The DOI matches its Crossref record; 66 of the 69 references it cites were found in a registry or an index; none of the 39 sources its claims cite is checked for support yet.
Evaluating Dopamine Reward Pathway in ADHD: Clinical Implications
Open accessAbstract
We used positron emission tomography to measure dopamine synaptic markers (transporters and D2/D3 receptors) in 53 nonmedicated adults with ADHD and 44 healthy controls. For both ligands, statistical parametric mapping showed that specific binding was lower in ADHD than in controls in regions of the dopamine reward pathway in the left side of the brain. The mean for DAT in the nucleus accumbens for controls was 0.71 vs 0.63 for those with ADHD and in the midbrain for controls was 0.16 vs 0.09 for those with ADHD. For D2/D3 receptors, the mean in the caudate for controls was 2.80 vs 2.67 for those with ADHD; and in the accumbens for controls was 2.85 vs 2.68 for those with ADHD.
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22 Sources not found · 17 Own result · 12 Own method · 9 Own interpretation · 1 No basis given
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In the paper
“for D2/D3 receptors, the mean accumbens for controls was 2.85 vs 2.68 for those with ADHD (95% CI, 0.06–0.30, P=.004)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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In the paper
“differences in D2/D3 in the hypothalamic region, with controls having a mean of 0.12 vs 0.05 for those with ADHD (95% CI, 0.02–0.12; P=.004)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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In the paper
“but the reductions in left hypothalamic region were not significantly different (Table 2).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine Transporters
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“and in the midbrain for controls was 0.16 vs 0.09 for those with ADHD (95% CI, 0.03–0.12; P ≤ .001)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“and in the midbrain, it was for controls 0.28 vs 0.18 for those with ADHD (95% CI, 0.02–0.17, P=.01)”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The correlations with reflectivity or impulsivity and the PET dopamine measures were not significant”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
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In the paper
“However, despite this limitation, significant differences in the latter regions between controls and participants with ADHD was shown.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
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In the paper
“For both ligands, statistical parametric mapping showed that specific binding was lower in ADHD than in controls (threshold for significance set at P<.005) in regions of the dopamine reward pathway in the left side of the brain.”
- Also stated in: § Dopamine D2/D3 Receptors · plain
“Statistical parametric mapping analysis of the [11C]raclopride distribution volume ratio images revealed 1 cluster with lower D2/D3 availability in ADHD participants than controls in the left hemisphere.”
- Also stated in: § Dopamine Transporters · plain
“Statistical parametric mapping analysis of the [11C]cocaine distribution volume ratio images revealed a cluster in the same location as manifested in the [11C]raclopride images.”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
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- Also stated in: § Dopamine D2/D3 Receptors · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean (95% CI for mean difference) of the K1 measures for [11C]cocaine did not differ in the left caudate with 0.49 among the controls vs 0.48 among those with ADHD (95% CI, −0.05 to 0.03) or in left accumbens region with a respective difference of 0.49 vs 0.51 among those with ADHD (95% CI, −0.02 to 0.07).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine Transporters
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast the K1 measures for [11C]raclopride (transport of radioligand from plasma to tissue) did not differ either in left caudate with the both groups having a mean 0.11 (95% confidence interval [CI], −0.01 to 0.006 mean difference) or in left accumbens region with the controls having a mean of 0.12 vs a mean of 0.11 for those with ADHD (95% CI, −0.01 to 0.005).”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine D2/D3 Receptors
plain- Asserted: passes — The authors put it forward as true.
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- The quote only partly states this claim. 1
- Probably not a substantial claim. 18
- It may state two separate claims as one. 12
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There were no regions that were higher in ADHD participants than in controls.”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Dopamine D2/D3 Receptors
plain- Asserted: passes — The authors put it forward as true.
