Hypoxic Syncope in a Competitive Breath-Hold Diver with Elevation of the Brain Damage Marker S100B

The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., “static apnea” (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 μg/l at the start of apnea to 0.083 μg/l after the apnea ( P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.

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Rehabilitation of Attention

Zeitschrift für Neuropsychologie ◽

10.1024/1016-264x.14.3.165 ◽

2003 ◽

Vol 14 (3) ◽

pp. 165-170 ◽

Cited By ~ 2

Author(s):

Ian H. Robertson

Keyword(s):

Brain Damage ◽

Dependent Plasticity ◽

Attention Systems ◽

The Brain

Abstract: In this paper, evidence is reviewed for separable attention systems in the brain, and it is argued a) that attention may have a privileged role in mediating experience dependent plasticity in the brain and b) that at least some types of attention may be capable of rehabilitation following brain damage.

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Aetiologies and anatomy of confabulation

10.1093/oso/9780198789680.003.0004 ◽

2017 ◽

Author(s):

Armin Schnider

Keyword(s):

Brain Damage ◽

Limbic Encephalitis ◽

Artery Aneurysm ◽

Anterior Communicating Artery ◽

Brain Areas ◽

Anatomical Basis ◽

Korsakoff Syndrome ◽

Hypoxic Brain ◽

Degenerative Dementia ◽

The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

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Zingiber officinaleMitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2011/429505 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 35

Author(s):

Jintanaporn Wattanathorn ◽

Jinatta Jittiwat ◽

Terdthai Tongun ◽

Supaporn Muchimapura ◽

Kornkanok Ingkaninan

Keyword(s):

Cognitive Function ◽

Cerebral Ischemia ◽

Brain Damage ◽

Focal Cerebral Ischemia ◽

Infarct Volume ◽

Neuroprotective Effect ◽

Morris Water Maze Test ◽

Brain Infarct ◽

Ginger Rhizome ◽

The Brain

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

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Race and Rorschach Signs of Brain Damage in Cerebral Thrombosis

Perceptual and Motor Skills ◽

10.2466/pms.1966.22.2.655 ◽

1966 ◽

Vol 22 (2) ◽

pp. 655-662 ◽

Cited By ~ 1

Author(s):

Ray B. Evans ◽

Jessie Marmorston

Keyword(s):

Myocardial Infarction ◽

Brain Damage ◽

Cerebral Thrombosis ◽

The Brain ◽

Item Scale

In an attempt to identify Rorschach signs which would differentiate the brain-damaged regardless of race, a study was made of 225 Caucasian and 127 Negro patients between 40 and 80 yr. of age. There was known brain damage (cerebral thrombosis) in 204 patients, and no known brain damage in 148 patients (myocardial infarction). Each of 31 Rorschach signs of cerebral impairment was studied to determine its power in discriminating Caucasian damaged from nondamaged and Negro damaged from nondamaged patients. A combination of 13 signs was thereby selected in which race did not appear to be a significant factor. The 13-item scale differentiated brain-damaged from nondamaged Caucasian, Negro, and combined Caucasian-Negro groups, all at levels below .001. The 13-item scale correctly classified 71% of the patients, compared with 73% when all 31 signs were used.

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GANGGUAN BERBAHASA PADA PENDERITA CEREBRAL PALSY SEBUAH KAJIAN LINGUISTIK KLINIS

Humanitatis : Journal of Language and Literature ◽

10.30812/humanitatis.v6i2.677 ◽

2020 ◽

Vol 6 (2) ◽

pp. 175-186

Author(s):

Agus Syahid

Keyword(s):

Cerebral Palsy ◽

Brain Damage ◽

Language Disorders ◽

Motor Center ◽

The People ◽

Children With Cerebral Palsy ◽

The Brain ◽

Motor Disturbances

This study describes language disorders in the people with cerebral palsy and what kind of treatments to people with cerebral palsy related to language disorders. Cerebral palsy is a series of disorders with problems regulating muscle movements where it is as a result of some damage to the motor centers in the brain. Damage to the motor center in the brain that causes cerebral palsy can occur prenatal (before birth), perinatal (during the birth), or even postnatal (immediately after birth). There are several main problems that are often found and faced by children with cerebral palsy, they are: (1) difficulty in eating and swallowing caused by motor disturbances in the mouth, (2) difficulty in speaking, (3) difficulty in hearing, and (4) language disorders.

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Intracerebral Injection of Heme Induces Lipid Peroxidation, Neuroinflammation, and Sensorimotor Deficits

Stroke ◽

10.1161/strokeaha.120.031911 ◽

2021 ◽

Author(s):

Luiz Ricardo C. Vasconcellos ◽

Letícia Martimiano ◽

Danillo Pereira Dantas ◽

Filipe Mota Fonseca ◽

Hilton Mata-Santos ◽

...

