Ultrastructural alterations of choroid plexuses of lateral ventricles of rats (rattus norvegicus) submitted to experimental chronic alcoholism

Adult male rats (Wistar lineage) were alcoholized with sugar cane liquor diluted at 30° GL during 300 days and sacrificed every 60 days in 5 stages. Samples of choroid plexuses of lateral ventricles were collected and examined at transmission electronic microscope to detect possible ultrastructural alterations and to raise possible pathological correlations. Gradual changes were observed in these animals during all the experiment: dilatation and enlargement of cisternae of Golgi complex, dilatation of RER, presence of digestive vacuoles and a large amount of pinocytic vesicles as well as vesicles with electronlucent content throughout cytoplasm, as well as an enlargement of intercellular space between basolateral interdigitation of the cells and of the connective tissue. The changes observed in the epithelium and connective tissue of choroid plexuses specially in 240 and 300 days of treatment are presumably due to a disturbance in hydroelectrolitic homeostasis, contributing to several morpho-functional disturbs of central nervous system. No changes were observed in the control group animals.

Lateral ventricle differences between first-episode schizophrenia and first-episode psychotic bipolar disorder: A population-based morphometric MRI study

Objectives. The extent to which psychotic disorders fall into distinct diagnostic categories or can be regarded as lying on a single continuum is controversial. We compared lateral ventricle volumes between a large sample of patients with first-episode schizophrenia or bipolar disorder and a healthy control group from the same neighbourhood. Methods. Population-based MRI study with 88 first-episode psychosis (FEP) patients, grouped into those with schizophrenia/schizophreniform disorder (N = 62), bipolar disorder (N = 26) and 94 controls. Results. Right and left lateral ventricular and right temporal horn volumes were larger in FEP subjects than controls. Within the FEP sample, post-hoc tests revealed larger left lateral ventricles and larger right and left temporal horns in schizophrenia subjects relative to controls, while there was no difference between patients with bipolar disorder and controls. None of the findings was attributable to effects of antipsychotics. Conclusions. This large-sample population-based MRI study showed that neuroanatomical abnormalities in subjects with schizophrenia relative to controls from the same neighbourhood are evident at the first episode of illness, but are not detectable in bipolar disorder patients. These data are consistent with a model of psychosis in which early brain insults of neurodevelopmental origin are more relevant to schizophrenia than to bipolar disorder.

A segmentation-based and partial-volume-compensated method for an accurate measurement of lateral ventricular volumes on T-1-weighted magnetic resonance images

Lateral ventricular volumes based on segmented brain MR images can be significantly underestimated if partial volume effects are not considered. This is because a group of voxels in the neighborhood of lateral ventricles is often mis-classified as gray matter voxels due to partial volume effects. This group of voxels is actually a mixture of ventricular cerebro-spinal fluid and the white matter and therefore, a portion of it should be included as part of the lateral ventricular structure. In this note, we describe an automated method for the measurement of lateral ventricular volumes on segmented brain MR images. Image segmentation was carried in combination of intensity correction and thresholding. The method is featured with a procedure for addressing mis-classified voxels in the surrounding of lateral ventricles. A detailed analysis showed that lateral ventricular volumes could be underestimated by 10 to 30% depending upon the size of the lateral ventricular structure, if mis-classified voxels were not included. Validation of the method was done through comparison with the averaged manually traced volumes. Finally, the merit of the method is demonstrated in the evaluation of the rate of lateral ventricular enlargement. (C) 2001 Elsevier Science Inc. All rights reserved.

