Download Annual Review of Psychology, vol 51 2000 by Janet T. Spence PDF

By Janet T. Spence

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Such exaggerated pain states naturally occur in situations involving infection, inflammation, or trauma of the skin, of peripheral nerves, and of the central nervous system itself. Implications for human pain conditions are discussed. 00 29 30 WATKINS Ⅲ MAIER INTRODUCTION Annu. Rev. Psychol. 51:29-57. org by Ball State University on 01/08/09. For personal use only. Interactions between the central nervous system and the body have generally been regarded as involving regulation of peripheral processes by the brain.

Indeed, TNF has been linked to demyelination and degeneration of axons (Redford et al 1995, Said & Hontebeyrie-Joskowicz 1992), leading to the suggestion that peripheral demyelinating neuropathies and multiple sclerosis may be linked to TNF release (Myers et al 1999). Such findings in laboratory animals again suggest examination of human conditions involving infection, inflammation, and damage involving or contacting peripheral sensory nerves. Some of these sites of proinflammatory cytokine production may be less than obvious.

Although no studies of animal models of arthritis have yet examined spinal cord glial activation, the prolonged sensory pain fiber activity known to be induced by such conditions would cause prolonged release of pain transmitters into the spinal cord dorsal horns. As noted previously, this pattern of effects predicts glial activation at spinal levels. In none of these cases has the effect Annu. Rev. Psychol. 51:29-57. org by Ball State University on 01/08/09. For personal use only. 48 WATKINS Ⅲ MAIER of drugs that disrupt glial function or specific glial mediators yet been tested.

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