors, and also behavioural and cognitive factors, and these may dominate the experience of chronic pain, which is ultimately primarily subjective (Box 1.1).
There are many similarities in the symptoms and impact of chronic pain between most individuals who experience chronic pain, irrespective of its cause. Consequently, there are also many similarities in approaches to preventing or managing chronic pain of different aetiological or diagnostic backgrounds. This has led some to propose the existence of a ‘chronic pain syndrome’, and certainly for many clinical and research purposes, there is considerable merit in regarding chronic pain as a single, global, clinical entity (while also paying suitable attention to individual, treatable causes of chronic pain).
It is the latter part of this definition that makes it such an important science in clinical medicine. The last twenty or so years have seen the publication of many good quality epidemiological studies of chronic pain that have enhanced our understanding of its causes, impact and approaches to management. Good epidemiological research on chronic pain can, and does, provide important information on its classification and prevalence and factors associated with its onset and persistence. This can inform the design and targeting of treatment and preventive strategies (Box 1.2).
Source: Adapted from Smith, BH, Smith, WC & Chambers, WA. (1996) Chronic pain – time for epidemiology. Journal of the Royal Society of Medicine, 89, 181–183
The prevalence of chronic pain depends on exactly where, when and how it is measured. There is no universally agreed cut-off point between acute and chronic pain, but in the absence of other information, three months is often taken as the point beyond which ‘normal tissue healing’ should have taken place, and when pain therefore becomes chronic. Around one in four or five adults is currently experiencing chronic pain. A comprehensive literature review found a weighted mean prevalence of chronic pain of 25.9%. This is broadly similar to a large European study of over 46 000 people using a 6-month cut-off point (19.0%), and other systematic reviews.
Some studies have examined more severe, perhaps more clinically relevant, chronic pain. For example, ‘chronic widespread pain’ (bilateral pain above and below the waist, including the axial skeleton) has consistently been found to affect at least 5% of adults, and perhaps more than 11% (Figure 1.1).
Figure 1.1 Pain diagram from patient with Chronic Widespread Pain.
A similar prevalence (5%) has been found for ‘severe chronic pain’ (intense, highly disabling, severely limiting pain). Pain with neuropathic features (which is often more severe and harder to treat than other pain) probably affects at least 6–8% of the population. These figures are similar to the prevalence rates of well-recognised conditions such as ischaemic heart disease and diabetes, for which health service resources are readily found. Chronic pain, however, generally attracts less attention and resource (perhaps because it is often regarded as a heterogeneous group of conditions, or as a symptom, rather than as a global entity requiring a global response) (Figure 1.2).
Figure 1.2 Chronic back pain is very common: around three out of four people will suffer from it at some point in their life.
The commonest location of chronic pain is in the back, followed by the large joints (knee and hip). Other common causes of chronic pain include headache, other joint pain, injury, and, importantly, neuropathic pain. The diagnosis of this is essential in order to initiate correct treatment (Chapter 6). In particular, persistent post-surgical pain (up to 30% of surgical patients experience pain beyond three months, and 5% experience severe chronic pain) may be under-recognised and, therefore, under treated. Additionally, most people (approximately 75%) with chronic pain report pain at more than one site, and 18% report it at five or more sites. Indeed, evidence suggests that it is the extent of chronic pain (i.e. the number of sites at which it occurs) that determines its impact (and therefore treatment required), rather than the specific cause or diagnosis. Furthermore, around 75% of people with chronic pain have had it for more than a year, and around half have had it for five years.
The duration and extent of chronic pain are relevant in considering its impact. There is a very strong association between the presence of chronic pain and poor general health, no matter how this is measured. Every dimension of health is worse in the presence of chronic pain, at a population level, compared with those who do not report chronic pain. There is a direct relationship between the severity of pain and poor health, with neuropathic pain being associated with the most adverse general health indicators. This includes physical, psychological and social aspects of health (Box 1.3). There is a strong link between chronic pain and depression, such that it frequently becomes impossible to separate the two: chronic pain without measurable depression is rare, and depression makes the presence of chronic pain much more likely. It is probable that there are common aetiological factors shared by chronic pain and depression.
While the prevalence of chronic pain tends to rise with age (at least to a certain age), some studies, however, report a lower prevalence in old and very old age groups. This phenomenon may be the result of a genuine reduction in prevalence (i.e. a protective effect of ageing), a survival effect or an artefact (i.e. older people not reporting chronic pain in surveys, thinking perhaps that is simply part of normal ageing); is the subject of current research. Cultural and geographical differences in the reported prevalence of chronic pain are also apparent, and have several potential and complex explanations (Box 1.4).
