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

In order to test the practicability and safety of whole-body cooling in term neonates with moderate-to-severe hypoxic-ischaemic encephalopathy (HIE) and to report outcomes, a prospective pilot study was carried out in 25 term infants (median postmenstrual age 38 weeks, range 36 to 41 weeks; 20 males, five females). Whole-body cooling, to a target core temperature of 33 to 34 degrees C, started within 6 hours of birth and was maintained for 72 hours. Of the 25 newborn infants (19 Sarnat II and six Sarnat III, 18 outborn), 18 survived, including 13 (72%) with normal cerebral signal by MRI. Temperature instability occurred during cooling in 15 infants, but neither severe haemodynamic instability nor renal failure was seen. Thrombocytopenia developed in 12 infants, including seven with biological disseminated intravascular coagulation. One patient had hypoxaemia with right-to-left shunting through the ductus arteriosus, and seven had limited meningeal or subdural bleeding. Whole-body cooling is feasible in term neonates, with no life-threatening adverse events. Improvements are needed to obtain stable hypothermia for 72 hours.
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PMID:Whole-body cooling after perinatal asphyxia: a pilot study in term neonates. 1255 98

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

The objective of this study was to evaluate the effects of a moderate, intraischemic hypothermia on the behavorial deficits up to 4 weeks after induction of a focal mass lesion. A focal epidural mass lesion was induced by an epidural balloon. The severity of the trauma was defined by the balloon volume and flattening of electroencephalography. Hypothermia (32 degrees C) was induced as soon as maximum balloon infIation was reached. Ischemia was extended over 30 min. After reperfusion, normothermic (n = 24) and hypothermic animals (n = 25) were monitored for 3 h followed by a rewarming of the cooled animals. Results were compared to sham-operated animals (n = 10). Behavioral deficits were assessed by postural reflex (PR), open field (OF), beam balance (BB), beam walking (BW), and water maze tests (WMT). MRI follow-up and histology was evaluated. Sham-operated rats showed normal test results. Rats with normothermia showed worsening of test performance (PR, p < 0.05; OF, p < 0.05; BB, p < 0.05; BW, p < 0.05; WMT, p < 0.05) compared to controls over the whole observation period. A significantly better behavioral outcome was observed in animals treated with hypothermia which showed no differences from controls 3-4 days after injury (PR, OF, BB, BW, WMT, p > 0.05). Lesion induced mortality was reduced in cooled animals but overall mortality rates were not influenced by this therapeutic measure. Neuronal cell loss in the CA1-CA4 region (p < 0.05) was reduced and the lesion size smaller (21%/p > 0.05) in hypothermic animals. Magnetic resonance imaging revealed that the lesion was more pronounced in the cortical grey matter after normothermia, whereas hypothermic animals showed more subcortical brain lacerations. In conclusion, intraischemic hypothermia significantly improved the behavioral outcome, and decreased lesion-induced mortality and the size of the lesion after an epidural focal mass lesion.
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PMID:Moderate hypothermia improves neurobehavioral deficits after an epidural focal mass lesion in rodents. 1290 39

To test the hypothesis that presence of metalloproteases (MMPs), their inhibitors (TIMPs) and their substrate laminin-5 differs between the ischemic core and the surrounding tissue, we examined the impact of middle cerebral artery occlusion/reperfusion (MCA:O/R) on these molecules in different regions of the infarct. We also investigated the influence of hypothermia on the progression of the ischemic lesion and MMP activity. Brain sections from 64 Wistar rats subjected to MCA:O/R were examined by means of cytohistochemistry and zymography. The artery was occluded for 2 h followed by 3, 5, 8 and 12 h of reperfusion. Well characterized antibodies against laminin-5, MMPs and TIMP-2 were used. A total of 32 rats were treated with hypothermia. The presence of each antigen was related to the following regions of interest: ischemic core with BBB breakdown (I(c)), surrounding ischemic tissue without BBB breakdown (I(r)), and the contralateral non-ischemic region (N). Regions of interest were defined by MRI. The I(c) increased over time at the cost of the I(r). BBB breakdown occurred early in the ischemic core and increased over time. Hypothermia reduced the BBB breakdown at all time points. A graded decreased presence of laminin-5 was observed with 16.5+/-3.7(N)>10+/-2.8(I(r))>4+/-1.4(I(c)) immunopositive microvessels/mm(2) at 3 h of reperfusion. MMP-9 showed a reverse pattern with 0 (N)<4+/-0.8(I(r))<10+/-1.5(I(c)) immunopositive microvessels/mm(2). Hypothermia decreased the MMP activity measured by zymography. Laminin-5 and MMP presence relate directly to the degree of postischemic injury. Hypothermia reduces the conversion from the I(r) to ischemic core and the degree of BBB as well as MMP abundance.
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PMID:Topographically graded postischemic presence of metalloproteinases is inhibited by hypothermia. 1293 40

