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PubMed1979

[Encephalomalacia in partridges, quails and pheasants raised in warrens].

With the introduction of industrial methods of breeding game animals, resp., birds in confinement some new diseases have arisen, such as encephalomalacia. Due to its peculiar character this disease was first referred to as B-complex avitaminosis, respective therapeutic measures being taken. Recent studies have ruled out avitaminosis, and the disease is now confirmed as encephalomalacia. In the case of partridges, rock partridges, and pheasants some drop was found of the levels of vitamin E and selenium. Accordingly, vitamtin E and selenium therapy produced a rapid curative effect.

Animals↗
PubMedDate not supplied

[E-vitamin activity of vitamin E derivatives with experimental encephalomalacia in chicks].

When adding pharmacopoeian alpha-tocopherylacetate, short-chain alpha-tocopherylacetate, alpha-tocopherylquinine, short-chain alpha-tocopherylquinone and alpha-tocopheronolactone to E-avitaminotic rations pharmacopoeian alpha-tocopherylacetate and alpha-tocopheronolactone manifest the highest E-vitamin activity in preventing encephalomalacia in chickens. The action of alpha-tocopheronolactone is not directly associated with changes in the content of vitamin E and ubiquinone in the brain and liver tissues. All the studied derivatives are effective in increasing resistance of erythrocytes to osmotic hemolysis. The data obtained evidence for a nonspecific function of vitamin E in preventing alimentary encephalomalacia in chickens as well as for the absence of disturbances in ubiquinone metabolism under conditions of the E-hypovitaminosis experimental model.

Animals↗
PubMed1980

[Protective effect of alpha-linolenic acid in encephalomalacia in chickens].

Encephalomacia is a vitamin E deficiency syndrome which affects the cerebellum of young chicks. The lesion includes degenerative alterations of cellular and fibrillar elements, apparently as the result of the ischaemia caused by thrombotic events in the microvascular system. A supply of linoleic acid, as fatty acid methyl esters prepared from safflower oil (Carthamus tinctorius), caused a high incidence of encephalomalacia. On the other hand, linseed oil esters, rich in alpha-linolenic acid, did not induce any symptoms and protected the chicks to a large extend against the development of signs produced by linoleic acid. Fatty acid esters of cod liver oil, rich in long-chain derivatives of alpha-linolenic acid, exerted a relatively weak protective effect. The analytical results show that a supply of alpha-linolenic acid led to an accumulation of eicosapentaenoic acid, 20:5 omega 3, and a reduced concentration of arachidonic acid in the phospholipds of liver and plasma. The results suggest that, under the conditions leading to encephalomalacia, the prostacyclin-thromboxane balance is shifted in direction of an excessive production of TXA2, causing thrombus formation in the capillaries of the cerebellum, alpha-linolenic acid, by modifying the PUFA profile, exerts a multiple action the main result of which appears to be an antithrombotic effect at the level of the microvascular system of the cerebellum.

Animals↗
PubMed2005

HPLC determination of free nitrogenous compounds of Centaurea solstitialis (Asteraceae), the cause of equine nigropallidal encephalomalacia.

Centaurea solstitialis (yellow star thistle) has been proven to cause equine nigropallidal encephalomalacia in horses. Over the last fifty years, nigropallidal encephalomalacia has been of interest to human medicine due to the possible connection with Parkinson's disease. Previous studies indicated the presence of neurotoxic nitrogenous compounds in polar extracts of the plant. In order to give a more detailed description of the nitrogen-containing fraction of C. solstitialis, various samples were collected at different development stages. Different aliquots of the same aqueous extract were directly derivatized with o-phthaldialdehyde and dansyl chloride and analyzed separately by reversed-phase HPLC. A complete profile of the free nitrogenous fraction of C. solstitialis was given and results obtained with the two derivatization procedures were compared. No particularly high level of free aspartic and glutamic acids, two potent neuroexcitotoxic amino acids, were found in polar extracts of the plant. Tyramine resulted to be the most important biologically active amine present in C. solstitialis (with a mean concentration of 2.0 mg/100 g of dry weight).

