The role of the striatum in impulsivity and self-awareness: neuropsychological and functional neuroimaging approaches

Complex cognitive functions require interactions within and between different brain regions by direct anatomical connections or synchronous activation. As such, damage to any region involved in a cognitive process has the potential to affect its function. Impulsivity is a multifaceted construct that, when dysfunctional, contributes to many psychiatric conditions. The striatum has been implicated as an integral part of the neural circuitry of impulsivity. The current work aims to contribute to the understanding of neural dysfunction underlying disorders of impulsivity by examining how striatal damage affects impulsive behavior. It also aims to improve our understanding of whether neural processes involved in impulsivity are also involved in maintaining awareness of one's thoughts and actions. No studies have systematically examined the extent to which damage to the striatum correlates with both changes in impulsive behavior and changes in self-awareness of impulsive personality.

In the first experiment, I examined the effects of focal unilateral striatal damage on self-awareness of impulsivity and other personality traits. I predicted that participants with striatal damage (SD) would have less self-awareness of changes in impulsivity and other personality traits after brain damage, as compared to brain damage comparisons (BDC), due to indirect disruption of neural networks responsible for self-referential processing. I tested this prediction using self and collateral versions of the Barratt Impulsiveness scale (BIS) and the Iowa Scales of Personality Change. In partial support of my hypothesis, there were mean differences in self- and collateral-reported impulsivity on the BIS, with self ratings higher than collateral ratings in the SD group. There were no significant differences in the correlations between self- and collateral-reports for current impulsivity, change in impulsivity, or change in other personality traits. In the second experiment, I examined the effects of focal unilateral striatal damage on laboratory measures of impulsivity. I predicted that participants with striatal damage would exhibit lower levels impulsivity than brain damaged comparisons due to structural loss of regions involved in reward/motivation and motor activity. I tested this using impulsive action tasks (Go/NoGo and Stop Signal Tasks) and impulsive choice tasks (Delay and Probability Discounting). In contrast to my hypothesis, SD participants did not exhibit less impulsive action or impulsive choice than BDC participants. In the third experiment, I examined the effects of focal unilateral striatal damage on the integrity of frontostriatal resting state functional connectivity. I predicted that participants with striatal damage would exhibit alterations in functional connectivity between the remaining regions of the frontostriatal network. I tested this by comparing the strength of functional connectivity of the caudate head and ventromedial prefrontal cortex. While my hypothesis was not directly supported, the data showed interesting trends that warrant further exploration. These included stronger caudate-vmPFC resting state functional connectivity on the lesion side, and weaker functional connectivity on the non-lesioned side in striatal participants compared to brain damaged comparisons.

Together, these experiments suggest that although unilateral striatal damage does not appear to affect subjective reports or laboratory measures of impulsivity, it may affect the underlying neural networks utilized by the striatum, as evidenced by changes in frontostriatal resting state functional connectivity. This work extends our understanding of the neurobiology of impulsive behavior and self-awareness, at systems level, and may help pave the way for treatments of those with brain injury, such as traumatic brain injury and stroke patients, or psychiatric disorders involving impulsivity.