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Objective/background Sleep-wake dysfunction is bidirectionally associated with the incidence and evolution of acute stroke. It remains unclear whether sleep disturbances are transient post-stroke or are potentially enduring sequelae in chronic stroke. Here, we characterize sleep architectural dysfunction, sleep-respiratory parameters, and hemispheric sleep in ischemic stroke patients in the chronic recovery phase compared to healthy controls. Patients/methods Radiologically confirmed ischemic stroke patients (n = 28) and matched control participants (n = 16) were tested with ambulatory polysomnography, bi-hemispheric sleep EEG, and demographic, stroke-severity, mood, and sleep-circadian questionnaires. Results Twenty-eight stroke patients (22 men; mean age = 69.61 ± 7.4 years) were cross-sectionally evaluated 4.1 ± 0.9 years after mild-moderate ischemic stroke (baseline NIHSS: 3.0 ± 2.0). Fifty-seven percent of stroke patients (n = 16) exhibited undiagnosed moderate-to-severe obstructive sleep apnea (apnea-hypopnea index >15). Despite no difference in total sleep or wake after sleep onset, stroke patients had reduced slow-wave sleep time (66.25 min vs 99.26 min, p = 0.02), increased time in non-rapid-eye-movement (NREM) stages 1–2 (NREM-1: 48.43 vs 28.95, p = 0.03; NREM-2: 142.61 vs 115.87, p = 0.02), and a higher arousal index (21.46 vs 14.43, p = 0.03) when compared to controls. Controlling for sleep apnea severity did not attenuate the magnitude of sleep architectural differences between groups (NREM 1-3= η p 2 >0.07). We observed no differences in ipsilesionally versus contralesionally scored sleep architecture. Conclusions Fifty-seven percent of chronic stroke patients had undiagnosed moderate-severe obstructive sleep apnea and reduced slow-wave sleep with potentially compensatory increases in NREM 1–2 sleep relative to controls. Formal sleep studies are warranted after stroke, even in the absence of self-reported history of sleep-wake pathology.

Hippocampal atrophy is seen in many neurodegenerative disorders and may be a cardinal feature of vascular neurodegeneration. We examined hippocampal volume (HV) in a group of ischemic stroke survivors with amyloid 18F-NAV4694 PET imaging three years after stroke. We compared HV between the amyloid-positive (n = 4) and amyloid-negative (n = 29) groups, and associations with co-morbidities using Charlson Comorbidity Indices and multi-way ANOVA. Amyloid status was not associated with verbal or visual delayed free recall memory indices or cognitive impairment. We found no association between amyloid status and HV in this group of ischemic stroke survivors.

Background Fatigue is associated with poor functional outcomes and increased mortality following stroke. Survivors identify fatigue as one of their key unmet needs. Despite the growing body of research into post-stroke fatigue, the specific neural mechanisms remain largely unknown. Aim This observational study aimed to identify resting state brain activity markers of post-stroke fatigue. Method Sixty-three stroke survivors (22 women; age 30–89 years; mean 67.5 ± 13.4 years) from the Cognition And Neocortical Volume After Stroke study, a cohort study examining cognition, mood, and brain volume in stroke survivors following ischemic stroke, underwent brain imaging three months post-stroke, including a 7-minute resting state functional magnetic resonance imaging. We calculated the fractional amplitude of low-frequency fluctuations, which is measured at the whole-brain level and can detect altered spontaneous neural activity of specific regions. Results Forty-five participants reported experiencing post-stroke fatigue as measured by an item on the Patient Health Questionnaire-9. Fatigued compared to non-fatigued participants demonstrated significantly lower resting-state activity in the calcarine cortex ( p FDR = 0.009, k = 63) and lingual gyrus ( p FDR = 0.025, k = 42) and significantly higher activity in the medial prefrontal cortex ( p FDR = 0.03, k = 45). Conclusions Post-stroke fatigue is associated with posterior hypoactivity and prefrontal hyperactivity reflecting dysfunction within large-scale brain systems such as fronto-striatal-thalamic and frontal-occipital networks. These systems in turn might reflect a relationship between post-stroke fatigue and abnormalities in executive and visual functioning. This whole-brain resting-state study provides new targets for further investigation of post-stroke fatigue beyond the lesion approach.

BACKGROUND: The apolipoprotein E (APOE) gene ɛ4 allele is a risk factor for Alzheimer's disease and cardiovascular disease. However, its relationship with cognition and brain volume after stroke is not clear. OBJECTIVE: We compared cognition and medial temporal lobe volumes in APOEɛ4 carriers and non-carriers in the first year after ischemic stroke. METHODS: We sampled 20 APOEɛ4 carriers and 20 non-carriers from a larger cohort of 135 ischemic stroke participants in the longitudinal CANVAS study. Participants were matched on a range of demographic and stroke characteristics. We used linear mixed-effect models to compare cognitive domain z-scores (attention, processing speed, executive function, verbal and visual memory, language, visuospatial function) and regional medial temporal lobe volumes (hippocampal, entorhinal cortex) between groups at each time-point (3, 12-months post-stroke), and within groups across time-points. APOE gene single nucleotide polymorphisms (SNPs; rs7412, rs429358) were genotyped on venous blood. RESULTS: APOEɛ4 carriers and non-carriers did not differ on any demographic, clinical, or stroke variable. Carriers performed worse than non-carriers in verbal memory at 3 months post-stroke (p = 0.046), but were better in executive function at 12 months (p = 0.035). Carriers demonstrated a significant improvement in verbal memory (p = 0.012) and executive function (p = 0.015) between time-points. Non-carriers demonstrated a significant improvement in visual memory (p = 0.0005). Carriers had smaller bilateral entorhinal cortex volumes (p

