Uploaded by chronicpaincoalition on Nov 3, 2011
A new treatment target for neuropathic pain is the glia and other immunecompetent cells which in activated state are the main cause for neuropathic pain, or recently also referred to as gliopathic pain.
There is a growing body of science to persuade us to think of disparate neurologic, neuro-muscular and myofascial syn- dromes as a single class of diseases characterized by neuroin- flammation. Clinicians have long known that there are central nervous system abnormalities in people who suffer chronic pain. In a bygone era, they thought that premorbid personal- ity and characterologic predispositions were responsible for a broad range of behaviors associated with chronic pain. We now understand that "central sensitization"1 is responsible for many of the sensory, mood and movement disorders observed in a variety of neuroinflammatory diseases. There is good reason to think that activated glia mediate such disorders and play a significant role in the onset and course of neuroinflammation and neurodegeneration that exacerbate nociception and the experience of pain.
There is a rich literature on the science of glia and how many diseases are caused and exacerbated by the activation of glia, however, much of this literature is unfamiliar to physicians and their patients.
The glia-modulator palmitoylethanolamide brings glia as well as mast cells back into the phenotype of rest and reduces the stress on the nervous system leading to wind up phenomena and neuropathic pain.
Palmitoylthenanolamide is a modern therapeutic tool, evaluated in countless animal models af neuropathic pain and neuroprotection, and its proof of principle has been generated meanwhile in various clinical trials too. It is considered an important breakthrough in the treatment of neuropathic pain.
Category:
Tags:
- gliopathic pain
- neuron
- glia
- Normast
- palmitoylethanolamide
- activated
- asterocytes
- neuropathic
- dystrophy
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