Provoking and Probing Adaptive and Maladaptive Pain Neuroplasticity
Often no apparent tissue changes can explain chronic pain, and if so, there is normally no association between the extent of the pathology and the pain intensity. Hypersensitivity due to maladaptive neuroplasticity in systems processing pain input may be the underlying mechanism of unexplained chronic pain.
The mechanisms of adaptive and maladaptive pain neuroplasticity may include neuronal reorganisation, increased gain of signal transduction or transmission, altered neuronal receptor functions, or changes in glial cell (supporting cells for the neurons) activation which may occur across the pain system. Specific approaches for provoking and probing the fundamental properties of such diverse human pain mechanisms are needed for progress in the field and to be able to translate fundamental animal findings into humans.
To study dynamic characteristics of human adaptive and maladaptive pain neuroplasticity, an original conception is system identification based provocation or probing approaches.
Provoking and Probing Advantageous Neuroplasticity
In contrast to maladaptive pain neuroplasticity, many neuroplastic key features are advantageous. The neuronal downstream control from the brain to reduce the pain input from the periphery is one example of advantageous neuroplasticity. Other examples include neuroplasticity of brain structures involved in memory or learning; the capacity to store, retain and subsequently retrieve information. Within neuroscience this is one of the most studied types of advantageous neuroplasticity.
From other research areas it is well known that neuroplastic changes can be induced by different downstream and upstream modulation approaches such as stimulation of the sensory system, cognitive interventions and motor-skill training. E.g., multichannel electrical stimulation of the hearing organ (cochlea implants) can normalise the neuroplasticity of the auditory cortex caused by a hearing deficit.
Provoking and probing advantageous neuroplasticity and exploiting its dynamics in pain neuroplasticity models is a fascinating new concept.
It is our ambition to identify and modulate key features of human pain neuroplasticity leading to prevention of maladaptive neuro-plasticity and promote advantageous neuroplasticity.
We keenly believe that this can be achieved through a systematic engineering approach, including provoking, probing and modulation of the dynamic neuroplastic properties of the pain system.