Cerebral Perfusion and the Occurrence of Nonfocal Transient Neurological Attacks

INTRODUCTION: Nonfocal transient neurological attacks (TNAs) are associated with an increased risk of cardiac events, stroke and dementia. Their etiology is still unknown. Global cerebral hypoperfusion has been suggested to play a role in their etiology, but this has not been investigated. We assessed whether lower total brain perfusion is associated with a higher occurrence of TNAs. METHODS: Between 2015 and 2018, patients with heart failure were included in the Heart Brain Connection study. Patients underwent brain magnetic resonance imaging, including quantitative magnetic resonance angiography (QMRA) to measure cerebral blood flow (CBF). We calculated total brain perfusion of each participant by dividing total CBF by brain volume. Patients were interviewed with a standardized questionnaire on the occurrence of TNAs by physicians who were blinded to QMRA flow status. We assessed the relation between total brain perfusion and the occurrence of TNAs with Poisson regression analysis. RESULTS: Of 136 patients (mean age 70 years, 68% men), 29 (21%) experienced ≥1 TNAs. Nonrotatory dizziness was the most common subtype of TNA. Patients with TNAs were more often female and more often had angina pectoris than patients without TNAs, but total CBF and total brain perfusion were not different between both groups. Total brain perfusion was not associated with the occurrence of TNAs (adjusted risk ratio 1.12, 95% CI 0.88-1.42). CONCLUSION: We found no association between total brain perfusion and the occurrence of TNAs in patients with heart failure

Blood pressure and body mass index in an ethnically diverse sample of adolescents in Paramaribo, Suriname

<p>Abstract</p> <p>Background</p> <p>High blood pressure (BP) is now an important public health problem in non-industrialised countries. The limited evidence suggests ethnic inequalities in BP in adults in some non-industrialised countries. However, it is unclear whether these ethnic inequalities in BP patterns in adults reflect on adolescents. Hence, we assessed ethnic differences in BP, and the association of BP with body mass index (BMI) among adolescents aged 12–17 years in Paramaribo, Suriname.</p> <p>Methods</p> <p>Cross-sectional study with anthropometric and blood pressure measurements. A random sample of 855 adolescents (167 Hindustanis, 169 Creoles, 128 Javanese, 91 Maroons and 300 mixed-ethnicities) were studied. Ethnicity was based on self-reported ethnic origin.</p> <p>Results</p> <p>Among boys, Maroons had a lower age- and height-adjusted systolic BP than Creoles, and a lower diastolic BP than other ethnic groups. However, after further adjustment for BMI, only diastolic BP in Maroons was significantly lower than in Javanese (67.1 versus 70.9 mmHg). Creole boys had a lower diastolic BP than Hindustani (67.3 versus 70.2 mmHg) and Javanese boys after adjustment for age, height and BMI. Among girls, there were no significant differences in systolic BP between the ethnic groups. Maroon girls, however, had a lower diastolic BP (65.6 mmHg) than Hindustani (69.1 mmHg), Javanese (71.2 mmHg) and Mixed-ethnic (68.3 mmHg) girls, but only after differences in BMI had been adjusted for. Javanese had a higher diastolic BP than Creoles (71.2 versus 66.8 mmHg) and Mixed-ethnicity girls. BMI was positively associated with BP in all the ethnic groups, except for diastolic BP in Maroon girls.</p> <p>Conclusion</p> <p>The study findings indicate higher mean BP levels among Javanese and Hindustani adolescents compared with their African descent peers. These findings contrast the relatively low BP reported in Javanese and Hindustani adult populations in Suriname and underscore the need for public health measures early in life to prevent high BP and its sequelae in later life.</p

Nonfocal transient neurological attacks are related to cognitive impairment in patients with heart failure

