Anything goes? Regulation of the neural processes underlying response inhibition in TBI patients
| Autor: | David K. Menon, Barbara J. Sahakian, Laura Moreno-López, Emmanuel Stamatakis, Anne E. Manktelow |
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| Přispěvatelé: | Sahakian, Barbara [0000-0001-7352-1745], Menon, David [0000-0002-3228-9692], Stamatakis, Emmanuel [0000-0001-6955-9601], Apollo - University of Cambridge Repository |
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Adult Male Traumatic brain injury methylphenidate Motor Activity Placebo Brain mapping 03 medical and health sciences Executive Function 0302 clinical medicine Double-Blind Method Dopamine Brain Injuries Traumatic Neural Pathways medicine Humans Pharmacology (medical) response inhibition Biological Psychiatry Default mode network Pharmacology Brain Mapping Cross-Over Studies medicine.diagnostic_test Methylphenidate traumatic brain injury functional connectivity Brain medicine.disease Crossover study Magnetic Resonance Imaging Psychiatry and Mental health Inhibition Psychological 030104 developmental biology Neurology Central Nervous System Stimulants Female Neurology (clinical) Functional magnetic resonance imaging Psychology Neuroscience 030217 neurology & neurosurgery medicine.drug |
| Popis: | Despite evidence for beneficial use of methylphenidate in response inhibition, no studies so far have investigated the effects of this drug in the neurobiology of inhibitory control in traumatic brain injury (TBI), even though impulsive behaviours are frequently reported in this patient group. We investigated the neural basis of response inhibition in a group of TBI patients using functional magnetic resonance imaging and a stop-signal paradigm. In a randomised double-blinded crossover study, the patients received either a single 30mg dose of methylphenidate or placebo and performed the stop-signal task. Activation in the right inferior frontal gyrus (RIFG), an area associated with response inhibition, was significantly lower in patients compared to healthy controls. Poor response inhibition in this group was associated with greater connectivity between the RIFG and a set of regions considered to be part of the default mode network (DMN), a finding that suggests the interplay between DMN and frontal executive networks maybe compromised. A single dose of methylphenidate rendered activity and connectivity profiles of the patients RIFG near normal. The results of this study indicate that the neural circuitry involved in response inhibition in TBI patients may be partially restored with methylphenidate. Given the known mechanisms of action of methylphenidate, the effect we observed may be due to increased dopamine and noradrenaline levels. |
| Databáze: | OpenAIRE |
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