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Biomedical subjects

F Lopera

Publications and source records attributed to F Lopera.

36 records · Page 2Linked to original sources
PubMedDate not supplied

[Image characterization of Alzheimer's disease associated with the E280A-PS1 mutation. Case-control study: MRI findings].

INTRODUCTION AND METHODS: In order to compare the magnetic resonance image characteristics of individuals belonging to pedigrees carrying the mutation E280A-PS1 associated to early onset Alzheimer disease, coming from Antioquia, Colombia, 78 individuals were studied. 47 of them were carriers of the mutation, 23 of those presented symptoms and 31 individuals being controls (non carriers of the mutation). RESULTS: In summary, significative differences were appreciated between symptomatic individuals and those asymptomatic. There was not significant difference between asymptomatic carriers and the controls. The presence of the perihippocampal fissure constituted a difference statistically significant between the symptomatic individuals and those carriers asymptomatic and between the symptomatic ones and the controls. The interuncal distance increased significantly was another difference between symptomatic and asymptomatic individuals and among symptomatic and control group. The lobar atrophy and the ventriculomegaly were found in symptomatic individuals and they correlate with the disorder graveness. There was not significance in the presence of infarcts and/or hippocampal hyperintensities. CONCLUSION: These results corroborate the statement that magnetic resonance image is very useful in the diagnosis and follow-up of individuals affected by early onset Alzheimer disease.

Age of Onset↗
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[Detection of antibodies to beta-amyloid in carriers of E280A mutation in the presenilin-1 gene].

OBJECTIVE: To investigate some immune component that could contribute to the pathogenesis of Alzheimer's disease associated with the E280A mutation of the presenilin-1 gene (PS-1). PATIENTS AND METHODS: Serum antibodies against both cardiolipin and beta-amyloid peptides (beta 1-40 and beta 1-42) were quantitated by means of an indirect ELISA technique in carriers of the mutation, either healthy or with Alzheimer's disease, as well as in normal controls without the mutation. RESULTS: Out of 19 patients with Alzheimer's disease only 2 had increased values of antibodies to cardiolipin, namely: one with 14.58 micrograms/ml of IgM and the other with 36.16 micrograms/ml of IgG. The remaining individuals revealed values under 10 micrograms/ml, considered normal, and there was no significant difference between the groups. Significant serum reactivity (p < 0.001) was detected against both beta-amyloid peptides in the mutation carriers, either with or without Alzheimer's disease, as compared to the control group. No correlation was detected between this antibody response and the mental or functional situation of the patients. CONCLUSION: beta-amyloid antibodies, present in the mutation carriers, may simply represent a marker of immune activation induced by beta-amyloid with no in vivo effect; however, despite the results, the possibility can not be ruled out of a pathogenic role of these antibodies in early onset Alzheimer's disease.

Adult↗
PubMedDate not supplied

[Procesing of faces: neurological bases, disorders and evaluation].

INTRODUCTION AND DEVELOPMENT: The processing of faces and recognition of familiar faces involves activity in many regions of the brain: 1. The visual association cortex in the act of constructing the perceived object; 2. Hippocampus and frontotemporal regions in the process of comparing what has been perceived with remembered images to activate sentiments of familiarity; 3. The temporoparietal regions in the semantic memory related to people, and 4. The left hemisphere in the activation of linguistic structures which codify information for access to the name. Lesions in any of these structures may give rise to alterations in the different steps of the cerebral processing of faces, amongst which prosopagnosia and prosopamnesia stand out. CONCLUSION: The psychophysiological and functional neuroimaging studies will permit, in the near future, evaluation and trial of cognitive models and advances in the understanding of cerebral processing of faces, their evaluation and disorders.

Facial Expression↗
PubMedDate not supplied

[Factorial and discriminant analyses of neuropsychological variables in familial and sporadic late onset Alzheimer disease].

INTRODUCTION: Prevalence of late onset Alzheimer's disease (LOAD) both familial and sporadic is increasing with the raising proportion of third-age population. There are evidences either supporting or rejecting the existence of differences in the behavior of neuropsychological variables between familial and sporadic cases of LOAD. OBJECTIVE: To identify neuropsychological variables discriminating between familial and sporadic cases of LOAD, in order to detect clinical manifestations that may provide information on the pathological process of the neurodegenerative process. PATIENTS AND METHODS: Using sequential sampling, we selected individuals affected by LOAD according to the criteria of the DSM-IV and NINCS-ADRDA. The following neuropsychological protocol was used: CERAD, Wisconsin, Phonological Fluency, Rey's Figure, Raven, A Cancellation Test, WAIS (Arithmetic); also used were: Global Deterioration Scale, Functional Assessment Staging of Reisberg (FAST), Barthel and Yesavage. Parametrical and non-parametrical univariate, factorial (principal components) and discriminant analyses were performed. In total, 52 patients were analyzed (average age: 74.8 years; mean age at onset of the disease: 69 years; time of disease's evolution: 5.7 years; average of educational level: 6.4 years). RESULTS: No significant statistical differences were found in clinical or neuropsychological variables between familial and sporadic cases of LOAD. Additionally, neither variables nor models were detected discriminating significantly between them. CONCLUSION: Familial and sporadic cases of LOAD present the same clinical and neuropsychological phenotype which makes very probable that sporadic cases are low penetrance familial ones.

