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

A retrospective study on 18 cases of DHF presented with jaundice and neurological signs which were considered unusual manifestation of DHF reveals that the causes or contributing factors are multifactorial. Most commonly found associated conditions were prolonged shock with metabolic acidosis and severe DIC that lead to hypoxia/ischaemia and resulted in both hepatic and brain dysfunction. Gross haemorrhage in the brain was noted in 6 of the 10 fatal cases while brain oedema was noted in 3 cases. Electrolyte disturbance such as hyponatremia could be another cause of brain oedema. It is certain from this study that there is no pathological evidence of encephalitis. Hepatic dysfunction found in associated with jaundice and encephalopathy is possibly caused by toxic substances, drugs and/or associated with underlying liver conditions. Reye's or Reye's-like syndrome was postulated in one case.
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PMID:Dengue haemorrhagic fever with unusual manifestations. 343 70

A series of patients with meningococcal infections have been studied and divided in two groups: Group I patients with meningococcal sepsis and group II, those with meningococcal meningitis. Patients in group I presented with more severe encephalopathy, shock, DIC and acute systemic complications. Both groups showed a marked hypoaminoacidemia compared with normal controls (other than for the sulfur containing amino acids and phenylalanine). The concentration of aromatic and basic amino acids, the phenylalanine/tyrosine ratio, the transaminase levels and the negative nitrogen balance were higher in group I patients. The ratio of branched chain to aromatic amino acids was lower in group I. All these differences were statistically significant. The close association between the metabolic derangements and clinical manifestations may help in the understanding of several physiopathological aspects of meningococcal infections.
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PMID:Significance of the changes in plasma amino-acid levels in meningococcal infection. 365 98

Two infants are described with a fulminant disorder characterised by profound circulatory collaps and shock, generalised convulsions and unremitting coma, bleeding due to severe DIC, fever, diarrhoea, metabolic acidosis and renal and hepatic failure. Both infants died shortly after onset of the symptoms. Autopsy mainly revealed haemorrhages in different organs, anoxaemic lesions in the brain and a normal structure of liver and pancreas. No causative agent could be demonstrated. We believe that both patients suffered from haemorrhagic shock and encephalopathy, a mostly fatal disorder which has recently been described. Although the clinical and biochemical features are very distinctive, this syndrome is probably heterogeneous and its differentiation from some other disorders may be difficult. Its pathogenesis is unknown but there are some indications that intravascular activity of trypsin may play a role. During a study of the two families we obtained abnormal results of immunologic tests in most members: the interpretation of this finding remains conjectural. Haemorrhagic shock and encephalopathy may occur more frequently than the restricted literature on this subject suggests. Future studies will have to deal with the question of identity and pathogenesis.
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PMID:Haemorrhagic shock and encephalopathy. 373 33

On the basis of examining the blood coagulation system and the pathomorphological changes in 20 patients with the epileptic status it is concluded that these patients have the disseminated intravascular coagulation syndrome (DIC-syndrome). It is supposed that the DIC-syndrome is the only possible pathology of the blood coagulation system in patients with the epileptic status not depending on the latter's cause. By blocking the microcirculation the DIC-syndrome is one of the main causes of the vasohypoxic encephalopathy which develops in epileptic status.
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PMID:[Syndrome of disseminated intravascular coagulation in the pathogenesis of vasculo-hypoxic encephalopathy in status epilepticus]. 729 80

