Multicystic encephalomalacia: An autopsy report of 4 cases

Multicystic encephalomalacia is varying sized cystic lesions in the brain encountered in developing fetuses or infants. These cysts start at the periventricular area and may extend onto the cortex. The cause of the formation of these cystic lesions is secondary to an ischemic or hypoxic insult, which leads to liquefactive necrosis and subsequent formation of gliotic cyst walls having an admixture of microglia. We discuss four autopsy cases that had multicystic encephalomalacia to highlight the scenarios in which these lesions are encountered.

Multicystic Encephalomalacia:Report of One Case / 中国医学科学院学报

The magnetic resonance imaging findings of multicystic encephalomalacia are featured by bilateral frontal large cystic lesion with corpus callosum involvement,evident heterogeneous enhancement of the lesion margin,ring hyperintensity on diffusion weighted imaging,and high choline peak and low N-acetylaspartate peak of the enhanced lesion margin on magnetic resonance spectroscopy.This article reports a case of multicystic encephalomalacia.

Bilateral Acute Retinal Necrosis and Encephalomalacia Due to Herpes Simplex Virus Infection in a Premature Infant

Herpes simplex virus (HSV) is a common pathogen, that causes a broad spectrum of diseases, ranging from minor skin infections to severe encephalitis and widespread infections. Acute retinal necrosis (ARN), one of the most serious manifestations of HSV infection, is defined as a rapidly progressing necrotizing retinopathy that presents discrete areas of circumferential retinal necrosis, along with signs of uveitis, vitreitis, and retinal vasculitis. We encountered a case of a female infant, born at 33 weeks of gestation with a body weight at birth of 2,080 g, who had ARN and encephalomalacia due to HSV infection. ARN associated with HSV infection should be suspected when nonspecific retinal exudates are observed in neonates, especially preterm infants.

Brain ultrasonographic findings of late-onset circulatory dysfunction due to adrenal insufficiency in preterm infants

PURPOSE: The aim of this study was to characterize the brain ultrasonographic findings of late-onset circulatory dysfunction (LCD) due to adrenal insufficiency (AI) in preterm infants. METHODS: Among the 257 preterm infants born at <33 weeks of gestation between December 2009 and February 2014 at our institution, 35 preterm infants were diagnosed with AI. Brain ultrasonographic findings were retrospectively analyzed before and after LCD in 14 preterm infants, after exclusion of the other 21 infants with AI due to the following causes: death (n=2), early AI (n=5), sepsis (n=1), and patent ductus arteriosus (n=13). RESULTS: Fourteen of 257 infants (5.4%) were diagnosed with LCD due to AI. The age at LCD was a median of 18.5 days (range, 9 to 32 days). The last ultrasonographic findings before LCD occurred showed grade 1 periventricular echogenicity (PVE) in all 14 patients and germinal matrix hemorrhage (GMH) with focal cystic change in one patient. Ultrasonographic findings after LCD demonstrated no significant change in grade 1 PVE and no new lesions in eight (57%), grade 1 PVE with newly appearing GMH in three (21%), and increased PVE in three (21%) infants. Five infants (36%) showed new development (n=4) or increased size (n=1) of GMH. Two of three infants (14%) with increased PVE developed cystic periventricular leukomalacia (PVL) and rapid progression to macrocystic encephalomalacia. CONCLUSION: LCD due to AI may be associated with the late development of GMH, increased PVE after LCD, and cystic PVL with rapid progression to macrocystic encephalomalacia.

Surto de intoxicação por sal em ovinos no estado do Pará / Salt poisoning outbreak in sheep in the state of Pará