Developmental vitamin D deficiency alters adult behaviour: An informative animal model of schizophrenia

Background: There is growing evidence that vitamin D is active in the brain but until recently there was a lack of evidence about its role during brain development. Guided by certain features of the epidemiology of schizophrenia, we have explored the role of vitamin D in the developing brain and behaviour using whole animal models. Methods: Sprague-Dawley rats were fed a vitamin D deficient diet (DVD) or control diet 6 weeks prior to mating and housed under UVB-free lighting conditions. On the day of birth all rats were fed a control diet for the remainder of the study. We observed behaviour at two timepoints; on the day of birth to study maternal behaviour, and at 10 weeks of age to study offspring behaviour in adulthood, under baseline and drug induced conditions (MK-801, haloperidol, amphetamine). Results: Prenatal vitamin D deficiency results in subtle alterations in maternal behaviour as well as long lasting effects on the adult offspring, despite a return to normal vitamin D levels during postnatal life. These affects were specific to transient prenatal vitamin D depletion as adult vitamin D depletion, combined prenatal and chronic postnatal vitamin D depletion, or ablation of the vitamin D receptor in mice led to markedly different outcomes. Conclusions: The developmental vitamin D (DVD) model now draws strength from epidemiological evidence of schizophrenia and animal experiments. Although the DVD model does not replicate every aspect of schizophrenia, it has several attractive features: (1) the exposure is based on clues from epidemiology; (2) it reproduces the increase in lateral ventricles; (3) it reproduces well-regarded behavioural phenotypes associated with schizophrenia (e.g. MK- 801 induced hyperlocomotion); and (4) it implicates a disturbance in dopamine signaling. In summary, low prenatal levels of vitamin D can influence critical components of orderly brain development and that this has a long lasting effect on behaviour.

Early pattern recognition in severe perinatal asphyxia: a prospective MRI study.

On the basis of MRI examinations in 88 neonates and infants with perinatal asphyxia, we defined 6 different patterns on T2-weighted images: pattern A--scattered hyperintensity of both hemispheres of the telencephalon with blurred border zones between cortex and white matter, indicating diffuse brain injury; pattern B--parasagittal hyperintensity extending into the corona radiata, corresponding to the watershed zones; pattern C--hyper- and hypointense lesions in thalamus and basal ganglia, which relate to haemorrhagic necrosis or iron deposition in these areas; pattern D--periventricular hyperintensity, mainly along the lateral ventricles, i.e. periventricular leukomalacia (PVL), originating from the matrix zone; pattern E--small multifocal lesions varying from hyper--to hypointense, interpreted as necrosis and haemorrhage; pattern F--periventricular centrifugal hypointense stripes in the centrum semiovale and deep white matter of the frontal and occipital lobes. Contrast was effectively inverted on T1-weighted images. Patterns A, B and C were found in 17%, 25% and 37% of patients, and patterns D, E and F in 19%, 17% and 35%, respectively. In 49 patients a combination of patterns was observed, but 30% of the initial images were normal. At follow-up, persistent abnormalities were seen in all children with patterns A and D, but in only 52% of those with pattern C. Myelination was retarded most often in patients with diffuse brain injury and PVL (patterns A and D).

Redox dysregulation in schizophrenia : effect on myelination of cortical structures and connectivity

