Prevalence of MRI abnormalities in people with epilepsy in rural China.

OBJECTIVE: To assess the prevalence of brain MRI abnormalities in people with epilepsy in rural China and to compare it with that of individuals in the United Kingdom. METHODS: Brain MRI scans were obtained in people with epilepsy who participated in a rural community-based program in China between July 2010 and December 2012. Individual epileptogenic lesion types were reviewed and their associations with seizure control examined. The MRI findings were compared with 2 previous similar studies in the United Kingdom. RESULTS: Among the 597 individuals (58% male, median age 38 years) with MRI scans analyzed, 488 (82%) had active epilepsy. The MRI was abnormal in 389 individuals (65%), with potentially epileptogenic lesion in 224 (38%) and nonspecific abnormalities in 165 (28%), and 108 (18%) were potentially resectable. The potentially epileptogenic lesions were less frequently detected in children (<18 years old, 12 of 68, 18%) than in adults (212 of 529, 40%; p < 0.001). In people with potentially epileptogenic lesions, 67% (150 of 224) had failed ≥2 antiseizure medications. They had higher risk of uncontrolled epilepsy than those with normal MRI (risk ratio [RR] 1.25; p < 0.001) and those with nonspecific abnormality (RR 1.15; p = 0.002) after adjustment for age and sex. The diagnostic yield of MRI was similar to that reported in community- and hospital-based studies in the United Kingdom. CONCLUSIONS: More than one-third of people with chronic epilepsy in rural China have potentially epileptogenic lesions identifiable on brain MRI, with two-thirds fulfilling the definition of pharmacoresistance. These findings highlight the magnitude of the unmet needs for epilepsy surgery in China.

Bovine diseases causing neurological signs and death in Mexican feedlots.

The number of large feedlot operations, similar to that of USA and Canada, has notably increased in Mexico in the last three decades. Clinical and laboratory diagnoses of neurological diseases in feedlot cattle are crucial in Mexico and Central America because of the high incidence of bovine paralytic rabies (BPR). Because of its zoonotic potential, BPR must be promptly diagnosed and differentiated from other bovine neurological diseases such as thrombotic meningoencephalitis (TME), polioencephalomalacia (PEM) and botulism. More recently, BPR and botulism have been diagnosed with increasing frequency in Mexican feedlots. Neither BPR nor botulism has relevant gross lesions, thus post-mortem diagnosis without laboratory support is impossible. Herein, we describe five outbreaks of neurological diseases in Mexican feedlots in which BPR, botulism and PEM were diagnosed either independently or in combination. A diagram illustrating the most conspicuous pathologic findings and ancillary laboratory test required to confirm the diagnoses of these neurological diseases in feedlot cattle is proposed.

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.

Sulfur-associated polioencephalomalacia in cattle grazing plants in the Family Brassicaceae.

Polioencephalomalacia was diagnosed histologically in cattle from two herds on the Darling Downs, Queensland, during July-August 2007. In the first incident, 8 of 20 18-month-old Aberdeen Angus steers died while grazing pastures comprising 60%Sisymbrium irio (London rocket) and 40%Capsella bursapastoris (shepherd's purse). In the second incident, 2 of 150 mixed-breed adult cattle died, and another was successfully treated with thiamine, while grazing a pasture comprising almost 100%Raphanus raphanistrum (wild radish). Affected cattle were either found dead or comatose or were seen apparently blind and head-pressing in some cases. For both incidents, plant and water assays were used to calculate the total dietary sulfur content in dry matter as 0.62% and 1.01% respectively, both exceeding the recommended 0.5% for cattle eating more than 40% forage. Blood and tissue assays for lead were negative in both cases. No access to thiaminase, concentrated sodium ion or extrinsic hydrogen sulfide sources were identified in either incident. Below-median late summer and autumn rainfall followed by above-median unseasonal winter rainfall promoted weed growth at the expense of wholesome pasture species before these incidents.

A review of some of the health issues of captive black rhinoceroses (Diceros bicornis).