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The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and with DAT in the midbrain (r=0.37; 95% CI, 0.16–0.53; P ≤ .001).”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Lower than normal D2/D3 receptors and DAT availability in ADHD in the caudate was also demonstrated.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Genetic and environmental etiologies that implicate the neurotransmitter dopamine have been proposed for ADHD.3”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [3]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“The psychometric properties of the SWAN rating scale are superior to those of truncated symptom-severity ratings scales.22”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Clinical Scales
What the sources say
- Not matchedcites [22]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, this finding is preliminary and in need of replication.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“which could reflect that the scores were low and thus the sensitivity to observe such a correlation was lacking.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The preliminary finding reported herein of lower than normal dopamine D2/D3 receptor availability in the hypothalamic region of ADHD participants is intriguing because if replicated, it could hypothetically provide a neurobiological basis for the high co-morbidity of ADHD with signs and symptoms suggestive of hypothalamic pathology45 such as sleep disturbances,46 overweight or obesity,47 and abnor”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“the laterality effects should be interpreted as preliminary and in need of replication.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
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Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This study was not initially designed to evaluate hypothalamic dopamine involvement in ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Evidence from brain imaging studies have shown that brain dopamine neurotransmission is disrupted in ADHD5–9 and that these deficits may underlie core symptoms of inattention8 and impulsivity.9”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [6]
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- Not matchedcites [7]
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- Not matchedcites [8]
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- Not matchedcites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Morphological MRI images were not obtained and thus whether volumetric differences in striatum in those with ADHD that could account for these findings could not be ascertained since volumetric differences in striatum have been reported in ADHD.36–40”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
What the sources say
- Not matchedcites [36]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [37]
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- Not matchedcites [38]
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- Not matchedcites [39]
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- Not matchedcites [40]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In our study, the D2/D3 receptor measures in accumbens were correlated with the dimension of attention, which would implicate the dopamine reward pathway in the symptoms of inattention in ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“This pathway plays a key role in reinforcement-motivation and in learning stimuli-reward associations,51 and its involvement in ADHD supports the use of interventions to enhance the saliency of school and work tasks to improve performance.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [51]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
- Not matched
In the paper
“This rating system has been widely used in clinical and research settings and has well-established factor structure, reliability, and validity (Table 1).24”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Clinical Scales
What the sources say
- Not matchedcites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosted- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“The reward deficits in ADHD are characterized by a failure to delay gratification, impaired response to partial schedules of reinforcement, and preference for small immediate rewards over larger delayed rewards.31”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [31]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
In the paper
“Finally, because a low number of dopamine D2/D3 receptors in the nucleus accumbens have been associated with a greater risk for drug abuse,33 future work should determine if the lower than normal D2/D3 receptor availability in the accumbens region in ADHD underlies the higher vulnerability for substance abuse in this population.34”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [33]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
- Not matched
In the paper
“Both motivational interventions and contingency management have been shown to improve performance in ADHD patients.52”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [52]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Another study limitation was that measures of reward sensitivity were not performed. Thus, we can only infer that the decreases in the dopamine markers in the accumbens region could underlie the reward deficits that have been reported in patients with ADHD.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Multiple hypothalamic nuclei express dopamine D2 receptors,49 but the limited spatial resolution of a PET scan does not allow for localizing where the differences between the groups occurred.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
What the sources say
- Not matchedcites [49]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“low statistical power may have contributed to the lack of significant ADHD-normal differences in the right brain regions.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Definitions for significant difference for the outcome measures1 were that statistical parametric mapping comparisons for the DAT and the D2/D3 images had to be significant at P<.005 (cluster corrected > 100 voxels) and the regional findings had to be corroborated by independently drawn region of interests2; comparisons for these corroborative measures had to be significant at P<.053; correlations”
§ Evaluating Dopamine Reward Pathway in ADHD > METHODS > Image Analysis and Statistics
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The mesoaccumbens dopamine pathway, which projects from the ventral tegmental area (VTA) in the midbrain to the nucleus accumbens is critically involved in reward and motivation14 and has been hypothesized to underlie the reward and motivational deficits observed in ADHD.11,15”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [15]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Not matched
In the paper
“Alternatively it could reflect the involvement of frontal regions in impulsivity,57 which could not be measured with current PET radioligands; D2/D3 receptors and DAT levels in frontal regions are very low.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT > Limitations
What the sources say
- Not matchedcites [57]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: D2/D3 receptors and DAT levels in frontal regions are very low.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“There is also increased awareness that patients with ADHD may have reward and motivation deficits.10–12”
§ Evaluating Dopamine Reward Pathway in ADHD > Abstract > Conclusion
What the sources say
- Not matchedcites [10]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [12]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“but the limited spatial resolution of a PET scan does not allow for localizing where the differences between the groups occurred.”