O presente trabalho relata um surto de intoxicação por sal em ovinos no Brasil, em uma propriedade no estado do Pará. De um total de 545 ovinos, oito animais adoeceram (1,46%) e quatro destes morreram (50%). A avaliação das instalações e do manejo indicaram como fatores predisponentes a ingestão excessiva de mistura mineral e a restrição hídrica. Os principais sinais clínicos foram decúbito, diminuição ou ausência da sensibilidade cutânea, ausência dos reflexos de ameaça, palpebral e auricular, midríase, nistagmo, opistótono, espasticidade de membros, sonolência e estupor. Havia ainda, timpanismo, diarreia, taquipneia, taquicardia, desidratação e poliúria. A evolução do quadro clínico nos animais que morreram variou de duas horas e meia a 48 horas. As médias das concentrações séricas de sódio e de potássio de 31 ovinos do mesmo lote afetado pela intoxicação, em amostras colhidas durante o surto, revelaram hipernatremia (190mEq/l) e hipercalemia (8,2mEq/l). À necropsia, observou-se em um animal, achatamento das circunvoluções cerebrais. Microscopicamente, neste animal, evidenciou-se vacuolização moderada do neurópilo, particularmente nas lâminas intermediárias do córtex cerebral, com aumento dos espaços perineural e perivascular. Nessas áreas foram observados ainda, acentuada tumefação e edema dos astrócitos e necrose neuronal aguda. A dosagem de sódio no encéfalo de um ovino, revelou-se elevada com valor de 3.513ppm. O diagnóstico foi realizado com base na epidemiologia, nos sinais clínicos, nas lesões macro e microscópicas e nas dosagens de sódio no soro e no encéfalo dos ovinos.(AU)

This paper reports an outbreak of salt poisoning in sheep on a farm in the state of Pará, northern Brazil. Eight (1.46%) animals were affected from a total of 545 sheep and four (50%) of them died. The evaluation of the facilities and the handling indicated as predisposing factors excessive intake of the mineral supplement and water restriction. The main clinical signs were recumbency, decrease or absence of cutaneous sensibility, absence of auricular, palpebral and menace reflex, mydriasis, nystagmus, opisthotonus, spasticity of limbs, somnolence and stupor. Beside these signs bloat, diarrhea, tachypnea, tachycardia, dehydration and polyuria were observed. The course of the disease in animals that died ranged from two hours and a half to 48 hours. The medium of serum concentration of sodium and potassium of 31 sheep from the same group affected on samples collected during the outbreak revealed hypernatremia (190mEq/l) and hyperkalemia (8.2mEq/l). At necropsy, there was flattening of the cerebral gyri in one sheep; in this animal was found vacuolization of the neuropil in the cerebral cortex with moderate intensity in the intermediary and mild on the superficial layers, with increased perineural and perivascular spaces. In these areas there were markedly swollen nucleus of astrocytes with acute neuronal necrosis. The dosage of sodium in the brain of a sheep revealed a high value of 3.513ppm. The diagnosis was made based on the epidemiology, clinical signs, macro and microscopic lesions and in the dosages of sodium in serum and brain.(AU)

Long-Term Outcomes of Hemispheric Disconnection in Pediatric Patients with Intractable Epilepsy

BACKGROUND AND PURPOSE: Hemispherectomy reportedly produces remarkable results in terms of seizure outcome and quality of life for medically intractable hemispheric epilepsy in children. We reviewed the neuroradiologic findings, pathologic findings, epilepsy characteristics, and clinical long-term outcomes in pediatric patients following a hemispheric disconnection. METHODS: We retrospectively studied 12 children (8 males) who underwent a hemispherectomy at Asan Medical Center between 1997 and 2005. Clinical, EEG, neuroradiological, and surgical data were collected. Long-term outcomes for seizure, motor functions, and cognitive functions were evaluated at a mean follow-up of 12.7 years (range, 7.6-16.2 years) after surgery. RESULTS: The mean age at epilepsy onset was 3.0 years (range, 0-7.6 years). The following epilepsy syndromes were identified in our cohort: focal symptomatic epilepsy (n=8), West syndrome (n=3), and Rasmussen's syndrome (n=1). Postoperative histopathology of our study patients revealed malformation of cortical development (n=7), encephalomalacia as a sequela of infarction or trauma (n=3), Sturge-Weber syndrome (n=1), and Rasmussen's encephalitis (n=1). The mean age at surgery was 6.5 years (range, 0.8-12.3 years). Anatomical or functional hemispherectomy was performed in 8 patients, and hemispherotomy was performed in 4 patients. Eight of our 12 children (66.7%) were seizure-free, but 3 patients with perioperative complications showed persistent seizure. Although all patients had preoperative hemiparesis and developmental delay, none had additional motor or cognitive deficits after surgery, and most achieved independent walking and improvement in daily activities. CONCLUSIONS: The long-term clinical outcomes of hemispherectomy in children with intractable hemispheric epilepsy are good when careful patient selection and skilled surgical approaches are applied.

