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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothermia-induced platelet aggregation (HIPA) was previously reported in whole blood exposed to synthetic surfaces at 24 degrees-32 degrees C in one-third of normal subjects tested. Cardiopulmonary bypass, conducted with hypothermia, may lead to such aggregation, resulting in microvascular occlusion contributing to cognitive impairment. This pilot study was conducted to explore the relationship between HIPA and cognitive outcome at hospital discharge in patients undergoing coronary artery bypass graft (CABG) surgery as a first step toward a longer-term study. Patients (n = 45) undergoing mild to moderate hypothermia (32 degrees-28 degrees C) during CABG surgery underwent cognitive testing preoperatively and prior to hospital discharge. Tests included: visual and verbal memory, mental processing speed, executive function, language, and intellectual function. HIPA was identified using an in vitro assay in which blood flowing in polyvinychloride tubing was subjected to hypothermia, and platelet aggregates were detected using microscopy and passing the exiting blood through a 20-microm pore filter. Forty-four percent of patients exhibited HIPA. The entire cohort exhibited significant postoperative cognitive decline in verbal memory, mental processing speed and executive function. There was greater cognitive decline in the group with HIPA compared with the group not exhibiting this phenomenon. The patients with HIPA showed significant decline in four of five cognitive measures whereas patients not exhibiting this phenomenon declined in only two of five cognitive measures. HIPA appears to be associated with an added risk of cognitive decline immediately following CABG surgery employing mild to moderate hypothermia. The findings of our study suggest the long-term cognitive effects of hypothermia-induced platelet aggregation need to be explored.
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PMID:Hypothermia-induced platelet aggregation and cognitive decline in coronary artery bypass surgery: a pilot study. 1603 88

Epidural analgesia is widely used for postoperative pain in a variety of surgical operations and it is recognised to provide superior quality of analgesia when compared with systemic opioids. The combination of low doses of local anaesthetics and opioids appears to provide optimal analgesia with minimal motor blockade. However, side effects have been reported with epidural analgesia such as postoperative nausea and vomiting (PONV), respiratory depression and arterial hypotension. Although the incidence of these side effects is lower than those reported with the use of systemic opioids, they can contribute to a delay in discharging patients from PACU. Epidural analgesia is also associated with perioperative hypothermia. The incidence of cognitive dysfunction is not decreased by using postoperative epidural analgesia. Assessment of the quality of analgesia by using pain visual analogue score (VAS) at rest and with movements or on coughing remains the most preferred in PACU, although there are limitations with this measurement. Epidural failure due to technical failure or malposition of the catheter represents potential problems having direct consequence on the quality of analgesia provided. All epidural catheters have to be checked and the quality of analgesia assessed before patients are discharging from PACU to the surgical wards. With advances in pain pharmacology, multimodal interventions and adjuvants can be used safely with the intent of providing better analgesia and decreasing the side effects associated with one technique.
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PMID:Epidural analgesia in the Post-Anaesthesia Care Unit. 1630 58

Neurologic injury is a devastating complication of cardiac surgery. Cerebral cooling is an important aspect of hypothermic cardiopulmonary bypass in some patients, because hypothermia is the only reliable method of neuroprotection against injuries related to cerebral ischemia. Hypothermia may afford neuroprotection by a variety of mechanisms, including reduction in cerebral metabolic rate, decreased excitatory transmitter release, reduced ion influx, and reduced vascular permeability. Conversely, hyperthermia, even if mild (2-3 degrees C), is harmful; it aggravates ischemic neuronal injury and accelerates neuronal death. In patients with acute strokes, hyperthermia worsens prognosis with respect to stroke severity, infarct size, mortality, and outcome in survivors. The degree of temperature discrepancy among standard monitoring sites in individual patients is often striking. The differences between jugular bulb temperature and rectal or bladder temperature are particularly large. Blood temperature in the arterial line leading from the oxygenator may be the most consistently accurate indicator of cerebral temperature. When hypothermia is used to protect vital organs during cardiopulmonary bypass, the cooling phase should be adequate, and the rewarming phase must be carefully managed. Hyperthermia may be as hazardous during the postoperative period as during surgery, exacerbating the extent of tissue injury if an overt stroke has occurred. Postoperative hyperthermia correlates with a greater degree of cognitive dysfunction measured 6 weeks after cardiac surgery. In conclusion, cardiac anesthesiologists can reduce the risk of inadvertent hyperthermia by selecting the best sites for temperature monitoring, carefully controlling the rewarming process, and continuing temperature monitoring during the postoperative period.
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PMID:Management of temperature during and after cardiac surgery. 1642 89

