The Effects of Chronic Migraine And Tension Headache On Neuropsychological Functioning

The present study was designed to examine possible neuropsychological deficits in migraine and tension headache subjects. Past research has been inconclusive, with some studies indicating that chronic migraine headache sufferers do exhibit some neuropsychological deficits such as short-term memory difficulties, gross motor slowing, and verbal memory deficits, while other studies have indicated that no deficits are seen in this group Also examined were headache precipitant and headache-related behaviors that these groups partake in when experiencing headache pain. Past research has suggested that migraine headache sufferers tend to deal with their headache pain differently than tension headache sufferers. Ninety undergraduate psychology students took part in a 1 1/2 hour testing session where they completed a series of questionnaires about their headaches and neuropsychological testing. Analysis of questionnaire data revealed that both tension and migraine headache sufferers consistently attributed their headaches to the same types of precipitants, though they tended to cope with headache pain in different ways. Analysis of neuropsychological data revealed that once the effects of depression had been factored out by ANCOVA, no significant differences between migraine headache sufferers and the other groups existed. In fact, the migraine headache sufferers showed a tendency to perform better than the other groups while experiencing depression. Chisquare revealed a significant number of subjects from all three groups scored in the impaired range on many of the tests, though there were no significant differences between groups in the number of subjects scoring in the impaired range. It remains puzzling as to exactly why this is the case and findings certainly require replication. Future neuropsychological investigations of migraine conducted longitudinally would be helpful in delineating the neuropsychological changes that may or may not occur in migraine headache sufferers

SIGNIFICANTLY LOWER RIGHT MIDDLE CEREBRAL ARTERY BLOOD FLOW VELOCITY IN THE FIRST EPISODE OF PSYCHOSIS DURING NEUROCOGNITIVE TESTING

Background: Changes in cerebral hemodynamics have been reported in schizophrenia and proposed as underlying the cognitive deficits seen in patients. The objective of our study was to compare changes of the cerebral blood flow velocity (BFV) during neurocognitive tasks between the patients with the first episode of psychosis and healthy controls. Subjects and methods: We recruited 46 patients with the first episode of psychosis (FEP), admitted to the University Hospital Centre Zagreb during 2016-2017 and 41 control subjects. Transcranial Doppler ultrasonography monitoring of BFV in both middle cerebral arteries was recorded during 25-minute long neurocognitive assessment with Phonemic Verbal Fluency test, Trial Making Test B and Stroop test. Between every consecutive test resting periods were recorded. Results: After the adjustment for age, sex and education by quantile regression, patients with FEP had significantly lower BFV in middle cerebral arteries during the 3rd

The effects of hemodynamic lag on functional connectivity and behavior after stroke

Stroke disrupts the brain's vascular supply, not only within but also outside areas of infarction. We investigated temporal delays (lag) in resting state functional magnetic resonance imaging signals in 130 stroke patients scanned two weeks, three months and 12 months post stroke onset. Thirty controls were scanned twice at an interval of three months. Hemodynamic lag was determined using cross-correlation with the global gray matter signal. Behavioral performance in multiple domains was assessed in all patients. Regional cerebral blood flow and carotid patency were assessed in subsets of the cohort using arterial spin labeling and carotid Doppler ultrasonography. Significant hemodynamic lag was observed in 30% of stroke patients sub-acutely. Approximately 10% of patients showed lag at one-year post-stroke. Hemodynamic lag corresponded to gross aberrancy in functional connectivity measures, performance deficits in multiple domains and local and global perfusion deficits. Correcting for lag partially normalized abnormalities in measured functional connectivity. Yet post-stroke FC-behavior relationships in the motor and attention systems persisted even after hemodynamic delays were corrected. Resting state fMRI can reliably identify areas of hemodynamic delay following stroke. Our data reveal that hemodynamic delay is common sub-acutely, alters functional connectivity, and may be of clinical importance

The role of obstructive sleep apnea syndrome in the pathogenesis and evolution of dementia