Prediction of Chronic Subdural Hematoma in Minor Head Trauma Patients / 대한신경손상학회지

OBJECTIVE: Chronic subdural hematoma (CSDH) is relatively common in neurosurgical field. However not all patients develop CSDH after minor head trauma. In this study, we evaluate the risk factors of post-traumatic CSDH. METHODS: Two-hundred and seventy-seven patients were enrolled and analyzed in this study from January 2012 to December 2013. Of those, 20 participants had minor head trauma developed CSDH afterward. We also included 257 patients with minor head trauma who did not develop CSDH during the same follow-up period as the control group. We investigated the risk factors related to the development of CSDH after minor head trauma. RESULTS: Old age (p=0.014), preexisting diabetes mellitus (p=0.010), hypertension (p=0.026), history of cerebral infarction (p=0.035), antiplatelet agents (p=0.000), acute subdural hematoma in the convexity (p=0.000), encephalomalacia (p=0.029), and long distance between skull and brain parenchyma (p=0.000) were significantly correlated with the development of CSDH after trauma. Multivariate analysis revealed that only the maximum distance between the skull and the cerebral parenchyma was the independent risk factor for the occurrence of CSDH (hazard ratio 2.55, p=0.000). CONCLUSION: We should consider the possibility of developing CSDH in the post-traumatic patients with the identified risk factors.

Epilepsy Associated with Encephalomalacia in Children

PURPOSE: Encephalomalacia is one of the major causes of symptomatic epilepsy. However, no previous study has examined the correlation between encephalomalacia and epilepsy in children. In this study, we aimed to quantify the prevalence, clinical features, and risk factors of epilepsy associated with encephalomalacia. METHODS: We performed a retrospective review of the medical records of 95 patients who were diagnosed with encephalomalacia by neuroimaging techniques at Pusan National University Children's Hospital between November 2008 and July 2013. Patients were classified into two groups: epilepsy (Group A) and non-epilepsy (Group B). We compared the demographics, underlying causes, and distribution of encephalomalacic lesions of these two groups. RESULTS: Groups A and B comprised 35 (36.8%) and 60 (63.1%) patients, respectively. Compared to Group B, Group A showed shorter mean gestational period (35.99+/-4.63 vs. 38.09+/-3.70, P=0.02), lower birth weight (2.60+/-0.94 vs. 3.02+/-0.64, P=0.02), and earlier onset of encephalomalacia (2.74+/-3.52 vs. 5.60+/-5.96, P=0.01). In comparing the underlying cause of encephalomalacia, the occurrence of epilepsy was lower after cerebrovascular disease (P<0.01), but trended towards a higher incidence after a central nervous system infection (P=0.09). Multifocal encephalomalacic lesions were significantly higher in Group A (P=0.04). CONCLUSION: The risk factors for epilepsy associated with encephalomalacia are early gestational age, low birth weight, early onset of encephalomalacia, and multifocal encephalomalacic lesions. It may be necessary for clinicians to search for these risk factors, and make a particularly close observation on these patients.

Intrahepatic cholangiocarcinoma and encephalomalacia in a budgerigar [Melopsittacus undulatus]

Encephalomalacia is softening or loss of brain tissue following cerebral infarction; cerebral ischemia infection, craniocerebraltrauma or other injuries. Cholangiocarcinomas are malignant neoplasms of biliary epithelium, which usually arise from the intrahepatic ducts. A budgerigar was presented with a history of ataxia, decreased activity, neck weakness and weight loss. Supportive care was attempted, but the bird did not improve and euthanasia was elected. At necropsy, the liver was pale and large. There were two symmetrical pale areas on the cortical surface of cerebrum. Representative specimens from all tissues were fixed in 10% buffered formalin, embedded in paraffin and stained with hematoxylin and eosin [HE]. In gray matter of cerebral tissue, there were small clear vacuoles of varied size that formed in the cytoplasm of neuron cell bodies. Proliferation of capillaries was seen. The fluid-filled clear spaces were in the white matter especially in peduncles. There were a few thromboses in the vessels and neuronal necrosis of cerebrum. Neoplastic tissue was limited to the liver. There were numerous epithelial lined ducts with an associated dense fibrous stroma. Cholangiocarcinoma and encephalomalacia were confirmed based on the macroscopic and microscopic evidences. It seems that chronic exposure to a mycotoxin and vitamin E deficiency are probable causes of encephalpmalacia and cholangiocarcinoma in this bird

