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N+R_CP_vol1_e_2012_ES5

10 References 1. Freynhagen R et al. 2006 (See abstract on page 11) 2. Schmidt C et al. 2009 (See abstract on page 11) COMMENTARY Dr Bart Morlion – Leuven Centre for Algology and Pain Management, University Hospitals Leuven, Belgium Pain management can be extremely challenging. Many pain conditions can’t be classified to clear cut clinical categories. In my experience, especially chronic pain patients often suffer from mixed pain. Different pathophysiological mechanisms interplay. Moreover, in our chronic pain patients, the affective and evaluative dimensions of pain outgrow the sensory-discriminative dimensions, increasing the complexity for the physician and the suffering for the patient. Clinically, signs and symptoms of neuropathic pain are often present but not always assessed. Attention to detail is an important issue in pain management. By improving awareness and education on the issues of neuropathic and mixed pain, more physicians will pay attention to it. The search for the Holy Grail goes on. Magic bullets do not exist in chronic pain management. Chronic pain problems are not likely to be resolved by acute interventions. Effective pain management warrants careful titration of several powerful analgesic drugs, often leading to combination therapy. In theory, drugs targeting several receptor systems might be beneficial for our patients. They should be monitored and assessed regularly. Balancing pain relief to acceptable side effects means tightrope walking for the physician. For the benefit of our patients, more efforts are needed to shift pain management from an art to a science. Initiatives like CHANGE PAIN can contribute to these goals. Anticonvulsants were originally de- veloped for the treatment of epilepsy, and their analgesic action is thought to be related to their membrane-stabilizing effect, partly by blocking sodium channels and reduction of neuronal excitability which is often a typical feature of neuropathic pain. Newer anticonvul- sants interact with voltage-gated calcium channels to decrease exci- tatory neurotransmitter release. Tricyclic antidepressants (TCAs) in- hibit the neuronal reuptake of nor- adrenaline (NA) and serotonin (5-HT) from the synaptic cleft.The resultant increase in neurotransmitter con- centration intensifies activity in the descending inhibitory pain pathway, producing analgesia. TCAs also affect histaminergic, cholinergic, and glutaminergic neurotransmission and block sodium channels. Serotonin and noradrenaline reuptake inhibitors (SNRIs) can also produce analgesia by inhibiting pain transmission in the spinal cord by increasing levels of NA and/or 5-HT. Conclusion Improving the knowledge about the underlying pain-inducing mecha- nisms and specific mechanisms of action of current treatment options could lead to more fact-based treat- ment decision, resulting in more effective management of pain.

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