Mechanisms and New Targets for the Treatment of Chronic Pain

📖 The Scoop

Acute pain has a physiological protective role in preventing tissue damage. However,

pain can become chronic due to a multitude of pathophysiological states, such

as: trauma, inflammation, neural injury, viral infection, cancer, autoimmune diseases

and vascular and metabolic disorders. These pathological states can trigger alterations

of the pain pathways that can lead to hypersensitivity, and in such circumstances, pain

loses its protective role and instead, becomes persistent and debilitating affecting

seriously to the quality of life of patients.

Chronic pain is one of the most important health problems worldwide. It has

been estimated that 10% of adults are diagnosed with chronic pain each year.

However, despite the high prevalence of chronic pain, its management is still

no fully satisfactory probably due to the variety of chronic pain conditions with

different etiologies (neuropathic, visceral and musculoskeletal pain), and because

their pathophysiological mechanisms are only partially known. Therefore, there is

a huge need for new effective therapies for the control and/or prevention of the

different types of chronic pain.

Chronic pain is associated with plastic changes in pain circuits of the peripheral

and central nervous system, including changes in the expression of ion channels,

neurotransmitters and receptors. In addition, there is growing consensus on

non-neuronal mechanisms that can amplify or resolve chronic pain, and cells

traditionally thought to act just as coordinators of the inflammatory response (such

as immune and glial cells) are now accepted as real modulators of pain signaling.

In this regard, animal models of persistent pain, such as models of neuropathic and

visceral pain and models of arthritis, are helping to elucidate our understanding of the

pathogenesis of chronic pain and make it possible to test experimental treatments.

Genre: Science / General (fancy, right?)