So you did something, but didn't apply anything to getting survivors recovered. Useless. I'd fire you all.
Intracortical and intercortical networks in patients after stroke: a concurrent TMS-EEG study
Journal of NeuroEngineering and Rehabilitation volume 20, Article number: 100 (2023)
Abstract
Background
Concurrent transcranial magnetic stimulation and electroencephalography (TMS-EEG) recording provides information on both intracortical reorganization and networking, and that information could yield new insights into post-stroke neuroplasticity. However, a comprehensive investigation using both concurrent TMS-EEG and motor-evoked potential-based outcomes has not been carried out in patients with chronic stroke. Therefore, this study sought to investigate the intracortical and network neurophysiological features of patients with chronic stroke, using concurrent TMS-EEG and motor-evoked potential-based outcomes.
Methods
A battery of motor-evoked potential-based measures and concurrent TMS-EEG recording were performed in 23 patients with chronic stroke and 21 age-matched healthy controls.
Results
The ipsilesional primary motor cortex (M1) of the patients with stroke showed significantly higher resting motor threshold (P = 0.002), reduced active motor-evoked potential amplitudes (P = 0.001) and a prolonged cortical silent period (P = 0.007), compared with their contralesional M1. The ipsilesional stimulation also produced a reduction in N100 amplitude of TMS-evoked potentials around the stimulated M1 (P = 0.007), which was significantly correlated with the ipsilesional resting motor threshold (P = 0.011) and motor-evoked potential amplitudes (P = 0.020). In addition, TMS-related oscillatory power was significantly reduced over the ipsilesional midline-prefrontal and parietal regions. Both intra/interhemispheric connectivity and network measures in the theta band were significantly reduced in the ipsilesional hemisphere compared with those in the contralesional hemisphere.
Conclusions
The ipsilesional M1 demonstrated impaired GABA-B receptor-mediated intracortical inhibition characterized by reduced duration, but reduced magnitude. The N100 of TMS-evoked potentials appears to be a useful biomarker of post-stroke recovery.
Background
Transcranial magnetic stimulation (TMS) can transsynaptically excite pyramidal neurons by activating the excitatory and inhibitory interneurons located in layers II and III of the brain cortex [1]. A single pulse of TMS with adequate intensity applied to the primary motor cortex (M1) produces a neural transmission along the corticospinal descending pathway and evokes activity in the contralateral muscle –– activity that is termed motor-evoked potentials (MEPs) [1]. Therefore, TMS has been used as a tool for investigating the integrity of the corticospinal tract and the functional balance of excitatory and inhibitory circuits within the motor cortex.
Understanding post-stroke neurophysiological alteration using many TMS protocols have played an essential role in investigating the correlates of motor recovery with adaptive and maladaptive neurophysiological alteration, predicting prognosis, and guiding non-invasive brain stimulation for stroke. Compelling evidence indicates that corticospinal excitability of the contralesional M1 is comparable with that of healthy counterparts, but such is not the case for the excitability in the ipsilesional M1, which decreases with impaired contralateral motor function. The reduction of ipsilesional M1 excitability can be indexed by increased resting motor threshold (RMT) and decreased resting MEP amplitudes [2, 3]. By measuring short-interval intracortical inhibition (SICI) of the ipsilesional M1 of patients with stroke, paired-pulse studies have revealed dynamically changed GABA-A receptor-mediated intracortical inhibition. That inhibition is reduced at the acute stage post-stroke, which may imply a process of intracortical disinhibition, and it has returned to a normal level at the chronic stage [2]. GABA-B receptor-mediated intracortical inhibition has been extensively investigated, but studies have reported that long-interval intracortical inhibition (LICI, mediated by GABA-B receptors) either remained unchanged [4], reduced [5], or enhanced [6] in patients with stroke, leading to the question of how the GABAergic inhibitory circuits are altered after stroke?
Concurrent TMS and electroencephalography recording (TMS-EEG) is a novel approach that records the summation of postsynaptic excitatory and inhibitory potentials that occur in response to TMS pulses and are termed TMS-evoked potentials (TEPs). This approach enables assessments of local cortical excitability and connectivity between brain regions [7], and has been used to provide prognostic biomarkers that predict motor recovery after stroke [8]. Pharmacological studies have confirmed that the amplitudes of N45 and N100 are mediated by the GABA-A and GABA-B receptors, respectively [9, 10], thus establishing a close link between TEP peaks and GABAergic intracortical inhibition. In addition, TMS-EEG data offer a way to characterize impaired causal connectivity from the perturbed site to remote brain regions, in patients with neurological conditions [11]. Furthermore, by computing the phase synchronizations of neural oscillations, the cortical networks of possible interactions among different brain regions can be analyzed [12, 13].
A previous study in patients with acute stroke suggested that the absence of the N100 component was an indicator of severe motor impairment [8]. Another study showed that in a group of patients who were undergoing longitudinal recording, the TEP amplitudes decreased at the subacute stage post-stroke, and they gradually increased in parallel with motor recovery [14]. However, Gray et al. [15] found that the N100 amplitude in patients with chronic stroke was comparable with that in healthy controls, a finding that appears to differ from others obtained in the acute and subacute patient groups [8, 14]. Recently, researchers noted that different patterns of TEPs in terms of their morphologies could be observed separately from different neurological conditions and could even coexist within the same brain, depending on the site of stimulation [16, 17]. Specifically, stimulating the contralesional M1 of patients with stroke produced TEPs with small amplitudes, quickly changing deflections, and a complex spatial distribution, resembling those obtained from healthy awake individuals [16, 17]. TEPs with quickly changing deflections can be confirmed by inspecting whether ERSP in high-frequency bands (beta band) is retained [16]. In contrast, directly stimulating the perilesional region over the ipsilesional hemisphere has been found to produce TEPs that are characterized by large amplitudes, slow frequencies, and stereotypical EEG reactivity [16, 17] and are similar to those in healthy individuals during non-rapid eye movement sleep and in patients with unresponsive wakefulness syndrome [18]. Furthermore, slow-frequency TEPs seem to be associated with the severity of motor impairment due to stroke [17], and the occurrence of such TEPs is a pathological form of local cortical bistability [16]. However, it is noteworthy that the standard form of TEPs found in contralesional stimulation and healthy people can also be recorded in ipsilesional stimulation in patients with a small subcortical lesion [16, 17]. In view of possibly different mechanisms, the distinct morphologies of the TEPs that are identified in stroke should be disentangled carefully before any subgroup analyses and interpretations are conducted.
To the best of our knowledge, although previous studies with many TMS protocols have provided informative investigation into post-stroke neurophysiology, largely inconsistent findings were reported, particularly in GABA-B receptor-mediated intracortical inhibition. In addition to TEPs characterized by large amplitudes and slow frequencies, ipsilesional stimulation can also produce a TEP pattern similar to that in contralesional stimulation and healthy people, but the characteristics of this TEP pattern in terms of peaks, oscillations, and connectivity are inconclusive. The objective of this study, therefore, was to conduct a comprehensive neurophysiological examination of patients with stroke, using TMS-EEG and MEP-based measures to address previous inconclusive findings in patients with chronic stroke.
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