Introduction Nonfocal transient neurological attacks (TNAs) are associated with an increased risk of future dementia, but it is unclear whether TNAs are also associated with concurrent cognitive impairment. We hypothesized that recent TNAs are related to worse cognitive functioning. We tested our hypothesis in patients with heart failure, as these patients are at risk of cerebral hypoperfusion, which might play a role in the etiology of TNAs. Methods We performed neuropsychological testing in all patients with heart failure enrolled in the Heart Brain Connection study. We assessed global cognition, attention-psychomotor speed, executive functioning, memory and language. All patients were interviewed with a standardized questionnaire on the occurrence of TNAs in the preceding 6 months. We studied associations between TNAs and cognitive functioning with linear and logistic regression analyses, adjusted for age, sex and education. We performed additional analyses in patients without previous stroke or TIA and in patients without brain infarction on MRI. Results Thirty-seven (23%) of 158 patients (mean age 70 years, 67% men) experienced one or more TNAs. Patients with a recent TNA were more likely to be impaired on≥1 cognitive domains than patients without TNAs [41% vs. 18%, adjusted odds ratio 4.6, 95% confdence interval (CI) 1.8–11.8]. Patients with TNAs performed worse than patients without TNAs on global cognition (mean diference in z scores −0.36, 95% CI −0.54 to −0.18), and on the cognitive domains attentionpsychomotor speed (mean diference −0.40, 95% CI −0.66 to −0.14), memory (mean diference −0.57, 95% CI −0.98 to −0.15) and language (mean diference −0.47, 95% CI −0.79 to −0.16). These associations were independent of cardiac output and volume of white matter hyperintensities. Subgroup analyses in patients without previous stroke or TIA or brain infarction on MRI (n=78) yielded comparable results, with the exception of the cognitive domain language, which was no longer diferent between patients with and without TNAs. Conclusion Among patients with heart failure, TNAs are associated with cognitive impairment, which warrants the need for more clinical awareness of this problem

Transient neurological attacks

Nonfocal transient neurological attacks (TNAs) are episodes with an acute onset of unexplained nonfocal symptoms that cannot be attributed to a specific territory of the brain, such as unsteadiness or bilateral weakness. These attacks are considered benign, possibly because the etiology of TNAs is still unknown. However, recent publications show that TNAs are not at all benign as they are associated with an increased risk of stroke, cardiac events and dementia. This thesis has tried to gain more insight in the etiology and cognitive consequences of TNAs. Given the nonfocal nature of TNAs, it was first hypothesized that they result from global brain hypoperfusion. Our results showed that TNAs are related to the presence of carotid artery occlusion. However, subsequently, we found no difference in 24-hour blood pressure characteristics between patients with and without TNAs, nor did we find a relation between TNAs and total brain perfusion. Therefore, our results do not support the hypothesis that TNAs are caused by global brain hypoperfusion. An alternative hypothesis is that TNAs are the result of focal brain ischemia. We investigated which mechanisms are involved in this process. We found that TNAs are related to lacunes and white matter hyperintensities on brain MRI, which suggests that a disease of the small brain vessels plays a role in the etiology of TNAs. Furthermore, we found that patients with a recent TNA are more often cognitively impaired than patients without TNAs

Transient neurological attacks

Nonfocal transient neurological attacks (TNAs) are episodes with an acute onset of unexplained nonfocal symptoms that cannot be attributed to a specific territory of the brain, such as unsteadiness or bilateral weakness. These attacks are considered benign, possibly because the etiology of TNAs is still unknown. However, recent publications show that TNAs are not at all benign as they are associated with an increased risk of stroke, cardiac events and dementia. This thesis has tried to gain more insight in the etiology and cognitive consequences of TNAs. Given the nonfocal nature of TNAs, it was first hypothesized that they result from global brain hypoperfusion. Our results showed that TNAs are related to the presence of carotid artery occlusion. However, subsequently, we found no difference in 24-hour blood pressure characteristics between patients with and without TNAs, nor did we find a relation between TNAs and total brain perfusion. Therefore, our results do not support the hypothesis that TNAs are caused by global brain hypoperfusion. An alternative hypothesis is that TNAs are the result of focal brain ischemia. We investigated which mechanisms are involved in this process. We found that TNAs are related to lacunes and white matter hyperintensities on brain MRI, which suggests that a disease of the small brain vessels plays a role in the etiology of TNAs. Furthermore, we found that patients with a recent TNA are more often cognitively impaired than patients without TNAs

Nonfocal transient neurological attacks in patients with carotid artery occlusion