Amino Acids↗
PubMed1981

Multicystic encephalomalacia due to fetal viral encephalitis.

Two children, aged 2 weeks and 2 months, with multicystic encephalomalacia aer described. Although computerized tomography (CT) scan was used for the diagnosis, the value of the simple method of transillumination is stressed. The mother of one child had mumps with meningitis at 26 weeks' gestation. The other child had an echovirus 11 isolated from the cerebrospinal fluid and herpesvirus hominis (HVH) from the skin at 8 weeks. We speculate that the changes in the brains of these babies may be due to the respective viruses causing a fetal encephalitis.

Echovirus Infections↗
PubMed1992

Cystic encephalomalacia and intrauterine herpes simplex virus infection.

Cystic encephalomalacia occurred in two preterm infants who had proven intrauterine herpes simplex virus type 2 infection. Calcification was evident in the basal ganglia. Follow-up scans indicated that the cysts had resolved over a period of two months in one infant, while in the case of the other, the cysts became progressively larger with significant ventricular dilatation developing. While cystic changes in the brain of preterm infants are usually due to periventricular leukomalacia, intrauterine infection needs to be considered as a possible cause. Antiviral treatment may be of benefit to infants with herpes simplex virus infection.

Brain Diseases↗
PubMed1978

Avian encephalomalacia in Barbados, West Indies: a description of spontaneous field cases with feed analyses.

The clinical, necropsy and histopathological findings in four natural outbreaks of encephalomalacia are reported. Feed analyses implicated low levels of vitamin E as the probable cause of the condition. Treatment with vitamin E has proved to be very effective. The instability of vitamin E in animal feed ingredients during long periods of shipment into the Caribbean may be important in the pathogenesis of the disease.

Animal Feed↗
PubMed1988

Ultrasound diagnosis of multiple cystic encephalomalacia.

Following bacterial meningitis thirty cases of enlarging head were evaluated on ultrasound to find out the cause. Nine out of 30 patients had multiple cystic lesions in both cerebral hemispheres with or without ventriculomegaly. Three patients showed debris in the cysts suggesting pus, which was confirmed on ultrasound-guided aspiration in two and on surgery in one case. Seven out of nine patients had died at the time of writing this communication, suggesting the need for its early detection and timely family counselling. It is stressed that multiple cystic encephalomalacia has a characteristic appearance on ultrasound and all patients with meningitis should be screened routinely so as to detect it at an early stage.

Brain Diseases↗
PubMed2003

Multicystic encephalomalacia.

Antepartum death of a fetus in a multiple gestation can be associated with mortality or major morbidity in the survivor. This article reports a rare case of multicystic encephalomalacia that occurred in the survivor twin with antepartum death of its co-twin. Its pathology and pathogenesis are discussed with review of literature.

Brain↗
PubMed1991

Cerebral lymphoma and HIV encephalitis in a case of paediatric AIDS, with pre-existing multicystic encephalomalacia.

A case of intracerebral malignant B cell lymphoma associated with encephalitis typical of Human Immunodeficiency Virus (HIV) infection is described in a 4 year old child, with post-transfusion Acquired Immune Deficiency Syndrome (AIDS) and severe pre-existing cystic encephalomalacia. This report further documents B cell lymphoma as the commonest cause of an intracerebral mass, and an important cause of death in paediatric AIDS. That more than one pathological process may be responsible for neurological symptoms in paediatric AIDS is also emphasised.

AIDS Dementia Complex↗
PubMed1993

Lipoxygenase and other enzymes of arachidonic acid metabolism in the brain of chicks affected by nutritional encephalomalacia.

