Ítem


Neuroplasticity of Supraspinal Structures Associated with Pathological Pain

Peripheral nerve and spinal cord injuries, along with other painful syndromes such as fibromyalgia, diabetic neuropathy, chemotherapeutic neuropathy, trigeminal neuralgia, complex regional pain syndrome, and/or irritable bowel syndrome, cause several neuroplasticity changes in the nervous system along its entire axis affecting the different neuronal nuclei. This paper reviews these changes, focusing on the supraspinal structures that are involved in the modulation and processing of pain, including the periaqueductal gray matter, red nucleus, locus coeruleus, rostral ventromedial medulla, thalamus, hypothalamus, basal ganglia, cerebellum, habenula, primary and secondary somatosensory cortex, motor cortex, mammillary bodies, hippocampus, septum, amygdala, cingulated and prefrontal cortex. Hyperexcitability caused by the modification of postsynaptic receptor expression, central sensitization and potentiation of presynaptic delivery of neurotransmitters, as well as the reduction of inhibitory inputs, changes in dendritic spine, neural circuit remodeling, alteration of gray matter, and upregulation of pro-inflammatory mediators (e.g. cytokines) by reactivation of astrocytes and microglial cells are the main functional, structural and molecular neuroplasticity changes observed in the above supraspinal structures, associated with pathological pain. Studying these changes in greater depth may lead to the implementation and improvement of new therapeutic strategies against pathological pain

© Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 2017, vol. 300, núm. 8, p. 1481-1501

Wiley

Autor: Boadas i Vaello, Pere
Homs, Judit
Reina de la Torre, Francisco
Carrera Burgaya, Ana
Verdú Navarro, Enrique
Resum: Peripheral nerve and spinal cord injuries, along with other painful syndromes such as fibromyalgia, diabetic neuropathy, chemotherapeutic neuropathy, trigeminal neuralgia, complex regional pain syndrome, and/or irritable bowel syndrome, cause several neuroplasticity changes in the nervous system along its entire axis affecting the different neuronal nuclei. This paper reviews these changes, focusing on the supraspinal structures that are involved in the modulation and processing of pain, including the periaqueductal gray matter, red nucleus, locus coeruleus, rostral ventromedial medulla, thalamus, hypothalamus, basal ganglia, cerebellum, habenula, primary and secondary somatosensory cortex, motor cortex, mammillary bodies, hippocampus, septum, amygdala, cingulated and prefrontal cortex. Hyperexcitability caused by the modification of postsynaptic receptor expression, central sensitization and potentiation of presynaptic delivery of neurotransmitters, as well as the reduction of inhibitory inputs, changes in dendritic spine, neural circuit remodeling, alteration of gray matter, and upregulation of pro-inflammatory mediators (e.g. cytokines) by reactivation of astrocytes and microglial cells are the main functional, structural and molecular neuroplasticity changes observed in the above supraspinal structures, associated with pathological pain. Studying these changes in greater depth may lead to the implementation and improvement of new therapeutic strategies against pathological pain
Format: application/pdf
Cita: 026305
ISSN: 1932-8486 (versió paper)
1932-8494 (versió electrònica)
Accés al document: http://hdl.handle.net/10256/13745
Llenguatge: eng
Editor: Wiley
Col·lecció: Versió postprint del document publicat a: http://dx.doi.org/10.1002/ar.23587
Articles publicats (D-CM)
És part de: © Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 2017, vol. 300, núm. 8, p. 1481-1501
Drets: Tots els drets reservats
Matèria: Dolor
Pain
Neuroplasticitat
Neuroplasticity
Títol: Neuroplasticity of Supraspinal Structures Associated with Pathological Pain
Tipus: info:eu-repo/semantics/article
Repositori: DUGiDocs

Matèries

Autors