For many people, pain is a temporary warning signal—an acute alarm that sounds when an injury occurs and quietens once the body has healed. This kind of pain is protective, signaling a broken bone or a fresh surgical incision that needs attention and rest. When discomfort persists well beyond the expected recovery time, typically lasting for more than three to six months, it transitions into a different state known as chronic pain. This persistent condition represents a complex shift where the body’s alarm system remains “on,” even when the initial threat is long gone, making the experience of “always hurting” a frustrating biological reality.
Understanding the Physical Roots of Ongoing Pain
Persistent discomfort often begins with tangible, peripheral issues in the body’s tissues, which create an environment that encourages ongoing pain signaling. One common mechanism is the presence of unresolved, low-grade chronic inflammation, which can sustain the activation of pain receptors known as nociceptors. These nociceptors become hyper-responsive because of the continuous presence of pro-inflammatory chemicals. The constant chemical irritation lowers the threshold at which these receptors fire, meaning they send pain signals to the brain much more easily than they should.
Lingering effects from past physical trauma or surgery can also maintain peripheral pain through structural changes. When tissues are damaged, the body repairs them by laying down new collagen fibers in a disorganized, fibrotic manner to form scar tissue. Unlike healthy tissue, this dense, less elastic collagen can restrict the smooth gliding of muscles and fascia, creating abnormal mechanical tension.
This stiff, adhered tissue can sometimes entrap or irritate local nerves, contributing to continuous discomfort. Furthermore, issues like poor posture or repetitive strain injuries can lead to the gradual accumulation of this fibrotic tissue and put chronic stress on muscles and tendons. The resulting biomechanical compensation, where other areas of the body move incorrectly to account for the restricted area, often shifts the pain to distant, seemingly unrelated locations.
When the Nervous System Becomes Hypersensitive
For many individuals, the reason the pain continues is not the original tissue damage but a profound change within the central nervous system itself. This mechanism is termed central sensitization, a state where the spinal cord and brain become overly efficient at processing and amplifying pain signals. The distinction is important: nociception is the detection of a potential threat, while pain is the conscious experience created by the brain. In central sensitization, the pain alarm system effectively gets stuck in the “on” position, long after the initial injury has resolved.
Spinal neurons subjected to prolonged, high-intensity pain signals undergo a process known as the “wind-up” phenomenon. This wind-up describes the progressive increase in the excitability of these neurons, causing them to fire more frequently and intensely in response to subsequent stimuli. This change involves molecular alterations that strengthen the synaptic connections that transmit pain. The nervous system learns the pain pathway so well that it becomes overly responsive, a form of maladaptive neuroplasticity.
This heightened state of reactivity results in two common clinical signs of chronic pain: hyperalgesia and allodynia. Hyperalgesia is the experience of an exaggerated pain response to a mildly painful stimulus. Allodynia occurs when a normally non-painful stimulus, such as light touch or the gentle pressure of clothing, is perceived as painful. This demonstrates that the brain and spinal cord are interpreting non-threatening input as danger.
The Interplay of Emotional Health and Persistent Discomfort
The pain experience is deeply intertwined with emotional and mental states, which can significantly amplify the intensity and persistence of physical discomfort. Chronic pain and emotional health issues like anxiety and depression exist in a bidirectional relationship, where one often feeds into the other. The brain regions involved in processing pain, such as the prefrontal cortex and amygdala, are the same areas that regulate mood and emotion. Chronic stress serves as a powerful modulator of the pain system through the hypothalamic-pituitary-adrenal (HPA) axis, which governs the body’s stress response.
Sustained exposure to stressors leads to the release of stress hormones, including cortisol. While cortisol is a potent anti-inflammatory hormone in the short term, chronic stress can lead to HPA axis dysregulation. This dysregulation can impair cortisol’s ability to suppress inflammation, allowing pro-inflammatory cytokines to persist and sensitize the nervous system further. High levels of stress hormones also increase the overall nervous system arousal, which effectively lowers the pain threshold.
Poor sleep quality, which is common in chronic pain, further exacerbates this cycle. Inadequate sleep impairs the body’s natural repair processes and interferes with the central nervous system’s ability to modulate pain signals. This combination of poor sleep, emotional distress, and nervous system hypersensitivity maintains and intensifies the experience of persistent discomfort.