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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Acute liver failure results in encephalopathy and brain edema that is characterized by astrocytic cell swelling. Molecular biological techniques have led to the identification of alterations in expression of several genes coding for key astrocytic proteins in acute liver failure. Such proteins include amino acid transporters, structural proteins, the endothelial cell glucose transporter GLUT-1, the mitochondrial "peripheral-type" benzodiazepine receptor, and the water channel protein aquaporin IV. Magnetic resonance spectroscopic studies reveal increased brain lactate concentrations that are positively correlated with severity of encephalopathy and brain edema in acute liver failure, suggesting a deficit of cellular oxidative capacity and impending brain energy failure. Mild hypothermia prevents brain edema in acute liver failure, and mechanisms responsible for this beneficial effect include reduced blood-brain ammonia transfer as well as normalization of astrocytic amino acid transport and brain energy metabolism. Further elucidation of the molecular mechanisms responsible for brain edema and encephalopathy in acute liver failure will undoubtedly lead to novel treatment strategies for these complications.
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PMID:Molecular neurobiology of acute liver failure. 1452 78

Influenza encephalopathy and related disorders such as Reye's syndrome, acute necrotizing encephalopathy and acute hemorrhagic encephalopathy are still undefined clinical entities because the pathophysiology is not clearly established. Even Reye's syndrome which has been extensively studied during the last two decades, its real picture has not been well established. Moreover, Reye's syndrome is going to disappear just like Ekiri syndrome. Acute necrotizing encephalopathy and acute hemorrhagic encephalopathy need further investigation to be recognized as single clinico-pathological entity because decreased cerebral blood flow is closely linked with brain edema including basal ganglia lesion and hepato-renal dysfunction.
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PMID:[Influenza encephalopathy, related disorders and differential diagnosis]. 1461 38

The principal cause of mortality in patients with acute liver failure (ALF) is brain herniation resulting from intracranial hypertension caused by a progressive increase of brain water. In the present study, ex vivo high-resolution 1H-NMR spectroscopy was used to investigate the effects of ALF, with or without superimposed hypothermia, on brain organic osmolyte concentrations in relation to the severity of encephalopathy and brain edema in rats with ALF due to hepatic devascularization. In normothermic ALF rats, glutamine concentrations in frontal cortex increased more than fourfold at precoma stages, i.e. prior to the onset of severe encephalopathy, but showed no further increase at coma stages. In parallel with glutamine accumulation, the brain organic osmolytes myo-inositol and taurine were significantly decreased in frontal cortex to 63% and 67% of control values, respectively, at precoma stages (p<0.01), and to 58% and 67%, respectively, at coma stages of encephalopathy (p<0.01). Hypothermia, which prevented brain edema and encephalopathy in ALF rats, significantly attenuated the depletion of myo-inositol and taurine. Brain glutamine concentrations, on the other hand, did not respond to hypothermia. These findings demonstrate that experimental ALF results in selective changes in brain organic osmolytes as a function of the degree of encephalopathy which are associated with brain edema, and provides a further rationale for the continued use of hypothermia in the management of this condition.
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PMID:Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia. 1474 28

The purpose of this paper is to describe brain pathology in neonates after major traffic trauma in utero during the third trimester. Our patient cohort consisted of four neonates born by emergency cesarean section after car accident in the third trimester of pregnancy. The median gestational age ( n=4) was 36 weeks (range: 30-38). Immediate post-natal and follow-up brain imaging consisted of cranial ultrasound ( n=4), computed tomography (CT) ( n=1) and post-mortem magnetic resonance imaging (MRI) ( n=1). Pathology findings were correlated with the imaging findings ( n=3). Cranial ultrasound demonstrated a huge subarachnoidal hemorrhage ( n=1), subdural hematoma ( n=1), brain edema with inversion of the diastolic flow ( n=1) and severe ischemic changes ( n=1). In one case, CT demonstrated the presence and extension of the subarachnoidal hemorrhage, a parietal fracture and a limited intraventricular hemorrhage. Cerebellar hemorrhage and a small cerebral frontal contusion were seen on post-mortem MRI in a child with a major subarachnoidal hemorrhage on ultrasound. None of these four children survived (three children died within 2 days and one child died after 1 month). Blunt abdominal trauma during pregnancy can cause fetal cranial injury. In our cases, skull fracture, intracranial hemorrhage and hypoxic-ischemic encephalopathy were encountered.
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PMID:Fetal trauma: brain imaging in four neonates. 1515 44

We addressed the incidence of influenza-associated acute encephalopathy, which is distinct from Reye syndrome, in children in Japan. Eighty-nine children with a mean age of 3.8 years were reported to have developed this disease during eight influenza seasons (December 1994-April 2002) in Hokkaido, Japan. None of them had received aspirin. Most of the patients rapidly became comatose with or without convulsions with a mean interval of 1.7 days from the onset of fever to the onset of central nervous system symptoms. Thirty-three (37.1%) patients died and 17 (19.1%) patients had neurological sequelae. A total of 53 (59.6%) cases were proved to have an influenza virus infection. Interleukin-6 and tumor necrosis factor-alpha were markedly elevated in serum and cerebrospinal fluid samples from two patients who died after a rapid, fulminant course. A post-mortem examination of one fatal case revealed vasogenic brain edema with generalized vasculopathy, suggesting that the generalized impairment of vascular endothelial cells caused by highly activated cytokines plays a central role in the pathophysiology of this disease. We conclude that influenza-associated acute encephalopathy may be an underestimated syndrome and is another reason to promote vaccination against influenza in infants and younger children.
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PMID:Influenza-associated acute encephalopathy in Japanese children in 1994-2002. 1516 92

