Back pain is a major health problem costing more than $24 billion annually in this country alone. Chronic 'idiopathic' back pain, which by definition has no clinically detectable origin in terms of tissue pathology, is particularly expensive and difficult to treat. With the present lack of understanding of the physiological basis for idiopathic pain, such pains are commonly attributed by default to either ongoing, undetectable nociception or to psychosocial factors. Another, previously untested hypothesis is proposed here - that nociceptor-induced sensitization of spinal pain pathways can persist over long periods of time, and this sensitization contributes to idiopathic back pain. This hypothesis is consistent with clinical findings that idiopathic pains exist in the absence of detectable pathology, are associated with allodynia/hyperalgesia, and are relatively insensitive to opiates. The experiments proposed here will incorporate a new animal model of persistent idiopathic back pain. This model, developed and evaluated in preliminary experiments, permits testing for both behavioral and neuronal correlates of persistent sensitization of central pain pathways weeks after single or repeated periods of transient inflammation in low back tissues.
The specific aims are as follows:
Specific Aim l: To determine the persistence of low back pain following repeated transient periods of inflammation in paraspinal tissues.
Specific Aim 2 : To determine the persistence of sensitization of spinal pain pathways induced by repeated transient periods of inflammation in lumbar paraspinal tissues and to determine the correlation between sensitization and pain behaviors.
Specific Aim 3 : To determine the persistence of changes in the numbers and spatial distribution of spinal sensory neurons activated by standardized non-noxious and noxious stimuli following repeated transient periods of inflammation in lumbar paraspinal tissues and to determine the correlation between such changes and pain behaviors. All experiments will utilize adult rats subjected to transient inflammation of either lumbar paraspinal or cervical subcutaneous tissues; each will be tested behaviorally for indicators of low back pain. Experiments for Aim 2 will involve single unit recordings from functionally identified spinal neurons to test for responding to standardized somatic stimuli. Experiments for Aim 3 will use immunocytochemical methods to label neurons that express c-fos in response to activation by standardized noxious or non-noxious stimuli. Our long term objective is to understand the physiological processes responsible for persistent idiopathic low back pain and to apply that knowledge toward improved prevention and care.
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