While we are unable reasonably to intervene on some biological and social risk factors for chronic pain identified by epidemiological research (age, sex, location and culture), other risk factors consistently reported are potentially amenable to intervention. Notable among these is the strong association between deprivation and the presence, extent and severity of chronic pain. This suggests that, whatever else is done to improve chronic pain, political support is required. The most imoprtant risk factor for chronic pain is pain, either acute pain, or chronic pain elsewhere in the body. This highlights the need for healthcare professionals to take all reports of pain seriously, addressing these to prevent future long-term ill health.
Early suggestions that the elimination of acute post-surgical pain minimises the risk of future chronic pain are encouraging, particularly if this can be extrapolated to other forms of acute pain. With other risk factors for chronic pain there is more variability but there are some that are potentially important for the design of interventions. Generally speaking, interventions based on these are at an early stage of design and evaluation, but the potential is there and the possible benefits great (Figure 1.3).
Figure 1.3 Reducing chronic pain by addressing some of the risk factors potentially amenable to intervention.
The societal costs of chronic pain are difficult to gauge. One study of the economic burden of back pain in the United Kingdom estimated that it cost £10.7 billion, over than a decade ago. Some £1.6 billion of this was attributable to direct healthcare costs (the remainder being accounted for by lost productivity, benefits etc.; there is a demonstrable link between severity of chronic pain and the inability to remain or function in employment). It is estimated that around one in five consultations with a general practitioner (GP) is for a chronic pain-related reason, and that people with chronic pain consult their GP five times more frequently than those without.
In summary, therefore, chronic pain is a very common and important clinical condition, affecting individuals, the health services and society in diverse and adverse ways. The rest of this book explores some of the ways in which the problem can and must be addressed, and there is much good work currently underway to this effect in the clinical, educational and research arenas. This has been, and must continue to be, supported by epidemiological research, for ‘one's knowledge of science begins when he can measure what he is speaking about and express it in numbers’ (Lord Kelvin).
Breivik, H, Collett, B, Ventafridda, V, Cohen, R & Gallacher, D (2006) Survey of chronic pain in Europe: Prevalence, impact on daily life, and treatment. Eur J Pain, 10, 287–333.
Doth, AH, Hansson, PT, Jensen, MP & Taylor, RS (2010) The burden of neuropathic pain: a systematic review and meta-analysis of health utilities. Pain, 149 (2), 338–344.
Maniadiakis, N & Gray, A (2000) The economic burden of back pain in the UK. Pain, 84, 95–103
McBeth J, Jones K. Epidemiology of chronic musculoskeletal pain. Best Practice & Research in Clinical Rheumatology21: 403–425, 2007.
Smith, BH & Torrance, N (2008) Epidemiology of Chronic Pain. In: McQuay, HJ, Kalso, E & Moore, RA (eds), Systematic Reviews in Pain Research: Methodology Refined. Seattle: IASP Press, pp. 247–273.
Smith, BH, Elliott, AM & Hannaford, PC (2004) Is chronic pain a distinct diagnosis on primary care? Evidence from the Royal College of General Practitioners Oral Contraception Study. Family Practice, 21, 66–74.
Verhaak, PF, Kerssens, JJ, Dekker, J, Sorbi, MJ & Bensing, JM (1998) Prevalence of chronic benign pain disorder among adults: A review of the literature. Pain, 77, 231–239.
Chapter 2
Pain Mechanisms
Carole Torsney and Susan Fleetwood-Walker
College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, UK
Overview
Chronic pain can occur following tissue injury or damage to the nervous system and, unlike acute pain, serves no useful function
Injury modifies both peripheral and central components of the somatosensory nervous system, leading to misprocessing of sensory information and subsequent development of chronic pain syndromes
Under normal conditions pain sensation is only evoked by painful stimuli; patients with chronic pain, however, may display pain sensation in the absence of sensory stimuli (spontaneous pain), exaggerated pain sensation to painful stimuli (hyperalgesia) and pain in response to touch (allodynia)
Peripheral nervous system changes include heightened sensitivity of peripheral nerve terminals to sensory stimuli (peripheral sensitisation) and altered transmission of sensory signals to the spinal cord
Central nervous system (spinal cord and brain) changes include distortion of spinal cord processing of sensory inputs, which increases spinal cord excitability and intensifies responses to sensory input (central sensitisation)
These injury-induced changes are complex; they vary dependent on the type of injury, are influenced by factors such as genetic variability, and can also cause autonomic and affective changes
Pain has its uses! It tells us to avoid situations that can cause serious damage to our bodies. That information is essential but when patients suffer from chronic, continuing pain it no longer serves any useful purpose and is an unpleasant and aversive experience.
Chronic pain states arise following tissue damage or injury to the peripheral and or central nervous system and are broadly termed ‘inflammatory’ or ‘neuropathic’, respectively. Both inflammatory and neuropathic pain states are characterised by spontaneous pain, hyperalgesia (exaggerated pain) and allodynia (touch evoked pain) (Figure 2.1). These symptoms may encourage behavioural adjustments that promote repair and recovery by limiting contact with, for example, wounded tissue. However, if these symptoms persist beyond tissue healing, these chronic pain symptoms can be extremely debilitating and greatly reduce quality of life.
