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.

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