To date, the primary treatments for Alzheimer's disease with proven efficacy have been acetylcholinesterase inhibitors that prevent the hydrolysis of acetylcholine (ACh) in the synaptic cleft, thereby prolonging its activity. Although these agents have some benefit in alleviating cognitive impairment, they have limited clinical utility because of insufficient efficacy and marginal tolerability. Within the last decade, there has been much experimental support for the use of therapeutics that directly target nicotinic ACh receptors (nAChRs) to improve cognitive function and slow neurodegenerative disease progression. These findings have spurred considerable research efforts to develop ligands selective for nAChRs, such as ABT-418 (Arneric et al., 1995), SIB-1553 (Bontempi et al., 2001), TC-2403 (Lippiello et al., 1996), and TC-2559 (Bencherif et al., 2000). There is abundant evidence that nAChR modulators have the potential to alleviate cognitive impairment in demented states. In addition to improving cognitive function, a large body of research implicates a role for nAChRs in neuroprotection, suggesting potential for disease modification. An impact of nAChR agonists on disease progression would provide an advantage over currently available treatments for memory loss. The profile of previous nAChR-targeted clinical candidates has not been adequate to warrant further development owing to poor oral bioavailability, side effects, and/or lack of efficacy. Thus, a challenge in nAChR drug design and development has been the reduction of undesirable effects that result from activity at specific nAChRs in the CNS and PNS, including cardiovascular toxicity, emesis, seizures, and hypothermia.
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PMID:Ispronicline: a novel alpha4beta2 nicotinic acetylcholine receptor-selective agonist with cognition-enhancing and neuroprotective properties. 1719 10

Postoperative cognitive dysfunction, confusion, and delirium are common after general anesthesia in the elderly, with symptoms persisting for months or years in some patients. Even middle-aged patients are likely to have postoperative cognitive dysfunction for months after surgery, and Alzheimer's disease (AD) patients appear to be particularly at risk of deterioration after anesthesia. Several investigators have thus examined whether general anesthesia is associated with AD, with some studies suggesting that exposure to anesthetics may increase the risk of AD. However, little is known on the biochemical consequences of anesthesia on pathogenic pathways in vivo. Here, we investigated the effect of anesthesia on tau phosphorylation and amyloid precursor protein (APP) metabolism in mouse brain. We found that, regardless of the anesthetic used, anesthesia induced rapid and massive hyperphosphorylation of tau, rapid and prolonged hypothermia, inhibition of Ser/Thr PP2A (protein phosphatase 2A), but no changes in APP metabolism or Abeta (beta-amyloid peptide) accumulation. Reestablishing normothermia during anesthesia completely rescued tau phosphorylation to normal levels. Our results indicate that changes in tau phosphorylation were not a result of anesthesia per se, but a consequence of anesthesia-induced hypothermia, which led to inhibition of phosphatase activity and subsequent hyperphosphorylation of tau. These findings call for careful monitoring of core temperature during anesthesia in laboratory animals to avoid artifactual elevation of protein phosphorylation. Furthermore, a thorough examination of the effect of anesthesia-induced hypothermia on the risk and progression of AD is warranted.
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PMID:Anesthesia leads to tau hyperphosphorylation through inhibition of phosphatase activity by hypothermia. 1737 70

Two healthy breast-fed term infants were admitted to the neonatal unit with symptomatic hypoglycaemia and seizures. In both patients, risk factors (i.e. hypothermia) and symptoms ofhypoglycaemia went unrecognised until apnoea or seizures developed. Both patients required antiepileptic medication for neonatal seizures. One patient had isolated restricted growth in head circumference in the first year of life. Follow-up at II years showed cognitive impairment and epilepsy. The other patient had normal head circumference and mild global delay in neurological development at the age of 36 months. Severe symptomatic hypoglycaemia in healthy breast-fed term infants may cause severe brain damage. Early recognition of risk factors such as hypothermia lasting more than 3 hours is essential to preventing hypoglycaemia. The presence of risk factors warrants additional bottle-feeding to maintain sufficient intake until breastfeeding is adequately established. Any uncertainty regarding the symptoms of hypoglycaemia should be investigated promptly.
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PMID:[Cerebral damage due to hypoglycaemia in otherwise healthy breast-fed term infants]. 1902 71

