Efectos del envejecimiento y la neuromodulación sobre la corteza somatomotora

Zusammenfassung

Neuronal plasticity is the ability of the central nervous system to respond to internal and external stimuli through structural and functional reorganization. However, plastic changes can also negatively interfere with brain function and behavior in some neurological conditions. This process is known as maladaptive plasticity and refers to plastic changes in the central nervous system that disrupt proper brain function. In this sense, the present doctoral thesis explores the plastic changes associated with aging and the use of neuromodulation-based techniques to reverse the maladaptive plastic changes caused by chronic pain. Specifically, the main objectives of the thesis were: 1) to examine whether aging is associated with changes in the inhibitory mechanisms associated with the processing of somatosensory information, and 2) to examine whether the self-regulation of sensorimotor activity through the training of Neurofeedback can reverse the plastic changes seen in chronic pain on motor and somatosensory cortices. To achieve these goals, three studies were conducted using EEG recording (event-related potentials and brain oscillations) and functional magnetic resonance imaging (fMRI) (studies 2 and 3 only). The first study explored the somatosensory activation phenomenon caused by repetitive tactile stimulation in healthy young and older participants. The results showed significant reductions in somatosensory activation in the middle and late stages of somatosensory information processing in older participants, suggesting reduced efficiency of inhibitory mechanisms during cognitive assessment (attention and memory processes), but not during the early coding of irrelevant and repetitive tactile stimuli. The second study demonstrated that most healthy participants were able to self-regulate sensorimotor activity through neurofeedback training, and that these plastic changes were related to increased functional connectivity between the motor and somatosensory brain areas at rest. Finally, the third study revealed that only half of the patients with chronic pain (fibromyalgia syndrome) were able to self-regulate their sensorimotor rhythm. Furthermore, the results demonstrated that good responders to neurofeedback training significantly reduced pain and increased functional connectivity of motor and somatosensory brain areas. Interestingly, those patients who learned self-regulation of sensorimotor activity were also characterized by having a lower impact of fibromyalgia and pain symptoms, as well as a better health-related quality of life compared to those who were unable to learn. In conclusion, the present doctoral thesis provides new data on the plastic changes in somatosensory processing related to aging and chronic pain, and shows that these changes could be partially reversed through neurofeedback training. Future research should further explore whether neurofeedback training could also be useful in reducing the impact of aging and pain on somatosensory processing over time.