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At least 307 records · Page 17Linked to original sources

PubMed1977

Cellular events during partial cerebral ischemia. I. Electron microscopy of feline cerebral cortex after middle-cerebral-artery occlusion.

The feline right cerebral hemisphere was subjected to regional (incomplete) ischemia after clipping the middle cerebral artery for 5, 10, 15, 30 or 60 min, respectively. After each ischemic episode, a 10-min recirculation period was allowed, following which the brain was fixed and processed for electron microscopy. The earliest alterations, detected in the cerebral cortex after 15 min, increased in severity with longer ischemic episodes and were distributed multifocally. There was: (a) marked neuronal mitochondrial matrical swelling and progressive condensation of cytoplasm and nucleoplasm; (b) cytoplasmic swelling of astrocytes with preservation of glial mitochondrial volume; (c) capillaries, oligodendrocytes, myelin sheaths and axis cylinders did not change significantly, even after the longest interval studied: 60 min. This type of tissue reaction appears to be common for those forms of cerebral ischemia, in which circulation is either sustained partially (via collateral arteries) or restored after a period of absolute ischemia. Under these conditions, as yet undefined permeability changes in cell membranes lead to pronounced volumetric alterations of cellular compartments. Although no softening is detectable by digital examination, we suggest that such a set of structural abnormalities constitutes encephalomalacia, or the earliest stage of a lesion which is designated infarction, once it reaches irreversibility.

Animals↗

PubMed2001

A case of pulmonary hypoplasia associated with intrauterine brainstem necrosis.

UNLABELLED: An infant with intrauterine brain death accompanied by pulmonary hypoplasia is reported. The fetus was delivered after 36 weeks gestation, 5 weeks after fetal movements ceased. The child died 4 h after birth. Pulmonary hypoplasia and remote brainstem necrosis associated with multicystic encephalomalacia were found at autopsy. CONCLUSION: These findings suggest that damage to brainstem respiratory centres had led to pulmonary hypoplasia through the absence of fetal respiratory movement.

Adolescent↗

PubMed1983

Unilateral subdural hematoma without midline shift.

Two cases of radiographically isodense subdural hematoma are presented in which absence of displacement of midline cerebral structures was due not to bilateral lesions, but rather to "balancing" of the volumetric effect of a unilateral lesion by preexisting encephalomalacia. Attention to the past medical history and the computed tomography scan which showed evidence of unilateral loss of brain substance led to the proper diagnosis.

Adult↗

PubMed1975

The neuropathology of stroke.

Vascular-circulatory derangements affecting the function of the central nervous system may result in parenchymal lesions that are hemorrhagic, ischemic, or mixed. Most nontraumatic intraparenchymal brain hemorrhages are found in asssociation with cerebral arteriolar sclerosis and other stigmata of hypertensive disease, such as hypertrophy of the left cardiac ventricle and granular kidneys. Global temporary ischemia, the type that exists during severe and transient hypotension, results in a wide variety of parenchymal lesions that may be bilateral, hypotension, results in a wide variety of parenchymal lesions that may be bilateral, unilateral, supratenorial, or infratentorial. The cerebral and cerebellar cortices, white matter, basal ganglia, brain stem, and spinal cord may be involved simulatenously or there may be isolated, focal lesions that are confined occasionally to any one of these areas. Regions ischemia, the type induced through the occlusion of a major intracranial artery, evolves through a stage of acute encephalomalacia, during which the morphologic change consists of alternating cellular swelling and shrinkage. This is followed by leukocytic inflammation at three to four days and the beginning of resolution at about the tenth day after arterial occlusion. In the evolution of this form of abnormal circulation, after a few minutes, some neurons in the most distal arterial territories show the first recognizable changes. In these neurons the mitochondria swell massively. Astrocytes and neurites in the same foci are selectively swollen, whereas oligodendrocytes and capillaries remain structurally unchanged during the initial stages of ischemic injury.

Animals↗

PubMed1983

[Diagnoses to consider in newborn infants with inactive EEG tracings].

Thirty-one neonates without any electroencephalographic activity detectable on the first EEG before day 5 were studied. In the first group (20 neonates) the first EEG was performed on day 0. Signs of foetal and/or perinatal anoxia were observed. In the second group (11 neonates), the first EEG was performed between day 1 and day 4. In 7 cases, the neonate was considered normal during a period varying between a few hours and a few days. Various aetiologies other than foetal or perinatal anoxia were found: cardiac arrest, metabolic disease, polycystic encephalomalacia.

Brain Diseases↗

PubMed1998

Motor organization after early middle cerebral artery stroke: a PET study.