Premessa e scopo. Il sonno è coinvolto nel mantenimento dell’ integrità anatomica e funzioni cerebrale attraverso meccanismi diversi, tra cui la promozione della plasticità sinaptica, il consolidamento della memoria e l'attività scavenger. Studi epidemiologici suggeriscono che la sindrome delle apnee ostruttive del sonno (OSAS) può aumentare il rischio di deterioramento cognitivo. Una conoscenza più approfondita del legame fisiopatologico tra OSAS e demenza e la dimostrazione che l’OSAS è in grado di influenzare direttamente lo sviluppo di alterazioni cognitive, potrebbe portare ad un miglioramento delle strategie di prevenzione e trattamento. L'obiettivo principale di questo studio è stato quello di valutare la correlazione tra deficit cognitivo e la presenza / gravità dell’OSAS, così come la possibile influenza di fattori vascolari. Soggetti e metodi. Sono stati arruolati 41 soggetti senza demenza affetti da OSAS, diagnosticata con una polisonnografia. Al basale, tutti i soggetti sono stati sottoposti ad uno screening vascolare completo e standardizzato, incluso uno studio della reattività cerebrovascolare mediante il calcolo dell’indice di apnea volontaria (BHI) sulla base della valutazione con Doppler transcranico. E’ stata inoltre eseguita una valutazione neuropsicologica per studiare i principali domini cognitivi. Come controlli, sono sati arruolati e sottoposti allo stesso protocollo di valutazione vascolare e cognitiva soggetti con caratteristiche anagrafiche simili, non affetti da OSAS. Tutti i pazienti con OSAS sono stati sottoposti al miglior protocollo di trattamento in base alle raccomandazioni delle linee guida internazionali e rivalutati dopo 6 mesi. In questo momento, ogni paziente ha ripetuto gli esami polisomnografici, neuropsicologici e ultrasonografici. Risultati. Al basale, le prestazioni cognitive erano più basse nei pazienti rispetto ai controlli nei seguenti compiti: Stroop test T1 e T2 e E1 ed E2 (p = 0,001), test delle parole di Rey per l’apprendimento verbale a breve termine / lungo termine (p = 0,0001 e 0,001, rispettivamente) e test di fluenza semantica e fonetica (p = 0,001). Considerando la reattività cerebrovascolare, una differenza significativa tra pazienti e controlli era presente per il BHI medio (p <0.05). Alla valutazione a 6 mesi, sulla base dei risultati del confronto tra le due valutazioni polisonnografiche, 21 pazienti presentavano un miglioramento della gravità dell’OSAS (gruppo 1) e 20 erano rimasti stabili (gruppo 2). Nel gruppo 1 è stato trovato un miglioramento significativo nel BHI sinistro (p = 0.001) e medio (p = 0.001) e nel test delle parole di Rey per l’apprendimento verbale a breve termine (p = 0.02) e a lungo termine (p = 0,001). Nessun cambiamento nella reattività cerebrovascolare e nel profilo cognitivo è stato rilevato nei pazienti del gruppo. Conclusioni. Il dato più significativo di questo studio riguarda la dimostrazione di una significativa associazione tra OSAS e riduzione dell’efficienza in alcuni compiti cognitivi in pazienti senza una storia di demenza. Il legame tra la riduzione delle prestazioni cognitive e le alterazioni emodinamiche cerebrali suggerisce un possibile ruolo patogenetico di una condizione circolatoria sfavorevole nel sostenere la disfunzione cerebrale nell’OSAS. La possibilità di migliorare le alterazioni vascolari e cognitive con trattamenti specifici merita una attenta considerazione per una strategia terapeutica completa e tempestiva nei pazienti con OSAS al fine di ridurre il rischio di sviluppo di un deterioramento cognitivo.ABSTRACT Background. Sleep is involved in maintaining cerebral anatomic integrity and functions through different mechanisms including promotion of synaptic plasticity, memory consolidation and scavenger activity. Epidemiological studies suggest that obstructive sleep apnea syndrome (OSAS) may increase the risk of cognitive impairment. A deeper knowledge of the pathophysiological link between OSAS and dementia and the demonstration that OSAS may directly influence the development of cognitive alterations, would improve prevention and treatment strategies. The main aim of this study was to evaluate the correlation between cognitive impairment and presence/severity of OSAS, as well as the possible influence of vascular factors. Subjects and methods. Forty-one non demented subjects with OSAS, diagnosed with an all-night polysomnography were enrolled. At baseline, all subjects underwent a complete and standardized vascular screening including a study of cerebrovascular reactivity by means of the breath-holding index (BHI) calculation based on transcranial Doppler evaluation. A neuropsychological evaluation to study main cognitive domains was also performed. As controls, an age- and sex-matched group of subjects without OSAS were enrolled and submitted to the same protocol of vascular and cognitive assessment. All OSAS patients were submitted to the best treatment protocol according with International specific guidelines and re-evaluated after 6 months. At this time, each patient repeated polisomnographic, neuropsychologic and transcranial Doppler assessment. Results. At baseline, the cognitive performances were lower in patients with respect to controls in the following tasks: Stroop Test T1 and T2 and E1 and E2 (p=0.001), Rey auditory verbal learning test (AVLT) short-term/long-term (p=0.0001 and 0.001, respectively) and semantic and phonetic fluency test (p=0.001). Considering cerebrovascular reactivity, a significant difference between patients and controls was present in mean BHI (p<0.05). At the 6-month evaluation, based on the results of the comparison between the polisomnographic evaluations, 21 patients had an improvement of OSAS severity (group 1) and 20 remained stable (group 2). In group 1 patients, a significant improvement was found in left and mean BHI (p=0.001) and in short-term (p=0.02) and long-term Rey AVLT (p=0.001) No change in cerebrovascular reactivity and cognitive profile was detected in group 2 patients. Conclusions. The main finding of the present study was the demonstration of a significant association between OSAS and reduced efficiency in some cognitive tasks in patients without a history of dementia. The link between reduced cognitive performances and alteration in cerebral hemodynamics suggests a possible pathogenic role of unfavorable circulatory changes in sustaining the cerebral dysfunction in OSAS. The possibility to improve vascular and cognitive alterations with specific treatments deserves full consideration for a comprehensive and timely therapeutic strategy in OSAS patients in order to reduce the risk of cognitive impairment

