Post-stroke sleep disturbance is common, with pooled prevalence estimates of roughly 50% to 53% in recent meta-analyses, while post-stroke cognitive impairment varies according to case definitions, assessment methods, population and time since stroke. Greater sleep fragmentation and lower sleep efficiency have been associated with poorer post-stroke cognitive performance. Executive dysfunction is especially consequential because problems with working memory, cognitive flexibility and conflict monitoring can slow functional gains, limit rehabilitation participation and hinder reintegration into community life. These observations nevertheless leave three possibilities open: disturbed sleep may contribute to cognitive impairment, it may emerge as a parallel consequence of brain injury, or both processes may be influenced by inflammation, circadian disruption, mood symptoms, medication and reduced daytime activity.

The clinical problem is also more complex than a single complaint about “poor sleep.” Insomnia, repeated awakening, obstructive sleep apnea, daytime hypersomnolence and circadian misalignment have different biological drivers. Obstructive sleep apnea, for example, involves recurrent arousals and intermittent hypoxia and has been associated with inflammation, oxidative stress and vascular dysfunction. Insomnia and fragmented sleep are more closely tied to hyperarousal and unstable sleep continuity. Likewise, executive dysfunction covers several cognitive domains that cannot be represented accurately by a single screening score. A targeted synthesis is therefore more informative than treating sleep disturbance and cognition as interchangeable symptoms, although the available literature often groups them this way and depends heavily on subjective questionnaires and global cognitive measures.

Stroke is increasingly understood not simply as focal tissue loss but as an event that damages communication across distributed systems. Focal lesions can coexist with diaschisis, disruption of long-range white-matter pathways and altered coordination among large-scale networks. The triple-network model focuses on interactions among the salience network, which is thought to help detect behaviorally relevant signals and switch between internally and externally directed states; the default mode network, which supports internally oriented cognition; and the frontoparietal network, which contributes to working memory, task-set maintenance and top-down control. Efficient executive behavior depends on the ability to disengage default-mode processing and recruit frontoparietal control when external demands rise. Stroke-related injury may therefore create a structural vulnerability that sleep disturbance could amplify at a functional level.

Post-stroke neuroimaging supports the presence of that vulnerable network architecture. One study of 118 patients with internal capsule stroke and 57 healthy controls found increased static coupling between the salience and default mode networks but reduced dynamic interactions between the executive control network and other systems. Patients with right-sided lesions also showed lower modularity and longer persistence of a state with strongly positive connections across all three networks, demonstrating that stronger connectivity can coexist with poorer differentiation. In another study, 17 patients with post-stroke cognitive impairment and 24 controls showed reduced static connectivity between the ventral default mode and salience networks. Patients spent longer in one recurring connectivity state, and longer dwell time correlated with lower Mini-Mental State Examination scores, although the association involved global rather than domain-specific cognition.

Directional analyses provide a further complication. Using spectral dynamic causal modelling, researchers comparing 41 patients with post-stroke cognitive impairment and 41 controls found increased effective influence from the posterior cingulate cortex to bilateral dorsolateral prefrontal regions and from the right insula to the right dorsolateral prefrontal cortex. Greater effective connectivity was associated with poorer cognitive scores. Lesion evidence also points to the salience network: in 144 patients with acute stroke, left insular lesions were associated with poorer set-switching even after accounting for the visual-spatial and motor demands of the task. Together, these studies show that stronger or more persistent communication is not automatically beneficial. They do not, however, reveal whether sleep disturbance causes, follows or amplifies the observed network abnormalities.

Sleep research from populations without stroke supplies biological plausibility but not direct proof. In 26 healthy adults scanned after normal sleep and approximately 24 hours without sleep, total sleep deprivation reduced connectivity within the default mode network and weakened its anticorrelation with task-positive regions during rest and a visual attention task. A separate study of 22 healthy participants found that 36 hours of sleep deprivation coincided with poorer working-memory performance, increased coupling between dorsal attention and default mode regions, and decreased coupling between frontoparietal and default mode regions. Insomnia findings point to reduced flexibility rather than necessarily altered average connectivity: 65 people with insomnia and 65 matched controls showed less temporal variation in connectivity between the anterior salience and left executive control networks. The authors note that experimental sleep loss is not equivalent to chronic post-stroke insomnia, apnea or fragmentation.