The brain organization for movement in a 20-year-old man with a history of intrauterine or perinatal right middle cerebral artery stroke was studied. [(15)O]-water positron emission tomography demonstrated a normal pattern of activation during finger movement in the right hand. Movement of the hemiparetic left hand was associated with activation in the supplementary motor area bilaterally and in the left premotor cortex. Blood flow increase was observed in the right temporal lobe adjacent to an extensive area of encephalomalacia, suggesting atypical motor function in the temporal lobe.

Adult↗

PubMed2001

Neuroimaging abnormalities in children with an apparent first unprovoked seizure.

OBJECTIVE: To determine the incidence and type of neuroimaging abnormalities in children presenting with a first seizure. METHODS: In a prospective observational study, 411 children with a first afebrile seizure were seen between 1983 and 1992. Imaging studies were performed in 218 (53%). For this analysis we examined the most sensitive neuroimaging study performed which included 159 computed tomography scans and 59 magnetic resonance imagings (MRI). RESULTS: Four children were found to have lesions requiring intervention (brain tumor in two, neurocysticercosis in two). The remaining 407 were enrolled in a follow-up study of children with a first unprovoked seizure. After a mean follow-up of >10 years, none have developed clinical evidence of a tumor. In these 411 children, 45 (21%) of 218 imaging studies were abnormal. The most common abnormalities were focal encephalomalacia (n=16) and cerebral dysgenesis (n=11). Although children with partial seizures were more likely to be imaged (64%) than children with generalized seizures (43%) (P<0.001), the fraction of abnormal imaging studies was similar in both groups. Six children with a normal neurological examination who were initially classified as cryptogenic were subsequently found to have errors of cerebral migration on MRI. The incidence of lesions requiring acute intervention in children presenting with a first seizure is low. A significant proportion will have neuroimaging abnormalities particularly on MRI. CONCLUSIONS: Neuroimaging should be considered in any child with a first seizure who does not have an idiopathic form of epilepsy.

Adolescent↗

PubMed2006

Cardiotocographic and Doppler ultrasonographic findings in a fetus with brain death syndrome.

OBJECTIVE: The diagnosis of brain death syndrome by cardiotocography (CTG) and Doppler ultrasonography (US) is reported in a fetus at 35 weeks of gestation. CASE REPORT: A 23-year-old, gravida 2, para 0, woman was referred to our hospital because of the absence of fetal movements. CTG showed fixed fetal heart rate (FHR) pattern. A detailed Doppler US examination of the fetus showed extensive cystic lesions of both cerebral hemispheres, polyhydramnios, total absence of neuromuscular parameters of biophysical profile (BPP) and the cessation of cerebral blood flow. Umbilical cord artery blood gas analysis showed pH 7.3, PaO2 30 mmHg and PaCO2 35 mmHg. A floppy male infant weighing 2,450 g was delivered vaginally at 36 weeks of gestation and the Apgar scores were 1 and 1 at 5 and 10 minutes, respectively. The neonate died 2 days after delivery. Postmortem examination of the brain showed diffuse, anoxic changes with multicystic encephalomalacia in both hemispheres and the brain stem. No other maternal or placental abnormalities were seen. CONCLUSION: The possibility of intrauterine brain death should be considered in all cases of prolonged fixed FHR pattern, accompanied by absence of neuromuscular parameters of BPP, polyhydramnios and demonstrated cessation of cerebral blood flow by Doppler US. Increased awareness of this event may prevent unnecessary emergency cesarean section.

Adult↗

PubMed1977

[Epilepsia partialis continua of Kozevnikov (author's transl)].

Continuous myoclonus in a localised area of the body was observed in three patients. In two cases the myocloni sometimes developed into motor Jacksonian convulsions. All three patients had neurological signs on the same side as their continuous twitching indicating a lesion of the contralateral hemisphere. The surface EEG did not show changes which could be directly correlated with continuous convulsions in any of the cases. The cause was found to be a malformation of the hemisphere in one case, a recent encephalomalacia in the second and a severe hyperosomolar diabetic electrolyte imbalance in the third. Epilepsia partialis continua Kozevnikov differs from motor Jacksonian epilepsy in the continuous non-attack character and the absence of a "march of convulsions". Pathophysiologically they are both forms of focal cortical status epilepticus.

Adult↗

PubMedDate not supplied

[Severe late-onset group B streptococcal infection. A case report].

