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Bipolar disorder (BD) affects over 1% of the population and is characterized by deficits in response inhibition. Response inhibition, a crucial component of executive functions, involves the ability to suppress or withhold a planned or ongoing response that is no longer required or appropriate in a given context. Response inhibition may be dissociated into three subcomponents: interference inhibition, action withholding, and action cancellation. These subcomponents are assessed using the hybrid response inhibition (HRI) task. Previous research has shown that inhibitory control is strongly lateralized to the right hemisphere. Specifically, the right inferior frontal gyrus (rIFG) is a key node underpinning response inhibition and might be amenable to neuromodulation using repetitive transcranial magnetic stimulation (rTMS). This proof-of-concept study aimed to investigate the effects of rTMS targeting the rIFG on response inhibition in individuals with BD and controls.
Methods
We investigated HRI performance scores in individuals with BD (n = 12) and sex-/age-matched controls (n = 12) immediately before and after intermittent theta-burst stimulation (iTBS) and continuous TBS to modulate cortical excitability of the rIFG.
Results
The response inhibition subcomponent “action withholding” was significantly improved in the HRI task following iTBS in the BD group. No other significant effects were observed in the results.
Conclusions
Our study is the first to show that iTBS to the rIFG neuromodulated a specific subcomponent of response inhibition in BD. Further research investigating the potential therapeutic effect of neuromodulation of the rIFG in BD is warranted.
Parkinson’s disease (PD) chronic L-Dopa treatment often triggers motor complications, such as L-Dopa-induced dyskinesias (LID). LID are reported to be associated with abnormal glutamatergic activity between the striatum and primary motor cortex (M1), resulting in M1 hyperactivation. Beneficial noninvasive brain stimulation (NIBS) paradigms were reported to normalize glutamatergic activity. The objective of the present study was thus to set up a NIBS paradigm in parkinsonian monkeys to investigate motor behavior under basal conditions and with L-Dopa treatment-inducing dyskinesias.
Methods:
Motor behavior was investigated in five 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) dyskinetic female Macaca fascicularis monkey models of PD, allowing us to monitor the administration of NIBS and drugs. NIBS used were inhibitory protocols, that is, cathodal transcranial direct current stimulation (c-tDCS) and continuous theta-burst stimulation (cTBS). A procedure of three weeks was developed to progressively acclimate animals to the experimental conditions, equipment and noise of c-tDCS and cTBS before stimulating them with either vehicle or L-Dopa.
Results:
One session of c-tDCS with L-Dopa yielded no effect, whereas five sessions briefly reduced LID but decreased the duration of L-Dopa anti-PD effects. cTBS alone improved (decreased) parkinsonian scores as compared to sham stimulation or vehicle alone. Two sessions of cTBS with L-Dopa decreased LID without affecting L-Dopa anti-PD effects.
Conclusion:
This is the first study testing c-tDCS and cTBS on the motor behavior of MPTP dyskinetic monkeys. As compared to medicated patients, MPTP monkeys offer the opportunity to evaluate NIBS after-effects in drug-free and LID conditions, which are critical in the search for new PD treatment.
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