Microstructural Change of the Brain in Chronic Obstructive Pulmonary Disease: A Voxel-Based Investigation by MRI

Ryu, Chang‐Woo; Jahng, Geon‐Ho; Choi, Cheon Woong; Rhee, Hak Young; Kim, Minji; Kim, Sun Mi; Kim, Eui Jong; Choi, Woo Suk

doi:10.3109/15412555.2012.752808

Cited by 25 publications

(23 citation statements)

References 33 publications

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“…Cluster labels correspond to those given in Table 2. SFG=superior frontal gyrus, dmPFC=dorsomedial prefrontal cortex, Pre-SMA=pre-supplement motor area neuroimaging study also did not find any local WM volume reduction in the patients with COPD (Ryu et al 2013). Our findings are, at least partly, consistent with previous VBM studies, which reported gray matter volume reductions in prefrontal, temporal and motor cortices (Zhang et al 2012(Zhang et al , 2013.…”

Section: Discussionmentioning

confidence: 92%

Reduced cortical thickness, surface area in patients with chronic obstructive pulmonary disease: a surface-based morphometry and neuropsychological study

Chen

Lin

Zhang

et al. 2015

Brain Imaging and Behavior

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Neural impairments accompanying chronic obstructive pulmonary disease (COPD) have received growing research attention. Previous neuroimaging studies exclusively used volumetric methods to measure cortical volume as a whole rather than focusing on anatomical and neuropathological distinct indices. Here we decomposed the cortical architecture into cortical thickness (CTh), surface area (SA), and gyrification, for the first time, to provide a more integrative profile of brain damage in COPD. Clinical T1-weighted MRI scans were acquired in 25 stable COPD patients (mean age 69) and 25 age-matched controls. Images were processed using surface-based morphometry to obtain cortical parameters enabling more accurate measurement in deep sulci and localized regional mapping. Demographic, physiological, and cognitive assessments were made and correlated with cortical indices. Compared to controls, COPD patients showed significantly reduced CTh broadly distributed in motor, parietal, and prefrontal cortices, together with more circumscribed SA reduction in dorsomedial prefrontal cortex and Broca's area (cluster-level P < 0.05 corrected). No abnormal gyrification was detected. Decreased CTh in parietofrontal networks strongly correlated with visuospatial construction impairment in COPD patients. Furthermore, thinner dorsolateral prefrontal cortex (DLPFC) best predicted poorer performance (r (2) = 0.315, P = 0.004), and was associated with lower arterial oxygen saturation. These data indicate that cortical thinning is a key morphologic feature associated with COPD that could be partly attributed to oxygen desaturation and contributes to COPD visual memory and drawing deficits. Surface-based morphometry provides valuable information concerning COPD, and could ultimately help us to characterize the neurodegenerative pattern and to clarify neurologic mechanisms underlying cognitive dysfunction in COPD patients.

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Section: Discussionmentioning

confidence: 92%

Reduced cortical thickness, surface area in patients with chronic obstructive pulmonary disease: a surface-based morphometry and neuropsychological study

Chen

Lin

Zhang

et al. 2015

Brain Imaging and Behavior

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“…Reduced WM integrity in the superior and middle frontal gyri and right occipital subcortical WM was shown in patients with moderate COPD [32]. WM integrity was more reduced in the bilateral frontal subcortical areas, right temporal lobe and pons in severe compared to moderate COPD.…”

Section: Longitudinal Studiesmentioning

confidence: 88%

“…CI is associated with global and/or specific cerebral abnormalities, and many studies have found structural or functional abnormalities in patients with COPD, along with elevated serum levels of S100B, a putative marker for brain damage [28]. Cortical degeneration [29][30][31][32], increased occurrence of small vessel disease [33] or abnormal functional activation on a global level is uncommon in COPD, with a few exceptions. Two studies found overall increased white matter (WM) lesion volumes and decreased WM integrity [30,31], and cortical thickness and volume were globally reduced in patients who were hospitalized for 30-45 days following an exacerbation [34].…”

Section: Longitudinal Studiesmentioning

confidence: 99%

Cognitive impairment in chronic obstructive pulmonary disease: disease burden, determinants and possible future interventions

Beers

Janssen

Gosker

et al. 2018

Expert Review of Respiratory Medicine

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Introduction: Cognitive impairment (CI) is an important but an under-recognized extra-pulmonary feature of chronic obstructive pulmonary disease (COPD). It is related to the burden of disability, worse health outcomes, and impaired self-management. Areas covered: CI includes deterioration of a wide range of cognitive functions, such as memory and various executive functions. Risk of hospitalization might be higher in patients with COPD compared to those without, with CI negatively impacting the wellbeing of patients with COPD. Disease-specific factors such as hypoxemia and inflammation, lifestyle factors such as dietary insufficiencies and lack of physical activity, and comorbidities such as obstructive sleep apnea and depression are likely to synergistically contribute to the development of CI in COPD. Tailored interventions can possibly improve CI in COPD, but this needs further investigation. Expert commentary: Further research is warranted involving the optimization of neuropsychological testing for screening and outcome assessment, longitudinal studies to investigate the development of CI in COPD over time, and randomized clinical trials to test the feasibility and efficacy of promising interventions.

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“…Furthermore, lower neural drive to the muscle can be ascribed to at least three mechanisms, which have never been questioned in the context of muscle weakness in COPD. First, decreased excitation from the brain is strongly expected in these patients given the decreased gray matter density in the motor and prefrontal cortex [22,23] and the presence of white matter lesions in the pyramidal neurons [24]. Second, lengthened latency and lower amplitude of the maximal compound muscle action potential (Mmax) have also been described in COPD patients and suggest impaired neuromuscular transmission at the motor neuron and/or the motor plate level [25][26][27][28].…”

Section: Introductionmentioning

confidence: 99%

Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness

Alexandre

Héraud²,

Tremey³

et al. 2020

BMC Pulm Med

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Background: Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness. Methods: Twenty-two patients with quadriceps weakness (COPD MW), 18 patients with preserved quadriceps strength (COPD NoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA peripheral) and transcranial magnetic (VA cortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions. Results: COPD MW exhibited lower VA cortical and lower MEP/Mmax compared with COPD NoMW (p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA cortical and MEP/Mmax. Conclusions: COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.

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Microstructural Change of the Brain in Chronic Obstructive Pulmonary Disease: A Voxel-Based Investigation by MRI

Abstract: This study demonstrated that COPD could affect the axonal integrity in multiple brain regions, and change in DTI might be related with the severity of the COPD.

Cited by 25 publications

References 33 publications

Reduced cortical thickness, surface area in patients with chronic obstructive pulmonary disease: a surface-based morphometry and neuropsychological study

Reduced cortical thickness, surface area in patients with chronic obstructive pulmonary disease: a surface-based morphometry and neuropsychological study

Cognitive impairment in chronic obstructive pulmonary disease: disease burden, determinants and possible future interventions

Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness

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