§ Evaluating Dopamine Reward Pathway in ADHD > COMMENT
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
No prior study has directly measured synaptic dopamine markers in the accumbens region of individuals with ADHD.
“However, to our knowledge no study has directly measured synaptic dopamine markers in the accumbens region of individuals with ADHD.”
The paper relies on this without support.
D2/D3 receptors and DAT levels in frontal regions are very low.
“D2/D3 receptors and DAT levels in frontal regions are very low.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“using positron emission tomography (PET) we showed lower than normal availability of DA D2/D3 receptors (measured with [ 11 C]raclopride) and of DA transporters (measured with [ 11 C]cocaine) in the midbrain and in NAcc in drug naïve ADHD participants compared to non-ADHD control subjects 10 .”
From Motivation Deficit in ADHD is Associated with Dysfunction of the Dopamine Reward Pathway (2011) · cites this paper as [10]
In the citing paper
“As a number of researchers have described [106,149], substance-use disorders are typically accompanied by decreased reward motivation for typical and non-pathological rewards, a phenomenon that has been variously termed ‘motivational toxicity’ [150] and ‘reward-deficiency syndrome’ [151].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [149]
In the citing paper
“The immediate and marked response of ADHD symptoms to stimulant medications such as amphetamines and methylphenidate, which increase levels of synaptic dopamine, suggests that the main underlying pathophysiological process may involve deficits or imbalances in catecholaminergic, dopaminergic, and nicotinergic functioning [109-111].”
From European consensus statement on diagnosis and treatment of adult ADHD: The European Network Adult ADHD (2010) · cites this paper as [111]
In the citing paper
“It readily applies to ADHD because children with ADHD are at elevated risk of addiction, and both addiction and ADHD have been strongly associated with dysfunction in ascending dopaminergic systems that relate to reward response (Volkow et al., 2009, Volkow et al., 2011a, Volkow et al., 2011b).”
From Characterizing heterogeneity in children with and without ADHD based on reward system connectivity (2015) · cites this paper as Volkow et al., 2009
In the citing paper
“It readily applies to ADHD because children with ADHD are at elevated risk of addiction, and both addiction and ADHD have been strongly associated with dysfunction in ascending dopaminergic systems that relate to reward response (Volkow et al., 2009, Volkow et al., 2011a, Volkow et al., 2011b).”
From Characterizing heterogeneity in children with and without ADHD based on reward system connectivity (2015) · cites this paper as Volkow et al., 2009
In the citing paper
“Stimulant treatment, such as methylphenidate, is known to act directly on brain regions associated with disrupted dopamine reward pathways in ADHD [62,63] and may be responsible for the global effects seen with stimulant treatment in ADHD.”
From Will Working Memory Training Generalize to Improve Off-Task Behavior in Children with Attention-Deficit/Hyperactivity Disorder? (2012) · cites this paper as [63]
In the citing paper
“A subsequent study of ADHD subjects showed the same finding of reduced D2 receptor binding in the ventral striatum and caudate (Volkow et al., 2009), which correlated inversely with attention.”
From Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity (2014) · cites this paper as Volkow et al., 2009
In the citing paper
“Based on these results, this group hypothesized that decreased dopamine transmission plays a role in the motivation and reward deficits seen in ADHD, which are characterized by poor response inhibition and preference for small immediate rewards over larger delayed rewards (Volkow et al., 2009).”
From Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity (2014) · cites this paper as Volkow et al., 2009
In the citing paper
“A number of studies have shown that ADHD is associated with a motivational deficit due to a dopamine dysfunction in the basal ganglia [71–73].”