This case report describes a lipoma located in the pre-mamillary area that appeared in a 5-year-old child. The first symptom was very deep, transient hypothermia. Laboratory exams were normal. Diagnosis of a lipoma situated in the hypothalamic-mamillary area was made by brain MRI. The lipoma showed no signs of growth and hypothermia disappeared over the following 2 years. It is an unusual case of the body adapting to a new anatomic situation.
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PMID:Pediatric hypothalamic lipoma with hypothermia--case report. 1472 18

Thrombolysis (T) is limited by reperfusion-associated injury and the short therapeutic window after stroke onset. The present study investigates whether hypothermia alone or in combination with thrombolysis has beneficial effects after experimental thromboembolic stroke. Wistar rats (n = 60) were subjected to thromboembolic occlusion (TE) of the middle cerebral artery (MCA). Thrombolysis (T) was performed with intravenous recombinant tissue-plasminogen activator (rt-PA) 1 h (early T) or 3 h (late T) after TE. Hypothermia (Hy) was applied for 4 h at 33 degrees C started 1 h after TE. Experimental groups included control (C), early thrombolysis (ET), late thrombolysis (LT), hypothermia (Hy), early thrombolysis plus hypothermia (ET+Hy), and late thrombolysis plus hypothermia (LT+Hy). Animals were investigated by MRI and silver infarct staining (SIS) to assess the cerebral infarct size. All animals of group Hy survived, in contrast to 40% in group C (P < 0.05). ET+HY and LT+Hy showed a trend towards better survival as compared to ET and LT alone. PWI parameters were not significantly different between ET versus ET+HY and LT versus LT+Hy, but rt-PA administration led to improved cerebral perfusion in MRI. Significant differences in infarct volumes (T2/SIS) were found after 24 h in all treatment groups versus the control group (P < 0.05). The lesion volume calculated from T2 was significantly smaller in ET (16% +/- 5%), ET+Hy (10 +/- 4%), and LT+Hy (20% +/- 9%) after 5.5 h (10.8% +/- 4.8%) versus C (42% +/- 15%), (P < 0.05). These data indicate that hypothermia improves survival and decreases infarct volume. However, there were no significant differences between the use of rt-PA alone or in combination with hypothermia. Further studies are needed to confirm these effects, also several days after stroke onset.
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PMID:Combination therapy of moderate hypothermia and thrombolysis in experimental thromboembolic stroke--an MRI study. 1547 93

Acute stroke is the third most common cause of death and also the most common cause of permanent disability in industrialized countries. Ischemic stroke is caused by occlusion of a cerebral artery leading to a critical reduction in brain perfusion in the respective brain area (penumbra). Most acute stroke treatment strategies are based on the penumbra concept: attaining rapid and persistent reperfusion is followed by the protection of critically ischemic and not yet infarcted (penumbral) tissue by, e.g., neuroprotection. Examination of the acute stroke patient includes a brief history, neurostatus and imaging (CT or MRI) for the exclusion of intracerebral hemorrhage. The diagnostic standard is CT; modern stroke MRI protocols provide an improved selection in later time windows. Intravenous thrombolysis with rt-PA within 3 h of symptom onset is the only approved therapy with a proven significant benefit for the patient. The effect is smaller but still significant if treatment occurs up to 4.5 h, and may still be present in MRI selected patients up to 9 h. More aggressive forms of therapy include interventional reperfusion techniques and therapy of malignant MCA infarction such as hemicraniectomy and hypothermia, which at present, however, are not routine and are only performed in specialized centers.
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PMID:[Acute cerebral circulation problems]. 1597 Oct 52