In captivity, black rhinoceroses (Diceros bicornis) are beset by many disease syndromes not described in black rhinoceroses in the wild. Hemolytic anemia, hepatopathy, and ulcerative dermatopathy that lead to increased morbidity and mortality characterize these syndromes. It is uncertain whether these are separate disease syndromes with different etiologies or the same disease with different manifestations. This article offers a brief review of some of the health issues of concern for the captive black rhinoceros population and proposes some possible avenues of research for consideration.

Meningoencefalite e encefalomalacia por Herpesvírus bovino-5: distribuição das lesões no sistema nervoso central de bovinos naturalmente infectados / Bovine herpesvirus type-5 meningoencephalitis and malacia: histological lesions distribution in the central nervous system of naturally infected cattle

Para determinar a distribuição das lesões histológicas que ocorrem no sistema nervoso central (SNC) de bovinos naturalmente infectados por herpesvírus bovino-5 (BHV-5) foram estudados 12 bovinos provenientes de 10 surtos da enfermidade diagnosticados pelo Laboratório Regional de Diagnóstico (LRD) da Faculdade de Veterinária da UFPel, entre 1986 e 2003. A epidemiologia, história clínica e evolução da enfermidade foram obtidas dos arquivos do LRD. Cortes do SNC foram realizados nos materiais conservados em formalina 10 por cento, abrangendo as regiões frontal, parietal, temporal e occipital do córtex telencefálico, cápsula interna e núcleos da base, tálamo, colículo rostral, ponte, pedúnculos cerebelares, cerebelo, bulbo na altura do óbex e medula cervical. As secções foram processadas rotineiramente e coradas por hematoxilina e eosina. Foram avaliadas a distribuição e intensidade das lesões inflamatórias e de malacia, que foram relacionadas com os aspectos epidemiológicos e clínicos da doença. Surtos da enfermidade foram observados em todas as estações ano. Foram afetados bovinos de 2 a 24 meses, de diferentes raças e de ambos os sexos. Macroscopicamente, foram observadas áreas amareladas e deprimidas no córtex telencefálico de cinco bovinos necropsiados. Adicionalmente, essas lesões foram observadas no tálamo, núcleos da base e cápsula interna de dois bovinos. Congestão e hemorragias multifocais foram observadas na maioria dos casos. Em todos os bovinos estudados a lesão histológica caracterizou-se por meningoencefalite não-supurativa observada em todas os cortes, porém mais acentuada no córtex frontal. Areas de malacia focal ou difusa com presença de células "Gitter" foram observadas em todas as regiões do córtex cerebral e nos núcleos da base, cápsula interna e tálamo. Em alguns casos, lesões discretas de malacia foram observadas no colículo rostral, ponte, bulbo, cerebelo e medula cervical. Corpúsculos de inclusão intranucleares foram encontrados em todos os casos estudados nas diferentes regiões do córtex cerebral, preferentemente em áreas que apresentavam lesões inflamatórias e de malacia discretas a moderadas. Em dois casos estes corpúsculos foram observados, também, nos núcleos da base e tálamo. Foi observado que a intensidade das lesões histológicas não é proporcional ao curso clínico da enfermidade. A presença de lesões de malacia em diferentes regiões do SNC, aspecto não mencionado na maioria dos trabalhos anteriores sobre a doença, pode...

[Multicystic encephalomalacia: MR imaging findings and clinical correlation]. / Multikistik ensefalomalazi: MRG bulgulari ve klinik bulgularla korelasyonu.

PURPOSE: To review the MR imaging findings of multicystic encephalomalacia and to investigate the correlation between MR imaging and clinical findings. MATERIALS AND METHODS: Twenty-one patients who presented with convulsion, mental-motor retardation and microcephaly and had evidence of multicystic encephalomalacia on MR images were included in this study. MR imaging patterns and clinical findings were reviewed. Consequently, we correlated MR imaging findings and clinical outcome. RESULTS: All patients had cortical thinning, white matter destruction, atrophy and gliosis. Tetraplegia was seen in 17 out of 19 patients with mixed type cerebral palsy in two patients with diffuse or symmetric involvement on MR imaging. Both of the patients with mixed type cerebral palsy had basal ganglia involvement on MR imaging. Hemiplegia was seen in two patients with asymmetric involvement on MR imaging. Microcephaly was seen in 17 patients with diffuse or symmetrical, and in one patient with asymmetrical, involvement. Microcephaly and tetraplegia was seen in all patients with cerebellar and basal ganglion involvement. CONCLUSION: Microcephaly and spastic tetraplegia were developed mostly in patients with diffuse involvement, whereas hemiplegia was seen in patients with asymmetric involvement. The clinical outcome was worse in patients with cerebellar and brainstem involvement. Therefore, we supposed that the symmetry of lesions and cerebellar or brainstem involvement might be used as a prognostic indicator.