From The brain anatomy of attention-deficit/hyperactivity disorder in young adults—a magnetic resonance imaging study (2017) · cites this paper as [71]
In the citing paper
“Recent studies have further indicated deficits in the dopamine reward circuitry,3–5 as predicted by developmental neurobiological models of the disorder.6–8”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [5]
In the citing paper
“Neurochemical studies have demonstrated alterations in dopaminergic signaling in the striatum and the midbrain in ADHD, and linked such alterations with inattention symptoms and motivation problems in children and adults with ADHD.5,27–29”
From Striatal sensitivity during reward processing in attention-deficit/hyperactivity disorder (2012) · cites this paper as [5]
In the citing paper
“A recent set of case–control PET studies in adult medication-naïve patients found that ADHD is associated with reduced dopamine transporter and dopamine D2/D3 receptor availability in selected brain regions of the left hemisphere, including the nucleus accumbens, caudate and midbrain (Volkow et al., 2007a, b, 2009).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2007a, b, 2009
In the citing paper
“This question is particularly relevant because findings for both juvenile and adult ADHD have implicated functional and structural midbrain abnormalities in the pathophysiology of the disorder (Ernst et al., 1999; Jucaite et al., 2005; Volkow et al., 2009; Romanos et al., 2010), also consistent with experimental animal models of ADHD (Leo et al., 2003).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2009
In the citing paper
“This result is consistent with previous evidence implicating the left caudate in inattentiveness, not only in patients with ADHD, but also in healthy subjects (Schrimsher et al., 2002; Volkow et al., 2007a, b, 2009) and is also congruent with reports that lesions in the left caudate produce attentional deficits (Benke et al., 2003).”
From A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment (2013) · cites this paper as Volkow et al., 2007a, b, 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Correlation With ADHD Symptoms Dimensions
“The dimension of attention (from the SWAN) was negatively correlated with D2/D3 receptor availability in the left accumbens region (r=0.35; 95% CI, 0.15–0.52; P=.001)”
§ Evaluating Dopamine Reward Pathway in ADHD > RESULTS > Correlation With ADHD Symptoms Dimensions
“Because the SWAN scale rates symptoms with a positive scale (from 1 to 3) and the opposite of symptoms with a negative scales (from −1 to −3) the negative correlation indicates that the lower the dopamine measures, the greater the symptoms of inattention.”
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“…have fewer dopamine receptors and transporters available in the midbrain, where the majority of dopamine in the brain is produced, and in the nucleus accumbens, a structure that receives significant projections from the midbrain and is integral to the dopamine-reward pathway (Volkow et al., 2009).”
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“…several factors may contribute, including: (cid:129) Lower than normal dopamine D 2 /D 3 receptor availability in the hypothalamic region of ADHD (15) (cid:129) Norepinephrine and dopamine dysregulation which contributes to ADHD symptoms and arousal regulation (16) (cid:129) Core de fi cits in in…”
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“In impulsive individuals, these effects may foster behavioral conditioning and compulsive use, particularly in the context of reduced sensitivity to delayed rewards and hypofunction of the mesolimbic dopamine system (Faraone and Biederman, 2005; Volkow et al., 2009).”
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“Similarly, individuals with ADHD exhibit lower levels of DRD2/DRD3 in the hypothalamic region [11] and DRD2 polymorphism involvement [12].”
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“…implicated in disorders of attention, such as attention-deficit hyperactivity disorder (ADHD; Biederman and Spencer, 1999; Swanson et al., 2000; Volkow et al., 2009; Wu et al., 2012; Vanicek et al., 2014), and sex differences in dopamine and norepinephrine pathways may partially underlie…”
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Self-citationObsesif-kompulsif kişilik bozukluğunda etiyolojik yaklaşımlar: Biyopsikososyal bir inceleme
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“Impaired dopaminergic signaling is implicated in the neuropsychiatric disorders associated with higher PNMI (23–26), contributing to dysfunction in symptom domains such as anhedonia, avolition, impulsivity, and novelty-seeking (27–30).”
Cunff, A. L., Russell, C., & Dommett, E. J. (2026) · BMC Psychology · doi:10.1186/s40359-026-04504-7
Photobiomodulation and Cognitive Enhancement in ADHD: Translational Evidence
Schwartz, A. Y., Machado, L. D. S., Gonzalez-Lima, F., Salehpour, F., da Silva, S. G., Lopes‐Martins, R. Á. B., Salgado, A. S. I., & Cardoso, F. D. S. (2026) · Clinical and Translational Neuroscience · doi:10.3390/ctn10020010 · Cited by 1
“In this context, CCO-mediated bioenergetic modulation may contribute to optimizing dopaminergic and noradrenergic signaling efficiency, potentially compensating for the functional deficits observed in ADHD [31,35,36].”
