ArticleBrain : a journal of neurology2020
Local sleep-like cortical reactivity in the awake brain after focal injury.
Article in Brain : a journal of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05468268 (Leveraging the Neural Circuits of Hyper-Memory to Ameliorate Memory Dysfunction in Prodromal Alzheimer's Disease), which is not on this map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Leveraging the Neural Circuits of Hyper-Memory to Ameliorate Memory Dysfunction in Prodromal Alzheimer's Disease (pAD) - Noninvasive Brain Stimulation for pAD (pADmemory)
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
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- Case Report: Electro-cortical network effects of an acute stroke revealed by high-density electroencephalography.Frontiers in neuroscience · 2025Article
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- Evoked slow oscillations and dynamic network reorganization after stroke.Brain communications · 2025Article
- EEG focal delta slowing in focal epilepsy - A didactic review.Clinical neurophysiology practice · 2025Review
- Role of homeostatic plasticity in critical brain dynamics following focal stroke lesions.Scientific reports · 2024Article
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functional consequences of focal brain injury are thought to be contingent on neuronal alterations extending beyond the area of structural damage. This phenomenon, also known as diaschisis, has clinical and metabolic correlates but lacks a clear electrophysiological counterpart, except for the long-standing evidence of a relative EEG slowing over the injured hemisphere. Here, we aim at testing whether this EEG slowing is linked to the pathological intrusion of sleep-like cortical dynamics within an awake brain. We used a combination of transcranial magnetic stimulation and electroencephalography (TMS/EEG) to study cortical reactivity in a cohort of 30 conscious awake patients with chronic focal and multifocal brain injuries of ischaemic, haemorrhagic and traumatic aetiology. We found that different patterns of cortical reactivity typically associated with different brain states (coma, sleep, wakefulness) can coexist within the same brain. Specifically, we detected the occurrence of prominent sleep-like TMS-evoked slow waves and off-periods-reflecting transient suppressions of neuronal activity-in the area surrounding focal cortical injuries. These perilesional sleep-like responses were associated with a local disruption of signal complexity whereas complex responses typical of the awake brain were present when stimulating the contralesional hemisphere. These results shed light on the electrophysiological properties of the tissue surrounding focal brain injuries in humans. Perilesional sleep-like off-periods can disrupt network activity but are potentially reversible, thus representing a principled read-out for the neurophysiological assessment of stroke patients, as well as an interesting target for rehabilitation.
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