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M Castañeda

Publications and source records attributed to M Castañeda.

40 records · Page 3Linked to original sources
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[Diagnosis of mesial temporal sclerosis with magnetic resonance imaging].

INTRODUCTION: Mesial temporal sclerosis (MTS) is a progressive drug-resistant epileptic syndrome which requires rapid, effective diagnosis and treatment. Histologically there is atrophy and gliosis of the hippocampus. OBJECTIVE: To establish magnetic resonance (MR) imaging guidelines for correct diagnosis. PATIENTS AND METHODS: We made a prospective study of 78 patients with drug-resistant temporal lobe epilepsy (44 women and 34 men; age 6-66 years, mean 31 years). Using a magnet of 1.5 Teslas paracoronal sections were made of the hippocampus with T1 volumetric with inversion-recovery, FLAIR (fluid-attenuated inversion-recovery) and T2 relaxometry. A control group of 30 healthy volunteers was established. The reduction in volume and hippocampal T2 hyperintensity were considered to be MTS diagnosed on MR. RESULTS: No hippocampal differences were observed among the healthy volunteers. The confidence intervals (mean +/- 1.96 SD) were: right volume: 4.169-5.911 mm3; left volume: 4.097-5.940 mm3; time of T2 relaxation: 98-113 ms. MTS was observed in 42 patients (54%): 24 left, 14 right and four asymmetrical bilateral. The results of the diagnostic validity (sensitivity/specificity) were: T1 volumetric 91/92%, FLAIR 93.5/98% and T2 relaxometry 91/92%. There was atrophy of other extrahippocampal structures in five cases of MTS; 10 patients with MTS (23.5%) had another extrahippocampal lesion associated (dual pathology), particularly migration disorders; 21 patients (27%) had lesions without MTS (tumors, alterations of migration, nonspecific gliosis) and in 15 cases (19%) there were no abnormal findings. A total of 27 patients were operated on: 22 with MTS (21 had diagnostic MR, one case had no abnormal findings), four cases had tumors and one had cortical dysplasia. CONCLUSION: The combination of quantitative techniques (T1 volumetric with inversion-recovery and T2 relaxometry) and FLAIR optimize MTS diagnosis using MR.

Adolescent↗
PubMedDate not supplied

[Vascular hereditary dementia CADASIL type in Colombia. III. Linkage analysis to notch3 gene].

OBJECTIVE: To perform linkage analysis between the Short Tandem Repeats (STR) microsatellite markers D19S923, D19S929, D19S22, which are in strong genetic linkage to Notch3 gene in order to contrast the hypothesis that the vascular hereditary dementia phenotype described in a multigenerational extended pedigree from Colombia correspond to CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy). Even we know that using techniques as the Single Strand Conformational Polymorphisms (SSCP) could determine mutations in Notch3, the rationality of this approach is that intronic variations could not be defined and that we are interested in determine if some forms of the clinical presentation and its phenotypic variability make part of CADASIL. INTRODUCTION: The CADASIL phenotype is caused by mutations in the Notch3 gene. Clinical features of CADASIL are: 1. Recurrent cerebra-vascular episodes; 2. Migraine history; 3. History of transitory ischemic attack and, 4. Behavior changes and dementia. MATERIAL AND METHODS: By using SIMLINK we showed that the extended genealogy had the enough power to detect significant LOD (logarithm of oods) score values when Notch3 was considered the disorder cause. Linkage analysis was carried out by using parametric and non parametrical methods. The Elston-Stewart general method was used as the parametrical analysis and the sib pair method as the non-parametrical one. We perform simulations changing the affection status codification by including as affected or not including those individuals with migraine. Furthermore, in order to detect the stability of the results, we changed the penetrance values, the genetic frequencies on both, the marker loci and the affection locus. RESULTS: The maximum pair-wise LOD score was 2.04 which was detected at the marker D19S23 with q= 0.11cM. This distance correspond exactly with the Notch3 location. That is 100 times more probable that there is linkage that there is not. In other words this probability could be explained as if the phenotype correspond to CADASIL than to other vascular dementia. The non parametric results were compatibles with the parametric ones. When the migraine symptom was considered as a part of the affected status, the LOD score values showed not linkage. CONCLUSIONS: The results of the linkage analysis to these STR microsatellite markers suggest that the vascular hereditary dementia phenotype described in this family correspond to CADASIL caused by a polymorphism on the Notch3 gene. On the contrary, these same results suggest that the migraine phenotype is not a part of the progressive dementia.

CADASIL↗