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Central nervous system injury inflammatory response

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. [Pg.459]

NO has complex roles in immunological host responses against viruses, and especially against HIV-1 infection. In HIV-1 infection, NO cannot be rigidly classified as an anti-inflammatory or proinflammatory molecule, but it can be deemed a true inflammatory mediator. Many studies support a proviral effect of NO in HIV-1 infection, mainly based on stimulation of viral replication, and on toxic effects on various cells, including central nervous system cells, via oxidative injury that may cause cellular and organ dysfunction, and immunosuppression and immunopathology, especially in the central nervous system. [Pg.23]

Zhang J, Rivest S (2001) Anti-inflammatory effects of prostaglanding E2 in the central nervous system in response to brain injury and drculating Upopolysaccharide. J Neurochem 76 855-864 Zipp F, Aktas O (2006) The brain as a target of inflammation common pathways link inflammatory and neurodegenerative diseases. Trends Neurosci 29 518-527... [Pg.382]

There are several members of the family of cytokines that play important roles in the inflammatory responses in the central and peripheral nervous systems. Certain cytokines when secreted following injury to the spinal cord, the dorsal root ganglion (DRG), or other injured nerves lead to pain generated from abnormal spontaneous activity in the injured nerve or in compressed or inflamed DRGs. These cytokines are small proteins secreted by cells that control communication among cells. The subgroups include lymphokines, monokines, chemok-ines, and interleukins. The network and interactions of cytokines are extremely complicated, but the family members associated with inflammatory pain seem to be largely limited to IL-ip, IL-6, and TNFa. [Pg.434]


See other pages where Central nervous system injury inflammatory response is mentioned: [Pg.937]    [Pg.347]    [Pg.59]    [Pg.359]    [Pg.232]    [Pg.61]    [Pg.465]    [Pg.123]    [Pg.193]    [Pg.337]    [Pg.16]    [Pg.51]    [Pg.106]   
See also in sourсe #XX -- [ Pg.661 , Pg.662 ]

See also in sourсe #XX -- [ Pg.661 ]




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Central nervous system injury

Central nervous system response

Inflammatory response

Inflammatory system

Nervous system injury

Responsibilities Systems

Responsive systems

System response

System responsiveness

Systemic response

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