The Disease of Pain

The difference 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.

The disease 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 and neurophysiology.

Phenomenologically, 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.

Neurophysiological 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.