Johnson, D., Finegold, K. E., Page, D., & Wade, M. (2026) · Springer eBooks · doi:10.1007/978-3-032-03292-8_16
Li, X., Tang, L., Kang, C., Xu, F., & Ma, N. (2026) · Brain Science and Child Development · doi:10.1016/j.bscd.2026.100007
Nawarathna, G. S., Ariyasinghe, D. I., Balasooriya, N., Fernando, A., & Dassanayake, T. L. (2026) · Nutritional Neuroscience · doi:10.1080/1028415x.2026.2659148
Zeng, Y., Yang, L., Cui, Z., & Cao, Q. (2026) · Psychological Medicine · doi:10.1017/s003329172610405x
“…in the binding of neuroactive ligands, such as dopamine and norepinephrine, to their receptors can impair prefrontal control over subcortical regions like the basal ganglia and locus coeruleus, contributing to core symptoms such as inattention, hyperactivity, and impulsivity (Volkow et al., 2009).”
Koziel, J., Brammer, M. J., Goodwin, A., Fritz, A., Hermila, B., Murphy, D., Demurie, E., Seelemeyer, H., Roeyers, H., Buitelaar, J. K., et al. (2026) · Research Square · doi:10.21203/rs.3.rs-9564653/v1
Mocini, E., Maiolo, A., Aquila, V., Caligiuri, M., Greco, F., Emerenziani, G., Tinelli, E., Sabatini, U., Giannetta, E., & Tarsitano, M. G. (2026) · Women · doi:10.3390/women6020034
“Neurobiologically, dysregulated dopamine signaling has been proposed as a shared mechanism for altered reward sensitivity and reinforcement learning in ADHD and binge eating [20,21].”
Lorenz, C. (2026) · Springer eBooks · doi:10.1007/978-3-662-73257-1_6
Kawaharada, R., Kimura, R., Miyata, E., Noguchi, R., Toriumi, A., & Nakamura, A. (2026) · Nutrients · doi:10.3390/nu18111748
“…the hyperactivity-like behavior observed in this study may be closely related to impaired dopaminergic neurotransmission and reward-related signaling, particularly the dysfunction of dopamine transporters and dopamine receptor pathways associated with attention and motor regulation [53,54].”
Brezolin, C. L. D. M., & de Freitas, S. B. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1785088 · Cited by 1
“ADHD, due to dysregulation in dopaminergic gain (Volkow et al., 2009), is an Immediate Stimulus-Seeking machine (compensating for low cortical tone).”
Metadata
- Authors
- Volkow, N. D., Wang, G.-J., Kollins, S. H., Wigal, T. L., Newcorn, J. H., Telang, F., Fowler, J. S., Zhu, W., Logan, J., Ma, Y., Pradhan, K., Wong, C., & Swanson, J. M.
- Affiliations
- National Institute on Drug Abuse (US)
- Corresponding author
- Volkow, Nora D.
- ORCID
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2009-09-09
- Volume
- 302
- Issue
- 10
- Pages
- 1084
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC2958516
- OpenAlex
- W2071411087
- Semantic Scholar
- 73303180da9a733fdf01dc78501b5769db289660
- Cited by
- 728
- References
- 69
- Citations by year
- 2026: 67 · 2025: 46 · 2024: 36 · 2023: 27 · 2022: 35 · 2021: 37 · 2020: 37 · 2019: 29 · 2018: 29 · 2017: 40 · 2016: 29 · 2015: 39 · 2014: 62 · 2013: 52 · 2012: 61
- FWCI
- 33.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (ZIAAA000550)
- National Institute of Mental Health (R01MH066961)
- National Institute on Drug Abuse (K24DA023464)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- attention deficit hyperactivity disorder, dopamine reward pathway, dopamine transporter, D2/D3 receptors, nucleus accumbens, caudate nucleus, adult ADHD, neuroimaging biomarkers, cocaine binding, left hemisphere lateralization, inattention, hyperactivity/impulsivity
- MeSH terms
- Adult, Attention Deficit Disorder with Hyperactivity, Brain, Brain Mapping, Carbon Radioisotopes, Cocaine, Dopamine, Female, Humans, Male, Mesencephalon, Synaptic Transmission, Reward, Dopamine Agents, Receptors, Dopamine D2, Raclopride, Positron-Emission Tomography, Dopamine Plasma Membrane Transport Proteins
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