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Books on the topic 'Spinal cord computational model'

Author: Grafiati
Published: 10 March 2023

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1

National Consensus Conference on Catastrophic Illness and Injury (1989 Atlanta, Ga.). Spinal cord injury: The model. [S.l: s.n.], 1990.

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2

Chen, Hsiao-Yu. Developing a model of spinal cord injury rehabilitation nursing using Grounded Theoryy. [S.l: The Author], 2004.

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3

Joshi, Mital. Development and characterization of a graded, in vivo, compressive, murine model of spinal cord injury. Ottawa: National Library of Canada, 2000.

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4

Scheumann, Johannes. Staged approach prevents spinal cord injury in hybrid surgical-endovascular thoracoabdominal aortic aneurysm repair: An experimental model. [S.l: s.n.], 2014.

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5

Taehakkyo, Yŏnse. Noe, ch'ŏksu sonsang model esŏ chungch'u sin'gyŏng chaesaeng ŭl wihan chulgi sep'o rŭl iyong han tamyŏnjŏk ch'iryo kisul ŭi kaebal =: The multidisciplinary therapeutic strategies for CNS regeneration with stem cell transplantation in brain and spinal cord injury model. [Seoul]: Pogŏn Pokchibu, 2007.

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6

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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7

Becker, Catherina G., and Thomas Becker, eds. Model Organisms in Spinal Cord Regeneration. Wiley, 2006. http://dx.doi.org/10.1002/9783527610365.

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8

Model organisms in spinal cord regeneration. Weinheim: Wiley-VCH, 2007.

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9

(Editor), Catherina G. Becker, and Thomas Becker (Editor), eds. Model Organisms in Spinal Cord Regeneration. Wiley-VCH, 2007.

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10

Becker, Thomas, and Catherina G. Becker. Model Organisms in Spinal Cord Regeneration. Wiley & Sons, Incorporated, John, 2007.

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11

Becker, Thomas, and Catherina G. Becker. Model Organisms in Spinal Cord Regeneration. Wiley & Sons, Limited, John, 2007.

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12

Nelson, Audrey Lynn O'Brien. A MODEL FOR SPINAL CORD INJURY REHABILITATION. 1990.

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13

L, Stover S., DeLisa Joel A, and Whiteneck Gale G, eds. Spinal cord injury: Clinical outcomes from the model systems. Gaithersburg, Md: Aspen Publications, 1995.

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14

Barone, Stacey Hoffman. ADAPTATION TO SPINAL CORD INJURY (COPING, ROY ADAPTATION MODEL). 1993.

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15

Delisa, Joel A., S. L. Stover, and Gale G. Whiteneck. Spinal Cord Injury: Clinical Outcomes From the Model Systems. Aspen Publishers, 1995.

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16

Guillery, Ray. The pathways for action. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198806738.003.0003.

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Early nineteenth-century studies demonstrated, on the basis of clinical, experimental, and anatomical evidence, that a motor pathway, the corticospinal or pyramidal tract, passes from a specific area of the cortex, the precentral motor cortex, to the brainstem and spinal cord. The motor cortex can be seen as a topographic map of the movable body parts, and damage to the cortex or pathways produces correspondingly localized paralysis. However, there are a great many other pathways that link other areas of the cortex to parts of the brain active in the control of movements. These still play a puzzling role in the standard model where the control of movements focuses on cortical contributions to voluntary movements by the corticospinal pathways.
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17

Black, Sheila. The original description of central sensitization. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0040.

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Abstract:
The landmark study discussed in this chapter is ‘The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue injury’, published by Coderre and Melzack in 1992. Previous studies in this field implicate a contribution of excitatory amino acids (EAAs), specifically l-glutamate and l-aspartate, to injury-induced sensitization of nociceptive responses in the dorsal horn of the spinal cord. Repetitive stimulation of primary afferent fibres demonstrated that l-glutamate and NMDA can produce ‘wind-up’ of neuronal dorsal horn activity, and this is blocked by application of NMDA antagonists. This study uses the formalin test as a behavioural model to investigate the mechanisms underlying central sensitization and the role of EAAs, NMDA, their receptors, and their antagonists in this process.
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18

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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