Neuropathic pain is pain initiated or caused by a primary lesion or “dysfunction” in the nervous system. A more precise and practical definition includes those presentations in which there is an identifiable nervous system lesion, and excludes or recategorises those presentations in which the pain is considered to be due to central sensitisation.
Neuropathic pain is different to nociceptive pain, which is pain derived from threatened or actual tissue damage. Nociceptive pain can be further divided into somatic pain (pain from the musculoskeletal system) and visceral pain (pain from “viscera” such as liver, kidney, heart, intestine etc.).
Persistent nociceptive pain is accompanied by alteration in central nervous system excitability, called central sensitisation. Abnormal manifestations of such processes include severe persistent pain accompanied by pain descriptors similar to those of neuropathic pain states. This is the moot point concerning the definition of neuropathic pain. Of further confusion is the realisation that the mechanism of tissue damage can also damage nerves, and thus, persistent pain could have dual mechanisms in any case.
Neuropathic pain is characterised by particular pain descriptors. The most common are burning, shooting and shooting. Dysaesthesias, such as formication, and aberrant pain perception, such as abnormally heightened response to light stroking (brush allodynia) increase the probability of a clinical presentation being labelled neuropathic pain.
When vascular symptoms complicate the pain picture the terms Complex Regional Pain Syndrome (CRPS) type 1 (formerly known as reflex sympathetic dystrophy) and type 2 (formerly known as causalgia) are also used.
In CRPS type 2, where the definition demands nervous system damage, the association with neuropathic pain is clear if the pain descriptors are right. However, in CRPS type 1, where there is no clear nerve injury, the pathophysiology of the pain is not necessarily neuropathic, and could be considered under broader terms such as central sensitisation or disinhibition.
Treatment of neuropathic pain
1. General concepts
The first priority is to manage the underlying disease process causing the neuropathic pain. The second priority is to administer symptom control measures. These therapies should be run in parallel.
a. General Concepts
Neuropathic pain seems to be derived from multiple pathophysiological mechanisms. Thus, one drug does not fit all clinical presentations of neuropathic pain, and some patients may require more than one drug to obtain adequate pain relief.
It is essential to individualise the pharmacotherapy, as the effect, side-effect and toxicity profile for each drug shows marked variation from person to person.
Thus, each drug trialled should not be abandoned as being ineffective until the maximum possible dose that does not produce significant side-effects is reached.
It is not uncommon to see patients, labelled as pharmacotherapy non-responders, who have had inadequate trials of medication. To prevent this, the clinician needs to titrate doses of single medications so that the attainment of either pain relief or side-effects is clearly defined.
Once adequate pain relief is obtained, the dose should be maintained for a time that can be settled by negotiation with the patient. After some weeks or months it is not unreasonable to observe the effects of reduced dosage. In some instances, however, the therapy may need to be continued for years.
b. Medication prescription guidelines
Start with one medication
Commence with the lowest possible dose
Increase dosage slowly, such as increasing each unit each 3-7 days, and
Continue increasing the dose until a definite end-point is reached, be it adequate pain relief or intolerable side-effects. Where relevant, monitor for toxic serum levels.