Cognitive Inhibition

Selectively retrieving an item from long-term memory reduces the accessibility of competing traces, a phenomenon known as retrievalinduced
forgetting (RIF). RIF exhibits cue independence, or the tendency for forgetting to generalize to novel test cues, suggesting an inhibitory
basis for this phenomenon. An alternative view (Camp, Pecher, & Schmidt, 2007; Camp et al., 2009; Perfect et al., 2004) suggests that using novel
test cues to measure cue independence actually engenders associative interference when participants covertly supplement retrieval with practiced
cues that then associatively block retrieval. Accordingly, the covert-cueing hypothesis assumes that the relative strength of the practiced items at
final test – and not the inhibition levied on the unpracticed items during retrieval practice – underlies cue-independent forgetting. As such, this
perspective predicts that strengthening practiced items by any means, even if not via retrieval practice, should induce forgetting. Contrary to these
predictions, however, we present clear evidence that cue-independent forgetting is induced by retrieval practice and not by repeated study
exposures. This dissociation occurred despite significant, comparable levels of strengthening of practiced items in each case, and despite the use of
Anderson and Spellman’s original (1995) independent probe method criticized by covert-cueing theorists as being especially conducive to
associative blocking. These results demonstrate that cue-independent RIF is unrelated to the strengthening of practiced items, and thereby fail to
support a key prediction of the covert-cueing hypothesis. The results, instead, favor a role of inhibition in resolving retrieval interference.

Executive function (EF) deficit is a hallmark of Fetal Alcohol Spectrum Disorders (FASD), but the vast majority of available evidence comes from school-age children and adolescents. Very little is known about EF during the critical developmental period prior to 6 years of age in FASD. We evaluated EF in 39 children with FASD (3.0 – 5.5 years) and a comparison group of 50 age-matched, non-exposed controls. Measures included the EF Scale for Early Childhood and a Delay of Gratification task. Compared to age-matched controls, preschool children with FASD had impairments on the EF Scale and showed more impulsivity on the Delay of Gratification task. To confirm the EF Scale finding, FASD group performance was compared to a separate normative dataset (N=1,400). Those with FASD performed below normal (M= −0.57, SD=0.92). Within the FASD group, IQ was correlated with the EF Scale (partial r=.60, p=.001) and Delay of Gratification (partial r=.58, p=.005). EF Scale performance did not differ significantly across levels of FASD severity [fetal alcohol syndrome (FAS), partial FAS, or alcohol-related neurobehavioral disorder (ARND)]. However, compared to normative data, those with FAS had the largest deficits (M= −0.91 SD, SE=0.23), followed by partial FAS (M= −0.66 SD, SE=0.26), then ARND (M= −0.36 SD, SE=0.20). These novel data show that EF deficits manifest well before the age of 6 years in children with FASD, that they occur across the spectrum, and that EF may be most impaired in children with more severe forms of FASD and/or lower IQs.

Over a century ago, Freud proposed that unwanted memories can be excluded
from awareness, a process called repression. It is unknown, however, how
repression occurs in the brain. We used functional magnetic resonance imaging
to identify the neural systems involved in keeping unwanted memories out of
awareness. Controlling unwanted memories was associated with increased
dorsolateral prefrontal activation, reduced hippocampal activation, and impaired
retention of those memories. Both prefrontal cortical and right hippocampal
activations predicted the magnitude of forgetting. These results
confirm the existence of an active forgetting process and establish a neurobiological
model for guiding inquiry into motivated forgetting.

