Psychopharmacology of chronic pain

Chronic pain is a common problem. Neuropathic pain, ranging from diabetic peripheral neuropathy and postherpetic neuralgia to less well understood conditions such as fibromyalgia, affects approximately 3% of the world's population. The pathophysiology of these disorders, such as ion channel upregulation, spinal hyperexcitability, and descending facilitation, has been detailed through extensive research. Psychotropics such as antidepressants, anticonvulsants, and neuroleptics offer effective alternatives to conventional analgesics. Antidepressants typically block the reuptake of monoamines such as norepinephrine and serotonin. Increased amounts of these neurotransmitters are presumed to increase descending inhibition of nociception. Anticonvulsants possess more heterogeneity in their pharmacology. Many anticonvulsants block use-dependent sodium channels that are increased in number on damaged neurons. Other anticonvulsants modulate calcium channels required for the release of neurotransmitters at the synaptic cleft. Newer anticonvulsants affect other nociceptive components such as the γ-aminobutyric acid receptor complex, N-methyl-D-aspartate receptors, and protect neurons from free radical damage. Atypical neuroleptics can augment other medications through their actions at dopamine and serotonin receptors that likely interact with the opioid- and adreno-receptor systems. Benzodiazepines, while widely prescribed, generally cause more problems, such as cognitive impairment and physicial dependence, than benefits. However, significant pain relief can be achieved in a select group of patients.