|
Items in cart [0] |
Questions? Call 888-624-8373 |
PAPERBACK Free Resources |
||||||||||||||||
|
||||||||||||||||
The following HTML text is provided to enhance online readability. Many aspects of typography translate only awkwardly to HTML. Please use the page image as the authoritative form to ensure accuracy. were activated bilaterally (31% and 7.8%, respectively). During the late phase, these structures remained active but the hindlimb activation became bilateral. In addition, the intensity of periaqueductal gray activation increased to 20% and was joined by significant rCBF increases in the interpeduncular and paraventricular nuclei (66% and 30%, respectively), in the habenular complex (58%), anterior dorsal nucleus of the thalamus (30%), and the parietal cortex (30%) adjacent to the hindlimb cortex. The somatotopic organization of the somatosensory thalamus and the small number of neurons excited by hindlimb stimulation probably resulted in an underestimation of specific thalamic nuclei activity. Nonetheless, we detected blood flow increases in the ventral posterolateral thalamus (8.7%) and in the medial thalamus (9.0%) that did not reach statistical significance but did tend to be greater in the late phase compared with the early phase of the formalin test. These results show that specific structures known to be important in nociceptive processing and modulation are selectively activated in the awake rat during the formalin test. Activation of a structure may be related to nociception, antinociception, or both. The contralateral hindlimb cortex and midbrain periaqueductal gray received nociceptive input and were active during the early phase. In the late phase, bilateral activity was seen throughout the forebrain, with the recruitment of limbic system components, each of which has been shown to participate in mediating or modulating nocifensive behaviors. In addition to the well-known analgesic effect of periaqueductal gray stimulation, interpeduncular nucleus stimulation modulates antinociceptive circuitry in the medullary raphe nuclei ( 79 ), and stimulation of the paraventricular nucleus produces analgesia ( 80 ). Analgesia also follows the microinjection of morphine and electrical stimulation within the habenular complex ( 81 , 82 ). Activation of the cingulate cortex is consistent with the activation of one of its major inputs, the anterior dorsal thalamic nuclei, and is in accord with the limbic cortical activation seen in human PET studies. Overall, the bilateral activation of somatosensory and limbic structures agrees with 2-deoxyglucose studies of glucose uptake in rats with chronic constriction injures of the sciatic nerve ( 83 ). Here we show that rCBF analysis is useful in studying central responses to acute and chronic stimuli. The Future of Pain Imaging. This developing technology may undergo significant improvements in both spatial and temporal resolution. Currently, PET provides a quantitative, statistically reliable method for assessing the activity of large brain and brainstem regions. Hypotheses can then focus on the conditions necessary and sufficient to activate one or more regions in a group of subjects. Although it is now possible to obtain reliable and quantitative information from single subjects with PET, fMRI has the ability to focus with great precision on rCBF responses in specific regions. Working together in a complementary manner, the two procedures should help develop a more precise understanding of the functional organization of pain and nociceptive processing. This progress will be facilitated by the parallel use of animal models, allowing questions about dynamics and functional connectivity to be addressed by selective stimulation, lesion, and drug microinjection studies. The clinical impact of this effort will be apparent as we develop an understanding of how the central nervous system adapts to chronic nociceptive input and injury. The changes in nociceptive processing demonstrated at the spinal cord level in experimental animals are likely to affect nociceptive processing and hence pain at higher levels. Such studies may