Stroke-specific evidence remains limited but includes a small resting-state imaging study of patients with post-stroke insomnia. Among 23 retained participants, imaging showed abnormalities in cortical regions beyond the infarcts, including elevated low-frequency activity in parts of the default mode network, but the measures did not test network switching or whether default-mode activity failed to suppress during executive tasks. In a separate actigraphy study of 35 older adults with chronic stroke and 35 matched adults without stroke, the stroke group had greater objectively measured fragmentation despite similar subjective questionnaire scores, and cognitive differences were larger where fragmentation was greater or sleep efficiency lower. A polysomnography study of 86 patients evaluated within 14 days of minor ischemic stroke found that obstructive sleep apnea was more prevalent among those with cognitive impairment, while shorter sleep time and lower minimum oxygen saturation remained associated with impairment. These observational findings cannot determine causal direction or identify the relevant network process.

To test the proposed pathway, the review recommends studies that combine objective sleep phenotyping with dynamic or effective connectivity, task-based functional MRI, domain-specific executive tests and longitudinal or interventional follow-up in the same participants. A practical initial population would be medically stable adults with imaging-confirmed ischemic stroke assessed within a defined recovery period, although that window is a design proposal rather than an established requirement. Insomnia, fragmentation, obstructive sleep apnea and their coexistence should be measured separately. Lesion location, structural disconnection, stroke stage, vascular burden, medication, mood, pain, fatigue, rehabilitation exposure and premorbid cognition may act as confounders or modifiers, depending on the causal model. Sample size should be determined through simulation because detecting an indirect effect through network function may require more participants than detecting a direct sleep-cognition association.

The framework makes specific predictions that can be contradicted. Greater fragmentation or insomnia severity would be expected to accompany longer dwell time in default-mode-dominant states, fewer transitions toward task-relevant control states and weaker salience-mediated switching. Insufficient suppression of internal activity and delayed frontoparietal recruitment could then impair conflict monitoring, working memory, processing speed and cognitive flexibility. Lesions or disconnection affecting fronto-insular, cingulate or frontoparietal pathways might strengthen these associations. A finding linking objectively measured sleep disruption to executive impairment but not to the prespecified network measure would challenge the proposed bridge. Likewise, an intervention that improves sleep and executive function without producing the predicted network change would weaken the mediation claim, although it would not make the treatment clinically useless. Because evidence is dominated by heterogeneous, largely observational studies and mechanistic inferences from non-stroke populations, the proposed pathway remains a roadmap for direct testing rather than an established basis for treatment selection.

Subject of Research: A mechanistic hypothesis linking post-stroke sleep phenotypes, large-scale brain-network dysfunction and executive impairment.

Article Title: Poststroke sleep phenotypes and executive dysfunction: toward a sleep-network-executive framework

Article References: Xu, J., Zhang, Y., Lin, D., Yan, X., Xie, N., Si, S., & Yang, S. (2026). Poststroke sleep phenotypes and executive dysfunction: toward a sleep-network-executive framework. Frontiers in Neuroscience, 20, Article 1978796. https://doi.org/10.3389/fnins.2026.1978796

Image Credits: AI Generated

DOI: 10.3389/fnins.2026.1978796

Keywords: post-stroke sleep disturbance, executive dysfunction, salience network, default mode network, frontoparietal network, functional connectivity, stroke rehabilitation, sleep fragmentation, insomnia, brain imaging, Poststroke, sleep

The research team set out to characterize what neuropsychologists call dysexecutive behavioral changes, a term that describes disruptions in the suite of behaviors orchestrated by the frontal systems of the brain. Executive functions encompass the ability to initiate activity, sustain effort toward goals, inhibit inappropriate impulses, organize sequences of actions, and adapt behavior to changing circumstances. When these systems falter, the consequences show up not as failures on a laboratory puzzle but as changes in daily life: a person may become apathetic and lose the drive to begin tasks, may struggle to organize and complete multi-step activities, or may find themselves saying and doing things that a previously well-regulated sense of social restraint would have suppressed. The study’s central premise is that capturing these changes requires a multidimensional behavioral assessment, complementing the cognitive testing that has dominated much of the post-COVID literature to date.

To do this, the researchers conducted a cross-sectional study of 69 participants, dividing them into two groups according to their clinical trajectory after infection. Forty-five participants had a history of acute COVID-19, meaning they had been infected and had experienced the acute illness, while 24 participants had post-COVID-19 syndrome, the condition in which symptoms persist well beyond the acute phase. The instrument at the heart of the study was the Frontal Systems Behavior Scale, known in the field as the FrSBe. This standardized questionnaire is designed to quantify behaviors associated with damage or dysfunction in frontal brain systems, and it yields scores along three well-characterized dimensions: apathy, executive dysfunction, and disinhibition. Crucially, the scale asks respondents to rate behavior both before and after the event of interest, which in this case was SARS-CoV-2 infection, allowing each participant to serve as their own baseline for comparison.