Background and PurposeFatigue is associated with poor functional outcomes and increased mortality following stroke. Survivors identify fatigue as one of their key unmet needs. Despite the growing body of research into post-stroke fatigue, the specific neural mechanisms remain largely unknown.MethodsThis observational study included 63 stroke survivors (22 women; age 30-89 years; mean 67.5±13.4 years) from the Cognition And Neocortical Volume After Stroke (CANVAS) study, a cohort study examining cognition, mood, and brain volume in stroke survivors following ischaemic stroke. Participants underwent brain imaging 3 months post-stroke, including a 7-minute resting state fMRI echoplanar sequence. We calculated the fractional amplitude of low-frequency fluctuations, a measure of resting state brain activity at the whole-brain level.ResultsForty-five participants reported experiencing post-stroke fatigue as measured by an item on the Patient Health Questionnaire-9. A generalised linear regression model analysis with age, sex, and stroke severity covariates was conducted to compare resting state brain activity in the 0.01-0.08 Hz range, as well as its subcomponents - slow-5 (0.01-0.027 Hz), and slow-4 (0.027-0.073 Hz) frequency bands between fatigued and non-fatigued participants. We found no significant associations between post-stroke fatigue and ischaemic stroke lesion location or stroke volume. However, in the overall 0.01-0.08 Hz band, participants with post-stroke fatigue demonstrated significantly lower resting-state activity in the calcarine cortex (pFDR=0.009, k=63) and lingual gyrus (pFDR=0.025, k=42) and significantly higher activity in the medial prefrontal cortex (pFDR=0.03, k=45), attributed to slow-4 and slow-5 oscillations, respectively.ConclusionsPost-stroke fatigue is associated with posterior hypoactivity and prefrontal hyperactivity, reflecting dysfunction within large-scale brain systems such as fronto-striatal-thalamic and frontal-occipital networks. These systems in turn might reflect a relationship between post-stroke fatigue and abnormalities in executive and visual functioning. This first whole-brain resting-state study provides new targets for further investigation of post-stroke fatigue beyond the lesion approach.

Introduction Hippocampal subfield volumes are more closely associated with cognitive impairment than whole hippocampal volume in many diseases. Both memory and whole hippocampal volume decline after stroke. Understanding the subfields’ temporal evolution could reveal valuable information about post‐stroke memory. Methods We sampled 120 participants (38 control, 82 stroke), with cognitive testing and 3T‐MRI available at 3 months and 3 years, from the Cognition and Neocortical Volume after Stroke (CANVAS) study. Verbal memory was assessed using the Hopkins Verbal Learning Test‐Revised. Subfields were delineated using FreeSurfer. We used partial Pearson's correlation to assess the associations between subfield volumes and verbal memory scores, adjusting for years of education, sex, and stroke side. Results The left cornu ammonis areas 2/3 and hippocampal tail volumes were significantly associated with verbal memory 3‐month post‐stroke. At 3 years, the associations became stronger and involved more subfields. Discussion Hippocampal subfield volumes may be a useful biomarker for post‐stroke cognitive impairment.

Introduction Compared to healthy individuals, stroke patients have five times the rate of dementia diagnosis within three years. Aerobic exercise may induce neuroprotective mechanisms that help to preserve, and even increase, brain volume and cognition. We seek to determine whether aerobic fitness training helps to protect brain volume and cognitive function after stroke compared to an active, non-aerobic control. Methods In this Phase IIb, single blind, randomised controlled trial, 100 ischaemic stroke participants, recruited at two months post-stroke, will be randomly allocated to either the intervention (aerobic and strength exercise) or active control (stretching and balance training). Participants will attend one-hour, individualised exercise sessions, three days-per-week for eight weeks. Assessments at two months (baseline), four months (post-intervention), and one year (follow-up) post-stroke will measure brain volume, cognition, mood, cardiorespiratory fitness, physical activity, blood pressure and blood biomarkers. Study outcome: Our primary outcome measure is hippocampal volume at four months after stroke. We hypothesise that participants who undertake the prescribed intervention will have preserved hippocampal volume at four months compared to the control group. We also hypothesise that this group will have preserved total brain volume and cognition, better mood, fitness, and higher levels of physical activity, than those receiving stretching and balance training. Discussion The promise of exercise training to prevent, or slow, the accelerated rates of brain atrophy and cognitive decline experienced by stroke survivors needs to be tested. Post Ischaemic Stroke Cardiovascular Exercise Study has the potential, if proven efficacious, to identify a new treatment that could be readily translated to the clinic.