Sulfur-induced polioencephalomalacia in a herd of rotationally grazed beef cattle.

Central nervous system disease occurred in a herd of rotationally grazed beef cattle consuming water containing 3400 ppm sulfate. Clinical signs, pathologic findings, and high water sulfate levels confirmed the diagnosis of sulfur-induced polioencephalomalacia. The incidence of disease reduced when the herd was switched to a low sulfate water source.

Polioencephalomalacia in captive harbour seals (Phoca vitulina).

In a colony of 11 harbour seals (Phoca vitulina Linné 1758) two episodes of central nervous disorders occurred within 2 years causing fatalities in seven adult animals. Clinical signs comprised dyspnoea, anorexia, apathy, incoordination and lateral recumbency. Vitamin B complex therapy was successful once. Pathomorphological examination of seven carcasses revealed acute and subacute malacia of the cerebellar grey matter. Additional acute malacic lesions located in the cerebral cortices and basal ganglia were observed. Mesencephalic nuclei were less severely affected and displayed acute changes. Despite intense search for environmental toxins and infectious agents, the cause of the fatalities remained undetermined. However, the type and pattern of the lesions are most suggestive of a thiamine deficiency.

Effects of dietary sulfur concentrations on the incidence and pathology of polioencephalomalicia in weaned beef calves.

Fourteen heifer calves weighing 174.5+/-17.7 kg were used to evaluate the effects of 3 levels of dietary sulfur. Sodium sulfate added to basal diet made treatments designated moderate (3860 ppm sulfur), moderatey high (5540 ppm sulfur) and high (7010 ppm sulfur). Clinical polioencephalomalacia occurred in all calves assigned to the moderately high and high treatments. The calves did not acclimate to the dietary sulfur as polioencephalomalacia occurred in 4 animals on d 35 and in 1 calf on d 37. Microscopic lesions confirmed polioencephalomalacia in the calves on moderately high and high diets. Microscopic lesions also were present in 4 moderate diet calves although clinical signs were not seen. High dietary sulfur did not limit feed intake. Diets containing sulfur levels >4000 ppm sulfur produced polioencephalomalacia in 10 calves and sub-clinical brain lesions occurred in 4 calves consuming <4000 ppm sulfur.

Occipitoparietal epilepsy, hippocampal atrophy, and congenital developmental abnormalities.

PURPOSE: Diagnostic uncertainty may arise in patients with occipitoparietal epilepsy when there is neuroimaging evidence of a posterior quadrant lesion and coexistent hippocampal abnormalities ("dual pathology"). It is not known whether hippocampal atrophy (HA) in these patients results from seizure propagation to temporolimbic structures or whether it is part of the pathological process underlying the occipitoparietal epilepsy. Clarification of this issue may have a significant bearing on the management of these patients. METHODS: We studied 20 patients with occipitoparietal epilepsy and neuroimaging or pathologic evidence of a congenital developmental abnormality. Normalized hippocampal volumes were obtained in all patients. The medical records and video-EEG recordings were analyzed to correlate the MRI findings with clinical data, seizure semiology, and EEG findings. RESULTS: HA was found in seven patients (35%). Neuroimaging abnormalities concordant with the side of HA were seen in all cases. There was clinical or EEG evidence of temporal spread in 12 patients. There was no correlation between the presence of HA and temporal lobe spread. The only clinical factor associated with HA in this series was a younger age of seizure onset. CONCLUSIONS: HA in patients with occipitoparietal epilepsy due to congenital developmental abnormalities is most likely to be a marker of a more widespread process related to a common pathogenesis during prenatal or perinatal development. HA in these patients is unlikely to be the result of secondary spread from an extrahippocampal focus. Surgical treatment should be tailored toward the primary epileptogenic zone rather the site of seizure spread.

