Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We treated two children with influenza-associated acute encephalopathy by a combination of mild hypothermia and steroid pulse therapy. Case 1, a 2-year-and-3-month-old boy, admitted to our hospital 7 days after the onset of central nervous symptoms. The brain MRI-CT revealed laminar cortical necrosis and severe brain edema. EEG showed very low voltage. Brain edema improved by the combination therapy. He had sequelae, but was able to eat. Case 2, a 1-year-and-10-month-old boy, admitted to our hospital 5 days after the onset of central nervous symptoms. Brain MRI showed frontal dominant cortical edema. EEG showed high voltage delta bursts. The combination therapy was effective, but he remained mental handicapped. The outcome was better compared to our previous cases of acute encephalopathy. The combination therapy is intended to counteract cytokines, and was considered to be an effective treatment against acute encephalopathy associated with an influenza virus infection.
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PMID:[Effects of mild hypothermia and steroid pulse combination therapy on acute encephalopathy associated with influenza virus infection: report of two cases]. 1091 71

Two children with influenza A-related encephalopathy were treated with a combination of mild hypothermia (deep body temperature of the forehead: 35 degrees C) and anticytokine agents (high-dose methylprednisolone and ulinastatin), while receiving amantadine. One of the cases exhibited acute necrotizing encephalopathy on computed tomography (CT). Although no severe complications occurred, correctable hypokalemia and hyperglycemia occurred in both cases. Both patients recovered without any neurological sequelae. Our therapeutic protocol appears to be effective for managing influenza A-related encephalopathy.
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PMID:Combined therapy with hypothermia and anticytokine agents in influenza A encephalopathy. 1104 19

During the Winter or Influenza season in Japan, there has been an increase in the number of patients presenting with Central Nervous System complaints or symptoms. One of the causes is reported be Influenza encephalitis/encephalopathy. Some of these patients undergo a course of Reye's Syndrome, Acute Necrotizing Encephalopathy (ANE), or Hemorrhagic Shock and Encephalopathy(HSE), of which the pathologic features are still unknown. It is likely that the major underlying feature is cerebral edema, caused by impairments in the blood-brain barrier, which is mediated by inflammatory cytokines. Mild brain hypothermia may be an effective treatment in preventing cerebral edema by preventing the cytokine activation and elevations in brain temperature. A combination of mild brain hypothermia and high-dose corticosteroid therapy is thought to be effective in the treatment of influenza encephalitis/encephalopathy.
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PMID:[Mild brain hypothermia for influenza encephalitis/encephalopathy and its significance]. 1122 26

Interleukin (IL)-1 and tumor necrosis factor (TNF) promote slow-wave sleep (SWS), whereas IL-10 inhibits the synthesis of IL-1 and TNF and promotes waking. We evaluated the impact of endogenous IL-10 on sleep-wake behavior by studying mice that lack a functional IL-10 gene. Under baseline conditions, C57BL/6-IL-10 knockout (KO) mice spent more time in SWS during the dark phase of the light-dark cycle than did genetically intact C57BL/6 mice. The two strains of mice showed generally comparable responses to treatment with IL-1, IL-10, or influenza virus, but differed in their responses to lipopolysaccharide (LPS). In IL-10 KO mice, LPS induced an initial transient increase and a subsequent prolonged decrease in SWS, as well as profound hypothermia. These responses were not observed in LPS-treated C57BL/6 mice. These data demonstrate that in the absence of endogenous IL-10, spontaneous SWS is increased and the impact of LPS on vigilance states is altered. Collectively, these observations support a role for IL-10 in sleep regulation and provide further evidence for the involvement of cytokines in the regulation of sleep.
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PMID:Cytokine- and microbially induced sleep responses of interleukin-10 deficient mice. 1135 86