The three dimensions measured by the FrSBe map onto distinct aspects of frontal-lobe function. Apathy reflects a loss of motivation, initiative, and emotional engagement, and it is classically associated with damage to medial frontal regions and their connections to deep brain circuits involved in drive and reward. Executive dysfunction captures difficulties with planning, organization, working memory in the service of action, and the flexible shifting of strategies when circumstances change. Disinhibition, by contrast, reflects a failure of inhibitory control, manifesting as impulsivity, socially inappropriate behavior, and difficulty restraining emotional or appetitive responses. Because these dimensions can be affected independently, a profile-based assessment can reveal patterns that a single global measure of cognitive impairment would obscure. This is precisely the kind of granularity the Spanish team sought in comparing the two post-infection groups.

The findings were consistent in one broad respect and revealing in another. Across both groups, the mean standardized scores, expressed as z-scores, for the FrSBe behavioral dimensions increased in the period after infection compared with participants’ retrospective ratings of their own pre-infection functioning. In other words, on average, people in both the acute COVID-19 group and the post-COVID-19 syndrome group reported more dysexecutive behaviors after their infection than before it. This uniform direction of change suggests that SARS-CoV-2 infection, regardless of the subsequent clinical course, may be associated with perceived alterations in behaviors that depend on frontal systems, a conclusion that aligns with the broader literature documenting neuropsychological alterations, particularly executive dysfunction, as frequently reported consequences of the infection.

The differences between the groups, however, were where the study’s most clinically interesting signal emerged. Participants with post-COVID-19 syndrome showed significant increases in all three dysexecutive symptom dimensions, and their post-infection scores reached the range of clinical difficulty on the apathy and disinhibition dimensions. This means that individuals living with the persistent form of the illness not only noticed changes in their capacity for organized, goal-directed activity but also reported meaningful losses of motivation and initiative alongside weakened behavioral inhibition. For a condition whose day-to-day burden is often described in terms of fatigue and cognitive fog, the finding that apathy, a motivational rather than purely cognitive construct, features prominently offers a potentially important reframing: some of what patients experience as exhaustion or loss of drive may be measurable as a distinct frontal-systems behavioral syndrome.

The acute COVID-19 group presented a subtler picture. These participants, who had been infected but had not developed the persistent syndrome, exhibited slight perceived behavioral changes on the executive dysfunction dimension, and more marked changes on the dimension of disinhibition. The prominence of disinhibition in this group is noteworthy because it suggests that even people whose infection resolves without a chronic syndrome may perceive changes in impulse control and behavioral regulation. The authors’ interpretation, as reflected in their reported results, is that the two trajectories carry distinct patterns of self-reported alteration: a broader and clinically elevated profile in post-COVID-19 syndrome, and a narrower, milder profile dominated by disinhibitory features in those with a history of acute infection alone.

From these observations, the researchers draw two practical conclusions. First, they propose that SARS-CoV-2 infection may be associated with perceived changes in dysexecutive behavior, with distinct patterns across individuals on different post-infection trajectories. Second, they suggest that the Frontal Systems Behavior Scale may be a useful tool for identifying behavioral alterations across the different clinical spectra of the disease. The second point has real methodological weight. Much of the post-COVID assessment literature relies on neuropsychological batteries that measure cognitive performance under structured testing conditions, which can miss changes that manifest primarily in spontaneous, real-world behavior. A validated behavioral instrument with established norms and a built-in pre-post comparison offers clinicians and researchers a complementary lens, one that may be particularly sensitive to the motivational and inhibitory changes that patients themselves notice but that standard testing may not capture.

The authors are careful, appropriately, to frame their conclusions as exploratory. The study is a cross-sectional comparison with a modest sample size, and the FrSBe’s pre-infection ratings are retrospective, which means they depend on participants’ memory and self-perception of how they functioned before falling ill. Retrospective self-report is vulnerable to bias, particularly in a population experiencing fatigue, low mood, or cognitive complaints, and the design cannot establish that the behavioral changes were caused by the infection itself rather than by illness-related stress, lifestyle disruption, or other confounding factors. The researchers explicitly state that these exploratory findings should be interpreted with caution and justify further research using a more robust methodological approach, a caveat that responsible readers should take seriously. Larger longitudinal studies, ideally with pre-infection behavioral data collected prospectively, would be needed to confirm and extend the reported patterns.