Enhanced task-related brain activation and resting perfusion in healthy older adults after chronic blueberry supplementation

© 2017, Canadian Science Publishing. All rights reserved. Blueberries are rich in flavonoids, which possess antioxidant and anti-inflammatory properties. High flavonoid intakes attenuate age-related cognitive decline, but data from human intervention studies are sparse. We investigated whether 12 weeks of blueberry concentrate supplementation improved brain perfusion, task-related activation, and cognitive function in healthy older adults. Participants were randomised to consume either 30 mL blueberry concentrate providing 387 mg anthocyanidins (5 female, 7 male; age 67.5 ± 3.0 y; body mass index, 25.9 ± 3.3 kg·m−2) or isoenergetic placebo (8 female, 6 male; age 69.0 ± 3.3 y; body mass index, 27.1 ± 4.0 kg·m−2). Pre-and postsupplementation, participants undertook a battery of cognitive function tests and a numerical Stroop test within a 1.5T magnetic resonance imaging scanner while functional magnetic resonance images were continuously acquired. Quantitative resting brain perfusion was determined using an arterial spin labelling technique, and blood biomarkers of inflammation and oxidative stress were measured. Significant increases in brain activity were observed in response to blueberry supplementation relative to the placebo group within Brodmann areas 4/6/10/ 21/40/44/45, precuneus, anterior cingulate, and insula/thalamus (p < 0.001) as well as significant improvements in grey matter perfusion in the parietal (5.0 ± 1.8 vs-2.9 ± 2.4%, p = 0.013) and occipital (8.0 ± 2.6 vs-0.7 ± 3.2%, p = 0.031) lobes. There was also evidence suggesting improvement in working memory (2-back test) after blueberry versus placebo supplementation (p = 0.05). Supplementation with an anthocyanin-rich blueberry concentrate improved brain perfusion and activation in brain areas associated with cognitive function in healthy older adults

