Lesões traumáticas do lobo temporal: indicações cirúrgicas baseadas na tomografia computadorizada

BACKGROUND: The indication for surgical treatment of post-traumatic parenchymal lesions in the temporal lobe remains controversial. OBJECTIVE: We reviewd the tomographic parameters that might be useful in making surgical decisions. METHOD: The tomographic findings of 69 patients were analyzed in a retrospective manner considering: 1) the effects of the lesion (classified into 4 variables: midline shift, status of the cisterns, status of the ventricles, and status of the peripheral sulci); and 2) the characteristics of the lesion: anterior, posterior or anteroposterior location (as defined by a coronal plane tangent to the cerebral peduncles) and its mediolateral diameter. RESULTS: When none or only one of the aforementioned variables was found to be altered, conservative treatment was instituted (22 out of 38 lesions). In two cases, all four variables were altered, and surgery was performed in both. Anterior, anteroposterior and posterior lesions measuring 21, 23 and 28 mm in diameter, respectively, had a 50% chance of surgical removal. CONCLUSION: Amongst the patients who underwent surgical intervention, the more anterior the location of the temporal lobe lesion, the smaller the diameter.INTRODUÇÃO: A indicação do tratamento cirúrgico das lesões parenquimatosas temporais de origem traumática é controversa. Analisaram-se os parâmetros tomográficos que poderiam ser úteis nesta decisão terapêutica. MÉTODO: Os achados tomográficos de 69 patientes foram analisados retrospectivamente em relação a: 1) efeitos das lesões (classificados em 4 variáveis: desvio de estruturas medianas, estado das cisternas, dos ventrículos e dos sulcos periféricos); e 2) características das lesões: localização anterior, posterior ou ântero-posterior (definida por um plano coronal tangente aos pedúnculos cerebrais) e diâmetro médio-lateral. RESULTADOS: Quando nenhuma ou uma das variáveis acima mencionadas foi encontrada alterada, foi instituído o tratamento conservador (22 em 38 lesões). Em dois casos, as quatro variáveis estavam alteradas, sendo instituído o tratamento cirúrgico. Lesões anteriores, ântero-posteriores e posteriores medindo 21, 23 e 28 mm, respectivamente, tiveram 50% de chance de serem removidas. CONCLUSÃO: Nos casos operados, quanto mais anterior a lesão esteve no lobo temporal, menor foi seu diâmetro.FHEMIG Hospital João XXIIIUniversidade Federal de São Paulo (UNIFESP), Escola Paulista de Medicina (EPM)UNIFESP, EPMSciEL

Assessment of the Benefit of Intraoperative Cortical Stimulation in Patients with Lesions within Eloquent Brain Regions

Objective The present study sought to evaluate the benefits of intraoperative cortical stimulation (CS) for reducing morbidity in neurosurgery

Chemical and cytological analysis of cerebral spinal fluid after intrathecal injection of hypodense fluorescein

ABSTRACT INTRODUCTION: Intrathecal fluorescein has been effective for topographic diagnosis of rhinoliquorrhea. Nonetheless, there are no reports on the study of cerebral spinal fluid (CSF) after use of intrathecal fluorescein. OBJECTIVE: A prospective study attempting to evaluate CSF through chemical and cytological analysis, after injection of fluorescein. METHODS: Prospective analysis of 24 samples of CSF after intrathecal injection of fluorescein for topographic diagnosis of CSF fistulae, collected at the time of puncture and after 24 and 48 h, divided by cellularity: Group 1, up to five cells, and Group 2, with more than five cells. RESULTS: The yellow-greenish color of CSF remained after 48 h in 36%, evidencing permanence of fluorescein. No changes in protein and glucose levels were observed between 0-24 h and 0-48 h. In group 2, an increase in cell count was observed between 24 h and 48 h (p = 0.019). In both groups, there was an increase of neutrophils between 0 and 48 h (p = 0.048) and a decrease between 24 and 48 h (p = 0.05). CONCLUSION: Intrathecal fluorescein provoked discreet meningeal reactions, such as an increase of cells between 24 and 48 h and an increase of neutrophils at 24 h, with a subsequent decrease at 48 h with no correlation with symptomatology

Extensa falha cutânea e craniana em paciente com aplasia cutis congenita Large scalp and skull defect in patient with aplasia cutis congenita

Aplasia cutis congenita (ACC) é doença rara, caracterizada pela ausência de formação completa da pele. Geralmente ocorre no couro cabeludo, na linha mediana, e apresenta-se ao nascimento como uma ferida ulcerada que pode atingir diferentes profundidades e envolver o periósteo, crânio e dura-máter. Descrevemos o caso de menina recem-nascida que apresentava fácies dismórfica com defeito no couro cabeludo que abrangia a quase totalidade da abóbada craniana e apresentava falha óssea desde a base dos ossos frontais até os occipitais e mastóides. A dura-máter estava em sua maior parte exposta, sem sinais de fissuras. Devido à raridade da ACC e ao pequeno número de pacientes nas séries publicadas na literatura a padronização do tratamento ainda é incipiente. O que existem são recomendações. Ainda são necessários estudos que abordem desde a etiologia da doença até a avaliação dos métodos de tratamento e evolução de grupos maiores de pacientes.<br>Aplasia cutis congenita is a rare condition characterized by the absence of skin layers. It is most common on the scalp, middle line, and it can be seen as a congenital ulcer involving periosteum, skull and dura. We present the case of a female newborn infant with a dysmorphic facies, a large scalp and skull defect exposing the dura. There was no cerebrospinal fluid leakage. The rarity of cases with large defects and small series reported make difficult to determinate the ideal treatment for aplasia cutis congenita. More studies are necessary to define the etiology and best management of this patients

A novel complex neurological phenotype due to a homozygous mutation in FDX2

Defects in iron–sulphur [Fe-S] cluster biogenesis are increasingly recognized as causing neurological disease. Mutations in a number of genes that encode proteins involved in mitochondrial [Fe-S] protein assembly lead to complex neurological phenotypes. One class of proteins essential in the early cluster assembly are ferredoxins. FDX2 is ubiquitously expressed and is essential in the de novo formation of [2Fe-2S] clusters in humans. We describe and genetically define a novel complex neurological syndrome identified in two Brazilian families, with a novel homozygous mutation in FDX2. Patients were clinically evaluated, underwent MRI, nerve conduction studies, EMG and muscle biopsy. To define the genetic aetiology, a combination of homozygosity mapping and whole exome sequencing was performed. We identified six patients from two apparently unrelated families with autosomal recessive inheritance of a complex neurological phenotype involving optic atrophy and nystagmus developing by age 3, followed by myopathy and recurrent episodes of cramps, myalgia and muscle weakness in the first or second decade of life. Sensory-motor axonal neuropathy led to progressive distal weakness. MRI disclosed a reversible or partially reversible leukoencephalopathy. Muscle biopsy demonstrated an unusual pattern of regional succinate dehydrogenase and cytochrome c oxidase deficiency with iron accumulation. The phenotype was mapped in both families to the same homozygous missense mutation in FDX2 (c.431C 4 T, p.P144L). The deleterious effect of the mutation was validated by real-time reverse transcription polymerase chain reaction and western blot analysis, which demonstrated normal expression of FDX2 mRNA but severely reduced expression of FDX2 protein in muscle tissue. This study describes a novel complex neurological phenotype with unusual MRI and muscle biopsy features, conclusively mapped to a mutation in FDX2, which encodes a ubiquitously expressed mitochondrial ferredoxin essential for early [Fe-S] cluster biogenesis