A case of tacrolimus-induced encephalopathy after kidney transplantation / 소아과

We present a case of tacrolimus-induced encephalopathy after successful kidney transplantation. An 11-year-old girl presented with sudden onset of neurologic symptoms, hypertension, and psychiatric symptoms, with normal kidney function, after kidney transplantation. The symptoms improved after cessation of tacrolimus. Magnetic resonance imaging (MRI) showed acute infarction of the middle cerebral artery (MCA) territory in the right frontal lobe. Three days later, she had normal mental function and maintained normal blood pressure with left hemiparesis. Follow-up MRI was performed on D19, showing new infarct lesions at both cerebral hemispheres. Ten days later, MRI showed further improvement, but brain single photon emission computed tomography (SPECT) showed mild reduction of uptake in both the anterior cingulate gyrus and the left thalamus. One month after onset of symptoms, angiography showed complete resolution of stenosis. However, presenting as a mild fine motor disability of both hands and mild dysarthria, what had been atrophy at both centrum semiovale at 4 months now showed progression to encephalomalacia. There are two points of interest in this case. First, encephalopathy occurred after administration of tacrolimus and improved after discontinuation of the drug. Second, the development of right-side hemiplegia could not be explained by conventional MRI; but through diffusion tensor imaging (DTI) and diffusion tensor tractography (DTT) of white matter tract, visualization was possible.

Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul / Outbreak of polioencephalomalacia in cattle consuming high sulphur diet in Rio Grande do Sul, Brazil

Neste trabalho descreve-se surto de polioencefalomalacia em bovinos decorrente da ingestão de dieta com excessiva concentração de enxofre em uma propriedade no Rio Grande do Sul. O lote era composto por 30 bezerros, mantidos em um piquete com azevém (Lolium multiflorum) e suplementados com ração e sal mineral. Seis bezerros morreram e dois deles foram necropsiados; amostras de tecido hepático para dosagem de chumbo e fragmentos do sistema nervoso central para histopatológico foram colhidos. Um dos bezerros foi examinado antes da morte e sinais neurológicos encefálicos foram constatados. Foi estabelecido o teor de enxofre nos componentes da dieta e água, a produção de sulfeto de hidrogênio ruminal em cinco bovinos do mesmo lote e realizada PCR de um bloco de parafina para detecção de DNA do herpevirus bovino tipo 5. O consumo total de enxofre foi de 0,38 por cento da matéria seca fornecida aos animais e as dosagens de sulfeto de hidrogênio ruminal em animais do mesmo lote variaram de 1.000 a 2.500ppm. Os achados histopatológicos indicaram necrose laminar do córtex cerebral. Não foi detectado chumbo na amostra de tecido hepático e não foi identificado DNA do herpesvirus bovino tipo 5 no encéfalo. O quadro clínico de síndrome cerebrocortical associado aos elevados valores do sulfeto de hidrogênio ruminal, alta ingestão de enxofre na dieta e os achados histopatológicos permitem estabelecer o excesso de enxofre como causador da polioencefalomalacia.