Age of Onset↗
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[Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)].

INTRODUCTION: The department of Antioquia in Columbia is the main producer of gold in Columbia. In the gold-producing regions the population is exposed to high levels of mercury used in the processes of extraction and purification. Studies done in Columbia on neurotoxicity underline the hazards of mercury from the environmental and occupational-health point of view, but the effect of long-term exposure on cognitive function has not been studied. OBJECTIVE: To determine whether the miners of El Bagre (Antioquia, Columbia) have neuropsychological and/or behavior disorders as a result of occupational exposure to toxic mercury vapor. PATIENTS AND METHODS: The sample was made up of 22 right-handed men, residents of El Bagre, aged between 20 and 45 years old who had been exposed to mercury vapor for at least three years. The control group consisted of 22 men who lived in the non-mining regions of the department and had not been exposed to mercury, paired with the cases considered for age and educational status. Neuropsychological assessment, a medical examination and behavioral performance tests were applied to all the men (in both groups). RESULTS: In the study group alterations were seen and classified as: intellectual damage (mainly alteration of executive function and constructional praxis); emotional changes (symptoms of depression and anxiety) and neurological changes (amnesia, insomnia and tremor of the tongue). No changes were found in the control group. CONCLUSION: Exposure to mercury causes specific neuropsychological and behavior disorders in the absence of clinically detectable physical or physiological damage.

Adult↗
PubMedDate not supplied

[Clinical characteristics of hereditary cerebrovascular disease in a large family from Colombia].

INTRODUCTION: The cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations of the Notch3 gene in the chromosome 19p13.1. and is characterized by small-vessel disease of the cerebral. The clinical feature consists of migraine, recurrent strokes, mood changes and dementia. OBJECTIVE: To describe the clinical phenotype of a Colombian family with hereditary cerebrovascular disease. PATIENTS AND METHODS: We performed one pedigree with 268 individuals, neurologic examination to 57 members and magnetic resonance imaging (MRI) to 25 of them. RESULTS: Clinical analysis strongly support the diagnosis of CADASIL because 12 individuals had suffered recurrent stroke, five of them later developed subcortical dementia. Two patients developed dementia without preceding stroke. All affected individuals by stroke or dementia whom were tested with MRI had white matter hyperintensities and subcortical infarcts (nine cases). Others seven individuals have MRI signal abnormalities like CADASIL, four of them are asymptomatic, one had suffered ischemic transient attacks and two had suffered migraine. Other 22 individuals had only migraine. We outstand the high frequency of MRI signal abnormalities in corpus callosum that we found in five individuals with stroke or dementia, the patient with ischemic transient attack and one asymptomatic patient, either the presence of hearing loss in seven individuals with stroke or dementia. CONCLUSIONS: We describe one large family with hereditary cerebrovascular disease characterized by recurrent strokes, subcortical dementia, hearing loss, migraine, and MRI signal abnormalities typed leukoencephalopathy, subcortical infarcts and alterations in corpus callosum. Clinical analysis strongly support the diagnosis of CADASIL.

Adult↗
PubMedDate not supplied

[Confirmation of the high prevalence of attention deficit disorder in a Colombian community].

INTRODUCTION: Using a shortened rating scale, the prevalence of Attention Deficit Hyperactivity Disorder (ADHD) has been reported to be very higher in a Colombian population. However, these data require clinical confirmation. OBJECTIVE: To confirm clinically the prevalence of ADHD in Colombian children and adolescents. PATIENTS AND METHODS: A randomized sample of 4 to 17 year old children and adolescents--184 males and 157 females--was selected from the schools. Sample was stratified in two socioeconomic status: high (4, 5, 6) and low (1, 2, 3). Several parents' and teachers' rating scales for the diagnosis of ADHD, standardized and validated in the Colombian population, were applied to the sample. The diagnosis of ADHD was confirmed using a semi-structured psychiatric and neurological interview, and medical histories revisions. RESULTS: Analysis found that prevalence of ADHD is 17.1%. Distribution for ADHD types was: combined 9.4%, inattentive 6.7% and hyperactive-impulsive 1%. Prevalence for boys was significant higher (21.8%) than for girls (10.9%) (chi 2 = 11.8, p < 0.01). In male predominate combined type and in female inattentive. Higher prevalence was found in low socioeconomic strata. Preschool children have lower prevalence (6.2%) than school 6 to 11 year old children (22.6%) and adolescents (21.6%). CONCLUSION: A higher prevalence of ADHD was confirmed in Colombian population.

