Pain Beliefs and Intracortical Excitability During Experimental Pain

Pain is not only a sensory experience. It is also influenced by psychological, emotional, and contextual factors, including how people interpret pain and the threat they associate with movement. In the presence of pain, individuals often modify the way they move. These adaptations may be protective in the short term, but when maintained over time, they may contribute to persistent movement avoidance and disability.

Within the fear-avoidance framework, kinesiophobia, or fear of movement, is considered an important factor in the relationship between pain, movement, and disability. Individuals with higher kinesiophobia may perceive movement as threatening or potentially harmful. This may influence not only motor behavior, but also the way the nervous system prepares and controls movement. However, the neurophysiological mechanisms linking pain-related beliefs, experimental pain, and motor control remain incompletely understood.

The primary motor cortex is a key brain region involved in voluntary movement. Its excitability can be assessed using transcranial magnetic stimulation, a non-invasive brain stimulation technique. When applied over the primary motor cortex, transcranial magnetic stimulation can evoke motor responses that are recorded from a target muscle using surface electromyography. These responses provide information about corticospinal excitability and about intracortical inhibitory and facilitatory mechanisms.

Previous studies suggest that experimental pain can modify motor cortex excitability, but the direction and magnitude of these changes vary considerably between individuals. Pain-related beliefs, especially kinesiophobia, may partly explain this variability. This study therefore focuses on whether experimental pain changes intracortical excitability in the motor cortex and whether this response differs according to baseline kinesiophobia.

The main objective is to quantify changes in short-interval intracortical inhibition before and during experimental pain induced by topical capsaicin, with particular attention to whether these changes vary according to the participant's baseline level of kinesiophobia. Short-interval intracortical inhibition is used as the primary neurophysiological measure because it reflects inhibitory activity within the motor cortex.

Secondary objectives are to characterize other markers of motor cortex excitability during experimental pain. These include long-interval intracortical inhibition, intracortical facilitation, and corticospinal excitability assessed using input-output recruitment curves. These complementary measures are included to provide a broader characterization of inhibitory, facilitatory, and corticospinal responses to experimental pain.

Healthy adults will complete one experimental session. At the beginning of the session, participants will complete questionnaires assessing pain-related beliefs, including kinesiophobia. Baseline neurophysiological assessments will then be performed using transcranial magnetic stimulation applied over the primary motor cortex, with electromyographic recordings from the first dorsal interosseous muscle of the hand.

After baseline measurements, topical capsaicin cream will be applied to the forearm to induce temporary, moderate experimental pain. Pain intensity will be monitored using a visual analog scale. Once experimental pain is established, the same transcranial magnetic stimulation assessments will be repeated.

Each participant serves as their own control, with neurophysiological measures compared between the baseline condition and the experimental pain condition. The investigators hypothesize that changes in motor cortex excitability during experimental pain will vary between individuals. This variability is expected to be partly related to kinesiophobia, with individuals reporting higher kinesiophobia showing smaller changes in motor cortex excitability during capsaicin-induced pain.

• Change in Short-Interval Intracortical Facilitation [Time frame: At baseline (before capsaicin cream application); at pain stabilization (after capsaicin cream application)]
• Change in Pain Intensity [Time frame: From baseline through completion of the experimental session, an average of 2 hours]
• Change in Intracortical Facilitation [Time frame: At baseline (before capsaicin cream application); at pain stabilization (after capsaicin cream application)]
• Change in Long-Interval Intracortical Inhibition [Time frame: At baseline (before capsaicin cream application); at pain stabilization (after capsaicin cream application)]
• Change from baseline in corticospinal excitability [Time frame: At baseline (before capsaicin cream application); at pain stabilization (after capsaicin cream application)]