An outbreak of equine leukoencephalomalacia at Oaxaca, Mexico, associated with fumonisin B1.

Equine leukoencephalomalacia (ELEM), swine pulmonary oedema and human oesophageal cancer have been associated with fumonisine B1 (FB1) ingestion. For the first time in this study it is reported that FB1 was identified as being associated with an outbreak of ELEM at Oaxaca, Mexico. Symptoms of ELEM and Equine Venezuelan Encephalitis (EVE) are similar and a different diagnosis is obligatory. In the geographical area (Oaxaca, Mexico) where donkeys died showing a neurological syndrome, 14 corn samples were collected. With the use of TLC (Thin layer chromatography) and HPLC (High performance liquid chromatography) all collected samples resulted positive to FB1. In the area of study, this syndrome was reported to be the cause of death of 100 donkeys, after 3 postmortem examinations in which macroscopic and microscopic cerebral white manner liquefactive necrosis were observed, when FB1 concentration was determined in the samples collected, using HPLC and TLC. It was concluded that HPLC is a highly sensitive method for the detection of FB1 through the formation of an OPA derivative. However, the reverse phase TLC plate and the visualisation of the coloured reaction with the vanillin acidic solution is more objective. FB1 concentration in the studied samples ranged from 0.67 to 13.3 ppm. It was concluded that FB1 was the cause of leukoencephalomalacia reported in donkeys in the state of Oaxaca, Mexico.

Polioencephalomalacia.

Polioencephalomalacia (PEM) is a neuropathologic condition of ruminants that can be induced by a variety of neural metabolic disruptions. These include altered thiamine status, water deprivation-sodium ion toxicosis, lead poisoning, and high sulfur intake. Investigations of sulfur-related PEM have demonstrated that the onset of the clinical signs coincides with excessive ruminal sulfide production. A number of ruminal factors could modulate the production and absorption of ruminal sulfide. The development of a convenient method to estimate ruminal gas cap H2S has made it possible to identify cattle with high levels of ruminal H2S and evaluate their risk of developing PEM.

Application of research findings and summary of research needs: Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle.

Updated research findings with acidosis, feedlot bloat, liver abscesses, and sudden death syndromes were presented at the Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle. Possible industry applications include the need to establish guidelines for use of clostridial vaccines in feedlot cattle, further assessment of the relationship between acidosis and polioencephalomalacia, examination of the effects of various ionophores on the incidence of metabolic disorders, and evaluation of the effects of feed bunk management and limit- and restricted-feeding programs on the incidence of metabolic disorders. A multidisciplinary approach among researchers, consulting nutritionists and veterinarians, and feedlot managers will be required for effective progress in research and in the application of research findings. Areas suggested for further research include 1) assessment of feed consumption patterns and social behavior of cattle in large-pen, feedlot settings; 2) evaluation of the relationship between feed intake management systems (feed bunk management programs, limit- and programmed-feeding) and the incidence of metabolic disorders, including delineation of the role of variability in feed intake in the etiology of such disorders; 3) efforts to improve antemortem and postmortem diagnosis, and to establish standardized regional or national epidemiological databases for various metabolic disorders; 4) ascertaining the accuracy of diagnosis of metabolic disorders and determining the relationship of previous health history of animals to the incidence of metabolic disorders; 5) further defining ruminal and intestinal microbiology as it relates to metabolic disorders and deeper evaluation of metabolic changes that occur with such disorders; 6) continued appraisal of the effects of grain processing and specific feed ingredients and nutrients on metabolic disorders, and development of new feed additives to control or prevent these disorders; and 7) application of biotechnology to develop grain varieties with altered nutrient degradation profiles that decrease the propensity for disastrous acid loads in the rumen, feed-grade enzymes and probiotics that modify nutrient digestion or microbial profiles in the rumen and intestine, and specific strains of ruminal bacteria and protozoa that alter ruminal and metabolic conditions that may precipitate metabolic disorders.

Evaluation of ruminal sulfide concentrations and seasonal outbreaks of polioencephalomalacia in beef cattle in a feedlot.