Adolescent↗
PubMedDate not supplied

[Analysis of complex segregation in a large family with hereditary cerebrovascular disease in Antioquia, Colombia].

INTRODUCTION: Among different kinds of cerebrovascular diseases, few of them are caused by genetic disturbances, such as CADASIL (caused by Notch3 mutations), CARASIL, mitochondrial encephalopathy, MELAS and dementia typed Binswanger. However, to describe these type of cerebrovascular diseases related with genetic mutations could permit to determinate the causes of both hereditary and sporadic cerebrovascular diseases and then lead solutions. OBJECTIVE: To describe the genetic, environmental and cohort factors that determinate the presence of many affected people by a several cerebrovascular diseases in the pedigree of a large family from Antioquia (Colombia). PATIENTS AND METHODS: We performed one pedigree (268 individuals), through singular recruit and then complex segregation analysis with POINTER program. RESULTS: The model that more close to data is autosomal dominant mayor locus without influence of environmental factors. Frequency of allele of susceptibility to develop stroke or subcortical vascular dementia was 0.0006. Mayor gene is over epistatic effects or interactions with other gene. CONCLUSIONS: Described an autosomal dominant hereditary model through complex segregation analysis in a pedigree of patients with hereditary cerebral vascular diseases characterized by recurrent strokes, early onset subcortical dementia, hearing loss, antecedent of migraine and MRI signal abnormalities, subcortical infarcts and leukoencephalopathy. In this family the parameter calculated, autosomal dominant model, and clinical feature strongly support the diagnostic of CADASIL, linkage analysis and sequentiation will be performed to determinate if mutant gene is Notch3.

Adolescent↗
PubMedDate not supplied

[Clinical history in the study of a patient with dementia].

OBJECTIVES: To carry out a detailed review of the keys to diagnosis of different types of dementia whilst taking a clinical history. DEVELOPMENT: Dementia is a syndrome with many different aetiologies. Correct diagnosis depends on recording data of the history of the dementia, particularly of complaints regarding cognition and behavior. The keys to the clinical history should be based on questions about cognitive disorders, with emphasis on how they started, their evolution and particular form of dysfunction, Although Alzheimer's dementia is the most frequent, this diagnosis should only be made when the other forms of dementia have been ruled out. In this article we describe some of the keys to a good clinical history to facilitate the etiological and differential diagnosis of dementia. CONCLUSIONS: Establishment of a full clinical history is the first and most important step in the diagnosis of dementia and cognitive disorders. On this will depend the plan to be followed to study the aetiology and most suitable treatment. Success or failure in the study of a patient with dementia depends on the quality of the clinical history obtained.

Acute Disease↗
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[Perinatal factors associated with attention deficit/hyperactivity diagnosis in Colombian Paisa children].

INTRODUCTION: Some perinatal factors have been associated with attention d ficit/hyperactivity disorder (ADHD). OBJECTIVE: To estimate the association between perinatal factor and ADHD diagnosis in school, aged 6 to 11 years, children from Medell n city (Colombia). PATIENTS AND METHODS: A randomized sample of 200 cases, 6 to 11 year old, with standardized ADHD diagnosis was selected. A randomized sample of 200 control children, 6 to 11 year old, was selected from a data base of 70 schools of Medell n city. The same diagnostic protocol was administered to controls. A questionnaire with questions about pregnancy, delivery an neonatal period was given to the mothers. Data were analyzed using cross tabulation and stepwise logistic multiple regression analyses. RESULTS: Miscarriage symptoms, premature delivery symptoms, severe flu attacks (cold with fever, without virus confirmation), tobacco abuse, alcohol abuse (to become drunk), minor congenital malformations, neonatal seizures and hospitalizations during newborn period were factors associated with ADHD diagnosis (p< 0.05). However, stepwise logistic multiple regression analysis selected a block of variables formed by premature delivery symptoms, severe flu attacks and neonatal seizures as significant perinatal risk factors (p< 0.01) for ADHD diagnosis.

