Ventrolateral prefrontal cortex (VLPFC) is part of a network that exerts inhibitory control over the motor cortex (MC). Recently, we demonstrated that VLPFC was more activated during imagined maximum eccentric than during imagined concentric contractions in healthy participants. This was accompanied with lower activation levels within motor regions during imagined eccentric contractions. The aim was to test a novel hypothesis of an involvement of VLPFC in contraction mode-specific modulation of force. Functional magnetic resonance imaging was used to examine differences in VLPFC and motor regions during the concentric and the eccentric phases of imagined maximum contractions in a selected sample of subjects with stroke (n = 4). The subjects were included as they exhibited disturbed modulation of force. The previously demonstrated pattern within VLPFC was evident only on the contralesional hemisphere. On the ipsilesional hemisphere, the recruitment in VLPFC was similar for both modes of contractions. The findings support a hypothesis of the involvement of VLPFC in contraction mode-specific modulation of maximum force production. A disturbance of this system might underlie the lack of contraction mode-specific modulation commonly found among stroke subjects, often expressed as an increased ratio between eccentric and concentric strength.
An intriguing quality of our brain is that when actions are imagined, corresponding brain regions are recruited as when the actions are actually performed. It has been hypothesized that the similarity between real and simulated actions depends on the nature of motor representations. Here we tested this hypothesis by examining S.D., who never used her legs but is an elite wheel chair athlete. Controls recruited motor brain regions during imagery of stair walking and frontal regions during imagery of wheel chair slalom. S.D. showed the opposite pattern. Thus, brain simulation of actions may be grounded in specific physical experiences.
Depressive symptoms may occur after Deep Brain Stimulation (DBS) in the subthalamic nucleus. This is often explained by reduced pharmacological treatment after surgery, and not as a direct effect of DBS. Pallidal DBS seems not to be associated with such side effects and have not, to our knowledge, previously been reported. We present a patient with acute depressive symptoms induced by pallidal DBS. We believe this case strengthen the hypothesis that the basal ganglia and structures involved in the functional connectome of these nucleuses play a role not only in regulation of movement but also in regulation of mood.
Ear advantage during a dichotic listening task tends to mirror speech lateralization. Previous studies in stroke patients have shown that lesions in the dominant hemisphere often seem to produce changes in ear advantage. In this study six Parkinson's disease (PD) patients treated for motor symptoms with deep brain stimulation (DBS) of the left subthalamic nucleus (STN) were tested preoperatively and at approximately 6 and 18months postoperatively with a dichotic listening task. Results show a significant decline of the right ear advantage over time. In three of the patients a right ear advantage preoperativley changed to a left ear advantage 18months postoperatively. This suggests the possibility that additional longitudinal studies of this phenomenon could serve as a model for understanding changes in indirect measures of speech lateralization in stroke patients.