A 15-year-old girl presented with meningeal irritation and bilateral cerebral signs after contracting influenza. A lumbar puncture revealed bloody cerebrospinal fluid and polymorphonuclear predominant pleocytosis with an elevated protein level and normal glucose level. Computed tomography showed a hematoma in the right basal ganglia and lateral ventricles. Symmetrical low density areas were also noted in the bilateral white matter. The preliminary diagnosis was hemorrhagic cerebrovascular disease of unknown cause. However, her neurological condition deteriorated. Magnetic resonance (MR) imaging showed diffuse high intensity signals in the bilateral white matter and small spotty lesions, indicating hemorrhages in various stages. The final diagnosis was acute hemorrhagic leukoencephalitis (AHL). However, high-dose steroid administration and plasmapheresis failed to improve her condition. Hypothermia could not control her intracranial pressure and she died 12 days after admission. The neuroimaging findings indicated the histological characteristics of AHL, but the hematoma formation is rare. AHL is a fulminant form of brain demyelination and can be fatal, so early diagnosis and aggressive treatment are important for successful recovery. Therefore, early investigation by MR imaging is necessary.
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PMID:Possible acute hemorrhagic leukoencephalitis manifesting as intracerebral hemorrhage on computed tomography--case report. 1220 93

Viral infections induce excess non-rapid eye movement sleep (NREMS) in mice. Growth hormone-releasing hormone receptor (GHRH receptor) was previously identified as a candidate gene responsible for NREMS responses to influenza challenge in mice. The dwarf lit/lit mouse with a nonfunctional GHRH receptor was used to assess the role of the GHRH receptor in viral-induced NREMS. After influenza A virus infection the duration and intensity [electroencephalogram (EEG) delta power] of NREMS increased in heterozygous mice with the normal phenotype, whereas NREMS and EEG delta power decreased in homozygous lit/lit mice. Lit/lit mice developed a pathological state with EEG slow waves and enhanced muscle tone. Other influenza-induced responses (decreases in rapid eye movement sleep, changes in the EEG high-frequency bands during the various stages of vigilance, hypothermia, and decreased motor activity) did not differ between the heterozygous and lit/lit mice. GH replacement failed to normalize the NREMS responses in the lit/lit mice after influenza inoculation. Decreases in NREMS paralleled hypothermia in the lit/lit mice. Lung virus levels were similar in the two mouse strains. Lit/lit mice had a higher death rate after influenza challenge than the heterozygotes. In conclusion, GHRH signaling is involved in the NREMS response to influenza infection.
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PMID:Alterations in EEG activity and sleep after influenza viral infection in GHRH receptor-deficient mice. 1259 90

A 41-year-old man was admitted to our hospital suffering from generalized convulsion with a high fever and disturbed consciousness one week after exhibiting flu-like symptoms. We made a diagnosis of acute viral encephalitis, based on the clinical features and the evidence of pleocytosis with an increase in protein in the CSF. On admission, MRI was normal and CRP was negative. The levels of transaminase, ammonia, and blood sugar were normal, so that an adult Reye's syndrome could be ruled out. Herpes simplex encephalitis and influenza encephalopathy were also ruled out because of viral examinations, and specific agents could not be determined. Clinical symptoms subsided once after he was treated with dexamethasone, acyclovir, and anti-convulsants, until generalized convulsion accompanied by a high fever again occurred on the 9th day. On the 18th day, the patient showed anisocoria and ataxic respiration due to severe brain edema. Mild hypothermia therapy to rectal temperature 35 degrees C was induced under mechanical ventilation. Cranial CT taken 3 days after the therapy began to show the improvement of the brain edema. After 7 days of the therapy, his clinical symptoms began to recover dramatically. On the 46th day, he was discharged from hospital without showing almost any neurological symptoms. Mild hypothermia therapy should be considered for adult patients as well as non-adult patients suffering from acute encephalitis with severe intracranial hypertension.
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PMID:[Successful use of mild hypothermia therapy in an adult patient of non-herpetic acute encephalitis with severe intracranial hypertension]. 1283 82

