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Results for “ENCEPHALOMALACIA”

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PubMedDate not supplied

Oedipism in a patient with frontal lobe encephalomalacia.

There is a growing recognition of the role of the frontal lobes in the aetiology of severe behavioural aberrations. The authors describe a case of Oedipism in a patient who had MRI evidence of frontal lobe encephalomalacia. After discussing the function of the frontal lobes in modulating behaviour the authors suggest that the structural lesion seen on the MRI was in part responsible for the patient's self-destructive act. Treatment issues and the importance of recognizing underlying structural lesions in instances of extreme self-mutilation are discussed.

Adult↗
PubMed1995

The influence of dietary fatty acids and vitamin E on plasma prostanoids and liver microsomal alkane production in broiler chickens with regard to nutritional encephalomalacia.

Nutritional encephalomalacia (NE) in broiler chicken is considered as a peroxidative dysfunction caused by vitamin E-deficient diets. A feeding experiment was performed to investigate the consequences of feeding different fats in combination with increasing amounts of vitamin E on liver lipid peroxidation and plasma prostanoid pattern. Newly hatched chicks from hens on a vitamin E-poor diet were fed with either mainly linolenic, linoleic or oleic acid-rich oils in a vitamin E-deficient (5 ppm) basic diet. The animals were supplemented with vitamin E on three levels (0, 20 or 120 ppm). On appearance of the first symptoms of NE after 8 days post-hatching, the animals were examined. Typical symptoms with a high incidence only occurred in the group fed linoleic acid and 5 ppm vitamin E. Plasma prostanoids and microsomal alkane production in liver as a measure of endogenous lipid peroxidation were determined. The dietary conditions affected plasma prostaglandin E2 and thromboxane A2, but not prostacyclin. However, it seems unlikely that the prostanoids are involved in the pathogenesis of NE. Liver lipid peroxidation increased in vitamin E deficiency. The level of alkanes depended on the type of fat supplied. The consequences of the different dietary fats in combination with vitamin E deficiency on peroxidative metabolism of broiler chickens are evident, indicating that a high level of oxidative stress is imposed by the linoleic acid-rich fat.

Alkanes↗
PubMed1990

[Multicystic encephalomalacia in twin pregnancies].

Multicystic encephalomalacia (ME) is a rare entity in the pediatric age. In ME brain tissue in substituted by cavities of variable size. ME has different etiologies being asphyxia and circulatory alterations the most important factors. In monozygotic twins there is an increased incidence of structural anomalies than dizygotic twins. We present four twin patients with ME. Three of them had a prenatal dead sibling. The fourth pair of twins had a twin-twin transfusion. We want to stress the utility of brain echography in early diagnosis of ME.

Brain Diseases↗
PubMedDate not supplied

[Urinary uropepsin activity in patients with encephalomalacia as an index of the activity of the hypothalamo- hypophyseal-adrenal axis].

The determinations were carried out in 25 patients with thrombotic encephalomalacia. The changes in 24-hour urine uropepsin activity were studied after administration of metopirone and dexamethasone. The uropepsin activity in a sample of 24-hour urine was determined by the method of West, Ellis and Scott. A statistically significant fall of uropepsin activity was observed in 24-hour urine after metopirone, with a rise in the activity of this enzyme after dexamethasone administration.

Aged↗
PubMed1989

[Multicystic encephalomalacia in an adult--a case report].

A case of multicystic encephalomalacia found in adult life was described. A 35-year-old man was admitted to our hospital with a chief complaint of unsteadiness. He had developed normally until he fell into the shock state induced by mismatch blood transfusion at the age of 15 months. Since then he has been mentally retarded moderately and had clumsiness of the skillful movement in the right hand. The other neurological abnormality was hyperreflexia only. Laboratory examination failed to disclose metabolic defect. Both CT scan and MRI demonstrated numerous cystic lesions of various size spreading over bilateral cerebral white matter partially involving the inner layer of the cortex. On the contrary basal ganglia, cerebellum and brainstem were completely spared. The diagnosis of MCE was made from (1) anoxic-ischemic episode in infancy, (2) static clinical picture and (3) characteristic distribution of cystic lesions. It is well known that MCE results from perinatal hypoxia, but it is a polyetiologic condition caused by various damages to immature brain of early infancy and usually results in severe psychomotor retardation. Nonetheless, it is intriguing in our case that marked discrepancy was found between morphological change and neurological deficit. It is probable that at the age of 15 months the myelination of major projecting fibers was almost completed, but sufficient plasticity was preserved in immature brain. As a result, the patient had the neurological deficit in the minimum degree in spite of severe morphological change.

Adult↗
PubMedDate not supplied

Multicystic encephalomalacia associated with symmetrical necrotizing brain stem lesions in an infant: a case report.

The simultaneous occurrence of multicystic encephalomalacia of the cerebral hemispheres, and symmetric necrotizing lesions of diencephalic and infratentorial structures is described in a 15 month-old infant. The baby developed clonic jerks of four limbs a few hours after delivery. She attained no developmental milestones, and remained bed-ridden with hypertonic posture until her death. Multicystic cavities of the cerebral hemispheres were well evident at CT scan when she was 7 months old. The topographic distributions of the different pathological pictures are described; their relationship to the regional properties of the developing brain are commented upon. Etiological aspects of this case are discussed according to present knowledge of the pathophysiological mechanisms leading either to multiple cyst formation or to necrotizing lesions.