Injury to the perinatal brain is a leading cause of childhood mortality and lifelong disability. Cerebral palsy and cognitive impairment are usually related to periventricular white matter damage, which is seen chiefly in babies born before 32 wk gestational age, and to corticosubcortical lesions, which occur mainly in full-term infants. Despite recent improvements in neonatal care, no effective treatment for perinatal brain lesions is available. Several interventions, such as magnesium sulfate in preterm newborns and hypothermia in term newborns, are the focus of completed or continuing clinical trials. Improved understanding of the pathophysiological mechanisms involved in perinatal brain lesions helps to identify potential targets for neuroprotective interventions, as discussed in this review.
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PMID:Neuroprotective strategies for the neonatal brain. 1849 96

Cerebral palsy is the most prevalent cause of persisting motor function impairment with a frequency of about 1/500 births. In developed countries, the prevalence rose after introduction of neonatal intensive care, but in the past decade, this trend has reversed. A recent international workshop defined cerebral palsy as "a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain." In a majority of cases, the predominant motor abnormality is spasticity; other forms of cerebral palsy include dyskinetic (dystonia or choreo-athetosis) and ataxic cerebral palsy. In preterm infants, about one-half of the cases have neuroimaging abnormalities, such as echolucency in the periventricular white matter or ventricular enlargement on cranial ultrasound. Among children born at or near term, about two-thirds have neuroimaging abnormalities, including focal infarction, brain malformations, and periventricular leukomalacia. In addition to the motor impairment, individuals with cerebral palsy may have sensory impairments, cognitive impairment, and epilepsy. Ambulation status, intelligence quotient, quality of speech, and hand function together are predictive of employment status. Mortality risk increases incrementally with increasing number of impairments, including intellectual, limb function, hearing, and vision. The care of individuals with cerebral palsy should include the provision of a primary care medical home for care coordination and support; diagnostic evaluations to identify brain abnormalities, severity of neurologic and functional abnormalities, and associated impairments; management of spasticity; and care for associated problems such as nutritional deficiencies, pain, dental care, bowel and bladder continence, and orthopedic complications. Current strategies to decrease the risk of cerebral palsy include interventions to prolong pregnancy (eg, 17alpha-progesterone), limiting the number of multiple gestations related to assisted reproductive technology, antenatal steroids for mothers expected to deliver prematurely, caffeine for extremely low birth weight neonates, and induced hypothermia for a subgroup of neonates diagnosed with hypoxic-ischemic encephalopathy.
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PMID:Diagnosis, treatment, and prevention of cerebral palsy. 1898 5

Abnormal hyperphosphorylation and aggregation of microtubule-associated protein tau play a crucial role in neurodegeneration of Alzheimer's disease (AD). Anesthesia has been associated with cognitive impairment and the risk for AD. Here we investigated the effects of anesthesia on site-specific tau phosphorylation and the possible mechanisms. We found that anesthesia for short periods (30 sec to 5 min) induced tau phosphorylation at Thr181, Ser199, Thr205, Thr212, Ser262, and Ser404 to small, but significant, extents, which appeared to result from anesthesia-induced activation of stress-activated protein kinases. Anesthesia for a longer time (1~h) induced much more dramatic phosphorylation of tau at the above sites, and the further phosphorylation may be associated with hypothermia induced by anesthesia. Anesthesia-induced tau phosphorylation appears to be specific because the increased phosphorylation was only seen at half of the tau phosphorylation sites studied and was not observed in global brain proteins. These studies clarified the dynamic changes of tau phosphorylation at various sites and, thus, served as a fundamental guide for future studies on tau phosphorylation by using brains of anesthetized experimental animals. Our findings also provide a possible mechanism by which anesthesia may cause postoperative cognitive impairment and increase the risk for AD.
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PMID:Anesthesia induces phosphorylation of tau. 1927 56

Despite a half century of research and the implementation of various risk-reduction strategies among clinicians and basic scientists, patients continue to experience strokes and cognitive dysfunction related to the use of cardiopulmonary bypass (CPB) for cardiac surgery. One strategy to reduce these detrimental effects has been the use of hypothermia. Although numerous studies have addressed the issue, the question of whether the use of hypothermia during CPB attenuates the impact of central nervous system consequences remains unresolved. However, data clearly demonstrate that hyperthermia is to be avoided in the perioperative period, necessitating careful rewarming strategies if hypothermia is used during CPB. Selecting and understanding the impact of the temperature-monitoring site is important to accurately estimate cerebral temperature and to avoid inadvertent surges in brain temperature. In this article, we review the literature regarding the impact of hypothermia and rewarming rates during cardiac surgery.
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PMID:A core review of temperature regimens and neuroprotection during cardiopulmonary bypass: does rewarming rate matter? 1992 98


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