Abstract
Adjuvant analgesics are medications that do not reduce significantly an acute nociceptive pain, but may increase analgesic activity in true analgesics (nonopioid or opioid) and alone can decrease patients' perception of pain in certain circumstances, particularly in neuropathic pain. Neuropathic pain can be reduced by inhibition of sodium channels in peripheral neurons (carbamazepine, phenytoin, local anesthetics), lowering central senzitization ("wind up") in the spinal cord by blocking NMDA receptors (ketamine) or by a reduction of neuronal calcium currents (pregabaline), and by a potentiation of serotonergic and noradrenergic descendent inhibitory pathways (antidepressants inhibiting reuptake of serotonin and noradrenaline).
Newer anticonvulsants (gabapentin, pregabalin) and antidepressants (duloxetine, venlafaxin) do not show higher NNT values than the old ones ( carbamazepine and amitriptylin, respectively), but they are safer and better tolerated. Many other drugs can have adjuvant analgesic effects in pain, for example by increasing activity of analgesics (caffeine, guaifenesin), by reducing edema in brain tumours (corticoids), spasms of smooth muscles ( spasmolytics, antimuscarinics), pain in bone metastase (bisfosfonates, calcitonin, radioisotopes) or by reducing adverse pain side effects (anxiety, sleep disorders, unrest - anxiolytics, antipsychotics)