The blood coagulation and fibrinolysis of 33 patients with compensated liver cirrhosis and 31 patients with hepatocellular carcinoma were examined using several markers, namely thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC), antithrombin-III (AT-III) and prothrombin time, and the relationship between these markers, endotoxemia, and TNF-alpha was examined. These patients had no complications due to hepatic failure, such as infections, encephalopathy, ascites, G-I bleeding and clinical DIC. PIC was not elevated, but TAT tended to be elevated in LC and significantly elevated in HCC. AT-III was decreased in LC and HCC, and the blood endotoxin was partly positive in LC and HCC, but was not correlated with AT-III or PT. The TAT level in the blood-endotoxin-positive patients measured by endospecy methods was higher than that in the negative patients, and was significantly correlated with the blood endotoxin level in the LC and HCC patients (r = 0.57, r = 0.88, p < 0.01). No relationship was observed between TNF-alpha and blood endotoxin. In conclusion, (1) blood coagulability was activated already in compensated LC and HCC, but was not connected with fibrinolysis, (2) the activation of coagulability was closely related with endotoxemia, and (3) TNF-alpha was not correlated with blood endotoxin or TAT.
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PMID:[Blood coagulation and fibrinolysis in relation to endotoxemia in liver cirrhosis and hepatocellular carcinoma]. 756 21

An autopsy case of portal systemic encephalopathy and senile dementia of the Alzheimer type coexisting in a 77-year-old man is described. The patient had suffered recurrent episodes of delirium after a subtotal gastrectomy for gastric carcinoma. He died of DIC 45 months after the gastrectomy. A pathological examination revealed a vascular plexus around the liver which might have served as collateral circulation. Neuropathologically, spongy necrosis and Alzheimer type II changes of astrocytes were found in the basal ganglia and fronto-occipital cortices. In the same anatomical regions, only immunohistological staining using antibody against amyloid beta-protein and the periodic-acid methenamine silver method revealed abundant neuriticplaques, cerebral amyloid angiopathy and diffuse plaques. We discussed the clinicopathological findings in this case.
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PMID:An autopsy case of coexisting portal systemic encephalopathy and senile dementia of the Alzheimer type. 830 83

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
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PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91

