Impact of COPD exacerbation on cerebral blood flow

Yıldız, Sema; Kaya, Ihsan; Çeçe, Hasan; Gençer, Mehmet; Ziylan, Zeki; Yalçın, Funda; Türksoy, Özlem

doi:10.1016/j.clinimag.2011.08.021

Cited by 15 publications

(11 citation statements)

References 33 publications

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“…There is a very interesting mechanism for counteracting cerebral hypoxemia, the so-called cerebrovascular oxygen reactivity, which ensures blood low up to 200% in the conditions of oxygen desaturation produced by chronic hypoxemia, nocturnal or exercise induced. For this reason, cerebral blood low is much higher in hypoxemic than in non-hypoxemic COPD patients and even healthy controls [32,33]. The same mechanism also explains that during rapid eye movement (REM) sleep, which accounts for about 13% of total sleep time in COPD patients, there is no cerebral hypoxemia.…”

Section: Copd: Fundamental Pathophysiological Mechanisms Susceptible mentioning

confidence: 66%

Neurocognitive Impairment as Systemic Effects of COPD

Oancea¹,

Tudorache²,

Tudorache³

2018

COPD - An Update in Pathogenesis and Clinical Management

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Mild cognitive impairment (MCI), also known as incipient dementia, is characterized by the decline of cognitive function greater than expected for a certain age and educational level of the individual but not severe enough to interfere with their daily activities. However, this mild cognitive impairment afects several areas: visuospatial, memory, atention and luency and it is a signiicant concern because it decreases the quality of life and treatment adherence of these patients. On the other hand, evidence suggests that individuals with Chronic obstructive pulmonary disease (COPD) also present an important risk of falls: 46% of these patients experience a fall/year, sometimes with fatal consequences. Standard clinical balance measures can predict the risk of falls in this population. Moreover, increased inlammatory biomarkers are associated with the decrease of cognitive functions and a higher risk of falls in this population. Patients with COPD have a higher balance and cognitive impairment than their healthy peers Therefore, it is important to identify, assess and understand the relevance of these comorbidities in order to characterize the full clinical spectrum of COPD and adjust prevention strategies, given the devastating consequences of these problems.

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Section: Copd: Fundamental Pathophysiological Mechanisms Susceptible mentioning

confidence: 66%

Neurocognitive Impairment as Systemic Effects of COPD

Oancea¹,

Tudorache²,

Tudorache³

2018

COPD - An Update in Pathogenesis and Clinical Management

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“…However, the roles of inflammation and oxidative stress in this dysfunction were not examined. Studies measuring cerebral blood flow in COPD patients have revealed contradictory findings [ 165 – 168 ]. Indeed, some investigators have revealed that cerebral blood flow is reduced in COPD patients [ 165 , 166 ], whereas other report that it is increased [ 167 , 168 ].…”

Section: Potential Mechanisms Linking Copd and Stroke Riskmentioning

confidence: 99%

COPD and stroke: are systemic inflammation and oxidative stress the missing links?

et al. 2016

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Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function, and is currently the third largest cause of death in the world. It is now well established that cardiovascular-related comorbidities such as stroke contribute to morbidity and mortality in COPD. The mechanisms linking COPD and stroke remain to be fully defined but are likely to be interconnected. The association between COPD and stroke may be largely dependent on shared risk factors such as aging and smoking, or the association of COPD with traditional stroke risk factors. In addition, we propose that COPD-related systemic inflammation and oxidative stress may play important roles by promoting cerebral vascular dysfunction and platelet hyperactivity. In this review, we briefly discuss the pathogenesis of COPD, acute exacerbations of COPD (AECOPD) and cardiovascular comorbidities associated with COPD, in particular stroke. We also highlight and discuss the potential mechanisms underpinning the link between COPD and stroke, with a particular focus on the roles of systemic inflammation and oxidative stress.

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“…These results cannot be due to oxygen desaturation because the exercise did not induce SpO 2 changes. Similarly, it may not be explained by lower resting cerebral blood flow due to resting blood gases abnormalities because cerebrovascular reactivity to hypoxemia (increase in cerebral blood flow when PaO 2 decreases) is preserved in COPD [38], [39]. According to the neurovascular coupling principle (as previously explained in the methods section), the data thus obtained with the fNIRS technique suggest a smaller local hyperoxygenation at the cortex in COPD patients compared with healthy controls.…”

Section: Discussionmentioning

confidence: 81%

Cortical Implication in Lower Voluntary Muscle Force Production in Non-Hypoxemic COPD Patients

et al. 2014

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Recent studies have shown that muscle alterations cannot totally explain peripheral muscle weakness in COPD. Cerebral abnormalities in COPD are well documented but have never been implicated in muscle torque production. The purpose of this study was to assess the neural correlates of quadriceps torque control in COPD patients. Fifteen patients (FEV1 54.1±3.6% predicted) and 15 age- and sex-matched healthy controls performed maximal (MVCs) and submaximal (SVCs) voluntary contractions at 10, 30 and 50% of the maximal voluntary torque of the knee extensors. Neural activity was quantified with changes in functional near-infrared spectroscopy oxyhemoglobin (fNIRS-HbO) over the contralateral primary motor (M1), primary somatosensory (S1), premotor (PMC) and prefrontal (PFC) cortical areas. In parallel to the lower muscle torque, the COPD patients showed lower increase in HbO than healthy controls over the M1 (p<0.05), PMC (p<0.05) and PFC areas (p<0.01) during MVCs. In addition, they exhibited lower HbO changes over the M1 (p<0.01), S1 (p<0.05) and PMC (p<0.01) areas during SVCs at 50% of maximal torque and altered motor control characterized by higher torque fluctuations around the target. The results show that low muscle force production is found in a context of reduced motor cortex activity, which is consistent with central nervous system involvement in COPD muscle weakness.

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Impact of COPD exacerbation on cerebral blood flow

Cited by 15 publications

References 33 publications

Neurocognitive Impairment as Systemic Effects of COPD

Neurocognitive Impairment as Systemic Effects of COPD

COPD and stroke: are systemic inflammation and oxidative stress the missing links?

Cortical Implication in Lower Voluntary Muscle Force Production in Non-Hypoxemic COPD Patients

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