BACKGROUND: Group B Streptococcus (GBS) is a well-known cause of neonatal pneumonia, sepsis and meningitis. Peripartal antibiotic prophylaxis for early-onset GBS infection is in routine use since the beginning of the last decade, but strategies for effective prevention of late-onset GBS infections are still lacking. CASE REPORT: Few hours after discharge from a non-local maternity ward a 3-week-old boy was admitted to our hospital because of GBS meningitis with necrotizing encephalomalacia. Maternal mastitis, not a disease of the baby, had led to the first admission. DISCUSSION: Case history and negative maternal swabs and cultures for GBS led to the hypothesis of nosocomial infection. Screening and risk based peripartal antibiotic prophylaxis, better monitoring and improved therapeutic modalities have reduced the incidence and mortality of early-onset GBS infections, but peripartal prophylaxis failed to influence late-onset GBS infections. Up to 40 % of infants with late-onset meningitis develop neurological sequelae. Maternal vaccination with multivalent conjugate vaccines against GBS is a new strategy which may lead to passive protection of the infant. Further studies to examine the efficacy of vaccines are in progress.

Anti-Bacterial Agents↗

PubMed1987

The evolution of neonatal herpes encephalitis as demonstrated by cranial ultrasound with CT correlation.

Three neonates with herpes encephalitis had serial cranial ultrasound and CT studies performed during their hospitalization. Initially, subtle changes of diffuse brain edema were present but with no ventricular compression. A second phase revealed progressive brain edema with ventricular compression. A third phase with enlarging ventricles indicates developing encephalomalacia. Occasionally cyst formation may be noted within the cerebral white matter, a phenomenon initially more readily evident by ultrasound.

Brain↗

PubMed1984

Biopotency of vitamin E in barley.

Investigations were carried out to establish the total biopotency of the natural vitamin E isomers in barley compared with that of DL-alpha-tocopheryl acetate. The chick was used as an experimental animal. Prevention of nutritional encephalomalacia (NE) and chick liver-storage and plasma-storage assays of vitamin E were the methods used in the study. The individual tocopherols and tocotrienols, both in the tissue samples and in the grain and barley oil, were analysed using high-pressure liquid chromatography (HPLC) with fluorescence detection. The diagnosis of NE was based on careful clinical and histopathological observations. It can be concluded from the results that full protection against NE in the chicks was obtained with a supplementation level of 7.5 mg DL-alpha-tocopheryl acetate/kg diet (i.e. a total vitamin E content of 11.20 mg/kg diet) or with a supplement of 8.7 g barley oil/kg diet (i.e. a total vitamin E content of 22.99 mg from barley oil/kg diet). This gave a biopotency factor of 0.49 for barley for prevention of NE of the chicks, as compared to that of DL-alpha-tocopheryl acetate. Using regression analysis a statistically linear relationship could be observed between the total dietary vitamin E level and the response, as measured by the total vitamin E content in the liver and plasma, both in the groups supplemented with DL-alpha-tocopheryl acetate and in the groups supplemented with corresponding amounts of vitamin E in barley oil. The liver and plasma responses to the total vitamin E in the barley-oil diet compared with those of the DL-alpha-tocopheryl acetate reference diet gave identical values for the regression coefficients, i.e. in both liver-storage and plasma-storage assays the value for slopes of dose-response lines was 0.37. This means that the biopotency of the total vitamin E in barley was 37% of that of dietary DL-alpha-tocopheryl acetate. Thus, barley is not as rich a source of vitamin E as could be supposed on the basis of the chemical determination of its total vitamin E content. It was possible to verify this experimentally established biopotency of 0.37 for the total vitamin E in barley by converting the chemically determined amounts of the vitamin E isomers in barley into DL-alpha-tocopheryl acetate equivalents by multiplying them with internationally accepted potency factors for the individual natural isomers (DL-alpha-tocopheryl acetate 1.00, D-alpha-tocopherol 1.49, D-beta-tocopherol 0.60, D-gamma-tocopherol 0.15, D-alpha-tocotrienol 0.37).(ABSTRACT TRUNCATED AT 400 WORDS)

Animal Feed↗

PubMed1996

Phospholipid fatty acids of brain and liver are modified by alpha-tocopherol and dietary fat in growing chicks.

Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching. The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg alpha-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:1n-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5. 25 or 125 mg alpha-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg alpha-tocopherol/kg. In 1-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the order dietary linolenic > linoleic > oleic acid. In liver, also, the effect of alpha-tocopherol supplementation on phospholipid fatty acids was most pronounced. The unsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the alpha-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.

Animals↗

PubMed1980

Comparison in inducing effect on vitamin E deficiency symptoms in chicks between dilauryl succinate and unsaturated fatty acids.