OBJECTIVES: To measure concentrations of thiamine in blood and sulfide in ruminal fluid in cattle with polioencephalomalacia (PEM) and to evaluate temporal associations between PEM and risk factors. DESIGN: Epidemiologic analysis. SAMPLE POPULATION: 14 steers with acute signs of PEM, 26 clinically normal steers and records of all cattle in a feedlot for the past 6 years. PROCEDURES: Concentrations of thiamine in blood and sulfide in ruminal fluid were measured. Values were compared between healthy steers that had been in the feedlot for 3 weeks or 2 months. Records were used to estimate the incidence of PEM and the time when cattle were at greatest risk of developing PEM. RESULTS: Thiamine concentrations in steers with PEM were within reference ranges. Healthy steers had significantly greater sulfide concentrations 3 weeks after entering the feedlot, when the incidence of PEM was greatest, than 2 months after entering the feedlot, when risk of developing PEM was low. Thiamine concentrations were within reference ranges at these times. Annually recurrent outbreaks of PEM during the summer began after initiating use of a water well containing a high content of sulfate. CLINICAL IMPLICATIONS: Excessive ruminal sulfide production is an important factor in the pathogenesis of PEM, without concurrent thiamine deficiency. Most cases of PEM developed between 15 and 30 days after introduction to a high-sulfur diet. When water is an important source of dietary sulfur, risk of PEM may increase during hot weather.

Neonatal multifocal encephalomalacia and other lesions in the brains of Georgia chicks: 1991-95.

Outbreaks of neonatal multifocal encephalomalacia with sepsis have been reported among flocks of very young chicks in Belgium, Scotland, and the United States. The purposes of the present study were to describe intralesional bacterial cocci in chicks with this type of encephalomalacia and to determine its incidence during 1991-95, and to determine the importance of this lesion with respect to the frequency of all other brain lesions/ diseases during the same time period. All laboratory records of broiler chickens examined at the Georgia Poultry Laboratory from Jan. 1, 1991, through Dec. 31, 1995, where the histopathologic diagnoses included the letter string *encephal* were retrieved for further study. The leading etiology for brain disease was nutritional encephalomalacia (57%), followed by neonatal encephalomalacia (22%), septic meningoencephalitis (16%), and Marek's disease (14%), in turn followed by nonpurulent encephalitis (7%), avian encephalomyelitis (3%), and mycotic meningoencephalitis (3%). Diagnosis of neonatal multifocal encephalomalacia with sepsis in the brains of Georgia chicks is a perennial one. Microscopically, the condition is characterized by mild to maximal multifocal locally extensive fibrin thrombosis of blood capillaries, and necrosis (encephalomalacia, malacia) of surrounding zones of brain stem and/or cerebral hemisphere neuropile. In 44% of cases of neonatal encephalomalacia fibrin thrombosis of blood capillaries was accompanied by intralesional gram-positive coccoid bacteria that were most abundant in medium- and small-sized arterioles or venules. Only gram-positive coccoid bacteria are found in cases of neonatal encephalomalacia (P < 0.05), and only gram-negative rod-shaped bacteria are found in cases of septic meningoencephalitis (P < 0.05). Therefore, bacterial culture and routine light microscopic histopathology are sufficient for diagnosing the condition when the differential diagnosis for neurologic disease in chicks includes neonatal encephalomalacia.

Clinical and pathological aspects of an outbreak of equine leukoencephalomalacia in Spain.

In 1988 an outbreak of leukoencephalomalacia was diagnosed in equids that had eaten corn with a pinkish fungal growth. The fungus was then identified as Fusarium moniliforme. The main symptoms observed appeared acutely and were overexcitement, blindness, incoordination, facial paralysis and death within 24 h. The main pathological changes were restricted to the central nervous system. Macroscopically they consisted of hyperemia and haemorrhages, the consistency was friable and the gyri were somewhat flattened. Microscopically, the lesions were profuse and had extensive haemorrhages, and numerous neurons appeared in different stages of degeneration and necrosis, with satellitosis and neuronophagia. Perivascular cuffs formed by macrophages, plasma cells and lymphocytes were also observed. These lesions were present in both brain and cerebellum, with a marked oedema and massive necrosis of the Purkinje cell layer of the latter.