gerstmann-straussler-scheinker disease/hypoxia

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Wernicke's encephalopathy-like lesions in global cerebral hypoxia.

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We report a patient with severe hypoxic encephalopathy after cardiac arrest, in which lesions depicted on MRI involved mainly the periaqueductal brainstem, hypothalamus and mamillary bodies, and medial thalami. Hypoxia usually causes cerebro-cerebellar cortical damage. However, it may also cause

Hypoxia-ischemic encephalopathy in full-term neonate: correlation proton MR spectroscopy with MR imaging.

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BACKGROUND To evaluate 1H Magnetic Resonance Spectroscopy (1HMRS) in the diagnosis of hypoxia-ischemic encephalopathy (HIE) of full-term neonates correlated with Magnetic Resonance Imaging (MRI). METHODS Thirty-eight cases of full-term neonates diagnosed as HIE clinically were selected to perform

Experimental models of hypoxic-ischemic encephalopathy: hypoxia-ischemia in the immature rat.

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The development of experimental models to study the mechanisms of perinatal hypoxic-ischemic encephalopathy and stroke and effective therapies represents an important goal in perinatal medicine. However, due to the complexity of this pathological condition in humans, to date there is no ideal animal

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

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Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or

[Hypoxic-ischemic encephalopathy in the full-term newborn infant. Recent advances, markers of hypoxia and therapeutic options].

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BACKGROUND Hypoxic-ischemic encephalopathy is the neurological consequence of a nonprogressive encephalopathic clinical picture of the hypoxic-ischemic syndrome, caused by a mixture of reduced oxygenation of the blood with increased carbon dioxide (asphyxia) and a lack of tissue perfusion

Post-operative hyponatraemic encephalopathy: a successful outcome despite hypoxia.

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Hyponatraemia is the most common electrolyte disorder encountered in clinical practice. Symptomatic hyponatraemia reflects brain damage because of cerebral swelling. Some coexisting factors such as extreme ages, hypoxia and female sex are associated with poor prognosis. In this report, we describe

Influence of hypoxia and sex on hyponatremic encephalopathy.

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Over the past 20 years it has become increasingly apparent that hyponatremic encephalopathy is a major cause of inhospital morbidity and mortality, particularly in postoperative patients. The factors that may lead to death or permanent brain damage and the susceptible patient groups have been

[Intermittent hypoxia in the treatment of dyscirculatory encephalopathy].

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An influence of intermittent hypoxia (IH) on antioxidant enzymes activity was investigated in 42 patients, aged 48.2 +/- 1.8 years, with 1-2-nd stage of dyscirculatory encephalopathy (DE) in the presence of I-II stage of arterial hypertension (AH). Patients with arterial pressure below 145/85 mmHg

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats.

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Encephalopathy of prematurity (EoP) is a term that encompasses the central nervous system (CNS) abnormalities associated with preterm birth. To best advance translational objectives and uncover new therapeutic strategies for brain injury associated with preterm birth, preclinical models of EoP must

Neuronal self-injury mediated by IL-1β and MMP-9 in a cerebral palsy model of severe neonatal encephalopathy induced by immune activation plus hypoxia-ischemia.

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BACKGROUND Inflammation due to remote pathogen exposure combined to hypoxia/ischemia (HI) is one of the most common causes of neonatal encephalopathy affecting at-term or near-term human newborn, which will consequently develop cerebral palsy. Within term-equivalent rat brains exposed to systemic

Endogenous hypothermic response to hypoxia reduces brain injury: Implications for modeling hypoxic-ischemic encephalopathy and therapeutic hypothermia in neonatal mice.

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Hypothermia treatment (HT) is the only formally endorsed treatment recommended for hypoxic-ischemic encephalopathy (HIE). However, its success in protecting against brain injury is limited with a number to treat of 7-8. The identification of the target mechanisms of HIE in combination with HT will

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

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The perinatal period represents a time of great vulnerability for the developing brain. A variety of injuries can result in death or devastating injury causing profound neurocognitive deficits. Hypoxic-ischemic neonatal encephalopathy (HIE) remains the leading cause of brain injury in term infants

Hearing impairment and hypoxia ischaemic encephalopathy: Incidence and associated factors.

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OBJECTIVE To establish the local incidence of hearing loss in newborns with Hypoxic Ischaemic Encephalopathy (HIE) and to identify associated risk factors. METHODS Retrospective Cohort Study. Neonatal Intensive Care Unit (NICU) dual stage hearing screening protocol, including automated otoacoustic

Insulin Growth Factor 1 Protects Neural Stem Cells Against Apoptosis Induced by Hypoxia Through Akt/Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase (Akt/MAPK/ERK) Pathway in Hypoxia-Ishchemic Encephalopathy.

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BACKGROUND Insulin growth factor 1 (IGF-1) is reported to modulate cell growth and acts as potential therapy for traumatic brain injury. This study was designed to investigate the effect of IGF-1 on hypoxia-induced apoptosis in neural stem cells (NSCs). MATERIAL AND METHODS A hypoxia model was

Effect of creatine monohydrate supplementation on various hematological and serum biochemical parameters of male albino mice following neonatal hypoxia-ischemia encephalopathy.

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BACKGROUND Present study was designed to report the effect of 2% creatine monohydrate supplementation for 8, 12 and 15 weeks on hematology and serum biochemical profile of male albino mouse following hypoxic ischemic insult on postnatal day 10. METHODS 66 Blood samples (2% creatine monohydrate

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