In contrast, systems plasticity (when new CNS neuronal connections are formed in response to nerve injury) takes place over the months and years following nerve injury and is often irreversible. When we recognize NPP and intervene before system neuroplastic changes occur, it may be possible to prevent pain from becoming chronic (TABLE 15). In cases of nerve injury, researchers have long suspected that early and aggressive pain treatment within the first few months that may include sympathetic and peripheral neural blockade reduces the likelihood that the patient will have chronic pain.6,7
It’s time to update our understanding of pain
The International Association for the Study of Pain (IASP)—a group of health care providers, scientists, and policymakers seeking to improve pain relief worldwide—notes in its definition of pain that the complaint, “I hurt” does not necessarily imply that there is a painful stimulus in the form of tissue injury.8 Yet most of us have been taught to think of pain solely as the result of tissue pathology, and we assume that emotional factors merely modify how the physical damage is perceived. This traditional concept of pain is incomplete. It leads clinicians to misdiagnose the cause of pain, initiate expensive and unnecessary treatment, engage in well-meaning but misguided prescribing behavior, and miss opportunities to help patients.
From periphery to brain: The process of nociceptive pain1-4
The process by which noxious stimuli lead to the experience of sensory pain consists of 4 steps:
In transduction, nociceptors containing special molecular proteins respond to noxious modalities, such as thermal, mechanical, or chemical stimuli, and trigger nerve impulses in the nociceptive nerve fibers (nerves dedicated to pain sensation).
During transmission—the second stage of the process—information from the nociceptors in the periphery (skin, muscle, viscera) is relayed to the spinal cord mainly by 2 types of nociceptive neurons: C-fibers and A delta (Aδ) fibers. Both approach the spinal cord in a peripheral nerve and then enter the spinal cord in the dorsal root entry zone. Because Aδ fibers are thinly myelinated, they send impulses faster than unmyelinated C fibers. This is why when injury occurs, we first feel sharp, acute pain that then slowly diffuses into a duller ache.
Once the incoming signal is transmitted to the CNS at the spinal cord, primary afferent neurons synapse on second order neurons. From there, information travels on to the thalamus via multiple neurons that have the capacity to change their response patterns when activity of nociceptive fibers is sustained (as occurs in the setting of a tissue or nerve injury and perhaps in the setting of psychological trauma). This is known as modulation of the incoming nociceptive stimulus. During this step of the process, stimuli can be amplified, suppressed, or even transformed from one type to another (eg, a light touch can be modulated in such a way that it will be perceived as a burning sensation). Also, it is this step that is affected by many medications, by intrathecal drug infusions, and by spinal neurostimulators.
In perception, the thalamus then directs the pain sensation to multiple brain centers. At this step, the stimulus is finally consciously perceived as pain by the individual.
Cortical pain circuits can be activated without physical input (ie, no tissue damage, noxious stimuli, or nerve injury). This becomes important in understanding pain syndromes, such as fibromyalgia.