scholarly journals The hypothesis of the functional disintegration of the brain due to the persistence of benign epileptiform patterns on the electroencephalogram

2021 ◽  
Vol 16 (3) ◽  
pp. 34-45
Author(s):  
I. A. Sadekov ◽  
A. V. Polyakov ◽  
I. V. Sadekova ◽  
E. A. Tupikina ◽  
V. Yu. Kochmar ◽  
...  
Keyword(s):  
Nervous System ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Neuropsychiatric Disorders ◽  
Epileptiform Discharge ◽  
Functional Disorders ◽  
The Brain ◽  
Developing Nervous System

In this work, we have analyzed the results of observation of 200 children aged from 3 to 15 years old, who had various neuropsychiatric disorders in combination with benign childhood epileptiform patterns on the electroencephalogram. A hypothesis has been put forward about functional disorders of the developing nervous system with prolonged persistence of benign focal epileptiform discharge of childhood on electroencephalogram, mainly in slow-wave sleep. The possibilities of therapeutic correction of these disorders are discussed.

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

Increased Alpha (8–12 Hz) Activity during Slow Wave Sleep as a Marker for the Transition from Implicit Knowledge to Explicit Insight

2012 ◽  
Vol 24 (1) ◽  
pp. 119-132 ◽  
Author(s):  
Juliana Yordanova ◽  
Vasil Kolev ◽  
Ullrich Wagner ◽  
Jan Born ◽  
Rolf Verleger
Keyword(s):  
Slow Wave ◽  
Explicit Knowledge ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Implicit Knowledge ◽  
Specific Power ◽  
Specific Marker ◽  
Knowledge Representations ◽  
Beta Power ◽  
The Brain

The number reduction task (NRT) allows us to study the transition from implicit knowledge of hidden task regularities to explicit insight into these regularities. To identify sleep-associated neurophysiological indicators of this restructuring of knowledge representations, we measured frequency-specific power of EEG while participants slept during the night between two sessions of the NRT. Alpha (8–12 Hz) EEG power during slow wave sleep (SWS) emerged as a specific marker of the transformation of presleep implicit knowledge to postsleep explicit knowledge (ExK). Beta power during SWS was increased whenever ExK was attained after sleep, irrespective of presleep knowledge. No such EEG predictors of insight were found during Sleep Stage 2 and rapid eye movement sleep. These results support the view that it is neuronal memory reprocessing during sleep, in particular during SWS, that lays the foundations for restructuring those task-related representations in the brain that are necessary for promoting the gain of ExK.

scholarly journals Reconfigurations in brain networks upon awakening from slow wave sleep: Interventions and implications in neural communication

2021 ◽  
Author(s):  
Cassie J Hilditch ◽  
Kanika Bansal ◽  
Ravi Chachad ◽  
Lily R Wong ◽  
Nicholas G Bathurst ◽  
...  
Keyword(s):  
Long Range ◽  
Slow Wave ◽  
Path Length ◽  
Slow Wave Sleep ◽  
Mechanistic Explanation ◽  
Clustering Coefficient ◽  
Sleep Inertia ◽  
The Awakening ◽  
Beta Power ◽  
The Brain

Sleep inertia is the brief period of impaired alertness and performance experienced immediately after waking. While the neurobehavioral symptoms of sleep inertia are well-described, less is known about the neural mechanisms underlying this phenomenon. A better understanding of the neural processes during sleep inertia may offer insight into the cognitive impairments observed and the awakening process generally. We observed brain activity following abrupt awakening from slow wave sleep during the biological night. Using electroencephalography (EEG) and a network science approach, we evaluated power, clustering coefficient, and path length across frequency bands under both a control condition and a blue-enriched light intervention condition in a within-subject design. We found that under control conditions, the awakening brain is typified by an immediate reduction in global theta, alpha, and beta power. Simultaneously, we observed a decrease in the clustering coefficient and an increase in path length within the delta band. Exposure to blue-enriched light immediately after awakening ameliorated these changes, but only for clustering. Our results suggest that long-range network communication within the brain is crucial to the waking process and that the brain may prioritize these long-range connections during this transitional state. Our study highlights a novel neurophysiological signature of the awakening brain and provides a potential mechanistic explanation for the effect of light in improving performance after waking.

scholarly journals ­Glial and stem cell expression of Fibroblast Growth Factor Receptor 1 in the embryonic and perinatal nervous system

2017 ◽  
Author(s):  
Jantzen C Collette ◽  
Lisha Choubey ◽  
Karen Muller Smith
Keyword(s):  
Stem Cells ◽  
Nervous System ◽  
Neuropsychiatric Disorders ◽  
Fibroblast Growth ◽  
Fgf Signaling ◽  
Cell Type ◽  
Anterior Midline ◽  
Organ Systems ◽  
The Brain