Cette thèse traite du rôle qu'un facteur de risque génétique développé chez les patients souffrant de schizophrénie, à savoir un déficit de la synthèse du glutathion, peut jouer dans les anomalies de la connectivité cérébrale trouvées chez ces patients. L'essentiel du travail a été consacré à évaluer la structure de la substance blanche dans l'ensemble du cerveau chez un modèle animal par une méthode similaire à celle utilisée en recherche clinique avec l'imagerie par résonance magnétique (IRM). Cette approche de translation inverse chez la souris knock-out de glutamate-cystéine ligase modulateur sous-unité (Gclm KO), avait l'objectif d'étudier l'effet des défenses redox déficientes sur le développement des connexions cérébrales, tout en excluant celui des facteurs non liés au génotype. Après avoir établi le protocole de recherche, l'influence d'une manipulation environnementale a également été étudiée. Pour effectuer une analyse statistique fiable des données d'IRM obtenues, nous .avons d'abord créé un atlas du cerveau de la souris afin de l'utiliser comme modèle pour une segmentation précise des différentes régions du cerveau sur les images IRM obtenues in vivo. Les données provenant de chaque région d'intérêt ont ensuite été étudiées séparément. La qualité de cette méthode a été évaluée dans une expérience de simulation pour déduire la puissance statistique réalisable dans chaque région en fonction du nombre d'animaux utilisés. Ces outils d'analyse nous ont permis d'évaluer l'intégrité de la substance blanche dans le cerveau des souris durant le développement grâce à une expérience longitudinale, en utilisant l'imagerie du tenseur de diffusion (DTI). Nous avons ainsi observé des anomalies dans les paramètres dérivés du tenseur (diffusivité et anisotropie) dans la Commissure Antérieure et le Fimbria/Fornix des souris Gclm KO, par rapport aux animaux contrôles. Ces résultats suggèrent une substance blanche endommagée dans ces régions. Dans une expérience électrophysiologique, Pascal Steullet a montré que ces anomalies ont des conséquences fonctionnelles caractérisées par une réduction de la vitesse de conduction dans les fibres nerveuses. Ces données renforcent les conclusions des analyses d'imagerie. Le mécanisme par lequel une dérégulation redox affecte la structure de la substance blanche reste encore à définir, car une analyse immunohistochimique des protéines constituantes de la couche de myéline des fibres concernées n'a pas donné de résultats concluants. Nous avons également constaté un élargissement des ventricules dans les jeunes souris Gclm KO, mais pas chez les adultes et des anomalies neurochimiques déjà connues chez ces animaux (Duarte et al. 2011), à savoir une réduction du Glutathion et une augmentation de l'acide N-acétylaspartique, de l'Alanine et du ratio Glutamine/Glutamate. Nous avons ensuite testé l'effet d'un stress environnemental supplémentaire, l'élevage en isolement social, sur le phénotype. Ce stress n'a eu aucun effet sur la structure de la substance blanche évaluée par DTI, mais a réduit la concentration de myo-Inositol et augmenté le ratio de Glutamine/Glutamate dans le cortex frontal. Nous avons aussi reproduit dans ce groupe indépendant d'animaux les effets du génotype sur le profil neurochimique, sur la taille des ventricules et aussi sur les paramètres dérivés du tenseur de diffusion dans le Fimbria/Fornix, mais pas dans la Commissure Antérieure. Nos résultats montrent qu'une dérégulation redox d'origine génétique perturbe la structure et la fonction de la substance blanche dans des régions spécifiques, causant ainsi l'élargissement des ventricules. Ces phénotypes rassemblent certaines caractéristiques neuro-anatomiques de la schizophrénie, mais les mécanismes qui en sont responsables demeurent encore inconnus. L'isolement social n'a pas d'effet sur la structure de la substance blanche évaluée par DTI, alors qu'il est prouvé qu'il affecte la maturation des oligodendrocytes. La neurochimie corticale et en particulier le rapport Glutamine/Glutamate a été affecté par le dérèglement redox ainsi que par l'isolement social. En conséquence, ce ratio représente un indice prometteur dans la recherche sur l'interaction du stress environnemental avec le déséquilibre redox dans le domaine de la schizophrénie. -- The present doctoral thesis is concerned with the role that a genetic risk factor for the development of schizophrenia, namely a deficit in Glutathione synthesis, may play in the anomalies of brain connectivity found in patients. Most of the effort was devoted to perform a whole-brain assessment of white matter structure in the Glutamate-Cysteine ligase modulatory knockout mouse model (Gclm KO) using Magnetic Resonance Imaging (MRI) techniques similar to those used in state-of-the-art clinical research. Such reverse translational approach taking brain imaging from the bedside to the bench aimed to investigate the role that deficient redox defenses may play in the development of brain connections while excluding all influencing factors beside the genotype. After establishing the protocol, the influence of further environmental manipulations was also studied. Analysis of MRI images acquired in vivo was one of the main challenges of the project. Our strategy consisted in creating an atlas of the mouse brain to use as segmentation guide and then analyze the data from each region of interest separately. The quality of the method was assessed in a simulation experiment by calculating the statistical power achievable in each brain region at different sample sizes. This analysis tool enabled us to assess white matter integrity in the mouse brain along development in a longitudinal experiment using Diffusion Tensor Imaging (DTI). We discovered anomalies in diffusivity parameters derived from the tensor in the Anterior Commissure and Fimbria/Fornix of Gclm KO mice when compared to wild-type animals, which suggest that the structure of these tracts is compromised in the KO mice. In an elegant electrophysiological experiment, Pascal Steullet has provided evidence that these anomalies have functional consequences in form of reduced conduction velocity in the concerned tracts, thus supporting the DTI findings. The mechanism by which redox dysregulation affects WM structure remains unknown, for the immunohistochemical analysis of myelin constituent proteins in the concerned tracts produced inconclusive results. Our experiments also detected an enlargement of the lateral ventricles in young but not adult Gclm KO mice and confirmed neurochemical anomalies already known to affect this animals (Duarte et al. 2011), namely a reduction in Glutathione and an increase in Glutamine/Glutamate ratio, N-acetylaspartate and Alanine. Using the same methods, we tested the effect of an additional environmental stress on the observed phenotype: rearing in social isolation had no effect on white matter structure as assessed by DTI, but it reduced the concentration of myo-Inositol and increased the Glutamine/Glutamate ratio in the frontal cortex. We could also replicate in this separate group of animals the effects of genotype on the frontal neurochemical profile, ventricular size and diffusivity parameters in the Fimbria/Fornix but not in the Anterior Commissure. Our data show that a redox dysregulation of genetic origin may disrupt white matter structure and function in specific tracts and cause a ventricular enlargement, phenotypes that resemble some neuroanatomical features of schizophrenia. The mechanism responsible remains however unknown. We have also demonstrated that environmental stress in form of social isolation does not affect white matter structure as assessed by DTI even though it is known to affect oligodendrocyte maturation. Cortical neurochemistry, and specifically the Glutamine to Glutamate balance was affected both by redox dysregulation and social isolation, and is thus a good target for further research on the interaction of redox imbalance and environmental stress in schizophrenia.