Keyword(s):

Lipid Peroxidation ◽

Signaling Pathway ◽

Brain Damage ◽

Autologous Blood ◽

Mapk Signaling ◽

Heme Oxygenase 1 ◽

Dependent Manner ◽

In Vivo Models ◽

Sensorimotor Deficits ◽

The Brain

Background and Purpose: Heme is a red blood cell component released in the brain parenchyma following intracerebral hemorrhage. However, the study of the pathophysiological mechanisms triggered by heme in the brain is hampered by the lack of well-established in vivo models of intracerebral heme injection. This study aims to optimize and characterize a protocol of intrastriatal heme injection in mice, with a focus on the induction of lipid peroxidation, neuroinflammation and, ultimately, sensorimotor deficits. We also evaluated the involvement of NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3), an inflammasome sensor, in the behavior deficits induced by heme in this model. Methods: Mice were injected with heme in the striatum for the evaluation of neuroinflammation and brain damage through histological and biochemical techniques. Immunoblot was used to evaluate the expression of proteins involved in heme/iron metabolism and antioxidant responses and the activation of the MAPK (mitogen-activated protein kinase) signaling pathway. For the assessment of neurological function, we followed-up heme-injected mice for 2 weeks using the rotarod, elevated body swing, and cylinder tests. Mice injected with the vehicle (sham), or autologous blood were used as controls. Results: Heme induced lipid peroxidation and inflammation in the brain. Moreover, heme increased the expression of HO-1 (heme oxygenase-1), ferritin, p62, and superoxide dismutase 2, and activated the MAPK signaling pathway promoting pro-IL (interleukin)-1β production and its cleavage to the active form. Heme-injected mice exhibited signs of brain damage and reactive astrogliosis around the injection site. Behavior deficits were observed after heme or autologous blood injection in comparison to sham-operated controls. In addition, behavior deficits and IL-1β production were reduced in Nlrp3 knockout mice in comparison to wild-type mice. Conclusions: Our results show that intracerebral heme injection induces neuroinflammation, and neurological deficits, in an NLRP3-dependent manner, suggesting that this is a feasible model to evaluate the role of heme in neurological disorders.

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Mycobacterium of tuberculosis with defective cell wall, determined in the brain of the biological model with spongional changes

Reports of Vinnytsia National Medical University ◽

10.31393/reports-vnmedical-2019-23(1)-02 ◽

2019 ◽

Vol 23 (1) ◽

pp. 12-19

Author(s):

O.P. Lysenko ◽

V.V. Vlasenko ◽

H.K. Palii ◽

I.H. Vlasenko ◽

O.A. Nazarchuk

Keyword(s):

Central Nervous System ◽

Cell Wall ◽

Nervous System ◽

Mycobacterium Tuberculosis ◽

Brain Damage ◽

Molecular Genetic Study ◽

Central Nervous System Damage ◽

Infectious Dose ◽

Microbiological Methods ◽

The Brain

Mycobacterium tuberculosis is endowed with resistance to adverse factors and rapidly forms drug resistance. The aim is to study of the connection of tuberculosis infection and the development of brain damage with signs of spongymorphic changes. There were investigated canned 10% formalin fragments of the brain of 2 goats with signs of central nervous system damage by histological, microbiological methods. For microbiological examination, 3–5 years brain samples after were sowed on the MycСel DW nutrient medium with a growth stimulator. The molecular genetic study was performed using a polymerase chain reaction on a Molecular Imager GelDoc TM XR + (BioRad) device. The polypeptide profile was studied electrophoretically. In the goats, who died with symptoms of central nervous system damage, spongiform changes were detected in the brain. In the brain samples, DNA and mycobacterium tuberculosis with a defective cell wall have been detected, accumulation of mycobacterial antigens has been observed in the cells of the brain and in the intercellular space. Despite the fact that brain samples were in 10% formalin for 1 month, 3 years and 5 years, in all cases mycobacterium tuberculosis with a defective cell wall was isolated. Their viability was comparable to the infectiousness of prions. The isolation of mycobacterium tuberculosis with a defective cell wall from the brain did not differ in morphology and polypeptide composition from isolates from tuberculin, FLK-BLV, lymph nodes of cows, patients with tuberculosis. This indicates a high probability that mycobacterial infection, depending on the infectious dose, the characteristics of the strain and host genome, as well as the state of the immune system, can cause oncogenic action, cause active tuberculosis, brain damage, and the cardiovascular system.

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Mechanisms and evolution of the brain damage in neonatal post-hemorrhagic hydrocephalus

Child s Nervous System ◽

10.1007/bf00301763 ◽

1995 ◽

Vol 11 (5) ◽

pp. 293-296 ◽

Cited By ~ 12

Author(s):

F. Guzzetta ◽

E. Mercuri ◽

M. Span�

Keyword(s):

Brain Damage ◽

The Brain

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