Double-stranded (ds)RNA is made as a by-product of viral replication. Synthetic dsRNA induces virtually all of the same systemic symptoms as acute viral infections, such as fever and malaise. In order to develop a model of respiratory viral infections (such as influenza) suitable for use in gene knockout mice (where the deleted gene may affect viral replication), we examined C57BL/6 mouse body temperature and locomotor activity responses to the synthetic dsRNA polyriboinosinic.polyribocytidylic acid (poly[rI.rC]) introduced via the intratracheal (IT) route. We compared the IT poly[rI.rC] responses to the well-characterized intraperitoneal (IP) poly[rI.rC] responses. IT poly[rI.rC] failed to induce an acute phase response (APR) in mice, in contrast to IP poly[rI.rC]. However, addition of interferon (IFN)gamma to the IT poly[rI.rC] inoculum induced sustained hypothermia and suppressed locomotor activity responses with similar kinetics to those responses seen in acute mouse influenza. We further examined cytokine, antiviral, muscarinic M2 receptor and inducible nitric oxide synthase gene expression at 5 hr in the lungs of IT challenged mice. These studies suggested that priming the lung with IFNgamma could enhance proinflammatory (IL1beta, IL6, TNFalpha) cytokine gene expression and suppress interferon gene expression compared to IT poly[rI.rC] alone. No differences were detected for the other genes examined. While further molecular characterization of the model is required, we demonstrate that IT challenge with combined poly[rI.rC] and IFNgamma closely simulates the APR to an acute respiratory virus, and may serve as a suitable model for analyzing the molecular basis of the viral APR in gene knockout mice.
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PMID:Intratracheal double-stranded RNA plus interferon-gamma: a model for analysis of the acute phase response to respiratory viral infections. 1501 Feb 66

A 1-year-old girl with influenza-associated encephalopathy initially exhibited prolonged febrile convulsions and subsequent drowsiness. She became unconsciousness and experienced a cluster of seizures 4 days later. Diffusion-weighted magnetic resonance imaging (DWI) showed high signal intensity in the bilateral frontal white matter. This signal change migrated to the bifrontal cortical areas and the caudate nuclei within 10 days, when T2 elongation appeared over the gray and white matter of frontal lobes. Choreoathetosis and oculogyric crisis were transiently noted at this period. Frontal lobe signs, including the forded mouth opening response, after diminution of these movement disorders. The DWI signal change subsequently resolved and frontal cortical atrophy appeared thereafter. Levels of inflammatory cytokines in the cerebrospinal fluid were normal during the acute phase of clinical course. The biphasic clinical course with initial prolonged seizure, involvement of the frontal lobes, and the progression of signal change on DWI from white to gray matter, meets the characteristics of "status epilepticus-type acute encephalopathy" suggested by Shiomi et al. Although pentobarbital infusion, steroid pulse therapy and mild hypothermia did not show any apparent effects on the clinical course of this patient, further trial of these therapies may be warranted for the treatment of this type of encephalopathy.
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PMID:[Influenza-associated encephalopathy with onset of prolonged convulsion: a case report]. 1709 68

The role of type I interferons (IFNs) in mediation of acute viral symptoms (fever, somnolence, anorexia, etc.) is unknown. To determine the role of type I IFN in selected symptom development, body temperature and sleep responses to a marginally lethal dose of X-31 influenza virus were examined in mice with a targeted mutation of the IFN receptor type I (IFN-RI knockouts) and compared to wild-type 129 SvEv control mice. Mice were monitored for 48 h to determine baseline temperature and sleep profiles prior to infection, and then for 9 days following infection. Hypothermic responses to virus were perceptible beginning at 64 h post-infection (PI) and were more marked in KO mice until 108 h, when hypothermia became more exaggerated in wild-type controls. Temperatures of wild-type mice continued to decline through day 9 while temperatures in IFN-RI KO mice stabilized. Time spent in non-rapid eye movement sleep (NREMS) increased in KO mice when hypothermia was marked and then returned to baseline levels, while NREMS continued to increase in wild-type mice through day 9. Other sleep parameters [time spent in rapid eye movement sleep (REMS), relative NREMS EEG slow wave activity, NREMS EEG power density] were all reduced in wild-type mice compared to KOs from days 3 to 8 while REMS low frequency EEG power density increased in wild-type relative to KOs. In conclusion, our results indicate that the presence of functional type I IFN slightly ameliorates disease symptoms early in the X-31 infection while exacerbating disease symptoms later in the infection.
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PMID:Interferon type I receptor-deficient mice have altered disease symptoms in response to influenza virus. 1709 95


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