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Neuroplastix


Change the Brain; Relieve the Pain; Transform the Person

Brain-Body Loop


The brain-body loop describes the constant connection between body and brain. Where pain is concerned it involves both the suppression of acute pain and amplification of persistent pain. It is a two way communication between the Connective Tissue System and the Nervous System.

In acute pain, the nerve cells pain processing regions of the brain fire due to input from peripheral tissue. Some of these nerve cells send signals to the spinal cord to suppress the incoming signal. There is no pain when the injured tissue is at rest. Pain is re-experienced if a person stresses the injured tissue. Higher functioning regions of the brain send signals to stop the pain and return the tissue to healing. Inflammation in the peripheral tissue gradually stops and is replaced by an anti-inflammatory response. Growth factors are released to repair the extracellular matrix and local nerve endings. Once this occurs, pain signals to the brain desist. Use of that tissue returns to normal and painless function.

The brain-body loop works quite differently when pain becomes persistent. Signals coming in from the peripheral nervous system increase in the central nervous system. This is known as wind-up. A series of events occur leading to runaway firing of nerves with or without input from the part of the body that is injured. The brain tries to suppress the signal, but it is too powerful. Brain astrocytes release inflammatory molecules. Nerve cells release more of the main pain neurotransmitter, Substance-P. Higher levels of Substance-P expand the network of pain transmitting nerves. Higher functioning areas of the brain signal to stop using that part of the body, regardless of its state of repair. Inactivity and disuse lead to loss of function and local release of more inflammatory chemicals. Substance-P is sent out to the peripheral tissues, functioning as an inflammatory substance. Local anti-inflammatory responses are overwhelmed. This results in ongoing inflammation, increased pain signals to the brain and augmentation of the brain-body loop.

© 2012 Michael Moskowitz, Marla Golden Contact