Presentation and Management of Chronic Pain in Kids
Presentation and Management of Chronic Pain in Kids
The mechanisms underlying the presentation of chronic pain in childhood can best be explained using a developmentally appropriate biopsychosocial model, similar to that previously described by Gatchel. The complex nature of pain is illustrated by the fact that the severity and time course of chronic pain are frequently not directly or clearly related to underlying pathology or recovery from illness. Obvious examples of this disconnection include the childhood 'functional' pain syndromes, where it is sometimes concluded that pain is not due to a physical cause. However, it is also known that daily pain and pain-associated impairment of functioning also correlate poorly with disease control in children with better understood chronic illnesses involving tissue injury by mechanisms such as inflammation and/or hypoxia, including Juvenile Idiopathic Arthritis (JIA) and Sickle Cell Disease. In fact, scientifically supported biopsychosocial concepts of pain physiology do explain these observations without the need to attempt to inaccurately (and often arbitrarily) dichotomise the causes of chronic pain into 'physical' or 'psychological'.
Briefly, tissue injury leads to 'nociceptive' pain due to the activation of nociceptors and signal transmission by nociceptive pathways, it may be somatic or visceral. Nociceptors are sensitised, and therefore more easily activated, by inflammatory mediators and other substances generated by physical tissue damage or injurious chronic disease processes. This in turn can lead to central nervous system (CNS) sensitisation (central sensitisation) causing augmented, persistent and more widespread 'inflammatory' pain, although redness and local tissue swelling—the other components of the classic triad of inflammation—are not necessarily present.
When nervous tissue is damaged, pain is described as 'neuropathic'; nociceptor and CNS sensitisation also occur but the mechanisms, clinical characteristics, time course and pharmacological management are different. Pain perception in nociceptive, inflammatory and neuropathic states is strongly influenced by descending modulatory circuits from cortical, limbic and other brain areas, and by developmental, genetic and environmental factors that can blur the relationship between any initiating stimulus and subsequent pain. Pain symptoms, pain-related disability and prognosis in disease-related and idiopathic chronic pain, also show demonstrable associations with psychological distress, emotional functioning, parental attitudes, family illness models, cultural values and previous negative life events. Associated CNS changes and mechanisms linking these factors are clearly emerging, for example brain imaging studies in a number of chronic pain conditions have found significant changes in structure and functional connectivity compared with controls. The role of CNS plasticity in long-term pain, the regulation of pain during development and neuropathic pain in children have all been reviewed recently.
Sleep disturbance, anxiety and mood disorders are common comorbid problems in children with chronic pain. Compared to controls, children and adolescents with pain due to JIA, sickle cell disease, migraine/headache, functional abdominal pain, juvenile fibromyalgia syndrome, chronic musculoskeletal pain and mixed causes, all suffered from clinically damaging sleep impairment. Disordered sleep and pain sensitivity are closely inter-related, and studies show that treatment of sleep problems may improve pain symptoms, analgesic effectiveness, mood and quality of life. Clinically elevated levels of anxiety were reported in children with non-cardiac chest pain (56–81%), juvenile fibromyalgia (58%) and abdominal pain (45–79%). Chronic pain is also a risk factor for suicidal ideation in adolescents. Significant pain-related impairment of daily functioning, particularly school attendance, shows clear relationships with pain intensity, psychological and emotional functioning.
Given the importance of pain as a mechanism for survival, it is perhaps unsurprising that pain perception is clearly influenced by conscious and unconscious memory, cognitive and emotional functioning and contextual factors that are explicitly included in a biopsychosocial formulation of pain. It follows therefore that as chronic pain is the result of a complex interaction of biological, psychological and socially determined mechanisms, it should be assessed and managed within the framework of these three domains. In addition, it is essential to appreciate that suppression or treatment of underlying disease may not lead to resolution of pain and therefore pain should be managed independently and concurrently.
Pathophysiology of Chronic Pain: The Biopsychosocial Model
The mechanisms underlying the presentation of chronic pain in childhood can best be explained using a developmentally appropriate biopsychosocial model, similar to that previously described by Gatchel. The complex nature of pain is illustrated by the fact that the severity and time course of chronic pain are frequently not directly or clearly related to underlying pathology or recovery from illness. Obvious examples of this disconnection include the childhood 'functional' pain syndromes, where it is sometimes concluded that pain is not due to a physical cause. However, it is also known that daily pain and pain-associated impairment of functioning also correlate poorly with disease control in children with better understood chronic illnesses involving tissue injury by mechanisms such as inflammation and/or hypoxia, including Juvenile Idiopathic Arthritis (JIA) and Sickle Cell Disease. In fact, scientifically supported biopsychosocial concepts of pain physiology do explain these observations without the need to attempt to inaccurately (and often arbitrarily) dichotomise the causes of chronic pain into 'physical' or 'psychological'.
Briefly, tissue injury leads to 'nociceptive' pain due to the activation of nociceptors and signal transmission by nociceptive pathways, it may be somatic or visceral. Nociceptors are sensitised, and therefore more easily activated, by inflammatory mediators and other substances generated by physical tissue damage or injurious chronic disease processes. This in turn can lead to central nervous system (CNS) sensitisation (central sensitisation) causing augmented, persistent and more widespread 'inflammatory' pain, although redness and local tissue swelling—the other components of the classic triad of inflammation—are not necessarily present.
When nervous tissue is damaged, pain is described as 'neuropathic'; nociceptor and CNS sensitisation also occur but the mechanisms, clinical characteristics, time course and pharmacological management are different. Pain perception in nociceptive, inflammatory and neuropathic states is strongly influenced by descending modulatory circuits from cortical, limbic and other brain areas, and by developmental, genetic and environmental factors that can blur the relationship between any initiating stimulus and subsequent pain. Pain symptoms, pain-related disability and prognosis in disease-related and idiopathic chronic pain, also show demonstrable associations with psychological distress, emotional functioning, parental attitudes, family illness models, cultural values and previous negative life events. Associated CNS changes and mechanisms linking these factors are clearly emerging, for example brain imaging studies in a number of chronic pain conditions have found significant changes in structure and functional connectivity compared with controls. The role of CNS plasticity in long-term pain, the regulation of pain during development and neuropathic pain in children have all been reviewed recently.
Sleep disturbance, anxiety and mood disorders are common comorbid problems in children with chronic pain. Compared to controls, children and adolescents with pain due to JIA, sickle cell disease, migraine/headache, functional abdominal pain, juvenile fibromyalgia syndrome, chronic musculoskeletal pain and mixed causes, all suffered from clinically damaging sleep impairment. Disordered sleep and pain sensitivity are closely inter-related, and studies show that treatment of sleep problems may improve pain symptoms, analgesic effectiveness, mood and quality of life. Clinically elevated levels of anxiety were reported in children with non-cardiac chest pain (56–81%), juvenile fibromyalgia (58%) and abdominal pain (45–79%). Chronic pain is also a risk factor for suicidal ideation in adolescents. Significant pain-related impairment of daily functioning, particularly school attendance, shows clear relationships with pain intensity, psychological and emotional functioning.
Given the importance of pain as a mechanism for survival, it is perhaps unsurprising that pain perception is clearly influenced by conscious and unconscious memory, cognitive and emotional functioning and contextual factors that are explicitly included in a biopsychosocial formulation of pain. It follows therefore that as chronic pain is the result of a complex interaction of biological, psychological and socially determined mechanisms, it should be assessed and managed within the framework of these three domains. In addition, it is essential to appreciate that suppression or treatment of underlying disease may not lead to resolution of pain and therefore pain should be managed independently and concurrently.
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