The infectivity and pathogenicity of influenza virus are primarily determined by host cellular trypsin-type processing proteases which cleave the viral membrane fusion glycoprotein hemagglutinin (HA). Therefore the distribution of the processing protease is a major determinant of the infectious organ tropism. The common epidemic human influenza A virus is pneumotropic and the HA processing proteases tryptase Clara, mini-plasmin, tryptase TC30 and ectopic anionic trypsin have all been isolated from mammalian airways. However, the pneumotropic influenza virus occasionally causes severe brain edema, particularly in children presenting with Reye's syndrome treated with aspirin, or in children with influenza-associated encephalopathy without antipyretic treatment. We have observed that, after influenza virus infection, the accumulation of mini-plasmin in the cerebral capillaries in mice with a congenital or acquired abnormality of mitochondrial beta-oxidation mimicking the pathological findings of Reye's syndrome, causes an invasion and multiplication of the pneumotropic influenza virus at these same locations. From these findings, we hypothesize that the accumulated mini-plasmin modifies the brain capillaries from a non-permissive to a permissive state, thereby allowing multiplication of pneumotropic influenza virus. In addition, mini-plasmin proteolytically destroys the blood-brain barrier. These pathologic findings, consistent with encephalopathy in mice with a systemic impairment of beta-oxidation, may have implications for human influenza encephalopathy.
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PMID:Accumulation of mini-plasmin in the cerebral capillaries causes vascular invasion of the murine brain by a pneumotropic influenza A virus: implications for influenza-associated encephalopathy. 1525 80

On a cold winter morning, a 35-year-old male was unexpectedly found dead and therefore autopsied. Macro- and microscopically, the lungs were demonstrated bronchopneumonia. On the surface of brain, small blood vessels were slightly congested. Microscopically, brain edema was also observed, and proliferation of lymphocytes was observed around the capillary vessels of the hippocampus. These findings suggested a viral infection of the cerebrum. We conducted an immunohistochemical study with antibody against influenza virus. Influenza A virus antigen was detected in both the lungs and brain. Therefore, findings were compatible with influenza A encephalopathy. Even when serological inspection is not performed, it is useful to inspect localization of the virus antigen immunohistochemically. We considered that it is necessary to perform pathological examination for influenza encephalopathy in sudden death cases when influenza is epidemic.
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PMID:An adult autopsy case of acute encephalopathy associated with influenza A virus. 1536 51

A 71-year-old woman with Hashimoto's disease was admitted to our hospital because of involuntary movement, gait disturbance, and mental decline. Her consciousness was alert but her orientation about time and place was disturbed. She was mentally ill (HDS-R; 12/30, MMSE; 14/30), and could not walk because of truncal ataxia. Myoclonus was present in the upper extremities. Laboratory examinations showed hypothyroidism and very high titers of antithyroid antibodies (ATA) in serum. Head MRI showed no abnormal lesions. On electroencephalogram (EEG), the basic rhythm was slow and bursts of irregular slow waves (4-6 Hz) were present. Her conditions gradually ameliorated so that she was discharged. However, she was hospitalized again because of sudden worsening of the illness: her consciousness got disturbed and the myoclonus became marked. As the result, she got bed-ridden. At the time, thyroid function was almost normal, suggesting that the deterioration could not be attributed to hypothyroidism. The EEG findings were quite different from the former: complex of multiple spikes and slow waves was continuously present. Examination of the cerebrospinal fluid (CSF) revealed an elevated level of protein and IgG (cell 1/m3, protein 101 mg/dl, sugar 60 mg/dl ,Cl 124 mEq/l, IgG 20.4 mg/dl). IgG index was 0.57 and Q albumin (CSF-albumin/serum-albumin ratio) was 15.2 (9.0>) . After the second admission, she recovered from the bed-ridden state but was still unable to walk or communicate. She continued to need complete support for all daily lives. The diagnosis was made as Hashimoto's encephalopathy (HE), from the following points: 1) encephalopathy not due to hypothyroidism, 2) very high titers of ATA, 3) elevated CSF protein. The effectiveness of steroid therapy was so amazing that the neurological problems faded away very soon. Finally she completely recovered. As well as the clinical manifestations, the EEG findings were improved. At the stage in which excellent clinical improvement had achieved, head MRI revealed that T2/FLAIR high lesions without Gd-enhancement temporarily appeared diffusely and extensively in the cerebral white matter. They thereafter almost disappeared on follow-up MRI. Judging from the lesions being non-enhanced and reversible, they supposedly reflected brain edema. It is important to keep it in mind that MRI findings may change abruptly and drastically in HE. ATA was detected not only in serum but also in CSF. Either titer thereafter decreased along with the healing of the illness. Concerning the reason why ATA is present in CSF, we supposed leakage from blood through the disrupted blood-brain barrier, for the following reasons: 1) IgG index was normal, 2) Q albumin was elevated, 3) the change of CSF-ATA titer was almost parallel to that of serum-ATA titer, and 4) the white matter lesions, which presumably reflected brain edema, were observed.
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PMID:[Reversible white matter lesions and antithyroid antibodies in the cerebrospinal fluid in Hashimoto's encephalopathy: a case report]. 1538 4

We report the clinical and neuroradiological features of reversible encephalopathy syndrome and follow-up results in 12 patients. This syndrome seems to be the result of an acute encephalopathy showing with brain edema mainly in the white matter (vasogenic edema). Diffusion-weighted magnetic resonance images are useful to distinguish this entity from acute ischemia. Early recognition and treatment often lead to complete neurological recovery. If unrecognized, the patient's condition can progress to central nervous system failure.
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PMID:Reversible encephalopathy syndrome: report of 12 cases with follow-up. 1544 51


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