1. Prostaglandin endoperoxide synthetase (PES) and lipoxygenase (Lox) activities were compared in the cerebella and cerebra of vitamin E-sufficient young chicks and in chicks in which nutritional encephalomalacia (NE) was induced by a diet deficient in vitamin E. 2. Eicosanoid production patterns were qualitatively similar in the brains of both groups of chicks, but prostaglandin production was 50-60% less in cerebella of ataxic chicks, compared to control cerebella, while the opposite trend was observed in the cerebellar Lox pathway, as measured by radioimmunoassay of 15-HETE. 3. Cerebellar phospholipase A2 activity was twice that of the cerebrum but was not affected by NE. 4. Purification of Lox activity from the cerebellar homogenates produced a lower yield and enrichment when the starting material was taken from ataxic chicks, compared to the controls. 5. In addition there were qualitative differences in the purified fractions from both groups, as seen by pH optima and kinetics. 6. The results are consistent with the view that the cerebellum has less antioxidant protection than the cerebrum and that its higher phospholipase A2 activity and greater propensity to oxygenate arachidonic acid via the Lox pathway at the expense of the PES pathway may render this region of the brain particularly vulnerable to oxidative damage in NE.

Animal Nutritional Physiological Phenomena↗
PubMed1978

Multicystic encephalomalacia of infancy: clinico-pathological report of 7 cases.

Clinical follow up and complete neuropathological examination was made on seven cases of multicystic encephalomalacia of infancy. Etiological factors were carefully studied in all the cases. They consisted of prenatal injuries presenting as a cord prolapse, in 3 cases; prolonged labour with marked cyanosis; abdominal trauma during gestation, and various maternal infections at different stages of pregnancy. Pathological interest is centred on the variable involvement of different areas of the brain, generally sparing the cerebellum and brain stem, and being minimal or absent in the occipito-temporal areas. This distribution may be explained by a different effect of the "causal agency" on these different areas, or by a different capacity of these regions to react against injury. Among the etiological factors reviewed in the literature, the anoxic theory appears the most probable, as there was a close parallelism between lesions and vascular areas, mainly the carotid and vertebro-basilar systems.

Asphyxia Neonatorum↗
PubMed1985

Intra-uterine tachycardia associated with multicystic encephalomalacia (MCE).

Multiple cystic brain lesions in neonates have been described as a result of a variety of causes. All events described thus far in association with multicystic encephalomalacia (MCE) seem to point to hypoxic-ischaemic injury as the common factor for this particular form of central nervous system damage. We describe a neonate in whom repeated, prolonged episodes of intrauterine tachycardia had been documented. Congestive heart failure and fetal hydrops were present at birth and MCE at the age of 13 wk. The obvious relationship between this child's intrauterine tachycardia and his MCE points to the fact that any fetus with prolonged tachycardia should be considered at risk of severe brain damage.

Adult↗
PubMed1979

Multicystic encephalomalacia in liveborn twin with a stillborn macerated co-twin.

Computed tomography showed multiple cystic lesions in the brains of three infants with cerebral palsy. Each patient was the product of a twin pregnancy with a stillborn, macerated co-twin. In two patients angiography was performed and suggested that the cystic lesions were multicystic encephalomalacia due to perinatal arterial occlusion.

Arterial Occlusive Diseases↗
PubMed2000

Brain, liver and plasma unsaturated aldehydes in nutritional encephalomalacia of chicks.

Vitamin E deficiency and linoleic acid-feeding lead to nutritional encephalomalacia (NE) in chicks, affecting the cerebellum exclusively. The relevance of lipid peroxidation (LPO) products to the pathogenesis of the disease was studied. Laying hens received a diet low in vitamin E. Resulting chicks were assigned to four groups fed either with linoleic (C18: 2n-6) or linolenic (C18: 3n-3) acid together with 1 or 50 p.p.m. vitamin E. Nine days post-hatching NE occurred in the vitamin E-deficient group fed linoleic acid. With each chick showing NE, a healthy one from all four groups was killed. Unsaturated aldehydes were determined in plasma, liver, cerebrum and cerebellum. Results underlined that the type of dietary fat is decisive for the aldehyde pattern. In the liver of linoleic acid-fed animals total aldehydes were increased. Diseased animals had increased aldehydes stemming from n-3 fatty acids. In plasma, vitamin E deficiency led to higher malondialdehyde and OH-nonenal concentrations. In brain, neither vitamin E deficiency nor NE were accompanied by increased aldehyde concentrations. In consequence a direct role of unsaturated aldehydes for the development of NE in the cerebellum is not probable.

