Understanding Central Pain Sensitization

This is an excellent technical explanation of Central Pain Sensitization, which results in chronic pain. This is the cause of all chronic pain, no matter its original origin. The original cause of the pain can be different, but it becomes chronic through the process of Central Sensitization, which is the same for all kinds of chronic pain.

Expanding Our Understanding of Central Sensitization – from MedScape

Pain is a complex process involving both the peripheral nervous system (PNS) and the central nervous system (CNS). Tissue injury activates the PNS, which sends signals through the spinal cord to the brain, where pain perception occurs. Evidence suggests that chronic pain results from a combination of mechanisms, including neural “memories” of previous pain.

Nociception: The Simplest Path

Acute or nociceptive pain is the everyday experience of discomfort that occurs in response to a simple insult or injury.

The mechanisms that generate nociceptive pain include transduction, which converts the external traumatic stimulus into electrical activity in specialized nociceptive primary afferent nerves.

the information is transferred to those parts of the brain that are responsible for our perception

Nociceptive pain is a relatively simple response to a relatively simple, acute stimulus. But the mechanisms responsible for nociceptive pain cannot explain phenomena, such as pain that persists despite removal or healing of the stimulus

Pain and the Inflammatory Response

This physiologic “wind-up” phenomenon starts at the skin, is potentiated along the peripheral nerves, and culminates in a hypersensitivity response from the spinal cord (dorsal horn) and brain.

Following the incision or other trauma, a cascade of hyperexcitable events occurs in the nervous system.

Thus, the major features triggering inflammatory pain include damage to the high-threshold nociceptors (peripheral sensitization), modifications and modulation of the neurons in the nervous system, and amplification of the excitability of neurons within the CNS.

This represents central sensitization and is responsible for hypersensitivity, in which areas adjacent to those of the actual injury hurt as if injured. These tissues also can respond to stimuli that ordinarily do not produce pain, such as a touch, clothing, light pressure, or a hairbrush, as if they are painful (allodynia).

Other Mechanisms in the Pain Mix

Neuropathic pain results from an insult to the nervous system

The overexcitation of the nervous system is seen to be a problem in a number of different disorders. For example, overactivation of an NMDA receptor is also associated with affective disorders, sympathetic abnormalities, and even opiate tolerance.

With other types of chronic pain, such as fibromyalgia and tension-type headache, some of the mechanisms active in inflammatory and neuropathic pain may also produce similar changes in the pain system, including central sensitization, greater excitability of the somatosensory pathways, and reductions in CNS inhibitory mechanisms.

Peripheral Sensitization

Cyclo-oxygenase (COX) also plays an important role in both peripheral and central sensitizations

The COX-2 that is expressed within the dorsal horn neurons of the spinal cord produces prostaglandins, which act on the central terminals — the presynaptic terminals of nociceptive sensory fibers — to increase transmitter release

the prostaglandins produce an increase in excitability of neurons centrally.

Brain Plasticity and Central Sensitization

Central sensitization describes changes that occur in the brain in response to repeated nerve stimulation. Following repeated stimulation, levels of neurotransmitters and brain electrical signals change as neurons develop a “memory’ for responding to those signals. Frequent stimulation results in a stronger brain memory, so that the brain will respond more rapidly and effectively when experiencing the same stimulation in the future. The resulting changes in brain wiring and response are referred to as nerve plasticity (describing the ability of the brain to change easily) or central sensitization. Thus, the brain is activated or sensitized by previous or repeated stimuli to become more excitable.

Research in animals shows that repeated exposure to a painful stimulus will change the animal’s pain threshold and result in a stronger pain response

Implications for Pain Management

Once central sensitization is established, larger doses of analgesics are required to suppress it. Preemptive analgesia, or treatment before pain progresses, may reduce the impact of all these stimuli on the CNS. Woolf[3] demonstrated that the morphine dose needed to prevent central hyperexcitability, given before brief noxious electrical stimulation in rats, was one tenth the dose required to abolish activity after it had developed.

So by “toughing it out” for too long, a “normal” pain can actually become chronic – all the more reason for early and effective intervention as soon as pain develops.

When pain occurs as a consequence of injury or surgery, the spinal cord can reach a hyperexcitable state wherein excessive pain responses occur that may persist for days or weeks (or even years)

Conclusion

Tissue injury leads to a constellation of changes in spinal excitability, which includes elevated spontaneous firing, increased response amplitude and duration, decreased threshold, enhanced discharge to repeated stimuli, and expanded receptive fields.[3] The persistence of these changes, which are collectively termed central sensitization, appears to be fundamental to the prolonged enhancement of pain sensitivity that defines chronic pain