Visceral chronic pain mechanisms

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There are differences between the nociceptive processes involved in visceral pain compared to those in somatic pain. However, it is well established that central hypersensitivity changes can occur in both types of pain. The implications are that normal sensory stimuli can be perceived in a magnified form with the result that innocuous sensations may be perceived as pain or that normally unperceived sensory stimuli become perceived. The latter dysaesthesias may be the cause of urinary frequency and urgency in the bladder pain syndromes, the urge to defecate in bowel hyper-sensitivities and sensory changes associated with ejaculation in the prostate pain syndromes. These central changes may occur as a result of an acute painful insult such as associated with infection. The insult to the organ results in activation of normally silent,

"sleeping" afferents and in changes in the receptive fields of second-order neuronal pathways within the central nervous system.

Multiple chemical changes may be implicated in these changes. N-methyl-D-aspartic acid (NMDA) is implicated in central neuromodulation as NMDA blockade can reduce the visceral hyperalgesia response in both psychophysical and electrophysiologic investigations. Nerve growth factor (NGF) has direct and indirect effects upon primary afferents with the result that the primary afferents are more sensitive to stimuli; that is, more activity is generated in them per unit of stimulus. The tachykinins may be involved in sensitization of the micturition reflex following bladder inflammation and may have a significant role in the production of neurogenic edema, such as may be seen in certain subgroups of bladder pain syndrome. Adenosine triphosphate (ATP) acting upon the P2X1 receptors and agents acting on the sodium channel receptors have also been implicated. As well as chemical changes, structural and local cell genetic changes occur and as a result the changes of sensory perception associated with the organ may persist for many months or even years after the original insult.

Recent evidence points to the existence of both visceral-visceral hyperalgesias and dysesthesias as well as visceral-muscular hyperalgesias. Central changes throughout the neuraxis may occur as a result of an insult such as acute distension or inflammation of an organ. These central changes may alter the neuro-processing of signals from organs not involved in the primary pathology so that those organs become hypersensitive (visceral-visceral hyperalgesia) or affecting muscles (visceral-muscular hyperalgesia). Visceral-visceral hyperalgesia and hypersensitivity may explain why many patients have pain and sensory abnormalities associated with multiple organs.

A number of chronic perineal/pelvic pain syndromes may involve chronic infection or inflammation that cannot be identified. The evidence that such pathologies cause chronic pain is hotly debated and there is a general trend away from diagnoses which imply undected infection or inflammation.

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