Even with those limitations, the study makes a contribution that fits into a growing scientific effort to understand the full neurological and psychological footprint of SARS-CoV-2. Executive dysfunction has been widely reported after infection, but behavioral dimensions such as apathy and disinhibition have received less systematic attention. By showing that these dimensions can be measured, that they change in self-reported terms after infection, and that their profiles differ between acute and persistent clinical courses, Becerra-García and Laval provide a template for how behavioral neuropsychology can sharpen the characterization of post-COVID conditions. The work was funded by the Universidad Internacional de La Rioja’s call for grants for scientific publication, was approved by the institution’s research ethics commission, and is published open access, making the full report available to clinicians, researchers, and patients alike. As the field moves toward more rigorous designs, instruments like the FrSBe may help ensure that the behavioral consequences of COVID-19, not just its cognitive ones, are neither overlooked nor underestimated.

Subject of Research: Perceived dysexecutive behavioral changes after SARS-CoV-2 infection in acute COVID-19 versus post-COVID-19 syndrome

Article Title: Characterizing perceived dysexecutive behavioral changes following SARS-CoV-2 infection in individuals with different clinical trajectories

Article References: Becerra-García, J. A., & Laval, M. D. F. (2026). Characterizing perceived dysexecutive behavioral changes following SARS-CoV-2 infection in individuals with different clinical trajectories. Discover Psychology. https://doi.org/10.1007/s44202-026-00933-y

Image Credits: AI Generated

DOI: 10.1007/s44202-026-00933-y

Keywords: SARS-CoV-2, post-COVID-19 syndrome, dysexecutive behavior, executive dysfunction, apathy, disinhibition, Frontal Systems Behavior Scale, neuropsychology, behavioral assessment, frontal lobes, COVID-19, mental health

The research focused on a task that cognitive neuroscientists have refined over decades: the interleaved pro-saccade and anti-saccade paradigm. In a pro-saccade trial, a participant simply looks toward a sudden visual target, an almost reflexive action governed by ancient circuitry linking the retina to the superior colliculus in the brainstem. In an anti-saccade trial, the instruction reverses: the participant must suppress the reflexive pull toward the target and instead look in the exact opposite direction. That act of suppression is anything but trivial. It depends on top-down executive control implemented by frontal-subcortical circuits—the same prefrontal networks that degrade in depression and that underpin planning, inhibition, and working memory. Because the reflexive and voluntary components of eye movement can be measured with millisecond precision, the task offers a window into executive function that is fast, non-invasive, and largely immune to the practice effects and cultural biases that plague paper-and-pencil tests.

The study enrolled 29 older adults diagnosed with late-life depression and 19 cognitively healthy controls of comparable age. Depression severity was quantified with the Geriatric Depression Scale-15, a widely used screening instrument, while global cognitive status was assessed with the Montreal Cognitive Assessment, or MoCA, a sensitive measure of mild cognitive impairment. Each participant then completed the interleaved saccade task while a high-speed video-based eye tracker recorded the trajectory, timing, and direction of every eye movement. The researchers extracted a rich set of measures: the rate of direction errors in anti-saccade trials, saccadic reaction times, the frequency of short-latency responses, the kinematic metrics of the movements themselves such as velocity and amplitude, and a less familiar quantity called voluntary override time, or VOT, which captures how long the executive system takes to override the reflexive response.

The headline finding was unambiguous. Older adults with late-life depression made significantly more direction errors on anti-saccade trials than the healthy controls did. In other words, when the task demanded that they suppress the automatic urge to glance at a flashing target, their eyes betrayed them more often. This is precisely the signature one would expect from weakened prefrontal inhibitory control, because the anti-saccade error rate is one of the most reliable behavioral indices of frontal-lobe integrity in the cognitive neuroscience literature. Importantly, the deficit was selective. The basic machinery of eye movement appeared intact: saccade metrics such as peak velocity and amplitude did not differ reliably between the groups, suggesting that the depression-related impairment lay not in the motor periphery or the brainstem reflex circuit itself but in the higher-order control system that decides whether the reflex should be allowed to run.