Highlights • First-year hippocampal atrophy in stroke is more accelerated ipsi-lesionally. • Volume estimation is not impacted by hemisphere side, study group, or scan timepoint. • Segmentation method-hippocampal size interaction determines volume estimation. • FreeSurfer/Subfields and fsl/FIRST segmentations agreed best with manual tracing., We assessed first-year hippocampal atrophy in stroke patients and healthy controls using manual and automated segmentations: AdaBoost, FIRST (fsl/v5.0.8), FreeSurfer/v5.3 and v6.0, and Subfields (in FreeSurfer/v6.0). We estimated hippocampal volumes in 39 healthy controls and 124 stroke participants at three months, and 38 controls and 113 stroke participants at one year. We used intra-class correlation, concordance, and reduced major axis regression to assess agreement between automated and ‘Manual’ estimations. A linear mixed-effect model was used to characterize hippocampal atrophy. Overall, hippocampal volumes were reduced by 3.9% in first-ever stroke and 9.2% in recurrent stroke at three months post-stroke, with comparable ipsi-and contra-lesional reductions in first-ever stroke. Mean atrophy rates between time points were 0.5% for controls and 1.0% for stroke patients (0.6% contra-lesionally, 1.4% ipsi-lesionally). Atrophy rates in left and right-hemisphere strokes were comparable. All methods revealed significant volume change in first-ever and ipsi-lesional stroke (p

Objective:To examine associations between ischemic stroke, vascular risk factors, and MRI markers of brain aging.Methods:Eighty-one patients (mean age 67.5 ± 13.1 years, 31 left-sided, 61 men) with confirmed first-ever (n = 66) or recurrent (n = 15) ischemic stroke underwent 3T MRI scanning within 6 weeks of symptom onset (mean 26 ± 9 days). Age-matched controls (n = 40) completed identical testing. Multivariate regression analyses examined associations between group membership and MRI markers of brain aging (cortical thickness, total brain volume, white matter hyperintensity [WMH] volume, hippocampal volume), normalized against intracranial volume, and the effects of vascular risk factors on these relationships.Results:First-ever stroke was associated with smaller hippocampal volume (p = 0.025) and greater WMH volume (p = 0.004) relative to controls. Recurrent stroke was in turn associated with smaller hippocampal volume relative to both first-ever stroke (p = 0.017) and controls (p = 0.001). These associations remained significant after adjustment for age, sex, education, and, in stroke patients, infarct volume. Total brain volume was not significantly smaller in first-ever stroke patients than in controls (p = 0.056), but the association became significant after further adjustment for atrial fibrillation (p = 0.036). Cortical thickness and brain volumes did not differ as a function of stroke type, infarct volume, or etiology.Conclusions:Brain structure is likely to be compromised before ischemic stroke by vascular risk factors. Smaller hippocampal and total brain volumes and increased WMH load represent proxies for underlying vascular brain injury.

Objectives The aim of the current study was to examine trajectories of brain volume and cognition in ischaemic stroke patients in the first year after their events and compare results with age-matched controls. Methods In the Cognition And Neocortical Volume After Stroke (CANVAS) study, we assessed ischaemic stroke patients within six weeks of their events and at 12 months post-stroke, and compared their results to healthy, age-matched controls. All participants were without dementia. Brain volume was assessed with high-resolution 3T MPRAGE MRI. FreeSurfer v5.1 was used to obtain total brain, hippocampal and thalamic volumes. The Hopkins Verbal Learning Test-Revised (HVLT-R) was used to assess memory, and the computerised Cogstate Battery was used to assess processing speed, working memory and attention. Results Sixty-five stroke patients (51 male; age 65.98±11.6 years, education 12.71±3.9 years; baseline NIHSS 3.3±2.6; days post-stroke 26.83±9) and 38 controls (23 male; age 68.6±6.8; education 15.68±4.5 years) completed their assessments at baseline and 12 months. Oxfordshire classifications were PACI 31; POCI 25; LACI 9. Brain volumes were averaged across hemispheres for controls. Between baseline and 12 months, rates of decline in total brain volume, ipsilesional thalamic volume and ipsilesional hippocampal volume were significantly greater in stroke patients relative to controls (p 0.05). Rates of cognitive decline over the same period were comparable between groups (p>0.05). Conclusions Brain volume loss precedes cognitive decline in the first year after ischaemic stroke. Tracking brain volume after stroke is important because brain volume is predictive of cognitive decline and atrophy is a hallmark of dementia.

Q ualitative ratings of smooth pursuit eye movements were significantly worse for 14 undergraduates with DSM-III-R schizotypal personality disorder than for 1 8 comparison subjects. The groups did not differ on IQ, indicating that deficits in smooth pursuit eye movements in schizotypal personality disorder are not a function of cognitive deficits. (Am J Psychiatry 1993; 150:152-154)

Further understanding at neuroscientific and personality levels should considerably advance our ability to deal with individuals that have strong sociopathic tendencies. An analysis of neurodynamic responses to emotional stimuli will eventually be able to detect sociopathic tendencies of the brain. Such information could be used to enhance the options available to individuals at risk without limiting their personal freedoms.