have an important impact on descending modulatory influences, especially in forebrain-dominated animals such as humans. Evidence has accumulated showing that peripheral injury can profoundly affect thalamic and cortical sensory processes over long periods of time ( 84 – 86 ). In some cases, these plastic changes can be correlated with pain ( 87 ). A significant minority of patients with injury or disease of the central nervous system also suffer chronic, often unremitting pain as a consequence of the central lesion(s) ( 88 ). The pathophysiology of this condition is unknown, but the methods discussed here hold the promise for better solutions to the treatment and prevention of these chronic pain conditions. 1. Melzack, R. & Casey, K. L. ( 1968 ) in The Skin Senses , eds. Kenshalo, D. R. & Thomas, C. C. ( Thomas , Springfield, IL ), pp. 423–439 . 2. Head, H. & Holmes, G. ( 1911 ) Brain 34 , 102–254 . 3. Kenshalo, D. R., Jr. , & Isensee, O. ( 1983 ) J. Neurophysiol. 50 , 1479–1496 . 4. Foltz, E. L. & White, L. E. ( 1962 ) J. Neurosurg. 19 , 89–100 . 5. Hurt, R. W. & Ballantine, H. T. ( 1973 ) Clin. Neurosurg. 21 , 334–351 . 6. Sikes, R. W. & Vogt, B. A. ( 1992 ) J. Neurophysiol. 68 , 1720–1732 . 7. Price, D. D. ( 1988 ) Psychological and Neural Mechanisms of Pain ( Raven , New York ), pp. 1–241 . 8. Gerhart, K. D. , Yezierski, R. P. , Fang, Z. R. & Willis, W. D. ( 1983 ) J. Neurophysiol. 49 , 406–423 . 9. Yezierski, R. P. , Gerhart, K. D. , Schrock, B. J. & Willis, W. D. ( 1983 ) J. Neurophysiol. 49 , 424–441 . 10. Dubner, R. , Hoffman, D. S. & Hayes, R. L. ( 1981 ) J. Neurophysiol. 46 , 444–464 . 11. Hayes, R. L. , Dubner, R. & Hoffman, D. S. ( 1981 ) J. Neurophysiol. 46 , 428–443 . 12. Basbaum, A. I. & Fields, H. L. ( 1984 ) Annu. Rev. Neurosci. 7 , 309–338 . 13. Yuan, B. , Morrow, T. J. & Casey, K. L. ( 1986 ) J. Neurosci. 6 , 3611–3617 . 14. Shin, H. C. & Chapin, J. K. ( 1990 ) Somatosens. Mot. Res. 7 , 421–434 . 15. Alloway, K. D. , Johnson, M. J. & Wallace, M. B. ( 1993 ) J. Neurophysiol. 70 , 892–908 . 16. Liu, X. B. , Honda, C. N. & Jones, E. G. ( 1995 ) J. Comp. Neurol. 352 , 69–91 . 17. Swanson, L. W. ( 1995 ) Trends Neurosci. 18 , 471–474 . 18. Cheema, S. S. , Rustioni, A. & Whitsel, B. L. ( 1984 ) J. Comp. Neurol. 225 , 276–290 . 19. Ralston, D. D. & Ralston, H. J. , III ( 1985 ) J. Comp. Neurol. 242 , 325–337 . 20. Blinkov, S. M. & Glezer, I. I. ( 1968 ) The Human Brain in Figures and Tables ( Plenum , New York ). 21. Towe, A. L. ( 1995 ) J. Brain Res. 36 , 393–398 . 22. Liu, X.-B. , Honda, C. N. & Jones, E. G. ( 1995 ) J. Comp. Neurol. 352 , 69–91 . 23. Ogawa, S. , Lee, T.-M., Kay, A. R. & Tank, D. ( 1990 ) Proc. Natl. Acad. Sci. USA 87 , 9868–9872 . 24. Roy, C. S. & Sherrington, C. S. ( 1890 ) J. Physiol. (London) 11 , 85–108 . 25. Roland, P. E. ( 1993 ) Brain Activation ( Wiley-Liss , New York ). 26. Malonek, D. & Grinvald, A. ( 1996 ) Science 272 , 551–554 . 27. Wang, G. , Tanaka, K. & Tanifuji, M. ( 1996 ) Science 272 , 1665– 1668 . 28. MacVicar, B. A. ( 1997 ) Neuroscientist 3 , 381–388 . 29. Mraovitch, S. , Calando, Y. , Pinard, E. , Pearce, W. J. & Seylaz, J. ( 1992 ) Neuroscience 49 , 451–466 . 30. Adachi, K. , Takahashi, S. , Melzer, P. , Campos, K. L. , Nelson, T. , Kennedy, C. & Sokoloff, L. ( 1994 ) Am. J. Physiol. 267 , H2155– H2162 . 31. Dirnagl, U. , Niwa, K. , Lindauer, U. & Villringer, A. ( 1994 ) Am. J. Physiol. 267 , H296–H301 . 32. Seitz, R. J. & Roland, P. E. ( 1992 ) Acta Neurol. Scand. 86 , 60–67 . 33. Auker, C. R. , Meszler, R. M. & Carpenter, D. O. ( 1983 ) J. Neurophysiol. 49 , 1504–1516 . 34. Ter-Pogossian, M. M. , Eichling, J. O. & Davis, D. O. ( 1969 ) Radiology 93 , 31–40 . 35. Fox, P. T. & Raichle, M. E. ( 1984 ) J. Neurophysiol. 51 , 1109–1120 . 36. Talairach, J. & Tournoux, A. ( 1988 ) A Coplanar Stereotaxic Atlas of the Human Brain ( Thieme , New York ). 37. Minoshima, S. , Berger, K. L. , Lee, K. S. & Mintun, M. A. ( 1992 ) J. Nucl. Med. 33 , 1579–1585 . 38. Minoshima, S. , Koeppe, R. A. , Mintun, M. A. , Berger, K. L. , Taylor, S. F. , Frey, K. A. & Kuhl, D. E. ( 1993 ) J. Nucl. Med. 34 , 322–329 .
|
|
|||||||||||||||