Aldehydes↗
PubMed1987

Nutritional encephalomalacia in the chick: an exposure of the vulnerable period for cerebellar development and the possible need for both omega 6- and omega 3-fatty acids.

1. Cockerels (1-d-old) received over a period of 4 weeks, a balanced diet containing either safflower oil (diet S) or linseed oil (diet L) as a source of polyunsaturated fatty acids (PUFA). Body-weight, and weights of cerebrum and cerebellum increased at similar rates in the two dietary groups. The total fatty acids (FA) of the cerebellum differed from the cerebral FA by their higher PUFA and oleic acid contents and their lower stearic acid level. During the 3rd week of life there was a spurt in accretion of PUFA in the cerebellum, but not in the cerebrum. At the end of the experimental period phosphatidylethanolamine was present at twice the concentration in the cerebellum, compared with the cerebrum. 2. Diets S and L resulted in extensive mutual replacement of omega 6- and omega 3-FA in brain, without any significant change in the total PUFA. Brain oleic acid concentration was higher in the diet-L group than in the diet-S group, but saturated FA were not affected by the dietary treatments. 3. These results may be relevant to basic brain biology and to chick nutritional encephalomalacia (NE). This disease, which specifically affects the cerebellum and is readily induced by diets supplying linoleic acid but deficient in vitamin E, usually reaches its highest incidence during the 3rd week of life and may thus be related to the cerebellar PUFA spurt that occurs at that time. The fact that NE was induced by linoleic acid, while alpha-linolenic acid exerted a protective action, points to an overproduction of arachidonic-derived eicosanoids as a factor in the etiology of the cerebellar lesion and possibly a structural change due to a loss of docosahexaenoic acid and gain of arachidonic acid in the chicks given diet S.

Animals↗
PubMed1983

Effects of vitamin E and aspirin on the incidence of encephalomalacia, fatty acid status and serum thromboxane levels in chicks.

This study was initiated to examine the role of prostanoids (thromboxane) in the development of nutritional encephalomalacia (NE). Chicks were fed diets deficient in or supplemented with vitamin E in the presence or absence of a known prostaglandin inhibitor, acetylsalicylic acid (ASA). When the incidence of NE was approximately 50% in the vitamin E--deficient group without ASA supplement, the chicks were killed, and serum thromboxane B2 (TxB2) and serum and brain fatty acid (FA) composition were determined. The incidence of NE was not altered by ASA treatment. Plasma arachidonate levels were increased by ASA treatment on the vitamin E--deficient diet. Furthermore, the serum TxB2 levels in vitamin E--deficient versus vitamin E--adequate chicks, unlike changes noted for rats, were decreased. Aspirin treatment drastically reduced TxB2 levels in all groups but did not alter the incidence of NE. Therefore, it is unlikely that the development of NE is a result of thromboxane-mediated thrombosis.

Animals↗
PubMed1991

Chick nutritional encephalomalacia and prostanoid formation.

Nutritional encephalomalacia (NE) was induced in young chicks using a diet low in vitamin E and containing 8% ethyl esters derived from safflower oil fatty acids (S-E group). The same diet with added alpha-tocopheryl acetate (S+E) failed to produce the pathology, and chicks receiving aerated linseed oil--high in alpha-linolenic acid and low in alpha-tocopherol (L-E)--did not develop symptoms. Formation of metabolites from labeled arachidonic acid (AA) by thrombocytes was similar in the S+E and S-E groups, yielding thromboxane B2 (TXB2) and hydroxy fatty acids as the major products. Collagen-induced thrombocyte aggregation and TXB2 production were not significantly different in the S-E and S+E groups, but aggregation values and TXB2 synthesis were significantly less in the L-E group than in the ataxic S-E chicks. Prostaglandin E2 production by aortal rings was significantly influenced by the diet; S-E yielded the highest value and L-E the lowest. These results show that alpha-linolenic acid causes alterations in the AA metabolism and thrombocyte function in young chicks.

Animals↗