Neck Pain in Adults _________________________________________________________________________
for psychological intervention [84]. A study of whether social pain from rejection promoted social anxiety two days later identified a link between emotional and physical pain [85]. Participants rejected during an initial social situation had higher social anxiety before and during a second situation (versus those not rejected), fully mediated by initial social pain intensity. Next, all participants in a social situation were rejected, and randomized to acetaminophen or placebo before the next social situation. Acetaminophen lowered social anxiety before and during this exposure. Roughly 50% of this effect was mediated by, and specific to, reduction in social pain and not social anxiety [85]. Attachment insecurity (i.e., anxiety and/or discomfort in close relationships) is associated with physical symptoms, medically unexplained symptoms, and painful conditions. Medically unexplained chronic pain has been associated with attachment insecurity, after adjusting for depressive and anxiety disorders [86]. New Directions in Chronic Neck Pain Practice Fewer than half of patients with chronic pain achieve at least 50% pain reduction with any single drug or their combinations, a consequence of [70; 87; 88]: • Limitations of neuropathic pain definitions and the “nociceptive-neuropathic dichotomy” of chronic pain mechanisms • Standard practice guidelines based on clinical trials that assess analgesic efficacy in patients with specific under-lying pathologies, but not pain types • Multiple pain mechanisms in most chronic pain, but most drugs target one pain mechanism These flaws have prompted intensive efforts to overhaul chronic pain research and practice, leading to publications that expand and clarify chronic pain mechanisms to improve pain assessment and treatment. Many findings in chronic low back pain are relevant to chronic neck pain and are summarized here. Implementation in neck pain assessment and treatment is discussed in later sections. Neuropathic pain definitions are often over-restrictive, with pain strictly tied to a lesion or disease in nerve structures, such as peripheral nerves (e.g., post-herpetic neuralgia, diabetic neuropathy) or spinal nerve roots (e.g., radiculopathy). In this model, without evidence of nerve lesion or disease, signs or symptoms are insufficient [89; 90]. Current chronic low back pain guidelines class 85% to 90% of patients as nonspecific pain and a fraction as neuropathic pain, but many patients with chronic low back pain present with symptoms of a neuropathic component that goes undetected and untreated because nerve lesion or disease is absent [91; 92; 93; 94]. Their misclassing as nociceptive or nonspecific pain may lead to poor treatment outcomes [93; 94].
Neuropathic pain can develop when nerve fibers in any segment of the somatosensory system become dysfunctional or transmit signals inappropriately—without lesion or disease [95; 96]. The painDETECT questionnaire (PDQ) was developed to identify neuropathic components in patients with chronic low back pain considered nociceptive [67; 87; 97]. This tool characterizes “altered nociception” as a distinct pain phenotype in chronic low back pain. In these patients, neuropathic-like signs and symptoms reflect maladaptive nervous system functioning and central rather than peripheral pain mechanisms [94; 98]. Other advances are improving pain mechanism assessment. Sensory profile (pain-related sensory signs and symptoms) testing in 902 patients with diverse neuropathic pain etiologies identified distinct sensory profile subgroups: sensory loss (42%), thermal hyperalgesia (33%), and mechanical hyperalgesia (24%). All sensory profile subgroups occurred across etiologies, reflecting pain-related signs and symptoms that differ in neurobiologic mechanisms and treatment response [97]. With the nociceptive-neuropathic dichotomy of chronic pain mechanisms outdated, research has led to “altered nociception” as a proposed pain mechanism descriptor when chronic pain is neither nociceptive (tissue damage) or neuropathic (nerve pathology) [88; 93; 94; 99]. Maladaptive CNS neuroplasticity in chronic pain has been recognized since the early 2000s as a disease process of its own right, and translation into clinical practice is needed [100]. Recognizing this, in 2017, the International Association for the Study of Pain (IASP) introduced the term “nociplastic pain,” which is defined as “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain” [99]. Additionally, in 2021, the IASP released clinical criteria and a grading system for nociplastic pain affecting the musculoskeletal system [101].
ASSESSMENT AND DIAGNOSIS
PATIENT HISTORY Assessment of neck pain begins with a thorough history and physical exam. This information guides further diagnostics and clinical management. The top priority is to identify potentially serious underlying pathologies, termed “red flag” conditions ( Table 2 ). While infrequently encountered, neck pain-related signs or symptoms that suggest serious disease require immediate investigation and intervention. “Red flags” should be assessed throughout the evaluation process, and imaging confirmation is necessary when clinician suspicion remains [7; 102]. After obtaining basic patient demographics, a detailed history is taken [7; 8; 56; 102; 103].
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