Disease of Pain
of pain as a disease and pain as a symptom is an important clinical distinction
to make for physicians and patients. The symptom of pain is an essential fact
of life and helps guide us to imobilize an injured part of the body, seek
help, and direct care. Pain is one of the most common symptoms, aiding physicians
in diagnosis and treatment. It is also disturbing enough for most people who
have it, to require some action, usually a cessation of activity. Diseases
that extinguish the ability to perceive pain can have devastating consequences.
Successful treatment aimed at the source of the pain often eliminates it.
In fact, the body has physiologic mechanisms designed to diminsh pain quickly
after most tissue injuries.
of pain, however is quite diffferent. It is the underlying condition and the
extensive pathology of that condition that distinguishes the disease of pain
from the symptom of pain. Although there are definitions of pain becoming
chronic based upon time or nerve injury or frequency of flare-ups, the best
definition views the disease process from the standpoints of phemomenology
the disease of pain represents a concatenation of biological, psychological
and social events that disrupt the life of the patient. Cascades that occur
in each area result in the experience of chronic pain. To successfully treat
chronic pain, the physician must be prepared to intervene in all three areas.
changes that occur at the peripheral injury, dorsal horn of the spinal cord
and the brain, result in the disease of pain, also known as maldynia. This
is very different from the symptom of pain, eudynia. In Maldynia, pathological
processes developing at the site of the peripheral injury include excessive
activity of sodium channels, ectopy, and recruitment of non-neceptors proximal
and distal to the site of injury. At the Dorsal Horn of the spinal cord excessive
activity of excitatory amino acids results in wind up pain, driven by the
excessive peripheral input. Wind-up is the direct product of activation and
pairing of Non-NMDA glutamate and Neurokinin-1 receptors by glutamate and
Substance P respectively. This pairing results in removal of the Magnesium
block in NMDA receptors and activation of these receptors. Subsequently Calcium
moves rapidly through calcium channels into the hyperstimulated receptor terminals
and a cascade of events sets up a vicious positive feedback loop. The loop
consists of increased release of Glutamate and Substance-P at presynaptic
terminals, increased production and placement of NMDA receptors in terminal
membranes, and increased sensitization of NMDA receptors. Wind-up pain can
happen with nociceptive pain, neuropathic pain or sympathetically maintained
pain. Wind-up pain is the central factor in the biological basis for Maldynia,
the disease of chronic pain.