Toward a more precise pain language, or should it be less precise?
Life is such precious stuff and also downright dangerous.
On the one hand, we have conducted a crusade to ask doctors to stop kidding themselves that opiates stop central pain. On the other hand, we are poised on the threshold of new drugs for nerve injury pain which block the N-type Calcium channels, with prices at around $3000.00 per dose (eg. Prialt or Ziconotide), which do appear able to treat burning dysesthesia. (see below for dysesthesias which may not be burning).
Boivie’s Paradox regarding Central Pain is that “One must loose sensation in order to be a candidate for more severe pain”. As commonplace as this is in the experience of central pain, it may merely be a model for sensory impairment. Such as in hearing, for example.
Who is the weak link in the communication between doctor and patient on the symptoms of Central Pain. This author feels it is the patient.
This is a word that gets thrown around a lot, but what does it mean, actually. Here we ask Dr. House, as it were.
More and more, the difference between regular (nociceptive) and nerve injury pain (neuropathic) refuses to declare itself. The same chemicals seem to operate in both spheres. The primary difference is in the chronicity. The growth factors from glia take over the genes of the neuron and force it to make pain exciters, and KEEP ON MAKING THEM.
The Swedish, always very good in pain theory, have suggested that excess calcium allowed across the blood brain barrier by the action of Substance P and CGRP actually induces excessive pain synapses to form by causing glia to release factors which increase the number of synapses, which in turn increases calcium flow, etc. etc.. If true, it means the pipes for sending out pain could multiply and stay multiplied.