Encefalomalacia nutricional por hipovitaminose E em Gallus gallus domesticus / Nutritional encephalomalacia by hypovitaminosis E in Gallus gallus domesticus

A encefalomalácia nutricional é um distúrbio metabólico caracterizado por sinais clínicos neurológicos e sua etiologia é atribuída à hipovitaminose E. Atinge frangos jovens acarretando altos prejuízos aos criadores e agroindústrias pela sua alta morbidade e mortalidade. O objetivo do presente estudo foi relatar as alterações macroscópicas e histopatológicas de um caso de encefalomalácia nutricional. Um frango de corte com quatro semanas de vida, foi encaminhado ao Laboratório de Patologia Animal da Universidade Federal de Rondônia. Ao exame físico apresentou escore corporal 1 e sinais neurológicos como, ataxia, andar em círculos, lateralização da cabeça, prostração e hiperestesia, caracterizada por espasmos corporais iniciados após estímulos como sons altos e toque físico. Após eutanásia, realizou-se exame necroscópico e exame histopatológico. Para isto, foram coletados fragmentos de órgãos e fixados em formalina tamponada a 10%. No exame necroscópico constatou-se necrose coliquativa no encéfalo, o qual apresentou-se extremamente friável, com coloração pálida. Na análise histopatológica foram observadas alterações como vacuolização citoplasmática, degeneração de células de Purkinje e malácia focal extensa na substância cinzenta cortical e da substância branca do cerebelo. Pela história clínica e as observações necroscópicas e histopatológicas, o caso foi diagnosticado como encefalomalácia nutricional por hipovitaminose E.(AU)

Nutritional encephalomalacia is a metabolic disorder characterized by clinical neurological signs and its etiology is attributed to hypovitaminosis E. It affects young chickens causing high losses to breeders and agroindustries due to their high morbidity and mortality. The aim of the present study was to report macroscopic and histopathological changes in a case of nutritional encephalomalacia. A young chicken with four weeks of life conducted to the Animal Pathology Laboratory of Federal University of Rondônia. Physical examination showed poor body score and neurological signs, such as ataxia, circling, head lateralization, prostration and hypersensitivity, characterized by body spasms initiated after stimuli such as loud sounds and physical touch. After euthanasia, necroscopic examination was performed, organ fragments were collected and fixed in 10% buffered formalin. Necroscopic examination revealed collictive necrosis in the brain, which was extremely friable, with a pale color. In histopathological analysis, changes such as cytoplasmic vacuolization, Purkinje cell degeneration and extensive focal malacia in the cortical gray matter and white matter of the cerebellum were observed. From the clinical history and necroscopic and histopathological observations, the case was diagnosed as nutritional encephalomalacia by hypovitaminosis E.(AU)

Encefalomalacia nutricional por hipovitaminose E em Gallus gallus domesticus / Nutritional encephalomalacia by hypovitaminosis E in Gallus gallus domesticus

A encefalomalácia nutricional é um distúrbio metabólico caracterizado por sinais clínicos neurológicos e sua etiologia é atribuída à hipovitaminose E. Atinge frangos jovens acarretando altos prejuízos aos criadores e agroindústrias pela sua alta morbidade e mortalidade. O objetivo do presente estudo foi relatar as alterações macroscópicas e histopatológicas de um caso de encefalomalácia nutricional. Um frango de corte com quatro semanas de vida, foi encaminhado ao Laboratório de Patologia Animal da Universidade Federal de Rondônia. Ao exame físico apresentou escore corporal 1 e sinais neurológicos como, ataxia, andar em círculos, lateralização da cabeça, prostração e hiperestesia, caracterizada por espasmos corporais iniciados após estímulos como sons altos e toque físico. Após eutanásia, realizou-se exame necroscópico e exame histopatológico. Para isto, foram coletados fragmentos de órgãos e fixados em formalina tamponada a 10%. No exame necroscópico constatou-se necrose coliquativa no encéfalo, o qual apresentou-se extremamente friável, com coloração pálida. Na análise histopatológica foram observadas alterações como vacuolização citoplasmática, degeneração de células de Purkinje e malácia focal extensa na substância cinzenta cortical e da substância branca do cerebelo. Pela história clínica e as observações necroscópicas e histopatológicas, o caso foi diagnosticado como encefalomalácia nutricional por hipovitaminose E.

