What are the neurophysiological mechanisms in chronic low back pain (cLBP)?

Updated: Aug 22, 2018
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Answer

Answer

Peripheral mechanisms may reinforce nociception when the source of pain persists. If an ongoing pathological condition causes the peripheral pain stimulus, continuous nociception may induce repetitive stimulation and sensitization of pain receptors and nerve fibers so that they adversely respond to even mild or normal sensory stimuli (ie, allodynia). Furthermore, the liberation of algogenic and other substances from damaged tissues may induce changes in the microenvironment by means of neuroactive, biochemical, inflammatory, or vasoactive effects that activate or increase the sensitivity of nociceptors.

Peripheral-to-central processing may also modify nociception. Persistent tissue damage may stimulate afferent nerve fibers that project to internuncial neurons in the spinal cord and thereby set up neuronal loops of continuous, self-sustaining abnormal reverberating nociceptive activity. Peripheral inhibition, a mechanism for reducing the intensity of an afferent pain signal, may be impaired owing to persistently malfunctioning or diseased large peripheral myelinated fibers, which normally dampen nociception (eg, peripheral neuropathy, epidural scarring, chronic herniated disk material).

Ectopic impulse generation is a theoretical mechanism Wall and Gutnick proposed. [33] Damaged sensory nerves, affected by conditions such as neuromata or demyelinating lesions in peripheral nerves, produce aberrant signals. Deafferentation hypersensitivity also purportedly causes abnormal and chronic nociceptive firing patterns.

CNS bias of the signal may occur in the spinal cord, brainstem reticular formation, or cortex. The brainstem reticular formation acts to direct the attention of the CNS toward or away from central and peripheral stimuli. Depending on the degree of focus, or the lack thereof, the transmission of pain signals may be either enhanced or inhibited. Furthermore, cortical influences, such as cognitive and affective disorders, may affect the intensity of the processed pain signal.


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