Basal Ganglia↗
PubMedDate not supplied

Encephalomalacia associated with hypovitaminosis E in turkey poults.

Four-to-five-week-old turkey poults fed a diet markedly deficient in vitamin E (alpha-tocopherol) abruptly developed neurologic signs such as tremor, incoordination, and recumbency shortly after being moved to new quarters. Serum concentrations of alpha-tocopherol in birds on this diet were significantly lower than control values. Associated lesions included recent ischemic necrosis of the cerebellum and spinal cord. The condition closely resembled nutritional encephalomalacia of chicks. This report represents the initial published description of that entity in turkeys.

Animal Feed↗
PubMed1979

[Electron microscopic findings in the skeletal musculature of broilers with nutritional encephalomalacia].

Sings of myopathy were recorded by means of electron microscopy from the skeletal muscles of 20 broiler chickens, aged five and six weeks and suffering from spontaneous nutritional encephalomalacia. Focal deposits of osmiophilic, granular or amorphous matter, intermixed also with membrane fragments and condensed to homogenous osmiophilic bodies, were found quite often in the sarcoplasm. Those deposits were interpreted as lipoproteid complexes (pigmentation due to vitamin E deficit). Also observed were degenerative disorders of compensatory reactions of membraneous fibre organelles (sarcoplasmic reticulum, mitochondria) as well as decomposition of myofibrils and fibre hyalinization. Fibre regeneration and vascular damage occurred less often. Pathogenetically, the changes are interpreted particularly with regard to a membrane-stabilising anti-oxidant action of vitamin E and compared to the selenium-dependent myopathies of ruminants from which primary myofibrillar damage was recordable but no pigment accumulation.

Animals↗
PubMed1984

Multicystic encephalomalacia: CT appearance and pathological correlation.

Perinatal insults, including anoxia, may lead to a form of cerebral necrosis designated multicystic encephalomalacia. This common condition is characterized by (a) moderate atrophic ventricular dilatation, (b) intact ventricular walls with thickened subependymal glial layer, (c) multiple cysts of irregular size and shape distributed throughout the cerebral white matter and the inner layers of the cortex bilaterally, and (d) relative sparing of the orbital surfaces of the frontal lobes, the temporal lobes below the superior temporal gyri, the basal ganglia, the cerebellar hemispheres, and the spinal cord (except for secondary degeneration of corticospinal tracts).

Brain↗
PubMed1980

[Clinical course and CSF lactate in encephalomalacia (author's transl)].

LCS level of lactate and clinical status correlate well during the initial stage of encephalomalacia (2nd-4th day) and during a period of 12 to 14 days after infarction LCS level of lactate may, therefore, be regarded as important parameter for short-term prognosis of encephalomalcia. The use of a semiquantitative clinical score also permits predictions as to the extent of remission to be expected. The reliability of this model of prognosis is limited by the comparatively small number of patients so far examined, the assumption of a linear relation between clinical alterations and changes in LCS lactate, as well as by the difficulty of determining LCS lactate in most severe cases at the specific time requested by the examination programme.

Aged↗
PubMed1995

[Multivariate autoregressive analysis of carotid artery blood flow waveform in a newborn with multicystic encephalomalacia].

We analyzed the carotid artery blood flow waveform (CABFW) through multivariate autoregressive analysis in a case with multicystic encephalomalacia (MCE) after neonatal asphyxia and compared the result with those of 35 healthy newborns. The total power of CABFW was at the -2 SD level of the value for 35 healthy newborns, and the power, % power, bio-informing amounts and damping time of component 3 (damping frequency 11.15 Hz) were less than -2 SD of the values in 35 healthy newborns. The Pulsatility Index (PI) of anterior cerebral artery (ACA) was high (0.76). These results suggest that cerebral blood flow decreases because of cerebral vasoconstriction in MCE after neonatal asphyxia.

Brain Diseases↗
PubMedDate not supplied

Nutritional encephalomalacia in turkeys: diagnosis and growth performance.

An outbreak of neurological disease in 2 1/2-to-3 1/2-week-old male turkey poults was diagnosed morphologically as nutritional encephalomalacia. About 20 to 30% of the flock of 6360 showed clinical signs, which included going down with legs extended or hock-sitting and inability to get up, incoordination, weakness, staggering, trembling, torticollis, and opisthotonus. The most important gross postmortem changes were found in the brain, which consisted of an enlarged and swollen cerebellum with focal and/or diffuse hemorrhages. Major histopathological alterations included congestion, hemorrhages, necrosis, and malacia associated with hyaline capillary thrombi affecting the cerebellar cortex and adjacent white matter. Except for a slightly higher mortality, flock performance compared favorably with performance of other flocks grown in the same farm as well as with the national average for market tom turkeys.

