Sub-acute stroke demonstrates altered beta oscillation and connectivity pattern in working memory

 

Big fucking whoopee.

 

 But you tell us NOTHING ABOUT A SOLUTION Useless!

Sub-acute stroke demonstrates altered beta oscillation and connectivity pattern in working memory

• Lin Mao,
• Xianwei Che,
• Juehan Wang,
• Xiaorui Jiang,
• Yifan Zhao,
• Liliang Zou,
• Shuang Wei,
• Shuyi Pan,
• Dazhi Guo,
• Xueqiong Zhu,
• Dongxia Hu,
• Xiaofeng Yang,
• Zuobing Chen &
• Daming Wang 

Journal of NeuroEngineering and Rehabilitation volume 21, Article number: 212 (2024) Cite this article

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Abstract

Introduction

Working memory (WM) is suggested to play a pivotal role in relearning and neural restoration during stroke rehabilitation. Using EEG, this study investigated the oscillatory mechanisms of WM in subacute stroke.

Methods

This study included 48 first subacute stroke patients (26 good-recovery, 22 poor-recovery, based on prognosis after a 4-week period) and 24 matched health controls. We examined the oscillatory characteristics and functional connectivity of the 0-back WM paradigm and assessed their associations with prognosis.

Results

Patients of poor recovery are characterised by a loss of significant beta rebound, beta-band connectivity, as well as impaired working memory speed and performances. Meanwhile, patients with good recovery have preserved these capacities to some extent. Our data further identified beta rebound to be closely associated with working memory speed and performances.

Conclusions

We provided novel findings that beta rebound and network connectivity as mechanistic evidence of impaired working memory in subacute stroke. These oscillatory features could potentially serve as a biomarker for brain stimulation technologies in stroke recovery.

Introduction

Stroke is the third most common cause of morbidity and the second most common cause of dementia [1]. The most common symptoms of stroke include physical deficits (such as paralysis, and sensory loss) and dysfunction in learning, memory, and executive functions. When it comes to cognitive function, working memory (WM) has a fundamental role in performing complex behaviours and is associated with poor functional outcomes after a stroke [2, 3].

An abrupt, cliff-like decline in brain function represents a key difference between acute stroke and neurodegenerative cerebral disorders. More importantly, this pattern of cognitive decline exhibits reversibility within a defined temporal framework [4], which is critical for both neural restoration and clinical rehabilitation. In clinical practices, there is also evidence supporting the ability to regain partial functions or develop compensatory skills through the process of learning [5]. Notably, working memory underpins the learning processes [2], making it critical for neural restoration and clinical rehabilitation. It is therefore important to investigate the behavioural and neural dynamics of WM, offering insights for the development of more effective rehabilitation strategies.(WHOM SPECIFICALLY DID YOU CONTACT TO GET THAT RESEARCH DONE? NO ONE? So, you're a complete failure at doing your job?)

Working memory is defined as a multi-component system involved in goal-directed behaviours that involve retaining and manipulating information [6]. N-back task is a well-validated and widely used means of manipulating working memory capacity and its response requirements [7]. Among them, 0-back requires less workload, which is highly suitable for post-stroke individuals with significant cognitive impairment. It includes components such as sustained attention to a stimulus and continuous memory of the instructions. It is noted that clinical assessment of vascular cognitive impairment (VCI) predominantly relies on cognitive scales, with a paucity of concurrent evidence from cognitive tasks such as WM.

Using an electroencephalogram (EEG), previous studies have established the oscillatory mechanisms of WM. Most of the studies have identified increased power in the fast oscillatory ranges such as beta (13–30 Hz) and gamma (30–100 Hz) [8, 9]. In terms of the functioning, gamma oscillation is suggested to store memories, while beta oscillation is closely associated with attention and response selection [9,10,11]. However, the effects of stroke on neural oscillations underlying WM are largely unclear. A recent scoping review indicated a correlation between decreased fast waves (such as beta) and poor cognition following a stroke [12].

