Pain is pain caused by damage to actual nerve tissue. This can involve demyelination,
transection, pressure necrosis, entrapment, neuroma formation, inflammatory
nerve damage, infectious injury, infarction, autoimmune damage and sympathetic
coupling. This type of pain is usually quite severe and often involves non-dermatomal
patterns due to collateral nerve ectopy induction.
nerve stimulation occurs by two distinct processes, transduction and stimulus
encoding. Transduction involves the propagation of ion flows through transmembrane
channels that stimulate transmembrane electrical currents at axon end terminals.
The second process is stimulus encoding, which involves a cascade of stimuli
that builds up to cross a threshold, causing repetitive nerve cell firing.
Stimulus encoding involves generation of extra sodium channels in the damaged
end of the nerve axons.
is an important factor in Neuropathic pain. Ectopic firing of nerve cells
occurs when nerve fibers that normally do not transmit pain, A-ß touch
fibers, begin to be pain responsive. This sensitization occurs when Dorsal
Root Ganglion Cells become hypersensitive to nerve pain impulses. This is
further complicated by wind-up in the Dorsal Horn Cell bodies through
sprouting of A-ß mechanical and touch fibers into the superficial areas
of the Dorsal Horn and activation of Glutamate specific postsynaptic NMDA
receptors located there . Virtually all sustained neuropathic pain will cause
central sensitization (central pain). If touch fibers alone are affected the
patient experiences paresthesias only, but if their is recruiting of local
pain transmitting nerves (C fiber and A-Delta fibers), hyperpathia and allodynia
are experienced, with paroxysms of electrical or stabbing pain, quite prominent.
These paroxysms may represent stimulus encoding thresholds being exceeded
in bursts of activity.
for neuropathic pain can be as complex as the numerous underlying causes of
this pain. If there is surgically correctable disease, the pressure on the
nerve should be addressed and removed. If, on the other hand, the patient
has a demyelinating illness, treatment with tricyclic analgesics may be the
best place to start. In general, for non-progressive, neuropathic pain a combination
of opioids at higher doses and synaptic membrane stabilization makes the most
sense. Opioids need to be used at higher doses, because 65%-75% of opioid
receptors are pre-synaptically located and these are damaged in damaged nerves.
The remaining post-synaptic receptors need to be saturated and CNS wind-up,
caused by NMDA receptor proliferation, will induce opioid tolerance. Stabilizing
synaptic membranes is most often accomplished with a variety of medications,
such as Lidocaine, Anti Epilepsy Drugs, Amantadine, Mexillitine, NMDA receptor
blocking drugs and possibly tricyclic analgesics. If there is an inflammatory
component to the neuropathic pain from irritation of the nerve and subsequent
swelling of the injured nerve in a restrictive space, NSAID treatment can
be helpful. Alpha 2 agonists in an intrathecal pump may be quite effective,
but are not effective orally. Implantation of an intrathecal pump, after failure
of oral therapy, may be very helpful due to low side effects, avoidance of
first pass metabolism, and novel combinations of opioids, local anesthetics,
Clonidine and/or Baclofen. Blocks with a combination of local anesthetic and
steroids can provide diagnostic information and therapeutic relief.