Background. Fibroblast growth factors (FGFs) and their receptors (FGFRs) are involved in the development and function of multiple organs and organ systems, including the central nervous system (CNS). FGF signaling via FGFR1, one of the three FGFRs expressed in the CNS, stimulates proliferation of stem cells during prenatal and postnatal neurogenesis and participates in regulating cell-type ratios in many developing regions of the brain. Anomalies in FGFR1 signaling have been implicated in certain neuropsychiatric disorders. Fgfr1 expression has been shown, via in situ hybridization, to vary spatially and temporally throughout embryonic and postnatal development of the brain. However, in situ hybridization lacks sufficient resolution to identify which cell-types directly participate in FGF signaling. Furthermore, because antibodies raised against FGFR1 commonly cross-react with other members of the FGFR family, immunocytochemistry is not alone sufficient to accurately document Fgfr1 expression. Here, we elucidate the identity of Fgfr1 expressing cells in both the embryonic and perinatal mouse brain. Methods. To do this, we utilized a tgFGFR1-EGFPGP338Gsat BAC line (tgFgfr1-EGFP+) obtained from the GENSAT project. The tgFgfr1-EGFP+ line expresses EGFP under the control of a Fgfr1 promoter, thereby causing cells endogenously expressing Fgfr1 to also present a positive GFP signal. Through simple immunostaining using GFP antibodies and cell-type specific antibodies, we were able to accurately determine the cell-type of Fgfr1 expressing cells. Results. This technique revealed Fgfr1 expression in proliferative zones containing BLBP+ radial glial stem cells, such as the cortical and hippocampal ventricular zones, and cerebellar anlage of E14.5 mice, in addition to DCX+ neuroblasts. Furthermore, our data reveal Fgfr1 expression in proliferative zones containing BLBP+ cells of the anterior midline, hippocampus, cortex, hypothalamus, and cerebellum of P0.5 mice, in addition to the early-formed GFAP+ astrocytes of the anterior midline. Discussion. Understanding when during development and where Fgfr1 is expressed is critical to improving our understanding of its function during neurodevelopment as well as in the mature CNS. This information may one day provide an avenue of discovery towards understanding the involvement of aberrant FGF signaling in neuropsychiatric disorders.

D-C potential changes in rabbit brain during slow-wave and paradoxical sleep

1964 ◽  
Vol 207 (6) ◽  
pp. 1379-1386 ◽  
Author(s):  
H. Kawamura ◽  
C. H. Sawyer
Keyword(s):  
Reticular Formation ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Paradoxical Sleep ◽  
Reference Electrode ◽  
Reference Points ◽  
Rabbit Brain ◽  
Positive Side ◽  
The Brain ◽  
Stimulation Of

A study has been made of d-c potential changes in the brain during various states of sleep and wakefulness in the unrestrained unanesthetized rabbit with chronically implanted electroencephalogram and d-c electrodes. In preliminary acute experiments with an occipital bone reference electrode, the direction of the d-c potential change induced by stimulation of the midbrain reticular formation was the same in cortical and subcortical sites. With frontal and occipital bones as reference points the cortical d-c potential changes were similar to one another, but arousal stimuli readily elicited positive d-c shifts with the frontal reference electrode. In the chronic rabbit with an occipital reference electrode, cortical and hypothalamic d-c potentials shifted strongly to the positive side during slow-wave sleep and after injection of pentobarbital; from these conditions stimulation of the reticular formation induced a marked negative shift. During paradoxical sleep both cortical and subcortical d-c electrodes showed negative shifts similar to those seen during an arousal reaction. Grooming and eating elicited strong positive shifts in both cortical and hypothalamic d-c electrodes.

scholarly journals Spatiotemporal Patterns of Adaptation-Induced Slow Oscillations in a Whole-Brain Model of Slow-Wave Sleep

2022 ◽  
Vol 15 ◽  
Author(s):  
Caglar Cakan ◽  
Cristiana Dimulescu ◽  
Liliia Khakimova ◽  
Daniela Obst ◽  
Agnes Flöel ◽  
...  
Keyword(s):  
Slow Wave ◽  
Traveling Waves ◽  
Large Scale ◽  
Slow Wave Sleep ◽  
Brain Area ◽  
Optimization Approach ◽  
Whole Brain ◽  
Slow Oscillations ◽  
Lower Amplitude ◽  
The Brain