We assessed voluntary orientation and reorientation of visuospatial attention in 313 healthy 6- to 22-year-old participants, 30 children suffering from benign epilepsy with centrotemporal spikes (BECTS) and 13 children with Panayiotopoulos syndrome (PS). The developmental section highlights the late development of reorientingskills. Only childrenwith BECTS-R showed a strong tendency toward a rightward bias in attentional orientation. Additionally, a unilateral deficit of disengagement characterizes the patients with BECTS-R and comorbid ADHD.Right rolandic spikes seem to aggravate subclinical reorienting difficulties. Finally, children with PS failed to diffuse inhibition, except in the nearest area outside the attentional focus. This deficit could be attributed tothe typical occipital-to-frontal spreading of the spikes in PS. By showing distinct attentional deficiencies according to the epileptic syndrome and the epileptic focus lateralization in BECTS, the results provide newevidence for alterations of attentional mechanisms by interictal epileptic activity, which probably contributeto learning difficulties.

Tic disorders are childhood onset neuropsychiatric disorders characterized by motor and/or vocal tics. Research has demonstrated that children with chronic tics (including Tourette syndrome and Chronic Tic Disorder: TS/CTD) can suppress tics, particularly when an immediate, contingent reward is given for successful tic suppression. As a diagnosis of TS/CTD requires tics to be present for at least one year, children in these tic suppression studies had been living with tics for quite some time. Thus, it is unclear whether the ability to inhibit tics is learned over time or present at tic onset. Resolving that issue would inform theories of how tics develop and how behavior therapy for tics works. We investigated tic suppression in school-age children as close to the time of tic onset as possible, and no later than six months after onset. Children were asked to suppress their tics both in the presence and absence of a contingent reward. Results demonstrated that these children, like children with TS/CTD, have some capacity to suppress tics, and that immediate reward enhances that capacity. These findings demonstrate that the modulating effect of reward on inhibitory control of tics is present within months of tic onset, before tics have become chronic.

IMPORTANCE There is accumulating evidence relating maternal smoking during pregnancy to attention-deficit/hyperactivity disorder (ADHD) without elucidating specific mechanisms. Research investigating the neurobiological underpinnings of this disorder has implicated deficits during response inhibition. Attempts to uncover the effect of prenatal exposure to nicotine on inhibitory control may thus be of high clinical importance. OBJECTIVE To clarify the influence of maternal smoking during pregnancy (hereafter referred to as prenatal smoking) on the neural circuitry of response inhibition and its association with related behavioral phenotypes such as ADHD and novelty seeking in the mother's offspring. DESIGN, SETTING, AND PARTICIPANTS Functional magnetic resonance imaging was performed for the offspring at 25 years of age during a modified Eriksen flanker/NoGo task, and voxel-based morphometry was performed to study brain volume differences of the offspring. Prenatal smoking (1-5 cigarettes per day [14 mothers] or >5 cigarettes per day [24 mothers]) and lifetime ADHD symptoms were determined using standardized parent interviews at the offspring's age of 3 months and over a period of 13 years (from 2 to 15 years of age), respectively. Novelty seeking was assessed at 19 years of age. Analyses were adjusted for sex, parental postnatal smoking, psycho-social and obstetric adversity, maternal prenatal stress, and lifetime substance abuse. A total of 178 young adults (73 males) without current psychopathology from a community sample followed since birth (Mannheim, Germany) participated in the study. MAIN OUTCOMES AND MEASURES Functional magnetic resonance imaging response, morphometric data, lifetime ADHD symptoms, and novelty seeking. RESULTS Participants prenatally exposed to nicotine exhibited a weaker response in the anterior cingulate cortex (t 168 = 4.46; peak Montreal Neurological Institute [MNI] coordinates x = −2, y = 20, z = 30; familywise error [FWE]–corrected P = .003), the right inferior frontal gyrus (t 168 = 3.65; peak MNI coordinates x = 44, y = 38, z = 12; FWE-corrected P = .04), the left inferior frontal gyrus (t 168 = 4.09; peak MNI coordinates x = −38, y = 36, z = 8; FWE-corrected P = .009), and the supramarginal gyrus (t 168 = 5.03; peak MNI coordinates x = 64, y = −28, z = 22; FWE-corrected P = .02) during the processing of the NoGo compared to neutral stimuli, while presenting a decreased volume in the right inferior frontal gyrus. These findings were obtained irrespective of the adjustment of confounders, ADHD symptoms, and novelty seeking. There was an inverse relationship between inferior frontal gyrus activity and ADHD symptoms and between anterior cingulate cortex activity and novelty seeking. CONCLUSIONS AND RELEVANCE These findings point to a functional involvement of prenatal exposure to tobacco smoke in neural alterations similar to ADHD, which underlines the importance of smoking prevention treatments.

