Human Imaging Contributions
August 18, 2015 at 03:58 AM | categories: mri
Contents
1 Human imaging contributions
The literature on positron emission tomography (PET) imaging supports the dopamine (DA) hypothesis of attention-deficit/hyperactivity disorder (ADHD), but the specific details are not yet clear. Some studies support the dopamine transporter (DAT) excess hypothesis, which results in a DA deficit owing to increased reuptake of synaptic DA, whereas others suggest this is just DAT plasticity that resets density based on levels of synaptic DA, which may be low in stimulant-naïve individuals, but high in treated individuals taking methylphenidate (MPH), as a result of adaptation to treatment rather than the presence of the disorder [5].
On the basis of imaging studies, it has been hypothesized that stimulant medications may act by facilitating the engagement of a dorsal task-positive attention network and the deactivation of the ventral resting state network [6]. This may reflect in part improved filtering out of task-irrelevant stimuli by way of stimulant-mediated DA and norepinephrine (NE) release in the prefrontal cortex and anterior cingulate gyrus [1]. Recent findings from PET brain imaging studies have documented that the DA deficits in ADHD were most prominent in the ventral striatum (a crucial brain region for modulating reward and motivation) and in the midbrain (where most DA neurons are located), which highlights the relevance of the reward/motivational circuit in this disorder [7]. As a result of their ability to increase DA, stimulants appear to enhance the motivational saliency of cognitive tasks. MPH-induced DA increases modulate the perception of how interesting and engaging a task is, which may explain why stimulants improve performance of a boring task in normal healthy individuals as well as in ADHD individuals [3, 4] and why unmedicated children with ADHD are able to perform properly when the task is salient to them [2].
Acronyms
- ADHD
- attention-deficit/hyperactivity disorder
- DAT
- dopamine transporter
- DA
- dopamine
- MPH
- methylphenidate
- NE
- norepinephrine
- PET
- positron emission tomography
References
[1] A. F. T. Arnsten. Fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. J Clin Psychiatry, 67 Suppl 8:7–12, 2006.
[2] M. J. Groom, G. Scerif, P. F. Liddle, M. J. Batty, E. B. Liddle, K. L. Roberts, J. D. Cahill, M. Liotti, and C. Hollis. Effects of motivation and medication on electrophysiological markers of response inhibition in children with attention-deficit/hyperactivity disorder. Biol Psychiatry, 67(7):624–31, Apr 2010. doi: 10.1016/j.biopsych.2009.09.029.
[3] T. W. Robbins and B. J. Sahakian. ”paradoxical” effects of psychomotor stimulant drugs in hyperactive children from the standpoint of behavioural pharmacology. Neuropharmacology, 18(12):931–50, Dec 1979.
[4] B. J. Sahakian and T. W. Robbins. Are the effects of psychomotor stimulant drugs on hyperactive children really paradoxical? Med Hypotheses, 3(4):154–8, 1977.
[5] J. Swanson, R. D. Baler, and N. D. Volkow. Understanding the effects of stimulant medications on cognition in individuals with attention-deficit hyperactivity disorder: a decade of progress. Neuropsychopharmacology, 36 (1):207–26, Jan 2011. doi: 10.1038/npp.2010.160.
[6] N. D. Volkow, J. S. Fowler, G.-J. Wang, F. Telang, J. Logan, C. Wong, J. Ma, K. Pradhan, H. Benveniste, and J. M. Swanson. Methylphenidate decreased the amount of glucose needed by the brain to perform a cognitive task. PLoS One, 3(4):e2017, 2008. doi: 10.1371/journal.pone.0002017.
[7] N. D. Volkow, G.-J. Wang, S. H. Kollins, T. L. Wigal, J. H. Newcorn, F. Telang, J. S. Fowler, W. Zhu, J. Logan, Y. Ma, K. Pradhan, C. Wong, and J. M. Swanson. Evaluating dopamine reward pathway in adhd: clinical implications. JAMA, 302(10):1084–91, Sep 2009. doi: 10.1001/jama.2009. 1308.