Introduction: Nonfocal transient neurological attacks (TNAs) are episodes with atypical, nonlocalizing cerebral symptoms. We examined the prevalence of nonfocal TNAs, in patients with and without carotid artery occlusion (CAO). Methods: We included 67 patients with CAO and 62 patients without CAO. In both groups, patients had a history of transient ischemic attack (TIA) or nondisabling ischemic stroke in the anterior circulation that had occurred >6 months before inclusion. Patients without CAO did not have ipsilateral or contralateral carotid artery stenosis of ≥50%. All patients were interviewed with a standardized questionnaire on the occurrence of nonfocal TNA symptoms during the preceding six months. We calculated risk ratios (RRs) with 95% confidence intervals (CIs) for the occurrence of ≥1 and ≥2 different nonfocal TNAs after adjustments for age, sex, systolic blood pressure and time interval between most recent TIA or ischemic stroke and administration of the questionnaire. Results: Forty-three of all patients (33%) had had one or more nonfocal TNAs in the preceding six months. Nonrotatory dizziness (24%) was reported most often. The prevalence of ≥1 nonfocal TNAs was not significantly different between patients with and without CAO (39% vs. 27%; adjusted RR 1.47, 95% CI 0.83–2.61), but the prevalence of ≥2 or more different nonfocal TNAs was higher in patients with CAO (16% vs. 3%; adjusted RR 4.77, 95% CI 1.20–18.98). In patients with CAO who also had a contralateral carotid or vertebral artery steno-occlusion, nonfocal TNAs occurred more often than in patients without any carotid or vertebral artery steno-occlusion (46% vs. 27%; adjusted RR 2.22, 95% CI 1.08–4.60 for ≥1 and 21% vs. 3%; adjusted RR 8.27, 95% CI 1.83–37.32 for ≥2 nonfocal TNAs). Conclusions: Patients with CAO more often experienced multiple nonfocal TNAs than patients without CAO

Nonfocal transient neurological attacks in patients with carotid artery occlusion

Introduction: Nonfocal transient neurological attacks (TNAs) are episodes with atypical, nonlocalizing cerebral symptoms. We examined the prevalence of nonfocal TNAs, in patients with and without carotid artery occlusion (CAO). Methods: We included 67 patients with CAO and 62 patients without CAO. In both groups, patients had a history of transient ischemic attack (TIA) or nondisabling ischemic stroke in the anterior circulation that had occurred >6 months before inclusion. Patients without CAO did not have ipsilateral or contralateral carotid artery stenosis of ≥50%. All patients were interviewed with a standardized questionnaire on the occurrence of nonfocal TNA symptoms during the preceding six months. We calculated risk ratios (RRs) with 95% confidence intervals (CIs) for the occurrence of ≥1 and ≥2 different nonfocal TNAs after adjustments for age, sex, systolic blood pressure and time interval between most recent TIA or ischemic stroke and administration of the questionnaire. Results: Forty-three of all patients (33%) had had one or more nonfocal TNAs in the preceding six months. Nonrotatory dizziness (24%) was reported most often. The prevalence of ≥1 nonfocal TNAs was not significantly different between patients with and without CAO (39% vs. 27%; adjusted RR 1.47, 95% CI 0.83–2.61), but the prevalence of ≥2 or more different nonfocal TNAs was higher in patients with CAO (16% vs. 3%; adjusted RR 4.77, 95% CI 1.20–18.98). In patients with CAO who also had a contralateral carotid or vertebral artery steno-occlusion, nonfocal TNAs occurred more often than in patients without any carotid or vertebral artery steno-occlusion (46% vs. 27%; adjusted RR 2.22, 95% CI 1.08–4.60 for ≥1 and 21% vs. 3%; adjusted RR 8.27, 95% CI 1.83–37.32 for ≥2 nonfocal TNAs). Conclusions: Patients with CAO more often experienced multiple nonfocal TNAs than patients without CAO

Cerebral blood flow and cognitive functioning in patients with disorders along the heart–brain axis: Cerebral blood flow and the heart–brain axis

Introduction: We examined the role of hemodynamic dysfunction in cognition by relating cerebral blood flow (CBF), measured with arterial spin labeling (ASL), to cognitive functioning, in patients with heart failure (HF), carotid occlusive disease (COD), and patients with cognitive complaints and vascular brain injury on magnetic resonance imaging (MRI; ie, possible vascular cognitive impairment [VCI]). Methods: We included 439 participants (124 HF; 75 COD; 127 possible VCI; 113 reference participants) from the Dutch multi-center Heart–Brain Study. We used pseudo-continuous ASL to estimate whole-brain and regional partial volume-corrected CBF. Neuropsychological tests covered global cognition and four cognitive domains. Results: CBF values were lowest in COD, followed by VCI and HF, compared to reference participants. This did not explain cognitive impairment, as we did not find an association between CBF and cognitive functioning. Discussion: We found that reduced CBF is not the major explanatory factor underlying cognitive impairment in patients with hemodynamic dysfunction along the heart–brain axis.</p