title: The central role of the prefrontal cortex in directing attention to novel events.
abstract: The physiological basis for the striking decrease of attention to novel events following frontal lobe injury is poorly understood. In this study, event-related potentials (ERPs) were recorded from patients with frontal lobe damage and matched subjects, who controlled the duration of viewing of background, novel and target stimuli. Frontal lobe patients did not differ from normal controls in terms of age, education, estimated IQ or mood. However, they were judged to be more apathetic as measured by self-report and informants' ratings. Patients with frontal lobe damage exhibited markedly reduced amplitude of the novelty P3 response and the duration of viewing of novel stimuli. In contrast, injury to the frontal lobes had a limited impact on P3 amplitude and behavioural responses (viewing duration and reaction time) to target stimuli. A strong correlation was found between measures of apathy and both attenuated P3 amplitude and viewing duration in response to novel but not target stimuli. Differences in amplitude of the novelty P3 response explained a large portion of the variance associated with duration of viewing of novel stimuli. After controlling for the influence of P3 amplitude, there was no association between frontal lobe injury and reduced viewing of novel stimuli. The results of this study suggest that frontal lobe damage leads to diminished visual attention to novel events through its disruption of neural processes underlying the novelty P3 response. These processes appear to regulate the allocation of attentional resources and early exploratory behaviours, and are not limited to immediate orienting responses. Damage to the frontal lobes may prevent the generation of a signal which indicates that a novel event in the environment requires additional attention due to its potential behavioural significance. The disruption of these processes is likely to contribute to the apathy observed in patients after injury to the frontal lobes.
authors.affiliation: Brigham Behavioral Neurology Group and Laboratory of Higher Cortical Functions, Division of Cognitive and Behavioral Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA. kdaffner@partners.org
authors.forename: K R
authors.initials: KR
authors.lastname: Daffner
authors.forename: M M
authors.initials: MM
authors.lastname: Mesulam
authors.forename: L F
authors.initials: LF
authors.lastname: Scinto
authors.forename: D
authors.initials: D
authors.lastname: Acar
authors.forename: V
authors.initials: V
authors.lastname: Calvo
authors.forename: R
authors.initials: R
authors.lastname: Faust
authors.forename: A
authors.initials: A
authors.lastname: Chabrerie
authors.forename: B
authors.initials: B
authors.lastname: Kennedy
authors.forename: P
authors.initials: P
authors.lastname: Holcomb
mesh_terms: D000328:Adult; D000339:Affect; D000368:Aged; D001288:Attention / Q000502:physiology*; D001921:Brain / Q000502:physiology* / Q000503:physiopathology; D001931:Brain Mapping; D002544:Cerebral Infarction / Q000473:pathology / Q000503:physiopathology / Q000523:psychology*; D005071:Evoked Potentials / Q000502:physiology*; D005260:Female; D005556:Form Perception; D006801:Humans; D007360:Intelligence; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010775:Photic Stimulation; D017397:Prefrontal Cortex / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D012016:Reference Values; D014057:Tomography, X-Ray Computed