Apolipoprotein E and Recovery from Traumatic Brain Injury

The outcome from traumatic brain injury (TBI) is variable and only partly explained by known prognostic factors. This is especially true for predicting long-term outcome. Genetic factors may influence the brain`s susceptibility to injury or capacity for repair and regeneration. To examine the association of apolipoproteinE (apoE) genotype with long-term outcome, hippocampal volumes and general brain atrophy, we determined the apoE genotype from 61 TBI patients who had been injured over on average 31 years earlier. The long-term outcome was evaluated with repeated neuropsychological testing and by applying various measures of everyday functioning and quality of life. Magnetic resonance imaging (MRI) based volumetric analyses of the hippocampus and lateral ventricles were performed. In the prospective study, the purpose was to examine the association between apoE genotype and visibility of traumatic brain lesions during the first year after TBI and the ability of apoE genotype, the Glasgow Coma Score (GCS), MRI findings and duration of posttraumatic amnesia (PTA) to predict the one-year outcome. Thirty-three patients with TBI were studied and the outcome was evaluated with the Head Injury Symptom Checklist (HISC) and the Glasgow Outcome Scale extended version (GOS-E) scores one year after the injury. MRI and apoE genotyping were carried out. After three decades, neither hippocampal nor lateral ventricle volumes differed significantly in those patients with the apoE ε4 allele vs those without this allele, but the TBI patients with the apoE ε4 allele showed significantly poorer general cognitive level than those without this allele. This decline was wholly accounted for by a subgroup of patients who had developed incident or clinical dementia. In the prospective study the apoE genotype was not associated with visible MRI changes or outcome. The duration of PTA and acute MRI were the best predictors of one-year outcome in TBI. A portion of the TBI patients with the apoE ε4 allele seem to be at risk of long-term cognitive decline. This association may involve mechanisms other than those responsible for the development of brain atrophy. The early MRI and PTA have an important role in assessing the injury severity and prognosis.

