The acute postoperative pain score correlates with the risk of developing chronic pain. An efficient postoperative pain therapy is therefore absolutely crucial. To treat acute postoperative pain, it is important to find the optimal approach in order to comply with the surgical procedure, and the patients needs. The techniques we use include continuous loco-regional procedures, systemic analgesia which can be patient controlled, and the combination of these techniques. A goal of our unit is to constantly optimise therapies used in the clinic developing new approaches.
According to a recent survey, almost 20% of the adult European population suffer from chronic pain. In almost 60%, pain lasted for more than two years and almost two thirds of the patients were unsatisfied by their analgesic treatment for either insufficient pain relief or intolerable side-effects. Plenty of evidence indicates that chronic pain of both inflammatory or neuropathic origin is to a large extent due to plastic changes in the peripheral or the central nervous system and as such often refractory to treatment with classical analgesic drugs. Important new insights into the molecular basis of the underlying maladaptive neuroplasticity have been gained in recent years. In the peripheral nervous system, quantitative and quali-tative changes in the expression of voltage-gated Na+ channels in primary sensory nerve fibers are believed to be major factors contributing to the generation and maintenance of pain.
Projects of the unit
Effects of pain modulators on peripheral nerve excitability
A recently described method for recording multiple excitability parameters of human motor nerves has been adapted to the study of sensory nerves. The median nerve is stimulated at the wrist and the antidromic compound sensory nerve action potential (SNAP) is recorded from antidromically. This method provides quite different and complementary information about nerve function, compared to conventional conduction studies. Especially, this tool enables us to explore the physiology and pathophysiology of peripheral nerves and how they are modulated by drugs.
Activity dependent changes of nociceptor excitability
Unmyelinated fibers in peripheral nerves can display activity-dependent slowing of their impulse conduction. In our unit, we investigate the mechanisms that cause this phenomenon using a computerized threshold-tracking program in a skin nerve in-vitro model of rodent. This model allows recording from functionally identified single afferent units and their specific behaviour to different forms of stimulation of the receptive field or the axon, respectively.
Mechanisms of hyperalgesia
Under physiological conditions, activation of nociceptors leads to the release of vasoactive neuropepdides (CGRP, SP) by mechano-insensitive nociceptors (also called "silent nociceptors") at the nerve endings ("neurogenic inflammation"). Activation of those nociceptors evokes hyperalgesia, e.g. a hypersensitivity to painful thermal and mechanical stimuli of the receptive fields of the injured tissue, a sign which is caused by processes in the central nervous system.
In a 'human pain model', we evoke a pain sensation in human volunteers with electrical stimulation of pain nerve fibers underneath the skin. We are interested in which way, and to what extent, pain medication modulates the development of hyperalgesia.