The cognitive-energetic model: an empirical approach to attention-deficit hyperactivity disorder.

By J. Sergeant. Neuroscience and Biobehavioral Reviews, 2000

668 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/c3d75e5f4b9c026d8fb9977b1cf2b6fd6cace903

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In Cognitive Neuroscience

In Psychiatry and Mental health

Citations in the corpus

Behavioral and Brain Functions (2005, critical): “Second, the results provide no support for the state regulation account of ADHD [24].”
Executive “Brake Failure” following Deactivation of Human Frontal Lobe (2006, background): “It is possible, for instance, that a deficit of response selection, response execution, or sustained attention could yield an inhibitory deficit (Sergeant, 2000).”
Executive Brake Failure following Deactivation of Human Frontal Lobe (2006, background): “It is possible, for instance, that a deficit of response selection, response execution, or sustained attention could yield an inhibitory deficit (Sergeant, 2000).”
Theory‐ and Evidence‐Based Strategies for Children with Attentional Problems (2005, background): “If through this behavior children are still unable to produce an optimal state of arousal, then their attention, response preparation, motor inhibition, and ability to allocate effort to a task are compromised (Banaschewski et al., 2003; Sergeant, 2000).”
Insights into the neural basis of response inhibition from cognitive and clinical neuroscience. (2009, neutral): “Whether the remaining cases of ADHD can be explained via dysfunction in other cognitiveneuroanatomical systems, including attention, arousal (Sergeant, 2000), delay aversion (Sonuga-Barke et al., 2003) or reward reinforcement (Sagvolden et al., 2005) remains to be determined.”
Behavioral models of impulsivity in relation to ADHD: Translation between clinical and preclinical studies (2006, positive): “However, there is also evidence to suggest that ADHD is not solely a prefrontal disorder, but that subcortical structures within the basal ganglia may play an important role (Rieger et al., 2003; Sergeant, 2000).”