Cognitive Functions After Traumatic Brain Injury. A 30-year Follow-up Study

Many cognitive deficits after TBI (traumatic brain injury) are well known, such as memory and concentration problems, as well as reduced information-processing speed. What happens to patients and cognitive functioning after immediate recovery is poorly known. Cognitive functioning is flexible and may be influenced by genetic, psychological and environmental factors decades after TBI. The general aim of this thesis was to describe the long-term cognitive course after TBI, to find variables that may contribute to it, and how the cognitive functions after TBI are associated with specific medical factors and reduced survival. The original study group consisted of 192 patients with TBI who were originally assessed with the Mild Deterioration Battery (MDB) on average two years after the injury, during the years 1966 – 1972. During a 30-year follow-up, we studied the risks for reduced survival, and the mortality of the patients was compared with the general population using the Standardized Mortality Ratio (SMR). Sixty-one patients were re-assessed during 1998-2000. These patients were evaluated with the MDB, computerized testing, and with various other neuropsychological methods for attention and executive functions. Apolipoprotein-E (ApoE) genotyping and magnetic resonance imaging (MRI) based on volumetric analysis of the hippocampus and lateral ventricles were performed. Depressive symptoms were evaluated with the short form of the Beck depression inventory. The cognitive performance at follow-up was compared with a control group that was similar to the study group in regard to age and education. The cognitive outcome of the patients with TBI varied after three decades. The majority of the patients showed a decline in their cognitive level, the rest either improved or stayed at the same level. Male gender and higher age at injury were significant risk factors for the decline. Whereas most cognitive domains declined during the follow-up, semantic memory behaved in the opposite way, showing recovery after TBI. In the follow-up assessment, the memory decline and impairments in the set-shifting domain of executive functions were associated with MRI-volumetric measures, whereas reduction in information-processing speed was not associated with the MRI measures. The presence of local contusions was only weakly associated with cognitive functions. Only few cognitive methods for attention were capable of discriminating TBI patients with and without depressive symptoms. On the other hand, most complex attentional tests were sensitive enough to discriminate TBI patients (non-depressive) from controls. This means that complex attention functions, mediated by the frontal lobes, are relatively independent of depressive symptoms post-TBI. The presence of ApoE4 was associated with different kinds of memory processes including verbal and visual episodic memory, semantic memory and verbal working memory, depending on the length of time since TBI. Many other cognitive processes were not affected by the presence of ApoE4. Age at injury and poor vocational outcome were independent risk factors for reduced survival in the multivariate analysis. Late mortality was higher among younger subjects (age < 40 years at death) compared with the general population which should be borne in mind when assessing the need for rehabilitation services and long-term follow-up after TBI.

The origin of cortical neurons

Neurons of the mammalian cerebral cortex comprise two broad classes: pyramidal neurons, which project to distant targets, and the inhibitory nonpyramidal cells, the cortical interneurons. Pyramidal neurons are generated in the germinal ventricular zone, which lines the lateral ventricles, and migrate along the processes of radial glial cells to their positions in the developing cortex in an `inside-out' sequence. The GABA-containing nonpyramidal cells originate for the most part in the ganglionic eminence, the primordium of the basal ganglia in the ventral telencephalon. These cells follow tangential migratory routes to enter the cortex and are in close association with the corticofugal axonal system. Once they enter the cortex, they move towards the ventricular zone, possibly to obtain positional information, before they migrate radially in the direction of the pial surface to take up their positions in the developing cortex. The mechanisms that guide interneurons throughout these long and complex migratory routes are currently under investigation.

