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Updated: Jun 11, 2025

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Methylphenidate reduces spatial attentional bias by modulating fronto-striatal connectivity.

Leehe Peled-Avron1,2, Maryana Daood1, Rachel Ben-Hayun3,4

  • 1School of Psychological Sciences, University of Haifa, Abba Khoushy Ave 199, Haifa, 3498838 Haifa, Israel.

Cerebral Cortex (New York, N.Y. : 1991)
|September 27, 2024
PubMed
Summary

Methylphenidate (MPH) reduces spatial attention bias by enhancing fronto-striatal connectivity, particularly involving the medial superior frontal gyrus and caudate. This mechanism may explain how dopamine agonists improve attention.

Keywords:
attention networkscaudatedopamineorienting biasprefrontal cortex

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Area of Science:

  • Neuroscience
  • Cognitive Psychology
  • Neuroimaging

Background:

  • Spatial attention bias is linked to asymmetric dopamine signaling in the striatum.
  • Dopamine agonists can reduce spatial bias, but the mechanism remains unclear.

Purpose of the Study:

  • To investigate whether methylphenidate (MPH), a dopamine agonist, modulates fronto-striatal connectivity to reduce spatial orienting bias.
  • To explore the neural mechanisms underlying MPH's effect on attention.

Main Methods:

  • 54 adults with consistent spatial bias underwent fMRI while performing the greyscales task under MPH or placebo in a double-blind design.
  • Functional connectivity and activation in fronto-striatal regions were analyzed.

Main Results:

  • MPH significantly reduced spatial bias by increasing orienting towards the non-preferred hemispace.
  • MPH increased activation in the medial superior frontal gyrus (mSFG) and its functional connectivity with the caudate nucleus when attention shifted to the non-preferred hemispace.
  • MPH decreased mSFG activation and fronto-striatal connectivity for the preferred hemispace.

Conclusions:

  • Methylphenidate modulates spatial attention bias by enhancing functional connectivity between the medial superior frontal gyrus and the caudate.
  • This fronto-striatal connectivity modulation is a potential mechanism for the therapeutic effects of dopaminergic agonists on attention deficits.