This study was designed to investigate the oscillatory characteristics of working memory in subacute stroke patients. Patients in the subacute stroke underwent a visual-spatial WM 0-back with EEG recordings. They were further classified as good-recovery (n = 26) and poor-recovery (n = 22) according to the modified Rankin Score (mRS). We hypothesized that stroke patients would demonstrate lower power in beta and gamma range compared to healthy controls. Moreover, patients with a poor recovery would have a more prominent decrease in beta and gamma oscillation.

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Bilaterally Reduced Rolandic Beta Band Activity in Minor Stroke Patients

Well, you described something, but I see nothing here that is going to get survivors recovered.

 

Bilaterally Reduced Rolandic Beta Band Activity in Minor Stroke Patients

Joshua P. Kulasingham^1*, Christian Brodbeck², Sheena Khan³, Elisabeth B. Marsh^3† and Jonathan Z. Simon^1,4,5†

• ¹Department of Electrical and Computer Engineering, University of Maryland, College Park, MD, United States
• ²Department of Psychological Sciences, University of Connecticut, Storrs, CT, United States
• ³Department of Neurology, The Johns Hopkins School of Medicine, Baltimore, MD, United States
• ⁴Department of Biology, University of Maryland, College Park, MD, United States
• ⁵Institute for Systems Research, University of Maryland, College Park, MD, United States

Stroke patients with hemiparesis display decreased beta band (13–25 Hz) rolandic activity, correlating to impaired motor function. However, clinically, patients without significant weakness, with small lesions far from sensorimotor cortex, exhibit bilateral decreased motor dexterity and slowed reaction times. We investigate whether these minor stroke patients also display abnormal beta band activity. Magnetoencephalographic (MEG) data were collected from nine minor stroke patients (NIHSS < 4) without significant hemiparesis, at ~1 and ~6 months postinfarct, and eight age-similar controls. Rolandic relative beta power during matching tasks and resting state, and Beta Event Related (De)Synchronization (ERD/ERS) during button press responses were analyzed. Regardless of lesion location, patients had significantly reduced relative beta power and ERS compared to controls. Abnormalities persisted over visits, and were present in both ipsi- and contra-lesional hemispheres, consistent with bilateral impairments in motor dexterity and speed. Minor stroke patients without severe weakness display reduced rolandic beta band activity in both hemispheres, which may be linked to bilaterally impaired dexterity and processing speed, implicating global connectivity dysfunction affecting sensorimotor cortex independent of lesion location. Findings not only illustrate global network disruption after minor stroke, but suggest rolandic beta band activity may be a potential biomarker and treatment target, even for minor stroke patients with small lesions far from sensorimotor areas.

Introduction

Motor impairment is present in many stroke survivors (1), but does not always take the form of significant weakness. Patients with “minor stroke” (2) and low National Institute of Health Stroke Scale (NIHSS) scores can exhibit normal strength but have disabling deficits manifesting as slowed response times and limited dexterity. This is common even in high functioning patients (3) and typically occurs bilaterally and independent of lesion location (4). Unlike hemiparesis, the underlying neural mechanisms for these processes are less well-understood. These minor stroke patients also report difficulty with concentration and attention which, paired with decreased motor dexterity and slowed response times, hinder their ability to successfully return to work and reintegrate back into society. Previously, we found that such patients have low amplitude responses to visual stimuli that are temporally dispersed, possibly indicating a disruption of cortical networks (4). In this study we investigate neural responses in the sensorimotor cortex of the same cohort of minor stroke patients compared to age-similar controls, to determine if they display abnormal beta band activity, possibly linked to mechanisms underlying reduced motor dexterity and slowed response times.