Molecular mechanisms underlying deficient neurogenesis in Alzheimer’s disease

La neurogenèse est présente, dans le cerveau adulte, dans la zone sous-ventriculaire (ZSV) encadrant les ventricules latéraux et dans le gyrus dentelé (GD) de l’hippocampe, permettant l’apprentissage, la mémoire et la fonction olfactive. Ces micro-environnements possèdent des signaux contrôlant l’auto-renouvellement des cellules souches neurales (CSN), leur prolifération, leur destin et leur différenciation. Or, lors du vieillissement, les capacités régénératives et homéostatiques et la neurogenèse déclinent. Les patients atteints de la maladie d’Alzheimer (MA), comme le modèle animal reproduisant cette maladie (3xTg-AD), montrent une accélération des phénotypes liés au vieillissement dont une diminution de la neurogenèse. Notre hypothèse est que la découverte des mécanismes affectant la neurogenèse, lors du vieillissement et de la MA, pourrait fournir de nouvelles cibles thérapeutiques pour prévenir le déclin cognitif. Les études sur l’âge d’apparition et les mécanismes altérant la neurogenèse dans la MA sont contrastées et nous ont guidé vers deux études. L’examen des changements dans les étapes de la neurogenèse lors du vieillissement et du développement de la neuropathologie. Nous avons étudié la ZSV, les bulbes olfactifs et le GD de souris femelles de 11 et 18 mois, et l’apparition des deux pathologies associées à la MA : les plaques amyloïdes et les enchevêtrements neurofibrillaires. Nous avons découvert que les souris 3xTg-AD possèdent moins de cellules en prolifération, de progéniteurs et de neuroblastes, induisant une diminution de l’intégration de nouvelles cellules dans le GD et les bulbes olfactifs. Notons que le taux de neurogenèse chez ces souris de 11 mois est similaire à celui des souris de phénotype sauvage de 18 mois, indiquant une accélération des changements liés au vieillissement dans la MA. Dans la ZSV, nous avons aussi démontré une accumulation de gouttelettes lipidiques, suggérant des changements dans l’organisation et le métabolisme de la niche. Enfin, nous avons démontré que le déficit de la neurogenèse apparait lors des premières étapes de la MA, avant l’apparition des plaques amyloïdes et des enchevêtrements neurofibrillaires. A l’examen des mécanismes inhibant la neurogenèse lors de la MA, nous voyons que chez des souris de 5 mois, le déficit de la neurogenèse dans la ZSV et le GD est corrélé avec l’accumulation de lipides, qui coïncide avec l’apparition du déclin cognitif. Nous avons aussi découvert que dans le cerveau humain de patients atteints de la MA et dans les 3xTg-AD, des gouttelettes lipidiques s’accumulaient dans les cellules épendymaires, représentant le principal soutien des CSN de la niche. Ces lipides sont des triglycérides enrichis en acide oléique qui proviennent de la niche et pas d’une défaillance du système périphérique. De plus, l’infusion locale d’acide oléique chez des souris de phénotype sauvage permet de reproduire l’accumulation de triglycérides dans les cellules épendymaires, comme dans la MA. Ces gouttelettes induisent un dérèglement de la voie de signalisation Akt-FoxO3 dans les CSN, menant à l’inhibition de leur activation in vitro et in vivo. Ces résultats permettent une meilleure compréhension de la régulation de la neurogenèse par le métabolisme lipidique. Nous avons démontré un nouveau mécanisme par lequel l’accumulation des lipides dans la ZSV induit une inhibition des capacités de prolifération et de régénération des CSN lors de la MA. Les travaux futurs permettront de comprendre comment et pourquoi le métabolisme lipidique du cerveau est altéré dans la MA, ce qui pourrait offrir de nouvelles voies thérapeutiques pour la prévention et la régénération.

