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

Regional cerebral blood flow was measured by the xenon 133-inhalation method in a 40-year-old man during an acute exacerbation of intracranial vasculitis. Neurologic function was quantitated by the Halstead-Reitan Neuropsychological test battery. The patient was also studied during remission that was induced by steroid therapy. Vasculitis produced a diffuse encephalopathy with generalized reduction in cerebral blood flow. During remission, only local symptoms secondary to a small cerebral infarction remained and regional cerebral blood flow returned to the normal range. There seems to be a close correlation between the severity of symptoms in cerebral vasculitis and reduction of flow through diseased vessels.
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PMID:Effect of intracerebral vasculitis on regional cerebral blood flow. 50 25

Cerebral malaria is an acute diffuse encephalopathy associated only with Plasmodium falciparum. It is probably a consequence of the rapid proliferation of the parasites in the body of man in relation to red cell invasion, and results in stagnation of blood flow in cerebralcapillaries with thromobotic occlusion of large numbers of cerebral capillaries. The subsequent cerebral pathology is cerebral infarction with haemorrhage and cerebral oedema. The wide prevalence of P. falciparum in highly endemic areas results in daily challenges to patients from several infected mosquitoes. It is thus important to understand the characteristics of P. falciparum, since this is one of the most important protozoan parasites of man and severe infection from it constitutes one of the few real clinical emergencies in tropical medicine. One of the more important aspects of the practice of medicine in the tropics is to establish a good understanding of the pattern of medical practice in that area. This applies to malaria as well as to other diseases. The neophyte might be somewhat surprised to learn, for example that an experienced colleague who lives in a holoendemic malarious area such as West Africa, sees no cerebral malaria. But the explanation is simple when the doctor concerned has a practice which involves treating adults only. Cerebral malaria is rare in adults, because in highly endemic areas, by the age of 1 year most of the infants in a group under study have already experienced their first falciparum infection. By the time they reach adult life, they have a solid immunity against severe falciparum infections. In fact, "clinical malaria" could occur in such a group under only two circumstances: 1) in pregnancy, a patent infection with P. falciparum might develop, probably due to an IgG drain across the placenta to the foetus;2) in an individual who has constantly taken antimalarials and who may have an immunity at such a low level that when antimalarial therapy is interrupted, clinical malaria might ensue. The above examples emphasise the paramount importance of the clinician dealing with malaria having some insight into the complex immunity processes operative in the human host; these have been reviewed by McGregor.
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PMID:Cerebral Malaria. 109 94

Three different neuro-imaging studies were performed in 3 infants with hemorrhagic shock and encephalopathy syndrome (HSE). Areas of cerebral infarction were noted on CT. Single photon emission computed tomography (SPECT) showed decreased perfusion in these areas in one infant. Magnetic resonance imaging (MRI) also identified the areas of infarction, noted on CT, but provided additional information showing non-haem iron deposition in the thalami and basal ganglia.
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PMID:Computed cranial tomography, magnetic resonance imaging and single photon emission computed tomography in hemorrhagic shock and encephalopathy syndrome: a report of three cases. 156 13

Our hypothesis was that progressive subcortical vascular encephalopathy of Binswanger's type (PSVE) in the elderly can be induced by repeated hypotension or greater variability of blood pressure in hypertensives, regardless of antihypertensive therapy. We retrospectively studied PSVE blood pressure, and compared them with those in atherothrombotic cerebral infarction (ACI) or in hypertensive cerebral hemorrhage (HCH). During the last seven years prior to death, neither the annual variability nor the annual mean value of systolic or mean arterial blood pressures in PSVE was different from that in ACI or in HCH. The present study did not support our hypothesis.
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PMID:Does the variability of casual blood pressure contribute to progressive subcortical vascular encephalopathy of Binswanger's type? 204 93