Animal Feed↗
PubMedDate not supplied

Multicystic encephalomalacia in a surviving monochorionic twin.

From a recent monochorionic diamniotic twin pregnancy seen at this hospital, one of the twins died in utero at 37 weeks' gestation. The other twin, a male infant, was delivered by Cesarean section because of fetal distress, with resuscitation performed in the delivery room. The infant developed generalized tonic seizure shortly after stabilization, and was put on anticonvulsants. The initial brain echography was normal; follow-up echograms and CT scans performed at 8 and 12 days old, respectively, revealed diffuse low density over both side of cerebral hemisphere. At one month old, the infants's brain echogram showed diffuse cystic encephalomalacia. At four months, he was noted to be spastic and significantly delayed in neurodevelopment. Disseminated intravascular coagulation caused by fetal-to-fetal transfer of thromboplastic material from the dead fetus was considered as the most possible cause of the neurological complication in this patient. In addition, perinatal hypoxic-ischemic insult may also have been a superimposed, influencing factor.

Diseases in Twins↗
PubMed1993

[Multicystic encephalomalacia in a surviving twin after death of the other twin in utero].

A case of multicystic encephalomalacia in a twin is reported. The other twin died in utero at 32 weeks gestational age. Because there was no evidence of fetal distress the pregnancy was allowed to continue until 36 weeks gestational age. Injuries to the surviving twin due to disseminated intravascular coagulation (DIVC) and vascular thrombosis or to anoxia and ischemia may occur when there are anastomoses between the circulatory systems of the two twins, i.e., in monochorionic pregnancies. The classically recommended strategy is to wait for adequate maturity of the surviving fetus (36 weeks). It is suggested that this attitude may be overly expectant and may deserve reappraisal.

Diseases in Twins↗
PubMed1996

[Tissue lipid peroxidation in nutritional encephalomalacia of broiler chickens].

The consequences of different dietary fats in combination with two vitamin E levels on peroxidative tissue damage of chicken brain and liver and its meaning for development of nutritional encephalomalacia (NE) were investigated. A feeding experiment was performed with 1-day-old chickens from hens on a vitamin-E-poor diet. The animals received a vitamin-E-deficient basic diet containing 10% fat, rich in either C18:3n3-, C18:2n6- or C18:1n9-fatty acids. The fat was given either fresh or oxidized (peroxidation number: 250) and 0 or 50 ppm alpha-tocopherylacetate was added. Typical symptoms of NE occurred mainly in those groups fed with n6-fatty acids beginning on day 7. In order to evaluate oxidative tissue damage, conjugated dienes, fluorescent pigments and TBA-reactive substances were determined in liver, cerebrum and cerebellum. Brain was examined histologically. In liver and cerebrum, the feeding of oxidized fats led to a 20% increase in conjugated dienes. Fluorescent pigments could be determined only in the brain tissues. However, feeding conditions had no effect, although autofluorescence was observed histologically in the affected animals. TBA-reactive substances were heightened in cerebrum (30%) and liver (130%) as a result of feeding linolenic acid. Vitamin E deficiency doubled TBA-reactive substances only in the liver. The parameters measured did not show intensified lipid peroxidation in the cerebellum of the animals fed the NE producing diet. Rather, the liver seems to be affected by the oxidative stress.

Animals↗
PubMed1997

[Multicystic encephalomalacia. Review of 19 cases].

OBJECTIVE: Multicystic encephalomalacia (EMQ) is a pediatric entity where the brain tissue is substituted by cavities of variably sizes. PATIENTS AND METHODS: Nineteen children diagnosed of EMQ were studied retrospectively. We analyzed the etiology, diagnosis and the clinical and radiological evolution. RESULTS: There were three different etiologies: twin pregnancy, 12 cases; perinatal hypoxia, 4 cases; perinatal infection, 1 case; cardiac arrest, 1 case; and 1 patient with multiple embolism of unknown cause. The diagnosis of EMQ was made with cerebral ultrasonography (14 patients), computed tomography (19 patients) and magnetic resonance imaging (5 patients). We stress the utility of cerebral ultrasonography in early and reliable diagnosis of EMQ. The clinical development was unfavorable. We studied the outcome of 15 patients. Two children died. Eleven patients (73%) show severe consequences (mental retardation, microcephaly, spastic tetraplegia, and in 7 children epilepsy). In 2 cases, the radiological development was hydranencephaly. Examination of the 4 remaining children (26.66%) revealed a spastic hemiplegia. CONCLUSIONS: EMQ is a rare disease in childhood and has a very poor outcome, for this reason early diagnosis is very important. To this effect, cerebral ultrasonography is the imaging modality of choice.

Diseases in Twins↗
PubMed1998

Focal symmetrical encephalomalacia in a 6-month-old Dorset sheep.

Neurological examination of a sheep that had acute onset of recumbency and mental depression indicated a diffuse symmetrical thalamocortical lesion. Cerebrospinal fluid analysis suggested a degenerative central nervous system disease. Thiamin administration resulted in partial and temporary improvement. Brain histological lesions were typical of focal symmetrical encephalomalacia.

Animals↗