Cerebrovascular mental stress reactivity is impaired in hypertension

<p>Abstract</p> <p>Background</p> <p>Brachial artery reactivity in response to shear stress is altered in subjects with hypertension. Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.</p> <p>Purpose</p> <p>To compare (CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects.</p> <p>Methods</p> <p>We evaluated CA reactivity to mental stress in 10 young healthy human volunteers (aged 23 ± 4 years), 20 older healthy volunteers (aged 49 ± 11 years) and in 28 patients with essential hypertension (aged 51 ± 13 years). In 10 healthy volunteers and 12 hypertensive subjects, middle cerebral artery (MCA) PW transcranial Doppler was performed before and 3 minutes after mental stress.</p> <p>Results</p> <p>Mental stress by Stroop color word conflict, math or anger recall tests caused CA vasodilation in young healthy subjects (0.61 ± 0.06 to 0.65 ± 0.07 cm, p < 0.05) and in older healthy subjects (0.63 ± 0.06 to 0.66 ± 0.07 cm, p < 0.05), whereas no CA vasodilation occurred in hypertensive subjects (0.69 ± 0.06 to 0.68 ± 0.07 cm; p, NS). CA blood flow in response to mental stress increased in young healthy subjects (419 ± 134 to 541 ± 209 ml, p < 0.01 vs. baseline) and in older healthy subjects (351 ± 114 to 454 ± 136 ml, p < 0.01 vs. baseline) whereas no change in blood flow (444 ± 143 vs. 458 ± 195 ml; p, 0.59) occurred in hypertensive subjects. There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects. Mental stress caused a significant increase in baseline to peak MCA systolic (84 ± 22 to 95 ± 22 cm/s, p < 0.05), diastolic (42 ± 12 to 49 ± 14 cm/s, p < 0.05) as well as mean (30 ± 13 to 39 ± 13 cm/s, p < 0.05) PW Doppler velocities in normal subjects, whereas no change in systolic (70 ± 18 to 73 ± 22 cm/s, p < 0.05), diastolic (34 ± 14 to 37 ± 14 cm/s, p = ns) or mean velocities (25 ± 9 to 26 ± 9 cm/s, p = ns) occurred in hypertensive subjects, despite a similar increase in heart rate and blood pressure in response to mental stress in both groups.</p> <p>Conclusion</p> <p>Mental stress produces CA vasodilation and is accompanied by an increase in CA and MCA blood flow in healthy subjects. This mental stress induced CA vasodilation and flow reserve is attenuated in subjects with hypertension and may reflect cerebral vascular endothelial dysfunction. Assessment of mental stress induced CA reactivity by ultrasound is a novel method for assessing the impact of hypertension on cerebrovascular endothelial function and blood flow reserve.</p

Investigating the origin and evolution of cerebral small vessel disease: The RUN DMC - InTENse study

Background Neuroimaging in older adults commonly reveals signs of cerebral small vessel disease (SVD). SVD is believed to be caused by chronic hypoperfusion based on animal models and longitudinal studies with inter-scan intervals of years. Recent imaging evidence, however, suggests a role for acute ischaemia, as indicated by incidental diffusion-weighted imaging lesions (DWI+ lesions), in the origin of SVD. Furthermore, it becomes increasingly recognised that focal SVD lesions likely affect the structure and function of brain areas remote from the original SVD lesion. However, the temporal dynamics of these events are largely unknown. Aims (1) To investigate the monthly incidence of DWI+ lesions in subjects with SVD;(2) to assess to which extent these lesions explain progression of SVD imaging markers;(3) to investigate their effects on cortical thickness, structural and functional connectivity and cognitive and motor performance;and (4) to investigate the potential role of the innate immune system in the pathophysiology of SVD. Design/methods The RUN DMC - InTENse study is a longitudinal observational study among 54 non-demented RUN DMC survivors with mild to severe SVD and no other presumed cause of ischaemia. We performed MRI assessments monthly during 10 consecutive months (totalling up to 10 scans per subject), complemented with clinical, motor and cognitive examinations. Discussion Our study will provide a better understanding of the role of DWI+ lesions in the pathophysiology of SVD and will further unravel the structural and functional consequences and clinical importance of these lesions, with an unprecedented temporal resolution. Understanding the role of acute, potentially ischaemic, processes in SVD may provide new strategies for therapies