We evaluated the effect of posthypoxic glucose supplement in a neonatal hypoxic-ischemic animal model. Seven-day-old rats underwent bilateral ligation of the carotid arteries, followed by exposure to an 8% oxygen atmosphere for 1 hour. The extent of hypoxic-ischemic brain damage was assessed histologically 72 hours later. Glucose load immediately after the end of the hypoxic exposure reduced the volume of neocortical infarction to 37% of the unsupplemented value, and attenuated ischemic damage in the striatum and the dentate gyrus. At the end of the hypoxic exposure, the brain level of glucose was 0.3 mmol/kg and the level of lactate 9 mmol/kg. Glucose supplement produced a rapid rise in brain glucose level to 3 to 5 mmol/kg over the next 2 hours. Lactate in both brain and plasma gradually fell toward the baseline level during the first hour of recovery. Posthypoxic glucose supplement slightly retarded lactate restitution. At any period of this neonatal model, brain lactate levels did not exceed the toxic level, which is postulated to be responsible for cerebral infarction in adult ischemic models. These results illustrate the important role of glucose in the development of neonatal hypoxic-ischemic encephalopathy and the fact that full cortical infarction can develop even if brain lactate levels are low.
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PMID:Posthypoxic glucose supplement reduces hypoxic-ischemic brain damage in the neonatal rat. 222 42

In a prospective study conducted in the Emergency Area of a general hospital during a period of 6 months, the Neurology Service was consulted in 45 cases of acute confusional syndrome. Twenty nine of these patients had no immediate apparent etiology. Among the studied patients 5 had a subarachnoid hemorrhage, 4 suffered a central nervous system infection, 3 had a cerebral infarction, 3 presented a metabolic encephalopathy, and the remaining patients had variate etiologies. Clinical signs and symptoms were insufficient to establish the diagnosis and in several cases complementary tests were required (cerebral tomography and cerebrospinal liquid examination). Even in these cases the diagnosis could not be obtained in some patients. The clinical implications of the present findings were discussed.
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PMID:[Acute confusional syndrome of unknown cause. Prospective study in the emergency room]. 226 Nov 91

Of 1721 consecutive autopsies performed on patients over 60 years of age in Tokyo Metropolitan Geriatric Hospital, 550 (32% of all autopsied cases) revealed symptomatic cerebrovascular lesions. Among the 550 patients, intracranial hemorrhage was found in 19%, cerebral infarction in 75%, and coexisting cerebral hemorrhage and cerebral infarction in 6%. Twenty-eight percent of the cerebral infarctions were embolic infarctions of cardiac origin, half of which were caused by nonvalvular atrial fibrillation, and 69% were non-embolic infarctions of cardiac origin. Progressive subcortical vascular encephalopathy accounted for 15% of the cerebral infarctions. Two-thirds of all lobar cerebral hemorrhages were amyloid angiopathy-related. Nonvalvular atrial fibrillation is the most important cardiac source of embolic stroke. Progressive subcortical vascular encephalopathy is one of the characteristic features of ischemic lesions, and cerebral amyloid angiopathy is an important cause of lobar cerebral hemorrhage in the aged.
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PMID:Subtypes and proportions of cerebrovascular disease in an autopsy series in a Japanese geriatric hospital. 228 May 80

