Fatigue is one of the most pervasive symptoms present in several neurological disorders. It exerts negative influence on cognition and social interaction, greatly affecting the quality of life of individuals experiencing it. While it has engendered hundreds of investigations, a unified theory of fatigue is yet to emerge. In the current talk, I will synthesize neuroimaging evidence from healthy and neurological populations as well as evidence from pharmacological studies of fatigue and show that they point to a specific hypothesis of fatigue: the dopamine imbalance hypothesis. Specifically, in support of the dopamine imbalance hypothesis, neuroimaging studies suggest that fatigue results from the disruption of communication between the striatum and areas of the prefrontal cortex. These regions play a key role in learning and decision-making and are particularly sensitive to reward presentation, even during social behavior. Communication between the striatum and prefrontal cortex relies on dopamine, a modulatory neurotransmitter. Supporting the dopamine imbalance hypothesis, clinical trials have shown that medication that increases the amount of dopamine in the brain alleviates fatigue in several clinical populations, such as in individuals with traumatic brain injury and in cancer patients, where fatigue is also prevalent. Given the framework of dopamine imbalance, the field can move forward by testing specific aspects of the hypothesis.

We're looking forward to see you there (Frankel Leo u. 30-34) !