Wise Young
09-27-2001, 02:13 PM
The role of neuroinflammation and neuroimmune activation in persistent pain [Topical review]
Joyce A. DeLeo and Robert P. Yezierski
Pain, 2001, 90:1-2:1-6
Manuscript received 20 December 2000 Accepted 21 December 2000;
Abstract
There is no abstract for this article. The text below is the first paragraph of text within the article.
Interest in neuroinflammation and neuroimmune activation has grown rapidly in recent years with the recognition of the role of central nervous system (CNS) inflammation and immune responses in the etiology of neurological disorders such as AIDS-associated dementia and pain, Alzheimer's disease, stroke, Parkinson's disease, traumatic brain and spinal cord injury, and demyelinating diseases such as multiple sclerosis ( Ruffolo et al., 1999). One approach to the treatment of these conditions is the implementation of putative anti-inflammatory and/or immunosuppressant strategies, which includes the use of methylprednisolone or steroids without glucocorticoid properties (the 21 aminosteroids), and synthetic glycolipid GM-1 gangliosides that ultimately result in the protection or rescuing of neurons in the penumbral region of a pathological insult. These neuroprotective strategies (with anti-inflammatory or immunosuppressant components) are presently being used to treat acute and chronic neurological diseases including: stroke, subarachnoid hemorrhage, brain and spinal cord injury, hypoxic-ischemic encephalopathy, Parkinson's, Alzheimer's and Huntington's disease, amyotropic lateral sclerosis, and diabetic and toxic neuropathies ( Wood, 2000). Since some of these conditions are also associated with persistent pain states, it is possible that there is a connection between the neurodegenerative characteristics of these central disorders and the mechanisms responsible for chronic pain.
Joyce A. DeLeo and Robert P. Yezierski
Pain, 2001, 90:1-2:1-6
Manuscript received 20 December 2000 Accepted 21 December 2000;
Abstract
There is no abstract for this article. The text below is the first paragraph of text within the article.
Interest in neuroinflammation and neuroimmune activation has grown rapidly in recent years with the recognition of the role of central nervous system (CNS) inflammation and immune responses in the etiology of neurological disorders such as AIDS-associated dementia and pain, Alzheimer's disease, stroke, Parkinson's disease, traumatic brain and spinal cord injury, and demyelinating diseases such as multiple sclerosis ( Ruffolo et al., 1999). One approach to the treatment of these conditions is the implementation of putative anti-inflammatory and/or immunosuppressant strategies, which includes the use of methylprednisolone or steroids without glucocorticoid properties (the 21 aminosteroids), and synthetic glycolipid GM-1 gangliosides that ultimately result in the protection or rescuing of neurons in the penumbral region of a pathological insult. These neuroprotective strategies (with anti-inflammatory or immunosuppressant components) are presently being used to treat acute and chronic neurological diseases including: stroke, subarachnoid hemorrhage, brain and spinal cord injury, hypoxic-ischemic encephalopathy, Parkinson's, Alzheimer's and Huntington's disease, amyotropic lateral sclerosis, and diabetic and toxic neuropathies ( Wood, 2000). Since some of these conditions are also associated with persistent pain states, it is possible that there is a connection between the neurodegenerative characteristics of these central disorders and the mechanisms responsible for chronic pain.