A second, subtler result added an intriguing twist. Short-latency pro-saccades—reflexive glances toward the target—were actually faster in the depressed group than in the controls. Rather than a general slowing, which clinicians often associate with depression in the form of psychomotor retardation, the eye-movement data revealed a pattern of disinhibition: the reflexive pathway fired more quickly and the voluntary brake applied less effectively. This combination of faster reflexes and weaker suppression points toward an imbalance in the competitive interaction between the superior colliculus, which generates saccade commands, and the frontal cortical networks that modulate them. In computational terms, the threshold for triggering a reflexive response appears lower while the top-down signal that raises that threshold appears weaker, a double hit that compounds executive failure.

Perhaps the most clinically significant finding emerged from correlations within the depressed group. MoCA scores, which index global cognitive performance, were significantly associated with both anti-saccade error rates and voluntary override time, meaning that patients whose eye movements showed the weakest executive control also scored lowest on the standard cognitive assessment. Yet depression severity, as measured by the GDS-15, showed no correlation with any of the oculomotor measures. This dissociation is important. It suggests that the saccade abnormalities track the cognitive dimension of late-life depression rather than the mood symptoms themselves, positioning the eye-tracking paradigm as a potential probe of the executive dysfunction that predicts poorer treatment outcomes, greater functional decline, and elevated risk of progression to dementia in this population.

The implications reach beyond the clinic. Late-life depression affects millions of older adults worldwide and is increasingly understood not merely as a mood disorder but as a condition with genuine neurobiological consequences, involving vascular injury, inflammation, and neurodegeneration in frontal-subcortical circuits. Executive dysfunction is one of its most disabling features, undermining medication adherence, financial decision-making, and the ability to benefit from psychotherapy. Yet because mood symptoms fluctuate and self-report is unreliable, the cognitive component often goes unrecognized until it has already compounded disability. A two-minute eye-tracking test that could be administered in a general practitioner’s office would offer a way to detect this component early, monitor it over time, and potentially identify which patients need closer neuropsychological follow-up.

The authors are careful to frame their results as preliminary. The sample sizes were modest, with 29 patients and 19 controls, and the study design was cross-sectional, capturing a single snapshot rather than tracking change over time. Larger longitudinal cohorts will be needed to establish whether saccade measures are reliable across repeated testing sessions, whether they predict clinical trajectories such as conversion to dementia, and whether they respond to treatment as depression remits. Questions also remain about how the measures perform in patients taking different classes of antidepressant medication, in those with coexisting medical illness, and in populations with different educational backgrounds. The researchers themselves state that further work is required to establish the reliability and clinical utility of saccade-based assessment in late-life depression.

Even so, the study adds to a growing movement in neuroscience and psychiatry toward behavioral measures that bypass self-report entirely. Eye movements occupy a privileged position in this effort because the circuits that control them are well mapped, their timing can be resolved to the millisecond, and the tasks that engage them are simple enough for frail or cognitively impaired patients to complete. The anti-saccade task in particular has a long pedigree as a probe of frontal function, having revealed inhibitory deficits in schizophrenia, Parkinson’s disease, attention deficit hyperactivity disorder, and normal aging. Extending it to late-life depression connects that literature to one of geriatric psychiatry’s most pressing clinical problems and demonstrates that a disorder of mood leaves measurable fingerprints on one of the body’s fastest and most automatic behaviors.

What makes the finding resonate is its elegance: the same neural machinery that lets a person resist an impulsive glance at a flashing light also lets them resist impulsive decisions, hold plans in mind, and steer attention where it needs to go. When that machinery falters in late-life depression, the failure shows up first where it can be measured most precisely—in the eyes. If larger studies confirm the reliability of these saccade-based markers, the humble eye movement could become a routine vital sign of executive health in aging, transforming how clinicians detect, track, and ultimately treat the cognitive shadow that follows depression into later life.

Subject of Research: Executive dysfunction in late-life depression assessed through saccadic eye-movement control

Article Title: Altered saccade control reveals executive dysfunction in late-life depression

Article References: Lee, Y.-T., Tai, Y.-H., Huang, L.-K., Chen, K.-Y., Chen, T.-L., Chen, C., & Wang, C.-A. (2026). Altered saccade control reveals executive dysfunction in late-life depression. BMC Geriatrics. https://doi.org/10.1186/s12877-026-08427-1

Image Credits: AI Generated

DOI: 10.1186/s12877-026-08427-1

Keywords: late-life depression, saccades, anti-saccade task, executive control, eye tracking, superior colliculus, geriatric psychiatry, MoCA, cognitive control, prefrontal cortex, voluntary override time, BMC Geriatrics