Figure 2.1 Chronic pain states arise following injury and are characterised by the symptoms of hyperalgesia (exaggerated pain), allodynia (touch-evoked pain) as well as continuing or spontaneous pain.
Chronic pain states transform dramatically the somatosensory nervous system, from one in which pain normally serves as a warning signal, promoting life and survival, to one in which pain is evoked by everyday activities and is counter-productive. In this chapter, those nervous system components that transduce and process sensory information are examined, how these components change or malfunction following injury is described and how these alterations are thought to produce chronic pain is explained.
Sensory information is conveyed from the periphery to the central nervous system via primary sensory neurons. There are different types of sensory neurons (Table 2.1) but all have their cell bodies in the dorsal root ganglia (Figure 2.2).
Table 2.1 Some of the different types of peripheral nerve fibres*
Figure 2.2 Basic somatosensory pathways. Sensory information is carried from the periphery to the spinal cord by primary sensory neurons, which have their cell bodies in dorsal root ganglia. Sensory information is then processed in the dorsal horn of the spinal cord before it is sent to the brain. There are also descending influences from the brain.
The pain-sensing primary sensory neurons, or ‘nociceptors’ have naked peripheral endings that terminate in the skin, mainly in the epidermal layer. These ‘peripheral nociceptor terminals’ possess an array of receptors or ion channels that transduce mechanical, thermal and chemical stimuli into neural signals (Figure 2.3a). Following sensory transduction, neural signals are then transmitted via primary sensory neurons to the dorsal horn of the spinal cord – the first stage of central processing of sensory input (Figure 2.4a).
Figure 2.3 Pain detection by the peripheral nociceptor terminal and its amplification (peripheral sensitisation) in chronic pain states. (a) Noxious stimuli are transduced into electrical signals by specific receptors and ion channels. Our knowledge of pain detection has been transformed by the discovery of the TRP (Transient Receptor Potential) channels that are thermo- and chemo-sensitive. It is not fully understood which receptor or receptors are responsible for transducing mechanical pain. (b) Following injury, damaged tissue cells and inflammatory cells release inflammatory mediators. These activate intracellular signalling pathways that modify transducer receptor and ion channel function, which increases the sensitivity of the peripheral nociceptor terminal to sensory stimuli.
Figure 2.4 Representation of spinal cord processing of sensory input and its distortion (central sensitisation) in chronic pain states. (a) Incoming sensory information undergoes local and descending modulation in the spinal cord dorsal horn. (b) Dorsal horn sensory processing is distorted in chronic pain states. There is increased sensory input, increased local excitation, decreased local inhibition and altered descending control. Overall, this increases spinal cord excitability and amplifies responses to sensory input.
The processing of sensory information within the dorsal horn is complex, involving local excitatory and inhibitory influences, as well as descending modulation from the brain. Importantly, this dorsal horn sensory processing determines which sensory signals are sent to higher centres to be perceived, where they may also influence emotional and autonomic function.
Basic research focuses predominantly on animal models of pain states in the quest to comprehend the mechanisms underlying chronic pain. These include inflammatory, surgical nerve injury and more sophisticated models in rodents that mimic pain conditions in the clinic (for example, demyelination, bone cancer, viral infection and arthritis). Analysis of these models reveals a multitude of changes, occurring within both peripheral and central sensory pathways, that are thought to underlie the misprocessing of sensory information leading to chronic pain. Chronic pain is essentially a pathological functioning of peripheral and central sensory pathways. It is recognised increasingly as a long term chronic condition in its own right, and might perhaps be considered as a chronic disease process.
Inflammation or tissue injury releases a number of inflammatory mediators, for example prostaglandins, bradykinin, nerve growth factor, cytokines, adenosine triphosphate (ATP) and protons, from damaged tissue cells and inflammatory cells. Some directly activate nociceptors but many alter dramatically the sensitivity of nociceptors by activating intracellular signalling pathways, which can modulate transducer receptors locally and also ion channels in the sensory neurons that are crucial for the generation of neural signals (Figure 2.3b). This represents ‘peripheral sensitisation’. Local peripheral sensitisation mechanisms occur on a rapid timescale (a few minutes) allowing the somatosensory system to respond to tissue injury dynamically (Figure 2.5).
Figure 2.5 Example of factors leading to peripheral sensitisation.
Peripheral sensitisation also occurs over longer timescales by altering gene expression in nociceptors. Following sustained injury, the high levels of nociceptor activity and the binding of inflammatory mediators, such as NGF, to its receptor trigger signalling cascades that act to modify gene transcription in nociceptors. The resultant change in expression of transducer receptors and ion channels influences powerfully the flow of sensory information from the periphery to the spinal cord.