Nutritional encephalomalacia is a metabolic disorder characterized by clinical neurological signs and its etiology is attributed to hypovitaminosis E. It affects young chickens causing high losses to breeders and agroindustries due to their high morbidity and mortality. The aim of the present study was to report macroscopic and histopathological changes in a case of nutritional encephalomalacia. A young chicken with four weeks of life conducted to the Animal Pathology Laboratory of Federal University of Rondônia. Physical examination showed poor body score and neurological signs, such as ataxia, circling, head lateralization, prostration and hypersensitivity, characterized by body spasms initiated after stimuli such as loud sounds and physical touch. After euthanasia, necroscopic examination was performed, organ fragments were collected and fixed in 10% buffered formalin. Necroscopic examination revealed collictive necrosis in the brain, which was extremely friable, with a pale color. In histopathological analysis, changes such as cytoplasmic vacuolization, Purkinje cell degeneration and extensive focal malacia in the cortical gray matter and white matter of the cerebellum were observed. From the clinical history and necroscopic and histopathological observations, the case was diagnosed as nutritional encephalomalacia by hypovitaminosis E.

Early destructive lesions in the developing brain: clinical and electrographic correlates.

OBJECTIVE: Early brain insults can cause cavitary lesions including porencephaly (POR) and multicystic encephalopathy (MCE). The objective of this study was to investigate clinical and electrographic correlates associated to these types of destructive brain lesions. METHOD: Patients with POR and MCE were selected and submitted to clinical and Video-EEG monitoring. The following variables were analyzed: demographic data, type of lesion, presence of gliosis, perinatal complications, epilepsy, brain atrophy, and presence and frequency of epileptiform discharges. RESULTS: Twenty patients were included, 65% males, 35% females, ages ranging from 1 to 40 years, 14 with MCE and 6 with POR. Eighteen patients had hemiparesis, 19 had epilepsy (current or in the past), seven of them had refractory seizures, and 16 had epileptiform discharges. All patients with MCE had gliosis while only 2 with POR had it. CONCLUSIONS: No correlation was observed between type of lesion and clinical and electrographical outcome. However, a positive correlation was observed between frequency of discharges and presence of brain atrophy, and between MCE and gliosis.

Early destructive lesions in the developing brain: clinical and electrographic correlates

OBJECTIVE: Early brain insults can cause cavitary lesions including porencephaly (POR) and multicystic encephalopathy (MCE). The objective of this study was to investigate clinical and electrographic correlates associated to these types of destructive brain lesions. METHOD: Patients with POR and MCE were selected and submitted to clinical and Video-EEG monitoring. The following variables were analyzed: demographic data, type of lesion, presence of gliosis, perinatal complications, epilepsy, brain atrophy, and presence and frequency of epileptiform discharges. RESULTS: Twenty patients were included, 65 percent males, 35 percent females, ages ranging from 1 to 40 years, 14 with MCE and 6 with POR. Eighteen patients had hemiparesis, 19 had epilepsy (current or in the past), seven of them had refractory seizures, and 16 had epileptiform discharges. All patients with MCE had gliosis while only 2 with POR had it. CONCLUSIONS: No correlation was observed between type of lesion and clinical and electrographical outcome. However, a positive correlation was observed between frequency of discharges and presence of brain atrophy, and between MCE and gliosis.

OBJETIVO: Insultos cerebrais precoces podem causar lesões cavitárias incluindo porencefalias (POR) e encefalomalacias multicisticas (EMC). O objetivo deste estudo foi investigar correlatos clínicos e eletrográficos associados a estes dois tipos de lesões destrutivas. MÉTODO: Pacientes com POR e EMC foram selecionados e submetidos à avaliação neurológica e monitorização vídeo-eletrencefalográfica, analisando-se as seguintes variáveis: dados demográficos, tipo de lesão, presença de gliose, complicações perinatais, epilepsia, atrofia cerebral, presença e freqüência de descargas epilépticas. RESULTADO: Vinte pacientes foram incluídos, sendo 65 por cento do sexo masculino, 35 por cento do feminino, idades entre 1 e 40 anos, sendo 14 com EMC e 6 com POR. Dezoito pacientes tinham hemiparesia, 19 tinham ou tiveram epilepsia (7 deles refratários ao tratamento medicamentoso) e 16 deles tinham paroxismos epileptiformes. Todos com MCE tinham gliose associada, contra apenas 2 dos pacientes com POR. CONCLUSÃO: Não houve correlação entre tipo de lesão e evolução clínica e eletrográfica. Houve, entretando, correlação positiva entre freqüência de descargas epilépticas e presença de atrofia cerebral, e entre lesão do tipo EMC e presença de gliose.