An outbreak of polioencephalomalacia in cattle caused by ingestion of high sulphur diet, in Rio Grande do Sul, Brazil is described. One group of 30 calves was kept in Italian ryegrass (Lolium multiflorum) pasture and supplemented with concentrate and minerals. Six calves died, necropsy was performed in two of them and liver samples (for lead determination) and fragments of central nervous system were collected. Clinical and neurological examination was performed in one calf and confirmed brain involvement. Sulphur content on dietary components and water, ruminal hydrogen sulfide production in five calves of the same group and PCR from formalin-fixed paraffin-embedded cerebral tissues to detect bovine herpesvirus 5 DNA was perfomed. The total sulphur intake was 0.38 percent dry matter and the values of ruminal sulfide concentration ranged from 1,000 to 2,500ppm. Lead It was not detected in the liver samples and PCR was negative for bovine herpesvirus 5. The brain lesions were characterized by laminar neuronal necrosis. The clinical signs of cerebrocortical syndrome associated with high ruminal sulfide values, elevated intake of dietary sulphur and histological lesions confirmed that the excess of sulphur caused the polioencephalomacia in these calves.

Polioencefalomalacia experimental induzida por amprólio em bovinos / Experimentally amprolium-induced polio-encephalomalacia in cattle

Para estabelecer um modelo experimental para o estudo da etiologia, patologia e patogênese da polioencefalomalacia (PEM) em bovinos, a condição foi induzida em quatro novilhos pela administração oral de amprólio nas doses diárias de 500 e 350mg/kg de peso vivo, respectivamente por 22 e 26-28 dias. Todos os bovinos morreram espontaneamente ou foram eutanasiados in extremis após um curso clínico de 4-7 dias. Três bovinos que receberam 1.000mg/kg de amprólio e dois que receberam 500mg/kg morreram espontaneamente com quadro clínico agudo a subagudo sem desenvolverem sinais e lesões de PEM. Nos novilhos que PEM foi reproduzida, os sinais neurológicos incluíram marcada apatia, incoordenação, posição de cavalete, quedas ocasionais, hiperexcitabilidade, tremores musculares, cegueira, bruxismo, estrabismo, nistagmo, midríase, opistótono, decúbito lateral e movimentos de pedalagem. Os principais achados de necropsia eram restritos ao encéfalo e consistiam de tumefação, achatamento, amolecimento e amarelamento das circunvoluções cerebrais. Histologicamente, havia necrose neuronal segmentar e laminar (neurônios vermelhos) associada a edema, tumefação endotelial, separação das lâminas de neurônios do córtex telencefálico ou entre as substâncias cinzenta e branca e infiltração moderada a acentuada de macrófagos espumosos. Essas alterações eram mais acentuadas nos lobos telencefálicos frontal, parietal e occipital. Adicionalmente, lesões similares e moderadas foram detectadas no mesencéfalo e hipocampo. A necrose neuronal e o edema afetaram uniformemente as camadas de neurônios da substância cinzenta dos lobos telencefálicos frontal, parietal e occipital. Esse modelo experimental de PEM com administração oral de amprólio parece ser útil para o estudo da doença em bovinos, conforme observado anteriormente em ovinos.

In order to establish an experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia (PEM) in cattle, the condition was induced into four steers by oral administration of amprolium at daily doses of 500 and 350mg per kg of body weight respectively for 22 and 26-28 days. All steers died spontaneously or were euthanized in extremis after being sick for 4-7 days. Three steers that received the drug at 1,000mg/kg and two that received 500mg/kg died spontaneously with acute or subacute clinical signs and without lesions and signs of PEM. In those steers in which PEM was reproduced, the neurological signs included marked apathy, incoordination, sawhorse stance, occasional falls, hyperexcitability, muscle tremors, blindness, grinding of teeth, strabismus, nystagmus, mydriasis, opisthotonus, and lateral recumbency with paddling movements. Main gross lesions were restricted to the brain and included swelling, flattening, softening and yellow discoloration of the cerebral circumvolutions. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, cleavage of laminar neuronal layers or between gray and white matter and moderate to severe infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telencephalic lobes. Additionally, similar and moderate lesions were detected in the midbrain and hippocampus. Neuronal necrosis and edema affected uniformly the neurons layers of the grey matter of the frontal, parietal and occipital lobes. This experimental model of PEM with oral administration of amprolium may be useful for the study in cattle, as previously observed in sheep.

