Treatments for Neuropathic Pain: Up-to-Date Evidence and Recommendations
Highlights
- The International Association for the Study of Pain (IASP) defines NeP as 'pain caused by a lesion or disease of the somatosensory nervous system'. It is divided into central or peripheral NeP according to the site of the lesion (View Highlight)
- NeP is now regarded as a distinct clinical condition; patients present with similar hallmark characteristics: allodynia, hyperalgesia, and dysaesthesia (View Highlight)
- Choice of amitriptyline, duloxetine, gabapentin, or pregabalin as initial treatment (View Highlight)
- Sustained-release oxycodone and morphine are the opioids most studied. Long-term use may be associated with abuse, cognitive impairment, and endocrine and immunological changes (View Highlight)
- The tertiary amine TCAs (amitriptyline, imipramine, clomipramine) are not recommended at doses greater than 75 mg day−1 in >65 yr because of major anticholinergic and sedative adverse effects, and an increased risk of sudden cardiac death at doses >100 mg day−1 (View Highlight)
- The onset of therapeutic effects of antidepressants is delayed. Hence their action is thought to be via long-term molecular and neural plasticity, recruiting downstream mechanisms such as chromatin regulation, gene expression, recruitment of neurotrophins, and stimulating neurogenesis (View Highlight)
- The action of antidepressant drugs on noradrenaline is a crucial component in the treatment of NeP. There are two proposed mechanisms for this: recruitment of descending noradrenergic pathways and peripheral noradrenaline recruitment from sympathetic nerves in the dorsal root ganglia. They may also act indirectly on proinflammatory cytokines (View Highlight)