Hypoxic ischemic encephalopathy (HIE) is a severe consequence of cardiac arrest (CA) representing a substantial diagnostic challenge. We have recently designed a novel method for the assessment of HIE after CA. The method is based on estimating the severity of the brain injury by analyzing changes in the electroencephalogram (EEG) slow wave activity while the patient is exposed to an anesthetic drug propofol in a controlled manner. In this paper, Hilbert-Huang Transform (HHT) was used to analyze EEG slow wave activity during anesthesia in ten post-CA patients. The recordings were made in the intensive care unit 36-48 hours after the CA in an experiment, during which the propofol infusion rate was incrementally decreased to determine the drug-induced changes in the EEG at different anesthetic levels. HHT was shown to successfully capture the changes in the slow wave activity to the behavior of intrinsic mode functions (IMFs). While, in patients with good neurological outcome defined after a six-month control period, propofol induced a significant increase in the amplitude of IMFs representing the slow wave activity, the patients with poor neurological outcome were unable to produce such a response. Consequently, the proposed method offer substantial prognostic potential by providing a novel approach for early estimation of HIE after CA.
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http://dx.doi.org/10.1109/EMBC.2016.7591080 | DOI Listing |
Neuron
January 2025
Neuroscience Institute, Langone Medical Center, New York University, New York, NY, USA; Department of Physiology and Neuroscience, Langone Medical Center, New York University, New York, NY, USA; Department of Neurology, Langone Medical Center, New York University, New York, NY, USA. Electronic address:
Systems consolidation relies on coordination between hippocampal sharp-wave ripples (SWRs) and neocortical UP/DOWN states during sleep. However, whether this coupling exists across the neocortex and the mechanisms enabling it remains unknown. By combining electrophysiology in mouse hippocampus (HPC) and retrosplenial cortex (RSC) with wide-field imaging of the dorsal neocortex, we found spatially and temporally precise bi-directional hippocampo-neocortical interaction.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, California, USA.
Introduction: Sleep disturbances are associated with Alzheimer's disease (AD) and Alzheimer's disease and related dementias (ADRD), but the relationship between sleep architecture, particularly rapid eye movement (REM) sleep, and AD/ADRD biomarkers remains unclear.
Methods: We enrolled 128 adults (64 with Alzheimer's disease, 41 with mild cognitive impairment [MCI], and 23 with normal cognition [NC]), mean age 70.8 ± 9.
bioRxiv
January 2025
Yale School of Medicine, New Haven, CT, U.S.A.
Study Objectives: Sleep deficiency is associated with Alzheimer's disease (AD) pathogenesis. We examined the association of sleep architecture with anatomical features observed in AD: (1) atrophy of hippocampus, entorhinal, inferior parietal, parahippocampal, precuneus, and cuneus regions ("AD-vulnerable regions") and (2) cerebral microbleeds.
Methods: In 271 participants of the Atherosclerosis Risk in the Communities Study, we examined the association of baseline sleep architecture with anatomical features identified on brain MRI 13~17 years later.
Front Neurol
January 2025
Department of Neurology, Xuanwu Hospital Capital Medical University, Beijing, China.
Objective: To observe and measure the morphological and temporal evolutionary features of the hypersynchronous (HYP) pattern in the mesial temporal seizure.
Methods: The HYP patterns during preictal and interictal states of 16 mesial temporal epileptic patients were analyzed. The wave components of the HYP transients were firstly observed and measured.
Prog Neurobiol
January 2025
Department of Biomedicine, University of Basel, Klingelbergstrasse 50, Basel 4056, Switzerland. Electronic address:
The brain faces the challenging task of preserving a consistent portrayal of the external world in the face of disruptive sensory inputs. What alterations occur in sensory representation amidst noise, and how does brain activity adapt to it? Although it has previously been shown that background white noise (WN) decreases responses to salient sounds, a mechanistic understanding of the brain processes responsible for such changes is lacking. We investigated the effect of background WN on neuronal spiking activity, membrane potential, and network oscillations in the mouse central auditory system.
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