Is Nociceptive Processing Evoked by Heat Homeostatically Regulated: A Contact-heat Evoked Potentials Study
Status:
Completed
Trial end date:
2024-03-04
Target enrollment:
Participant gender:
Summary
Homeostatic plasticity is a mechanism that stabilizes neuronal activity to prevent excessive
nervous system excitability. This mechanism can be investigated in humans by applying two
blocks of non-invasive brain stimulation, such as transcranial direct current stimulation
(tDCS).
In healthy subjects, homeostatic plasticity induction over the primary motor cortex increases
the amplitude of motor-evoked potentials after the first block of excitatory tDCS, which then
decreases after the second block of excitatory tDCS. However, this mechanism is impaired in
chronic and experimental pain, demonstrated by an increase in excitability instead of a
reversal.
The role of homeostatic plasticity mechanisms in pain is yet to be unraveled, but homeostatic
plasticity may hold an important role in pain development or persistence.
Thus, the aim of this study is to investigate if the cortical nociceptive response reflected
by contact heat stimulation (CHEPs) is regulated by homeostatic mechanisms. For this,
homeostatic plasticity will be induced in both the primary motor (M1) and sensory cortices
(S1). The first research question will explore if the contact heat evoked potentials are
homeostatically regulated and if this regulation is occurring locally or globally in the
cortex. Additionally, it will be investigated if and how capsaicin-induced nociception
interacts and effects the homeostatic response as reflected by CHEPs.