Many aspects of attention decline with aging. There is a current debate on how aging also affects sustained attention. In this study, we contribute to this debate by meta-analytically comparing performance on the go/no-go Sustained Attention to Response Task (SART) in younger and older adults. We included only studies in which the SART had a low proportion of no-go trials (5%-30%), there was a random or quasirandom stimulus presentation, and data on both healthy younger and older adults were available. A total of 12 studies were suitable with 832 younger adults and 690 older adults. Results showed that older adults were slower than younger adults on go trials (g = 1, 95% CI [.72, 1.27]) and more accurate than younger adults on no-go trials (g = .59, 95% CI [.32, .85]). Moreover, older adults were slower after a no-go error than younger adults (g = .79, 95% CI [.60, .99]). These results are compatible with an age-related processing speed deficit, mostly suggested by longer go RTs, but also with an increased preference for a prudent strategy, as demonstrated by fewer no-go errors and greater posterror slowing in older adults. An inhibitory deficit account could not explain these findings, as older adults actually outperformed younger adults by producing fewer false alarms to no-go stimuli. These findings point to a more prudent strategy when using attentional resources in aging that allows reducing the false-alarm rate in tasks producing a tendency for automatic responding.

OBJECTIVE: Interference suppression and response inhibition are distinct effortful inhibitory processes. Yet they rely on partly overlapping neural substrates. Their independence was studied using an auditory paradigm. METHOD: Continuous EEG was recorded in 16 adults and event-related potentials (ERPs) were analyzed in a new dichotic listening - Go/Nogo task. Attention was directed either to the right dominant ear (forced-right blocks [FR]) or to the left ear (forced-left blocks [FL]). The Go/Nogo task required a motor response only to the standard word played to the selected ear; the nonselected ear was simultaneously presented with the same word (Go condition) or with a deviant (Incongruent Go condition). In the Nogo condition, a deviant was presented to the selected ear while the standard was played to the nonselected ear. Effortful interference suppression was expected only in the FL blocks to override the automatic processing of distractors in the dominant ear. RESULTS: When no effortful interference suppression was necessary (FR blocks) in the Nogo condition, the N2 and P3 increase probably reflected two subcomponents of response inhibition (response restraint and response cancellation) and the P2 decrease probably reflected an early inhibitory mechanism (sensory gating). When effortful interference suppression was necessary (FL blocks), there was no Nogo-N2 (i.e., no response restraint). Interference suppression (Incongruent Go condition minus Go condition) also increased the N2 and P3, but did not modulate the P2. CONCLUSIONS: This new paradigm confirms the partial overlap between response inhibition and effortful interference suppression and points out specific features of their subcomponents.

Background
Neurological illness can produce a disorganization of behavior, including verbal disinhibition, despite apparent preserved intelligence. Neuropsychological tests of such behavioral control mechanisms may predict real-world performance of healthy people, such as success or misbehavior in educational contexts.

Method
In two separate studies, we examined how the Hayling Test of verbal response suppression predicts grades and classroom misbehavior.

Results
Verbal suppression errors and spontaneous strategy use were significant predictors of undergraduate grades. Using a modified version of the Hayling Test designed to reduce strategic responding with high school students (mean age 16), higher grades were predicted by shorter response suppression latencies and better working memory scores, and classroom misbehavior was predicted by lower working memory scores.

Conclusion
Verbal response suppression and spontaneous strategy use, both closely linked to disorganized behavior in neuropsychological patients, predict academic achievement but seem unrelated to classroom misbehavior, which is associated with weakness in working memory.