Coagulation disorders are common in cancer patients. In patients with solid tumors, a low-grade activated coagulation can result in systemic and cerebral arterial or venous thrombosis. Cancer treatments may also contribute to this coagulopathy, which usually, but not exclusively, occurs in the setting of advanced malignant disease. There may be TIAs or cerebral infarctions. Because of the widespread distribution of cerebral thromboses, there may be a superimposed encephalopathy; sometimes this is the only sign. Concurrent systemic thrombosis is present in many patients and is a useful clue to the diagnosis. In cerebral venous occlusion, the initial symptom is usually a headache. Except for cerebral intravascular coagulation that is unassociated with NBTE, neuriomaging studies usually demonstrate one or more parenchymal infarctions. MRI or MRV may demonstrate venous thrombosis. The laboratory evidence of coagulopathy is difficult to distinguish from the asymptomatic coagulopathy that often accompanies advanced cancer, and the test results must be interpreted cautiously. NBTE can be diagnosed by transesophageal echocardiography. There is no established treatment for the thrombotic coagulopathy associated with cancer, but anticoagulation should be considered. In leukemia and lymphoma, the coagulopathy is typically acute DIC that can lead to systemic and brain hemorrhages. It is especially common in acute myelogenous leukemias. The clinical signs of cerebral hemorrhage are fulminant and may be fatal. The bleeding usually occurs in the brain or subdural compartment, and rarely in the subarachnoid space. The diagnosis can be suspected by the clinical setting and by systemic thrombosis or hemorrhage. It can be established by examination of the peripheral smear, the platelet count, and tests of coagulation function. Therapy of acute DIC is controversial and should be individualized for the clinical setting. Cerebrovascular disorders can complicate metastatic or primary tumor in the brain, skull, dura, or leptomeninges. The clinical signs of infarction are indistinguishable from other causes of stroke, except that tumor-related venous occlusion will usually first produce signs of increased intracranial pressure. The diagnosis of tumor-related infarction can usually be established by neuroimaging studies that show infarction and may show extracerebral sites of tumor. CSF examination is useful in diagnosing leptomeningeal metastasis. A search for lung or cardiac tumor should be performed when embolic tumor infarction is suspected. Primary or metastatic tumors in the brain or dura may hemorrhage, producing the initial clinical signs of the brain tumor or a change in chronic signs induced by the tumor. There are helpful clues to a neoplastic hemorrhage on brain CT or MRI scans. The brain hemorrhage may require evacuation and the underlying tumor will usually require additional antineoplastic treatment. Hyperleukocytosis (extreme elevation of the cell count) in acute myelogenous leukemia is a less common cause of brain hemorrhage in recent years because of improved methods to lower the cell count. Cerebral arterial or venous thrombosis is sometimes the result of cancer therapy. The attribution of thrombosis to chemotherapy in many published cases is only speculative, because carefully conducted prospective studies that include investigation for other thrombotic causes are not available. The best-known associations with thrombosis are L-asparaginase, which is typically used in the induction therapy of acute lymphocytic leukemia, and combination hormonal therapy and chemotherapy for breast cancer. Radiation to the head and neck, typically administered for head and neck epithelial cancers or lymphoma, may result in delayed carotid atherosclerosis. The distribution of stenosis or occlusion is within the radiation portal and is typically more extensive than is atherosclerosis that develops in the absence of radiation. Small clinical series suggest that surgical treatment is equally effective as in nonirradiated carotid atherosclerosis. In children, the cerebral vessels can be affected by brain radiation resulting in stenosis or occlusion. Brain hemorrhages can result from chemotherapy effects on the hemostatic system or a microangiopathic anemia. Hemorrhages from radiation-induced vascular abnormalities are rare. Opportunistic infections, especially fungal infections, can complicate cancer or its treatment. Septic cerebral emboli may result in focal cerebral signs, seizures, or encephalopathy. Sometimes there is an associated hemorrhagic vasculitis or cerebritis. Rarely, mycotic aneurysms may bleed. A high index of suspicion is needed to diagnose fungal infection because of the difficulty in culturing the organism from the blood or CSF. A clinician can usually establish the cause of stroke in the cancer patient by performing a careful review of the clinical setting--including the type and extent of cancer and the type of antineoplastic therapy--in which the stroke occurred. Systemic thrombosis, embolism, or hemorrhage can be a clue to the cause, and appropriate neuroimaging and coagulation studies to aid in the diagnosis are available. Therapy may ameliorate symptoms or prevent further episodes. The identification of one of these unusual stroke syndromes that leads to the diagnosis of an occult and treatable cancer can be particularly rewarding.
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PMID:Cerebrovascular complications in cancer patients. 1269 Jun 49

From the middle of 1990's, there repeated in winter season an outbreak of encephalopathy in Japan that appeared to be associated with influenza. A national survey was conducted, and a total of 507 patients was diagnosed as having influenza-associated encephalopathy during 1998-2002 on the basis of virologic analysis. Type A influenza was more pathogenic than type B, and A: H3 type was more invasive than A: H1 type. Encephalitis developed mainly in children below 5 years of age, either on the day that influenza signs appeared or on the next day. We hypothesized that the replicated viruses at nasopharyngeal epithelium disrupt the olfactory mucosa. Via olfactory nerve system, the stimuli may be transmitted to the brain eventually to activate glial cells, and to induce the production of pro-inflammatory cytokines. The cytokine storm results in neural cell damage as well as apoptosis of glial cells due to TNF-induced mitochondrial respiratory failure. The disruption of blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF.
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PMID:[Influenza-associated encephalopathy--pathophysiology and disease mechanisms]. 1461 37

Patients with a new type of influenza-associated encephalopathy with high mortality are increasing in Japan and the United States. We present three patients treated with methyprednisolone pulse treatment and plasma exchange to remove cytokines, and all three patients recovered without severe sequela. IL-6 decreased dramatically after the start of the plasma exchange and methyprednisolone. Therefore when influenza-associated encephalopathy is actually diagnosed, steroid pulse therapy should be started at an early stage, and when signs of DIC and/or MOF appear, plasma exchange is recommended to remove the cytokines and NOx.
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PMID:Efficacy of plasma exchange and methylprednisolone pulse therapy on influenza-associated encephalopathy. 1603 52


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