▪ Abstract The prefrontal cortex has long been suspected to play an important role in cognitive control, in the ability to orchestrate thought and action in accordance with internal goals. Its neural basis, however, has remained a mystery. Here, we propose that cognitive control stems from the active maintenance of patterns of activity in the prefrontal cortex that represent goals and the means to achieve them. They provide bias signals to other brain structures whose net effect is to guide the flow of activity along neural pathways that establish the proper mappings between inputs, internal states, and outputs needed to perform a given task. We review neurophysiological, neurobiological, neuroimaging, and computational studies that support this theory and discuss its implications as well as further issues to be addressed

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An integrative theory of prefrontal cortex function

We provide an “executive-attention” framework for organizing the cognitive neuroscience research on the constructs of working-memory capacity (WMC), general fluid intelligence, and prefrontal cortex (PFC) function. Rather than provide a novel theory of PFC function, we synthesize a wealth of singlecell, brain-imaging, and neuropsychological research through the lens of our theory of normal individual differences in WMC and attention control (Engle, Kane, & Tuholski, 1999; Engle, Tuholski, Laughlin, & Conway, 1999). Our critical review confirms the prevalent view that dorsolateral PFC circuitry is critical to executive-attention functions. Moreover, although the dorsolateral PFC is but one critical structure in a network of anterior and posterior “attention control” areas, it does have a unique executiveattention role in actively maintaining access to stimulus representations and goals in interference-rich contexts. Our review suggests the utility of an executive-attention framework for guiding future research on both PFC function and cognitive control.

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The role of prefrontal cortex in working-memory capacity, executive attention, and general fluid intelligence: An individual-differences perspective

Mild cognitive impairment is common in nondemented Parkinson's disease (PD) patients and may be a harbinger of dementia. In view of its importance, the Movement Disorder Society commissioned a task force to delineate diagnostic criteria for mild cognitive impairment in PD. The proposed diagnostic criteria are based on a literature review and expert consensus. This article provides guidelines to characterize the clinical syndrome and methods for its diagnosis. The criteria will require validation, and possibly refinement, as additional research improves our understanding of the epidemiology, presentation, neurobiology, assessment, and long-term course of this clinical syndrome. These diagnostic criteria will support future research efforts to identify at the earliest stage those PD patients at increased risk of progressive cognitive decline and dementia who may benefit from clinical interventions at a predementia stage.

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Diagnostic Criteria for Mild Cognitive Impairment in Parkinson’s Disease: Movement Disorder Society Task Force Guidelines

Individual differences in working-memory (WM) capacity predicted performance on the Stroop task in 5 experiments, indicating the importance of executive control and goal maintenance to selective attention. When the Stroop task encouraged goal neglect by including large numbers of congruent trials (RED presented in red), low WM individuals committed more errors than did high WM individuals on the rare incongruent trials (BLUE in red) that required maintaining access to the ?ignore-the-word? goal for accurate responding. In contrast, in tasks with no or few congruent trials, or in high-congruency tasks that followed low-congruency tasks, WM predicted response-time interference. WM was related to latency, not accuracy, in contexts that reinforced the task goal and so minimized the difficulty of actively maintaining it. The data and a literature review suggest that Stroop interference is jointly determined by 2 mechanisms, goal maintenance and competition resolution, and that the dominance of each depends on WM capacity, as well as the task set induced by current and previous contexts.

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Working-memory capacity and the control of attention: the contributions of goal neglect, response competition, and task set to Stroop interference.

Principles and Practice of Sleep Medicine

We read the article by Vendette et al. with great interest.1 We have been prospectively investigating patients with Parkinson disease (PD) without dementia with polysomnography (PSG)-confirmed or excluded REM sleep behavior disorder (RBD) and cannot uniformly confirm an association of cognitive impairment with the presence of RBD in PD (table e-1 on the Neurology ® Web site at www.neurology.org).

In a comprehensive neuropsychological assessment, patients with PD with RBD had lower scores in figural fluency, verbal and figural memory tests except for recognition, and had more difficulty with visuospatial tasks. Patients with PD also made more interference errors as in Vendette et al. ’s study, but patients with PD with RBD performed better in verbal fluency with fewer perseverations in the Goldenberg test, which evaluates concept learning and shifting.

Apraxia, visuoperceptual, and other cortical deficits were not found in either group but no quantitative measures had been performed. Compared to matched healthy controls (unpublished data), our patients with PD with and without RBD showed mild impairment of executive function and memory, which can be seen in the early stages of PD.2 In contrast, patients with PD without RBD and healthy controls …

http://www.zora.uzh.ch/id/eprint/14407/1/Cognitive_impairment_in_Parkinson%27s_disease.pdf

REM sleep behavior disorder predicts cognitive impairment in Parkinson disease without dementia

Numerous studies have assessed a wide range of cognitive deficits associated with obstructive sleep apnea syndrome (OSAS). The comparison of these various results, however, is hampered by the fact that different studies employ different neuropsychological tests, even when assessing the same function. The aim of this paper is to present a standardized neuropsychological test battery for the evaluation of OSAS patients. Following a description of the general characteristics of OSAS, we review the main cognitive functions reported as being impaired in OSAS patients. These include general intellectual functioning, attentional functioning, memory and learning abilities, executive functions, and motor performance. Based on this review, we propose a test battery designed to cover these cognitive processes while taking into account the time constraints present in most research and clinical centers. In addition to providing a comprehensive neuropsychological evaluation of OSAS patients, the proposed test battery should facilitate the comparison of results from different laboratories.

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Cognitive deficits associated with sleep apnea syndrome: a proposed neuropsychological test battery.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age- and gender-matched healthy subjects. During wakefulness, RBD patients showed a considerably higher theta power in frontal, temporal, and occipital regions with a lower beta power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, beta power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders.

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder

Cognitive impairment in obstructive sleep apnea

Background: Idiopathic REM sleep behavior disorder (iRBD) might be a stage in the development of neurodegenerative disorders, especially Parkinson disease and dementia with Lewy bodies. Recent studies showing a slowing of waking EEG in iRBD suggest that iRBD is associated with cognitive impairment. Objective: To compare patients with iRBD on measures of cognitive function and quantitative waking EEG. Methods: Fourteen patients with iRBD and 14 healthy control subjects matched for age and educational level were studied. Subjects underwent an extensive neuropsychological evaluation and waking EEG recordings. Results: Compared to controls, patients with iRBD showed a lower performance on neuropsychological tests measuring attention, executive functions, and verbal memory. Moreover, patients with iRBD showed EEG slowing (higher delta and theta power) during wakefulness in all brain areas compared to controls. However, no correlation was found between performance on cognitive tests and quantitative waking EEG in patients with iRBD. Conclusion: This study shows a co-occurrence of impaired cognitive profile and waking EEG slowing in patients with idiopathic REM sleep behavior disorder similar to that observed in early stages of some synucleinopathies.

Anne Décary

Papers

REM sleep behavior disorder predicts cognitive impairment in Parkinson disease without dementia

Cognitive deficits associated with sleep apnea syndrome: a proposed neuropsychological test battery.

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder

Cognitive impairment in obstructive sleep apnea

Executive dysfunction and memory impairment in idiopathic REM sleep behavior disorder.