A state of persistent, pathological hyperexcitability within the central nervous system, involving the spinal cord and brain, that results in an amplified response to both painful and non-painful stimuli. This neurological phenomenon is characterized by an abnormal increase in the gain of sensory processing, leading to allodynia (pain from non-painful stimuli) and hyperalgesia (increased pain from painful stimuli). It is a key mechanism underlying various chronic pain syndromes and can be exacerbated by hormonal and inflammatory dysregulation.
Origin
This clinical term originated in the field of pain research and neurophysiology, describing a change in the functional properties of neurons in the central nervous system following prolonged or intense peripheral noxious input. The concept of “sensitization” highlights the heightened state of neural responsiveness. Understanding this phenomenon is critical for moving beyond peripheral interventions to address the central neurological drivers of chronic pain.
Mechanism
The underlying mechanism involves long-term potentiation-like changes in the synaptic connections of the dorsal horn neurons in the spinal cord and higher brain centers. This is driven by the sustained release of excitatory neurotransmitters, such as glutamate, and the activation of NMDA receptors, which ultimately leads to an increased influx of calcium and subsequent gene expression changes. Hormonal imbalances, particularly low levels of inhibitory steroids like progesterone, can impair the central nervous system’s ability to dampen this excessive neural activity, perpetuating the sensitized state.
Prioritizing restorative sleep is the most effective intervention for pain, as it recalibrates the hormonal and neural systems that govern pain perception.
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