Focal symmetrical encephalomalacia in sheep / Encefalomalacia focal simétrica em ovino

Focal symmetrical encephalomalacia (FSE) is the most prominent lesion seen in the chronic form of enterotoxemia by Clostridium perfringens type D. This paper reports FSE in sheep in Brazil. Six deaths occurred within a seven days period in a flock of 70, four to 30-month-old Santa Inês sheep in the state of Paraíba in the Brazilian semiarid. The flock was grazing a paddock of irrigated sprouting Cynodon dactylon (Tifton grass), and supplemented, ad libitum, with a concentrate of soybean, corn and wheat. Nervous signs included blindness and recumbence. A 19 month-old sheep was examined clinically and necropsied after a clinical course of three days. Gross lesions were herniation of the cerebellar vermis and multifocal, bilateral, symmetric brownish areas in the internal capsule, thalamus and cerebellar peduncles. Histologic lesions were multifocal, bilateral malacia with some neutrophils, swelling of blood vessels endothelium, perivascular edema, and hemorrhages. The flock was vaccinated, before the outbreak, with only one dose of Clostridium perfringens type D vaccine. Two factors are suggested to be important for the occurrence of the disease: insufficient immunity due to the incorrect vaccination; and high nutritional levels by the supplementation with highly fermentable carbohydrates.

Encefalomalacia focal simétrica (EFS) é a lesão mais proeminente vista nas formas subaguda ou crônica da enterotoxemia por Clostridium perfringens tipo D. Este trabalho relata EFS em ovinos no semiárido do estado da Paraíba. Seis ovinos morreram, em um período de sete dias, dentro de um rebanho de 70 animais, da raça Santa Inês, entre 4-30 meses de idade, que pastavam em piquete de Cynodon dactylon (capim Tifton), que estava rebrotando. Os ovinos eram suplementados com um concentrado de soja, trigo e milho. Os sinais nervosos incluíam cegueira e decúbito lateral. Um ovino de 19 meses de idade foi examinado clinicamente e necropsiado, depois de um curso clínico de 3 dias. Macroscopicamente foram observadas herniação do cerebelo e áreas acastanhadas, multifocais, simétricas e bilaterais na cápsula interna, tálamo e pedúnculo cerebelar. Histologicamente observou-se malacia, bilateral e simétrica, com alguns neutrófilos, tumefação das células endoteliais dos vasos sanguíneos, edema perivascular e hemorragia. O rebanho foi vacinado, antes do surto, com umaúnica dose de vacina para Clostridium perfringens tipo D. Dois fatores são sugestivos quanto a importância da ocorrência da enfermidade: imunidade insuficiente devida à vacinação incorreta; e altos níveis nutricionais da suplementação com carboidratos altamente fermentáveis.

Experimental sulfur toxicosis in sheep II- pathologic evaluation of neural and extraneural lesions

Two equal groups, 3 of each, of adult female Balady sheep [8-9 months old] were fed a balanced diet with or without elemental sulfur [0.8% in diet] up to the appearance of neurologic signs including coma and animals were going to die [days 25, 26 and 28 of the experiments for the three intoxicated sheep, respectively]. Brain lesions were typical of polioencephalomalacia primarily of the neocortex and to less extent the cerebellar grey matter. The nonneural lesions included constant severe, diffuse periportal necrosis with centrilobular degeneration, pulmonary edema complicated into serofibrinous pneumonia because of germ invaders, nephrotoxic tubulonecrosis with tubular casts, cardiomyocyte degeneration and segmental necrosis as well as lymphocytic cell depletion of spleen white pulps. Both the gastrointestinal tract and skeletal muscles had no lesions. It could be concluded that the noticeable hepatic lesions may augment the toxic effect of dietary sulfur because of impairment of the hepatic detoxification system to the liberated toxic sulfide ions in the rumen