Dilauryl succinate (DLS) and unsaturated fatty acids (UFA) were compared for the effects of inducing vitamin E deficiency symptoms in chicks. Experimental diets containing DLS, UFA and DLS + UFA, respectively, were given to 1-day-old chicks for 28 days. The diet containing DLS but not UFA showed far less increase in peroxide value than those containing UFA or DLS + UFA when left in a battery brooder of 30 degrees. Vitamin E deficiency symptoms in chicks given DLS + UFA were more severe than those in chicks fed either DLS or UFA. No significant difference in vitamin E deficiency symptoms except incidence of encephalomalacia was observed between the chicks given DLS and UFA. Extracting UFA from the diet containing DLS + UFA resulted in the reduction of vitamin E deficiency induction to the same degree as the diet containing DLS. Synthetic antioxidants were effective in alleviating the vitamin E deficiency symptoms in the chicks fed UFA and DLS + UFA, while only slightly effective in those given DLS. It was found that the effects of DLS and UFA can be separated and combined technically and it was suggested that they have different mechanism in inducing vitamin E deficiency.

Animals↗

PubMedDate not supplied

Delayed radiation encephalopathy after radiotherapy for nasopharyngeal cancer: a CT study of 45 cases.

The CT features of 45 cases of delayed radiation encephalopathy (including radiation necrosis) following radiotherapy for nasopharyngeal carcinoma are reported. The brain lesions were uni- or bilateral and involved mainly the white matter and subsequently the gray matter of the lower portion of the brain included within the portals of irradiation and its vicinity. The lesions were edematous and hypodense on CT and showed postcontrast enhancement in 50% of the cases. Within the period of follow-up (1-5 years), the lesions showed remissions and exacerbations and in some cases stabilized. In addition, there was progressive cerebral atrophy, manifesting itself mainly as dilatation of the temporal horns, the neighboring cisterns, and sylvian fissures. In some cases that were followed for a long time, the cerebral lesions showed either foci of calcification or encephalomalacia and/or porencephaly.

Adrenal Cortex Hormones↗

PubMed1993

Biopotency of vitamin E in lucerne meal for chickens.

In order to estimate the biopotency of vitamin E in lucerne/alfalfa meal in comparison to that of dl-alpha-tocopheryl acetate (dl-alpha-Ta; all-rac-alpha-Ta) a study was conducted with newly hatched White Leghorn male chicks. An increase in the vitamin E level in the liver and plasma, and the prevention of nutritional encephalomalacia (NE) were used as criteria for biopotency. After a vitamin E depletion period of one week posthatching, the chicks continued on a semipurified, vitamin E free basal diet without vitamin E supplementation, or were repleted with graded levels of that vitamin for six weeks, provided as extracted lucerne oil or as dl-alpha-Ta. High performance liquid chromatography (HPLC) with fluorescence detection was used for the analysis of the vitamin E homologues. The diagnosis of NE was based on clinical and histopathological observations. A significant increase (P < 0.05) in vitamin E content in the liver and plasma was observed in response to dietary supplementation with both vitamin E sources. The linear increase both in the liver and plasma storage assays was associated with a reduced incidence of NE. The disease was totally prevented by a dietary supplement of 7.50 and 5.40 mg vitamin E/Kg feed provided as dl-alpha-Ta or lucerne oil, respectively. The natural biopotency of the vitamin E in lucerne meal compared with that of dl-alpha-Ta in the liver and plasma storage assays and in the prevention of NE was 123, 105 and 99%, respectively, as calculated by the slope ratio technique.

Animal Feed↗

PubMed1982

Cerebral, renal and splenic lesions due to fetal anoxia and their relationship to malformations.

Two newborn infants who suffered severe intra-uterine anoxia a few weeks before birth are described. Both died shortly after being born spontaneously and slightly prematurely. In one case the mother had attempted suicide by inhaling butane. The infant's kidneys were hypoplastic and resembled those seen in renal dysplasia, and the brain showed a severe encephalomalacia which would probably have developed into hydranencephaly. The other case was a twin who survived the intra-uterine death of her co-twin: she had hypoplastic kidneys similar to those in the first case, and a hypoplastic spleen. (The brain was not examined.) It is thought that intra-uterine anoxia may produce lesions in fetal organs which appear at birth as congenital developmental malformations. This mechanism is thought to account in particular for some cases of renal dysplasia and for hydranencephaly.

Adult↗

PubMed1997

Visual agnosia with bilateral temporo-occipital brain lesions in a child with autistic disorder: a case study.

A 2-year-old boy meeting the criteria for autistic disorder was diagnosed 2 years later with a visual agnosia characterised by a combination of certain aspects of associative and apperceptive agnosia. MRI then revealed a severe encephalomalacia of the right temporal lobe and bilateral temporo-occipital areas. This association is discussed in terms of a clinical and aetiological relation between autistic disorder and visual agnosia.

Agnosia↗