Systemic lupus erythematosus (SLE) can produce profound disturbances in the central nervous system, characterized by encephalopathy, focal neurologic deficits, cerebral infarction, psychosis, and seizures. We used 31P nuclear magnetic resonance (NMR) spectroscopy to determine the in vivo levels of high-energy phosphates in the central nervous system of 10 patients with SLE and 10 age-matched normal controls. 31P NMR spectroscopy was performed on a 1.5-Tesla unit equipped with a dual-tuned 1H-31P surface coil and a software-directed DRESS (depth resolved surface coil spectroscopy) pulse sequence. This procedure detected ADP, ATP, sugar phosphates, phosphocreatine (PCr), inorganic phosphate, phosphomonoesters, and phosphodiesters in the brain tissue of all study subjects. Levels of ATP in the deep white matter of 10 SLE patients were significantly decreased compared with the levels in 10 normal controls, as quantitated by the ratio of ATP:ATP + ADP (mean +/- SD 0.81 +/- 0.11 versus 0.91 +/- 0.05; P less than 0.02). In a subgroup of 4 patients, PCr levels were decreased to a greater extent than the ATP levels. NMR spectroscopic alterations were not related to obvious anatomic lesions, as determined by standard cranial proton magnetic resonance imaging. In 4 SLE patients with markedly abnormal 31P NMR spectra, treatment with prednisone (80 mg/day) normalized the levels of ATP and PCr. Restoration of a normal 31P profile was accompanied by an obvious improvement in the patients' mental status and clinical symptoms. 31P NMR spectroscopy is a powerful new technique for monitoring high-energy phosphate metabolism, and may be particularly useful for characterizing central nervous system disease in patients with neuropsychiatric SLE.
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PMID:Depletion of high-energy phosphates in the central nervous system of patients with systemic lupus erythematosus, as determined by phosphorus-31 nuclear magnetic resonance spectroscopy. 236 38

Positron emission tomography (PET) was performed in four patients with Rett syndrome (RS) to elucidate the cerebral blood flow and oxygen metabolism. Cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) were measured quantitatively with HEADTOME-IV using 15O2, C15O2 steady state inhalational technique. As to the correlation between CBF and CMRO2, these four patients were compared with nine cases with other neurological disorders. Case 1, the youngest girl among the patients, showed milder symptoms than others. In all patients, no abnormal findings except for mild brain atrophy were seen on CT. In case 1, values of CBF might be lower for her age than normal values by the report of Kety. OEF was markedly reduced in all regions of three patients with RS (cases 2, 3, 4). These decreased OEF might be caused by reduced oxygen metabolism. However, case 1 which was the youngest and had milder symptoms, showed almost normal values of OEF. The distribution of CBF and CMRO2 was thought not to be abnormal in all patients. On the other hand, there was no discrepancy between CBF and CMRO2 in nine neurological control subjects. Decreased value of OEF was known to be seen in mitochondrial encephalopathy as well as an early stage of cerebral infarction. In mitochondrial encephalopathy, OEF was thought to decrease by reduced oxygen metabolism due to disturbance of aerobic glycolysis. Although the cause of reduced oxygen metabolism in RS was obscure, these results suggested that in RS there was some disturbance of oxygen metabolism of the brain, and values of OEF might be related to clinical status of RS or age.
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PMID:[Cerebral blood flow and oxygen metabolism in Rett syndrome]. 236 59

Experimental evidence has shown that the amount of 5-HIAA in the CSF reflects the metabolism of serotonin in the brain if this metabolite is eliminated from the brain and flows into the CSF at a constant rate. We studied the concentration of 5-HIAA in the lumbar CSF in several neurological diseases to elucidate the alteration in abnormalities of serotonin metabolism. The concentration of 5-HIAA in the CSF was measured in 94 patients with cerebral infarction, 30 with vascular dementia, 25 with dementia of the Alzheimer type, 28 with Parkinson's disease and 6 with hypoxic encephalopathy. Patients with cerebral infarction were classified into 24 with a solitary cerebral infarct and 70 with multiple cerebral infarcts. Patients with Parkinson's disease were subdivided into 12 with various psychiatric symptoms including depressive state, hallucination and/or intellectual impairment and 16 without psychiatric symptoms. Patients with hypoxic encephalopathy consisted of 5 with apallic syndrome and one patient with Lance-Adams syndrome. The concentration of 5-HIAA in solitary cerebral infarct, multiple cerebral infarcts and vascular dementia did not exhibit a significant difference from that in control cases (54.6 +/- 23.1 ng/ml). But patients with dementia of the Alzheimer type (34.5 +/- 10.9, p less than 0.001) showed a significantly lower concentration. This fact seems to reflect the pathological finding that the number of large neurons is decreased and neurofibrillary tangles are increased in the nucleus raphe dorsalis of patients with Alzheimer type dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the lumbar cerebrospinal fluid (CSF) in neurological diseases]. 248 Aug 63


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