Attention Deficit Disorder with Hyperactivity↗
PubMedDate not supplied

[Neuronal DNA damage correlates with a positive detection of c-Jun, nuclear factor kB, p53 and Par-4 transcription factors in Alzheimer's disease].

INTRODUCTION AND OBJECTIVES: Alzheimer s disease is a neurodegenerative disorder characterized neuropathologically by beta amyloid plaques, neurofibrillary tangles, gliosis and neuronal loss. Recently, we have elucidated a molecular cascade of cell death induced by A beta 25 35 involving the activation of nuclear factor kappa B (NF kB), p53, and c Jun transcription factors in vitro. At present, no comparative reports have been published to establish a similar cell death signalization pathway in in vitro and in in vivo. The aim of this investigation was to determine if AD brains might activate NF kB, p53, c Jun, Par 4 transcription factors and to establish whether there exist a relationship between neuronal DNA damage and transcription factors activation. PATIENTS AND METHODS: We investigated Ab plaques, neurofibrillary tangles and NF kB, p53, and c Jun transcription factor activation in five cerebral regions from 3 normal subjects and from six demented patient with sporadic AD and one patient with AD familiar according to CERAD criteria. Using TUNEL we determine neuronal damage. RESULTS: We demonstrated neuronal damage in 17 out of 50 regions evaluated as TUNEL positive, and their distribution was heterogeneous in all brain regions evaluated; and the activation of NF kB, p53, c Jun and Par 4 transcription factors from case # 24 and #22, corresponding to TUNEL positive. CONCLUSIONS: We found a correlation between severity of DNA damage and nuclear activation of the transcription factors. These findings suggest that the AD brain may induce cell death by a molecular signalization similar to a non neuronal model by Ab exposure. This in situ study might validate previous Ab induced cell death observations in vitro.

Adult↗
PubMedDate not supplied

[A neuropsychological study of Huntington's disease in families in Antioquia, Colombia].

INTRODUCTION: Various neuropsychological studies have been conducted to determine the cognitive functioning of patients with Huntington s disease and their results have shown that the pattern of cognitive decline is thought to be typical of a frontal subcortical dementia. OBJECTIVES: To determine if significant differences exist between the cognitive performances of a group diagnosed with Huntington s disease and a group of healthy, at risk relatives on a series of neuropsychological tests, and to examine the extent to which the Huntington group s cognitive performance profile corresponds to frontal subcortical damage as reported in other studies. PATIENTS AND METHODS: The sample was comprised of a group of 18 subjects with a clinical diagnosis of initial stage Huntington s disease and a group of 15 healthy relatives at risk for Huntington s disease. A battery of tests (the CERAD) and additional neuropsychological tests were administered to all subjects. RESULTS: Compared to the at risk group, the Huntington s disease group scored significantly lower on 85.41% of the tests. CONCLUSIONS: The neuropsychological tests utilized in this study were useful to discriminate between diagnosed and at risk groups. The Huntington s disease group s global neuropsychological profile was similar to that of a frontal subcortical dementia in which the predominant features include executive functioning deficits, memory problems, visuo constructive alterations, attention deficits, verbal fluency problems and naming deficits.

Adult↗
PubMedDate not supplied

[Clinical and neuropsychological characteristics of Huntington's disease: a review].

INTRODUCTION: Huntington's disease is a dominant autosomic neurodegenerative disorder. This article's objective is to provide an up-to-date description of the clinical and neuropsychological manifestations over the course of the disease. METHOD: According to clinical studies, the main characteristics of Huntington's disease include motor deficits, psychiatric problems and cognitive deficits. Many investigations have shown that a fronto-subcortical circuit dysfunction is responsible for these deficits. As the disease progresses, patients tend to have more cognitive difficulties which include attention/concentration problems, slowed cognitive processing, memory and language deficits, visuo-spatial problems and executive functioning difficulties. CONCLUSION: Studies with asymptomatic carriers of Huntington's disease have shown that cognitive deterioration may begin long before a clinical diagnosis of the disease is possible.

Cerebral Cortex↗
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[Performance of carriers and non-carriers of the E280A mutation for familial Alzheimer's disease in a naming test].

