_________________________________________________________________________ Neck Pain in Adults
which are relayed to the dorsal horn of the spinal cord. In the dorsal horn, primary neurons synapse with second-order nociceptive neurons. The noxious stimuli signal is sent up ascending spinal pathways to the brain. The brain interprets pain signal intensity and location, assigns meaning, activates fear or anxiety, and initiates appropriate motor responses. The brain then signals back the spinal dorsal horn, via descending pathways, to inhibit or facilitate incoming nociceptive stimuli. Thus, pain transmission signals travel up the spinal cord for processing and interpretation in the brain, which responds by pain modulation signals down descending pathways to the spinal dorsal horn. This bi-directional feedback circuit balances signaling facilitation and inhibition; normal function is maintained. Chronic Pain Pathophysiology With normal somatosensory function, pain from tissue injury or damage resolves during or before tissue healing or resolution. In contrast, chronic pain develops as somatosensory function becomes pathologic [41; 68; 69; 70; 71]. Mechanical/ inflammatory injury of peripheral sensory nerve fibers activates the function of their ion channels (e.g., sodium, calcium). This increases excitatory synaptic transmission in dorsal horn neurons and nociceptive circuits. Intense nociceptive bombardment in the dorsal horn impacts synaptic activity, where primary neurons signal second-order neurons. The bombardment induces synaptic release of excitatory amino acids and neuropeptides (e.g., substance P, glutamate), which bind post-synaptic receptors of second-order neurons in the dorsal horn. In altered second-order spinal cord neurons, excessive N -methyl-D-aspartate (NMDA) and α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) signaling reflects a hyperexcitability state that amplifies sensory responses; central sensitization develops. In this state, brainstem control of descending pain modulatory pathways becomes impaired; balance between descending inhibition and excitation is altered, and excitation dominates. Pain perception is facilitated by ascending pain pathway sensitization and disinhibited by impaired descending inhibitory. The brain now receives altered, abnormal sensory messages. Pain Modulation Nociceptor activation does not necessarily produce pain. Some persons with marked spinal pathology are asymptomatic, while others experience severe, chronic, disabling pain without apparent structural pathology. Patient responses to analgesic therapy also vary substantially. A key factor in this pain response variability is how the pain message is modulated in the central nervous system (CNS). The pain signal can be augmented or diminished as it ascends from its dorsal horn entry point to the CNS and arrives in the cerebral cortex (which mediates awareness). An assumed correlation between peripheral tissue pathology and pain intensity is subject to modification and interference in the
various pathways [69; 72; 73; 74]. Without treatment, CNS pain modulation abnormalities persist and may become refractory to intervention [75; 76]. Transitions in Chronic Whiplash Pain Post-whiplash pain is the most-studied chronic neck pain condition, with cervical facet joints key pain contributors. Facet joint structure may pathologize as chronic post-whiplash pain develops [50]. Following acute tearing of the facet joint capsule or stretching beyond its limits, the joints fill with fluid and distend, causing pain and limiting cervical range of motion. In the subacute phase, inflammatory changes develop from vasodilation and invasion of inflammatory cytokines, promoting degeneration. Laxity from joint capsule hypertrophy and distention impinges a nerve root exiting the spinal canal or neuroforamen; radiating symptoms or radiculopathy develops. Chronic inflammation leads to central sensitization, with pain stimuli thresholds decreasing and pain signal firing rates increasing. Facet capsule fibrosis and osteophyte formation further restrict segmental motion. Psychological Factors in Chronic Neck Pain Psychological factors contribute to the development of chronic neck pain and disability in some patients. In the fear-avoidance model, key psychological processes, including emotions, cognitions, attention, and behaviors, converge to form fear-avoidance beliefs and behaviors, which become drivers of pain-related disability. Fear develops in response to negative cognitions, exaggerating both the potential threat of pain and the negative interpretation of pain-related health information. Pain catastrophizing refers to this exaggerated set of pain-related cognitions, often appearing as anticipation of the worst possible outcome [77; 78]. Fear focuses the attention on pain and related symptoms, leading to a hypervigilant state and avoidance of activities (e.g., occupational, social) and movements (e.g., walking, physical therapy) perceived to possibly worsen pain [79]. Evidence connects pain, stress response, and prognosis following whiplash. After whiplash injury, the presence of hyperalgesia (amplified pain sensitivity), stress-related symptoms, and pain catastrophizing is linked to higher initial pain and disability, and strongly predicts poor functional recovery [80]. Hyperalgesia is a consequence of inflammatory processes. Intense stress exposure (as with acute trauma) can release cytokines that signal infection or inflammation, and a relationship between catastrophizing and inflammation has been identified [81]. Hyperalgesia and stress-mediated responses/symptoms in whiplash-injured patients with poor prognosis suggests contribution of inflammatory processes [82; 83]. Other evidence expands the understanding of how psychological factors may influence pain. High levels of perceived injustice following whiplash injury have been associated with prolonged work disability at follow-up, suggesting a modifiable risk factor
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