Measurements of cortical activity using electroencephalography (EEG) or magnetoencephalography (MEG) indicate that rolandic beta band (13–25 Hz) responses are intricately linked to motor function (5–7). Spontaneous rolandic beta band activity may reflect multiple functional mechanisms in sensorimotor cortex including intracortical inhibition, communication, motor imagery and motor planning (8–10). Abnormal beta band activity has been observed in stroke (11, 12), Parkinson's disease (13) and other sensorimotor disorders (14). Stroke patients with motor deficits have been found to display reduced beta responses, especially in the ipsi-lesional hemisphere, possibly due to abnormal disinhibition and increased excitation (15). It is well-established that beta band activity reduces during movement planning and execution (Event Related Desynchronization or ERD), and increases afterwards (Event Related Synchronization or ERS) in sensorimotor cortex (8, 9, 16). Although the neural mechanisms involved in these changes are not clear, prior work suggests that beta ERD may reflect cortical excitability and downregulation of inhibition while ERS may reflect active inhibition or a return to status quo after movement (17–19). Stroke patients with hemiparesis have decreased beta ERD/ERS, with a greater reduction in the ipsi-lesional hemisphere (11, 20) and abnormal cortical patterns and latencies (21). However, it is unclear whether patients with small lesions without significant hemiparesis, would also display such abnormalities in beta band activity and beta ERD/ERS, and if abnormalities would occur independent of whether the lesion affected traditional motor pathways. We have reason to hypothesize this will be the case, and that abnormalities will be bilateral, given their observed clinical deficits.

This study involved MEG data collected from stroke patients with small lesions with minor impairments in motor dexterity but no hemiparesis, and was motivated by several research questions. First, we address whether stroke patients with small infarcts display abnormal rolandic beta activity compared to controls using relative beta power and beta ERD/ERS during button press responses. Next, we explore whether abnormalities improve with time, using a subset of the patient cohort who return for a second visit ~6 months later. Finally, we investigate whether the lesion location influences beta band activity by separately analyzing responses in ipsi- and contra-lesional hemispheres, and use the pattern of abnormal beta to draw conclusions regarding potential mechanisms and future treatment implications.

More at link.

 

Corticospinal Tract Microstructure Correlates With Beta Oscillatory Activity in the Primary Motor Cortex After Stroke

So what is the fix? No fix, you just wasted your research. 

Corticospinal Tract Microstructure Correlates With Beta Oscillatory Activity in the Primary Motor Cortex After Stroke

Robert Schulz

,

Marlene Bönstrup

,

Stephanie Guder

,

Jingchun Liu

,

Benedikt Frey

,

Fanny Quandt

,

Lutz A. Krawinkel

,

Bastian Cheng

,

Götz Thomalla

,

Christian Gerloff

Originally published20 Aug 2021https://doi.org/10.1161/STROKEAHA.121.034344Stroke. ;0:STROKEAHA.121.034344

Abstract

Background and Purpose:

Cortical beta oscillations are reported to serve as robust measures of the integrity of the human motor system. Their alterations after stroke, such as reduced movement-related beta desynchronization in the primary motor cortex, have been repeatedly related to the level of impairment. However, there is only little data whether such measures of brain function might directly relate to structural brain changes after stroke.

Methods:

This multimodal study investigated 18 well-recovered patients with stroke (mean age 65 years, 12 males) by means of task-related EEG and diffusion-weighted structural MRI 3 months after stroke. Beta power at rest and movement-related beta desynchronization was assessed in 3 key motor areas of the ipsilesional hemisphere that are the primary motor cortex (M1), the ventral premotor area and the supplementary motor area. Template trajectories of corticospinal tracts (CST) originating from M1, premotor cortex, and supplementary motor area were used to quantify the microstructural state of CST subcomponents. Linear mixed-effects analyses were used to relate tract-related mean fractional anisotropy to EEG measures.

Results:

In the present cohort, we detected statistically significant reductions in ipsilesional CST fractional anisotropy but no alterations in EEG measures when compared with healthy controls. However, in patients with stroke, there was a significant association between both beta power at rest (P=0.002) and movement-related beta desynchronization (P=0.003) in M1 and fractional anisotropy of the CST specifically originating from M1. Similar structure-function relationships were neither evident for ventral premotor area and supplementary motor area, particularly with respect to their CST subcomponents originating from premotor cortex and supplementary motor area, in patients with stroke nor in controls.