INTRODUCTION: Early preclinical diagnosis is the greatest challenge faced by researchers into dementia. Cognitive, neuroanatomical, neurophysiological and genetic markers have been reported. One of the preclinical cognitive markers is anomia and it is often assessed using visual naming tests. AIMS: The aim of this study was to analyse the type of mistakes made in a visual naming test in a group of carriers and non-carriers of the E280A PS1 mutation. PATIENTS AND METHODS: The sample was made up of 91 participants who were genotyped for the E280A PS1 mutation and divided into three groups: non-carriers (n = 30), asymptomatic carriers (n = 39) and sick carriers (n = 22). Selection was performed using the Minimental and the Fast and EDG scales and mistakes in the CERAD naming test were classified. The types of mistakes taken into account were: no answer, visual, semantic, phonological, the whole for the part, and not related. RESULTS: There is a significant difference in the number of semantic errors between non-carriers and asymptomatic carriers; on comparing the three groups, no statistically significant differences were found in visual mistakes. CONCLUSIONS: Visual mistakes are a general characteristic, even in healthy subjects and, therefore, these errors did not provide any information that could be used to classify patients with or without dementia. Semantic mistakes can be considered as being a preclinical sign in familial Alzheimer's disease (FAD). Both visual and auditory naming tests must be applied when evaluating patients with FAD.

Adult↗
PubMedDate not supplied

[Specific developmental language disorder: a theoretical approach to its diagnosis, aetiology and clinical symptoms].

AIM: This article presents an updated review about the definition, diagnostic criteria, classifications, etiology and the evolution of the specific language impairment (SLI). DEVELOPMENT: The specific language impairment is characterized by a developmental language delay and an impaired language, that persist over time and it is not explained by sensorial, motor and mental disabilities, neither by psycopathological disorders, socio-emotional deprivation, nor brain injury. The diagnosis is based on exclusional criteria. Some researchers propose different classifications considering the children performance in language comprehension and language production. Genetical linkage to the FOXP2 gen in the SPCH1 region of the chromosome 7 and to the chromosomes 13, 16 y 19 has been reported. The neuroimage studies have shown alterations in the volume and perfusion of some brain structures related to language. The manifestations of SLI may change during the development of the children and may disturb the self-esteem, the academic performance and the social abilities. CONCLUSIONS: The variability in the linguistic and cognitive performance, and the variety in the etiological findings in children with SLI, don't allow to settle the affected population as an homogeneous group. Different theoretical positions have emerged as a consequence of this condition.

Cognition↗
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[A description of semantic memory performance in a sample of the Antioquian population].

INTRODUCTION: Available treatments for Alzheimer disease allow that early diagnosis become an important issue, because treatment only are useful during the earliest stage, especially during the mild cognitive impairment (MCI), when the most of the cognitive function is preserved. AIM: To observe the performance on a shortened version of a Semantic Cue Recall Memory Test (SCRMT) from a group of adult aged over 50 years old, living in Medellin city and with dementia of Alzheimer type (DAT). SUBJECTS AND METHODS: The sample was constituted by 30 patients with DAT, 30 with MCI, and 59 healthy controls, which were matched by socio economic strata and school achievement. The SCRMT was administered to the sample. For the analyses two groups of age (50-69 and over 70 years) were conformed. RESULTS: Comparisons statistically significant differences between the groups (p < 0.05). The scores were not significant affected by age. A combination of low scores with the presence of intrusions on the free, immediate cue, and delay cue recalls suggested the diagnosis of DAT, which allow recommending a complete neuropsychological assessment. Statistically significant differences were preserved when the groups were divided by age. The effect of the gender could not determine because the small size of the male sample. CONCLUSION: The shortened version of the SCMRT would appear be useful for the DAT diagnosis.

Adult↗
PubMedDate not supplied

[Tumour of the corpus callosum: the association between interhemispheric disconnection and an anterograde amnesia syndrome].

INTRODUCTION: Sperry, or interhemispheric disconnection, syndrome was reported in patients who had undergone surgical section of the corpus callosum carried out in an attempt to control medication-resistant epilepsy. It has occasionally been linked to tumours of the corpus callosum and, although even more rarely, it has also been associated to an amnesic syndrome. In this paper we report the anatomical and neuropsychological findings in a patient with interhemispheric disconnection syndrome associated to a hippocampal-type amnesic syndrome, caused by a tumour in the splenius of the corpus callosum that extended into the fornix. CASE REPORT: A 52-year-old white male who visited because of loss of memory; on admission to hospital the physical examination revealed a certain degree of asomatognosia with regard to the left-hand side of the body. An axial tomography brain scan showed a dense central lesion in the brain that extended laterally and occluded the body of both lateral ventricles. A biopsy study revealed an undifferentiated astrocytoma that affected the corpus callosum and the fornix. CONCLUSIONS: Sperry, or interhemispheric disconnection, syndrome produced by a tumour in the splenius of the corpus callosum is very likely to course with an amnesic syndrome due to disconnection caused by destruction of the fornix. This association, which characterised our patient's clinical picture, has only previously been described in three cases.

Amnesia, Anterograde↗