During slow-wave sleep, the brain is in a self-organized regime in which slow oscillations (SOs) between up- and down-states travel across the cortex. While an isolated piece of cortex can produce SOs, the brain-wide propagation of these oscillations are thought to be mediated by the long-range axonal connections. We address the mechanism of how SOs emerge and recruit large parts of the brain using a whole-brain model constructed from empirical connectivity data in which SOs are induced independently in each brain area by a local adaptation mechanism. Using an evolutionary optimization approach, good fits to human resting-state fMRI data and sleep EEG data are found at values of the adaptation strength close to a bifurcation where the model produces a balance between local and global SOs with realistic spatiotemporal statistics. Local oscillations are more frequent, last shorter, and have a lower amplitude. Global oscillations spread as waves of silence across the undirected brain graph, traveling from anterior to posterior regions. These traveling waves are caused by heterogeneities in the brain network in which the connection strengths between brain areas determine which areas transition to a down-state first, and thus initiate traveling waves across the cortex. Our results demonstrate the utility of whole-brain models for explaining the origin of large-scale cortical oscillations and how they are shaped by the connectome.

Proving the Carry-over Effect of Slow-Wave Sleep by Mathematical Models

1991 ◽  
Vol 3 (2) ◽  
pp. 88-92
Author(s):  
Toshinori Kobayashi ◽  
◽  
Yoichi Tsuji ◽  
Yoshinobu Iguchi
Keyword(s):  
Mathematical Models ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Early Morning ◽  
Night Sleep ◽  
Sleep Episode ◽  
Carry Over ◽  
Daytime Nap ◽  
The Brain ◽  
Carry Over Effect

In order to study the psychophysiological function of ""slow wave sleep (SWS), we are trying to identify the control mechanism of SWS. It is well known that the amount of SWS found in a sleep episode depends upon the length of wakefulness prior to the sleep episode. But Karakan et al. (1970) and Miyashita et al (1978) reported that SWS of a sleep episode was also influenced by SWS of the preceding sleep episode. So, we examined the hypothesis that SWS of a sleep episode depended not only on prior wakefulness to the sleep episode but also on SWS of the preceding sleep episode by the use of mathematical models and the experiment. Two models were prepared to examine the hypothesis: one is MODEL (CO), in which SWS of a sleep episode depends upon both prior wakefulness and SWS carried over from the preceding sleep episode, the other is MODEL (nCO), in which SWS of a sleep episode depends on only prior wakefulness to the sleep episode. Four pairs of night sleep and dayti,me naps were recorded in the experiment for eight healthy university students (aged 18 to 25) as follows: (1) Morning nap (0900-1300) was recorded after the mid night sleep (23000300) or early morning sleep (0300-0700), and (2) evening nap (1700-2100) after mid night sleep or early morning sleep. We compared SWS of night sleep and daytime naps estimated by two models with those obtained by the experiment. There was close agreement between SWS estimated by MODEL (CO) and that obtained by the experiment. This result indicates that there is carry over of SWS from night sleep to daytime nap. So, SWS of a sleep episode depends on both prior wakefulness to the sleep episode and SWS carried over from the preceding sleep episode. SWS is accumulated in proportion to the length of wakefulness prior to a sleep episode during waking and is released according to sleep progression during sleep. When SWS is relatively large compared with the length of sleep episode, all SWS is not completely released in the sleep episode. A part of SWS remains in the brain. The remainder of SWS is carried over to the following sleep episode. When SWS is considered as an index of a kind of fatigue in the brain, it is accumulated during waking and is restored during sleep. When the fatigue is not fully restored in a sleep episode, it carries over into the following sleep episode.

scholarly journals IL-1 is a mediator of increases in slow-wave sleep induced by CRH receptor blockade

2000 ◽  
Vol 279 (3) ◽  
pp. R793-R802 ◽  
Author(s):  
Fang-Chia Chang ◽  
Mark R. Opp
Keyword(s):  
Hpa Axis ◽  
Slow Wave ◽  
Tumor Necrosis ◽  
Slow Wave Sleep ◽  
Central Administration ◽  
Regulatory Systems ◽  
The Central Nervous System ◽  
Factor Α ◽  
The Brain ◽  
Necrosis Factor