Experimental sulfur toxicosis in sheep I- the prophylactic potential of thiamine

Nine adult female Balady sheep [8-9 months old] were divided into 3 equal groups. Gp.1 was fed on a balanced diet containing 0.8% elemental sulfur, Gp.2 was fed on the same diet with 0.8% sulfur plus 0.025% pure thiamine, and Gp.3 was a control. Feeding on these diets continued until the appearance of neurologic signs which only appeared in GP.1 and started as anorexia and ended up with coma. Three animals from Gp.1 were dying on days 25, 26 and 28 of the experiment. Brain lesions of Gp.1 animals were typical of polioencephalomalacia [PEM] Primarily of the cerebral and to some extent of cerebellar cortices; however, similar lesions were restricted only to the cerebral grey matter in animals of Gp.2 despite absences of any signs of illness. The extraneural lesions were noticed in animals of Gps. 1 and 2 and included periportal necrosis, serofibrinous pneumonia, renal tubulonecrosis, myocardial segmental necrosis and lymphocytic cell depletion of the splenic corpuscles. It was evident that simultaneous supplementation of thiamine [0.025%] with excess sulfur [0.8%] only prevented the appearance of clinical signs associated with PEM despite the occurrence of the classic cerebral lesions. Also, the neural lesions were confined only to the cerebrum; however, the cerebellum was normal. Moreover, administration of thiamine did not prevent the appearance of extraneural lesions

Polioencefalomalacia em bovinos: epidemiologia, sinais clínicos e distribuição das lesões no encéfalo / Bovine polioencephalomalacia: epidemiology, clinical signs and distribution of lesions in the brain

Trinta e um casos de polioencefalomalacia (PEM) diagnosticados de 1999-2008 em bovinos do Sul (13 casos) e Centro-Oeste (18 casos) brasileiros foram estudados. As taxas de morbidade (0,04 por cento-6,66 por cento), mortalidade (0,04 por cento-6,66 por cento) e letalidade (50 por cento-100 por cento) foram semelhantes em ambas as regiões estudadas. Não houve uma associação clara entre os casos de PEM e a idade, sexo dos bovinos e sazonalidade. Os casos ocorreram principalmente em bovinos criados de forma extensiva em pastagem. Na Região Sul a doença afetou principalmente bovinos jovens (um ano de idade ou menos), enquanto que principalmente bovinos mais velhos (3 anos de idade ou mais) foram afetados no Centro-Oeste. Os sinais clínicos mais frequentemente observados incluíram cegueira, incoordenação, andar em círculos, opistótono, decúbito e movimentos de pedalagem. A evolução do quadro clínico variou de 12 horas a 8 dias (media 3 dias e meio). Em 11 encéfalos não foram observadas alterações macroscópicas; as principais alterações macroscópicas nos outros casos incluíam congestão com tumefação e achatamento das circunvoluções, amolecimento e amarelamento do córtex telencefálico, focos de hemorragia no tronco encefálico, cerebelo e telencéfalo e herniação cerebelar. As principais alterações histológicas ocorreram no córtex dos lobos telencefálicos occipital, parietal e frontal; no entanto, lesões menos acentuadas e menos frequentemente observadas ocorreram no hipocampo, núcleos da base, tálamo, mesencéfalo e cerebelo. O tipo de lesão microscópica cortical era consistente em todos os casos e incluía necrose neuronal (neurônio vermelho) laminar segmentar, espongiose, tumefação do núcleo das células endoteliais, astrócitos Alzheimer tipo II e infiltração por células gitter. Em 20 por cento dos casos havia um leve infiltrado celular linfo-histiocitário e em 13 por cento dos casos havia leve infiltrado de neutrófilos e eosinófilos. Adicionalmente, ...

Thirty one cases of polioencephalomalacia (PEM) diagnosed from 1999-2008 in cattle from the Southern (13 cases) and Midwestern (18 cases) Brazil were studied. Morbidity (0.04 percent-6.66 percent), mortality (0.04 percent-6.66 percent), and lethality (50 percent-100 percent) rates were similar in both regions studied. There was no clear association between PEM cases and age, sex or seasonality. Cases occurred mainly in cattle raised at pasture; in the Southern the disease affected mainly young cattle (one-year old or less) while mainly older cattle (three-year-old or older) were affected in the Midwest. Clinical signs more frequently observed included blindness, incoordination, circling, opisthotonus, recumbence and peddling movements. Clinical course varied from 12 hours to 8 days (average three days and a half). In 11 cases no gross changes were observed in the brain. Main gross findings in the brain of remaining cases included congestion with swelling and flattening of gyri, softening and yellow discoloration of cerebral cortex, hemorrhagic foci in the brain stem, cerebellum and telencephalon, and cerebellar herniation. The main histopathological changes were in the cortex of occipital, parietal and frontal telencephalic lobes; however less prominent and less frequently found lesions occurred in the hippocampus, basal nuclei, thalamus, midbrain, and cerebellum. The type of microscopic cortical lesions was consistent in all cases and included segmentar laminar neuronal necrosis (red neurons), spongiosis, swollen of vascular endothelial nuclei, Alzheimer type II astrocytes and infiltration of gitter cells. In 20 percent of the cases there was mild lymphohistiocytic cellular infiltrate and in 13 percent of the cases there was mild infiltrate by neutrophils and eosinophils. Additionally, mild to moderate necro-hemorrhagic lesions were observed in 49 percent of the cases in the basal nuclei, in 39 percent of the cases in brain stem and...