Conclusions:

These data suggest there might be a link connecting microstructure of the CST originating from M1 pyramidal neurons and beta oscillatory activity, measures which have already been related to motor impairment in patients with stroke by previous reports.

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The Effect of Neurofeedback Training Using Display After Stroke

 Your doctor should be able to afford the $113 to help her/his patients get better.
You will notice that no physical changes were described, only beta waves, nothing objective. 

The Effect of Neurofeedback Training Using Display After Stroke

Authors: Cho, Kihun; Yu, Jaeho

Source: Journal of Nanoelectronics and Optoelectronics, Volume 11, Number 1, February 2016, pp. 87-91(5)
Publisher: American Scientific Publishers

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Abstract:

This study investigates the changes in the brain wave of stroke patients through neurofeedback training (NFBT) using display. Thirty stroke patients were assigned to two group: 14 patients in the NFBT group, and 16 in the control group. NFBT group played the display game by watching the monitor with the poles attached, and his awakening level was controlled. The training time for this trial was set at 30 minutes, during which a 3-minute training module was conducted 10 times, and trained as five times a week for 6 weeks. Their brain waves were measured pre- and post-training through electroencephalography. In result, the frontal and parietal lobes in particular of NFBT group showed significant differences in activation after the test (p < 0.05). But there were no significant differences between before and after intervention in control group. This study suggests that rehabilitation by NFBT is effective in changing relative beta waves and improving cognitive function.

 

Comparative Analysis Electroencephalographic of Alpha, Beta and Gamma Bands of a Healthy Individual and One with Hemiparesis

I can see absolutely no use of this for survivors and I doubt your doctor will either.  Someone could enlighten us all.
Comparative Analysis Electroencephalographic of Alpha, Beta and Gamma Bands of a Healthy Individual and One with Hemiparesis

Dionis de Castro Dutra Machado^{1) 2) 4)}, Glenda Crispim Lima^{1) 2)}, Rodrigo Souza dos Santos^{1) 2)}, Amanda Júlia Bezerra Ramos^{1) 2)}, Cáio César Menezes de Sousa^{1) 2)}, Rayele Pricila Moreira dos Santos¹⁾, Karyna Kelly Oliveira Coelho^{1) 2)}, Mauricio Cagy⁴⁾, Marco Orsini³⁾, Victor Hugo Bastos^{1) 2)}

1) Department of Physical Therapy, Federal University of Piauí: Av. São Sebastião, 2819-64202-020, Parnaíba, PI, Brazil 2) Brain Mapping and Functionality Laboratory (LAMCEF), Federal University of Piauí, Brazil 3) Master Program of the Rehabilitation Science, UNISUAM, Brazil 4) Brain Mapping and Sensory Motor Integration Laboratory, Federal University of Rio de Janeiro (IPUB/UFRJ), Brazil

Released on J-STAGE June 30, 2014  

Keywords: Electroencephalography, Hemiparetic, Rehabilitation

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[Purpose] The study analyzed the electroencephalographic (EEG) data of the central cortical areas, during execution of the motor gestures of feeding, activation of the system of mirror neurons, and imagery between a right hemiparetic volunteer (RHV) and a healthy volunteer (HV). [Subjects and Methods] The volunteers’ EEG data were recorded with their eyes open for 4 minutes while they performed five experimental tasks. [Results] The alpha band, absolute power value of HV was lower than that of RHV. In the beta band, during the practice condition, there was an increase in the magnitude of the absolute power value of HV at T3, possibly because T3 is representative of secondary motor areas that work with cortical neurons related to planning and organizing sequence of movements performed by the hands. The gamma band is related to the state of preparation for movement and memory. The results of this study indicate that there was increased activation of the gamma frequency band of HV. [Conclusion] The findings of this study have revealed the changes in pattern characteristics of each band which may be associated with the brain injury of the hemiparetic patient. 

Even the 4 page full text did nor provide any understanding at all.