We describe a case of traumatic panhypopituitarism following head injury. Generally considered, posttraumatic hypopituitarism occurs in patients who have suffered from severe head injury. However there were a few case reports of panhypopituitarism due to mild and moderate head injury. A 51-year-old male presented with a history of blunt head injury caused by a concrete block hitting his head directly during work. On admission, initial Glasgow Coma Scale was 14. Open depressed skull fracture was suspected. Emergency craniectomy and debridement were performed. Ten days after surgery, hypothermia, lethargy and appetite loss were manifested. Endocrinological examination showed panhypopituitarism with diabetes insipidus. MRI revealed ruptured pituitary stalk and pituitary gland hemorrhage. Coronal and sagittal MRI was helpful for the diagnosis of traumatic panhypopituitarism. General condition was recovered by hormone replacement therapy. It is important for medical staff carefully to observe vital signs and clinical symptoms, even if mild brain injury. Pituitary function test should also be undergone, if panhypopituitarism was suspected from clinical condition.
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PMID:[Traumatic panhypopituitarism: case report]. 1668 92

Treatments for acute ischaemic stroke continue to evolve. Experimental approaches to restore cerebral perfusion include techniques to augment recanalising therapies, including combination of antiplatelet agents with intravenous thrombolysis, bridging therapy of combining intravenous with intra-arterial thrombolysis, and trials of new thrombolytic agents. Trials with MRI selection criteria are underway to expand the window of opportunity for thrombolysis. Sonothrombolysis and novel endovascular mechanical devices to retrieve or dissolve acute cerebral occlusions are being tested. Approaches to improve cerebral perfusion with other devices and induced hypertension are also being considered. Although numerous neuroprotective agents have not shown benefit, trials of hypothermia, magnesium, caffeinol, high doses of statins, and albumin are continuing. The findings of these randomised trials are anticipated to allow improved treatment of patients with acute stroke.
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PMID:Experimental treatments for acute ischaemic stroke. 1739 3

Reperfusion injury is a complication of recanalization therapies after focal cerebral ischemia. The disruption of the blood-brain barrier (BBB) caused by up-regulated metalloproteinases (MMPs) can lead to edema and hemorrhage. Middle cerebral artery occlusion (MCAO=90 min) and reperfusion (R=24 h vs. 5 days) was induced in male Wistar rats. Rats were randomized in four groups: (1) control (C), (2) twice daily minocycline (30 mg/kg bodyweight) every day (M), (3) hypothermia (33 degrees C) for 4 h starting 60 min after occlusion (H), (4) combination of groups 2 and 3 (MH). Serial MRI was performed regarding infarct evolution and BBB disruption, MMP-2 and MMP-9 were assessed by zymography of serum and ischemic brain tissue, and a functional neuroscore was done at 24 h and 5 days. M and H reduced both infarct sizes, volume and signal intensity of BBB breakdown and improved neuroscore at all points in time to the same extent. This was most likely due to inhibition of MMP-2 and MMP-9. The presence of MMP-9 at 24 h or MMP-2 at 5 days in brain tissue correlated with BBB breakdown whereas serum MMP-2- and -9 showed no relationship with BBB breakdown. The combination MH had a small but not significantly additional effect over the single treatments. Minocycline seems to be as neuroprotective as hypothermia in the acute and subacute phase after cerebral ischemia. One essential mechanism is the inhibition of MMPs. The combination therapy is only slightly superior. The net effect of MMPs inhibition up to 5 days after focal cerebral ischemia is still beneficial.
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PMID:Minocycline and hypothermia for reperfusion injury after focal cerebral ischemia in the rat: effects on BBB breakdown and MMP expression in the acute and subacute phase. 1803 17


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