Cistos subependimários diagnosticados pelo ultra-som transfontanelar

Objetivos: avaliar a evolução ultra-sonográfica de cistos subependimários (CSE) do ângulo externo dos ventrículos laterais, e a evolução clínica dos pacientes. Comparar os pacientes com CSE isolados e os com CSE associados a outras lesões. Métodos: foram diagnosticados um a vários cistos no ângulo externo de um ou de ambos os ventrículos laterais, por meio de ultra-som transfontanelar (US) de rotina, realizado nos primeiros dias de vida, caracterizando os CSE. Durante o período de 1981-2000, 66 recém-nascidos tiveram CSE evidenciados na UTI neonatal do Hospital de Port-Royal. Foram constituídos dois grupos: G-I, com CSE isolados (n=21), e G-II, com CSE associados a outras lesões (n=45). Resultados: os recém-nascidos do GI apresentaram maior maturidade, melhores condições de nascimento e menor morbidade respiratória em relação a GII. A incidência de malformações congênitas foi elevada em ambos os grupos. Houve baixa taxa de infecção bacteriana e ausência de infecção congênita. Os CSE foram uni ou bilaterais, únicos ou múltiplos (colar de pérolas), sem diferença entre os grupos estudados, e predominaram à esquerda. US seriados foram realizados em 49/66 pacientes (74%), mostrando aumento no tamanho do cisto em 21/49 (45%), no primeiro mês de vida, enquanto 12 CSE (24%) desapareceram. O óbito ocorreu em dez recém-nascidos com lesões neurológica graves (quatro leucomalácias periventriculares, cinco hemorragias peri e intraventriculares), e somente um com hérnia diafragmática não apresentava outras lesões ao US transfontanelar. Conclusões: as características dos CSE não diferiram quando esses estavam associados a outras lesões. O nítido predomínio no lado esquerdo sugere uma etiologia vascular. Foi encontrada uma alta taxa de malformações associadas, alertando para a possibilidade de uma etiologia malformativa. Ambas hipóteses sugerem um desvio de desenvolvimento, e não de uma fetopatia viral.

Trigone ventricular meningiomas surgical approaches

Objective: Report our experience with trigone ventricular meningiomas and review the surgical approaches to the trigone. Method: From 1989 to 2006, six patients with meningiomas of the trigone of the lateral ventricles underwent microsurgical resection. Their clinical features, image, follow up, and surgical approaches were retrospectively analyzed. Results: Five patients presented with large and one with small volume meningioma. Unspecific symptoms occurred in three patients; intracranial hypertension detected in three patients; homonymous hemianopsy in three; and motor deficit present in one patient. Three patients were operated by transparietal transcortical approach, two by middle temporal gyrus approach, and one by parieto-occipital interhemispheric precuneus approach. Total resection was achieved in all patients without additional deficits. Conclusion: Judicious preoperative plan, adequate knowledge of anatomy, and use of correct microsurgical techniques are fundamental in achieving complete resection of trigone meningioma with low morbidity.

Fourth ventricle computed tomography indexes: standardisation and characteristics in neurocysticercosis

OBJETIVOS: propor padrão de normalidade das dimensões do IVventrículo e estudar suas características em neurocisticercose. MÉTODO: em um grupo controle (GC) constituído de 114 indivíduos com tomografias normais e em outro grupo composto de 80 doentes com neurocisticercose (GN), mediram-se a distância fronto-polar de ventrículos laterais (FP) e os diâmetros craniano interno (Cr), ântero-posterior (AP) e látero-lateral (LL) do IVº ventrículo para a padronização de seis índices. RESULTADOS: AP/Cr, AP/LL e AP/FP foram os índices mais discriminatórios e apresentaram, em GC, valores médios de 0,063, 0,267 e 0,582, respectivamente. em GN os valores foram estatisticamente superiores a GC. Selecionaram-se 51 doentes do GN com índice> ou =2 desvios-padrão da média em GC. Neles, AP/Ll foi> ou =1 em 95% doentes com derivação liquórica e em 88% com depressão, ocorrendo em 73% com evolução satisfatória e todos que faleceram. CONCLUSÃO: AP/Cr, AP/LL e, principalmente, AP/FP são representativos das dimensões do IVventrículo.

Cisto coloide no terceiro ventrículo e morte súbita em jovem

Morte súbita de jovem, sexo masculino, 23 anos, assintomático, suscitou verificação de óbito. Antes queixou-se de cefaleia excruciante, em sala de aula, caindo sobre o computador. Encéfalo apresentou edema e congestão vascular. Sem herniações. Cortes coronais evidenciaram dilatação dos ventrículos laterais e nódulo aderido ao teto do terceiro ventrículo. À microscopia o diagnóstico foi cisto coloide do terceiro ventrículo. A ameaça de morte súbita em portadores de cisto coloide é sério problema diagnóstico na emergência médica. A relevância deste caso está em lembrar aos médicos que esta entidade deve permanecer como diagnóstico diferencial nas cefaleias em crianças, adolescentes e adultos jovens.