Severe Symptomatic Vasospasm following Intraventricular Hemorrhage from Arteriovenous Fistula

The authors present a rare case of severe vasospasm following the rupture of arteriovenous fistula. On initial CT scan, hematoma in the corpus callosum and left inferior frontal region with surrounding cerebromalacia and all ventricles without apparent subarachnoid hemorrhage were seen. Angiograms showed arterivenous fistula but did not show cerebral vasospasm. Thirteen days after admission the neurological state of patient suddenly deteriorated and bilateral motor weaknesses developed. Following angiograms revealed severe narrowing on the supraclinoid portion of bilateral internal carotid arteries, bilateral anterior cerebral arteries and bilateral middle cerebral arteries. Transluminal angioplasty and intra-arterial papaverine infusion were performed. The patient remained stable with moderate neurologic deficits.

A case of ventriculitis caused by Vancomycin-Resistant Enterococcus durans / 대한내과학회지

Infections associated with Enterococcus durans have been rare in humans until now. E. durans is a frequent component of the intestinal flora of several domestic animal species and may cause septicemia and encephalomalacia in chicks. We report a case of ventriculoperitoneal shunt infection caused by vancomycin-resistant E. durans in a 17-year-old woman with Dandy-walker syndrome. To the best of our knowledge, this is the first human case of ventriculitis caused by vancomycin-resistant E. durans.

A case of ventriculitis caused by Vancomycin-Resistant Enterococcus durans / 대한내과학회지

Infections associated with Enterococcus durans have been rare in humans until now. E. durans is a frequent component of the intestinal flora of several domestic animal species and may cause septicemia and encephalomalacia in chicks. We report a case of ventriculoperitoneal shunt infection caused by vancomycin-resistant E. durans in a 17-year-old woman with Dandy-walker syndrome. To the best of our knowledge, this is the first human case of ventriculitis caused by vancomycin-resistant E. durans.

Usefulness of Magnetic Resonance Imaging after Serial Cranial Ultrasound in the Neonates Graduating Neonatal Intensive Care Unit

PURPOSE: To evaluate usefulness of MR imaging after serial brain US in the high-risk neonates before discharge of the neonatal intensive care unit. MATERIALS AND METHODS: Retrospective comparison of 412 US and 121 MR scans in 121 neonates and young infants were performed. Grading of germinal matrix /intraventricular hemorrhage (GMH/IVH) was performed and presence of intracranial hemorrhage other than GMH/IVH and parenchyma lesions was also analyzed. RESULTS: Among the 242 lateral ventricles, Seven GMH and 46 IVH were additionally detected by MRI. On the other hand, 30 GMH were only detected by US. US demonstrated Grade 1/2/3/4 GMH/IVH in 24/8/13/0 ventricles each, while each grades were identified in 3, 49, 10, 2 ventricles on MR images. Other intracranial lesions additionally detected on MR images were cerebral hemorrhage (n=4), cerebellar hemorrhage (n=4), extraaxial hemorrhage (n=8), diffuse excessive signal change of the white matter (n=72), non-cavitary lesion (n=4), encephalomalacia (n=2), and ventriculomegaly (n=5). CONCLUSION: MR imaging could be an excellent complimentary study after serial brain US for additional detection of the intracranial pathology, particularly IVH and white matter lesions, though US would be better in follow-up of GMH in some neonates.