We hypothesize that corticotropin-releasing hormone (CRH), a regulator of the hypothalamic-pituitary-adrenal (HPA) axis, is involved in sleep-wake regulation on the basis of observations that the CRH receptor antagonist astressin, after a delay of several hours, reduces waking and increases slow-wave sleep (SWS) in rats. This delay suggests a cascade of events that begins with the HPA axis and culminates with actions on sleep regulatory systems in the central nervous system. One candidate mediator in the brain for these actions is interleukin (IL)-1. IL-1 promotes sleep, and glucocorticoids inhibit IL-1 synthesis. In this study, central administration of 12.5 μg astressin into rats before dark onset reduced corticosterone 4 h after injection and increased mRNA expression for IL-1α and IL-1β but not for IL-6 or tumor necrosis factor-α in the brain 6 h after injection. To determine directly whether IL-1 is involved in astressin-induced alterations in sleep-wake behavior, we then pretreated rats with 20 μg anti-IL-1β antibodies before injecting astressin. The increase in SWS and the reduction in waking that occur after astressin are abolished when animals are pretreated with anti-IL-1β. These data indicate that IL-1 is a mediator of astressin-induced alterations in sleep-wake behavior.

French Psychological Literature

1868 ◽  
Vol 14 (65) ◽  
pp. 132-142
Author(s):  
John Sibbald
Keyword(s):  
Nervous System ◽  
Delirium Tremens ◽  
Functional Disorders ◽  
Cerebral Lesions ◽  
Cerebral Disease ◽  
Organic Life ◽  
The Mind ◽  
External Stimuli ◽  
The Brain ◽  
Visceral Innervation

Pathology of the Brain in Cholera.—Dr. E. Mesnet devotes a paper to the consideration of the cerebral lesions observed in this disease. With the first period of the disease, that of prostration and enfeeblement, are associated functional disorders of the ganglionic nervous system; with the second, or reactive period, are associated those cerebral complications to which Mesnet directs our attention. In the cases of three persons who were seized with choleraic symptoms, while under the influence of alcoholic intoxication, the algidity and cyanotic symptoms did not come on. But about the tenth day of the disease a condition undistinguishable from delirium tremens made its appearance, and, after continuing three days, gave place to convalescence, which was inaugurated by an abundant and apparently critical perspiration. In general, he says, the discord between the nervous functions of animal life and those connected with relational existence is very striking. “There is nothing more affecting than the appearance of the asphyxie stage of collapse when the patient is in continual movement, when his features and skin are corpse-like, and visceral innervation appears to be extinguished, when all organic functions appear to have ceased, and when, nevertheless, his intellect is preserved and he can converse with us up to the last moment. The mind has no longer its natural vivacity; the con ceptions are languid; the memory requires to be stimulated; but when the patient is roused and the attention fixed, correct answers are obtained to questions put. The semi-comatose condition in which he is found is not the coma of cerebral disease, but a sort of drowsiness, which results from the general exhaustion of organic life. The benumbed condition of the senses is, in part, the cause of slowness of cerebral action; less sensitive to external stimuli, they transmit imperfect impressions, which are followed by obscure sensation. The hearing is almost lost, vision enfeebled, and sensi bility in general obtuse. As soon as the collapse begins to pass off, and reaction supervenes, the intellectual faculties recover from the torpidity to which we have referred, and the patient, who is more or less aware of his condition, becomes conscious of what is going on around him, and directs a restless attention to it.

scholarly journals On Catalepsy, with Cases. Treatment by High Temperature and Galvanism to Head

1887 ◽  
Vol 33 (142) ◽  
pp. 259-267
Author(s):  
Alex. Robertson
Keyword(s):  
Nervous System ◽  
High Temperature ◽  
Rare Disease ◽  
Short Duration ◽  
Considerable Proportion ◽  
Functional Disorders ◽  
Males And Females ◽  
Lunatic Asylums ◽  
The Brain ◽  
Organic Lesions

Catalepsy is one of the most striking of the great group of functional disorders of the nervous system. In this country it is a rare disease, except in lunatic asylums, where, at least in a modified form, it is by no means uncommon. Among the recorded cases a considerable proportion occurred in women of a hysterical disposition. It has, however, been observed in many other conditions. Thus in some individuals it has been associated with gross organic lesions of the brain, such as tumours and softening; but these may be regarded as accidental coincidences, and not as essential to the disease. Malaria would seem to have been the agent in its production in a number of instances, this opinion being supported by the fact that the patients recovered under the use of quinine and other remedies with similar properties. A curious case is recorded by Vogt of an Alpine village near Würzburg, in which half of the population, both males and females, suffered from this disease. He states that the inhabitants had been much given to intermarriage, and that generally they are, or at least were—for his account was published in 1863—a small and deformed race. The seizures were of short duration, not generally lasting longer than five minutes. They were preceded by a chill, which was soon followed by a strange sensation in the arms and legs. Then the sufferers became deadly pale, while their limbs got stiff, and continued in the position they were in when the attack commenced.

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