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A menudo, el diagnóstico de demencia ha sido facilitado a través de pruebas psicométricas. El deterioro de las habilidades en estos pacientes, puede ser evaluado desde tests de screening a baterías neuropsicológicas. Actualmente, existen muchas investigaciones que han estudiado la necesidad de estos instrumentos en el diagnóstico de demencia. El siguiente artículo es un estudio sobre los tests que evalúan el deterioro cognitivo y el declive funcional en actividades de la vida diaria en pacientes con posible demencia. (AU)

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El diagnóstico de demencia considera una pérdida de habilidades intelectuales que interfiere con la función social y ocupacional. Esto es muy importante en términos humanos. asimismo es díficil de determinar la proporción del coste económico gastado en el cuidado de estos pacientes. Actualmente, muchos estudios han investigado la prevalencia y la incidencia de la demenmcia en la población anciana, posiblemente debido al incremento dramático en los países de mayor desarrollo económico (AU)

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El propósito de esta investigación fue estudiar el poder discriminante de las pruebas neuropsicológicas de la "Batería Abreviada Grganada de Evaluación Neuropsicológica" (BAGEN). Los resultados sugieren que la prueba de memoria y la prueba de cálculo son las más importantes en el diagnóstico de la demencia (AU)

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BAGEN fue diseñada para evaluar demencias en pacientes con bajo nivel educativo. Evalúa orientación, lenguaje, memoria, praxias y atención. El principal objetivo de este estudio fue determinar los ítems con mayor poder discriminante entre demencia y otros trastornos cognitivos. Dos grupos, formaron un total de 144 sujetos. Todos los sujetos incluidos en el informe habían completado todas las pruebas neuropsicológicas. El diagnóstico de demencia estuvo basado en un examen clínico. El resultado de esta investigación sugiere que algunos ítems pueden ser eliminados de la batería (AU)

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We analyzed the amino acid concentrations and aminopeptidase activities in plasma and the cerebrospinal fluid (CSF) of Alzheimer patients. Correlations were calculated between these parameters and the degree of cognitive impairment, duration of the disease and age. In comparison with a control group, no changes were found in the levels of amino acids in CSF or plasma of Alzheimer patients. Alanyl-aminopeptidase activity was significantly lower in the CSF of Alzheimer patients, whereas no differences in CSF were detected as regards the remaining aminopeptidases. The plasma/CSF ratio for aminopeptidase activities was higher in AD patients than in controls, although the difference was only significant for alanyl-aminopeptidase. Amino acid ratios did not show this general tendency. The correlations between plasma aspartate and glutamate concentrations and the stage of the disease, measured with the Mini Mental State Examination, were studied. Changes in aminopeptidase activities and their role in protein dysfunction underlying Alzheimer disease are discussed.

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The case of a 25-year old man who presented with meningoencephalitis as the sole clinical manifestation of Q fever is described. Serological studies revealed the presence of IgM and IgG antibodies to Coxiella burnetii. The patient responded favourably to a ten-day course of i.v. ceftriaxone and was discharged without any neurological sequelae.

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An electro-neuro-physiological, biochemical and hematological study was carried out in 3 groups of non-symptomatic drinkers: those in group A had a daily alcohol intake of less than 40 grams of alcohol; group B had a daily intake of between 40 and 80 grams of alcohol and those in group C had an intake greater than 80 grams of alcohol per day. The aim of this study was to demonstrate that all the parameters evaluated show quicker alterations when the intake of ethanol is chronic. Electroneuro-physiological parameters were less sensitive than the following indexes: VCM, GGT, GOT, GPT. However, in 50.9% of the patients there were changes in conduction speed, which is an important point to take into account when making a therapeutic decision.

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Alterations in nervous transmission might be an early feature of diabetic peripheral polyneuropathy, even in the subclinical stage. We performed a study on 100 diabetic patients. Those with possible endogenous or exogenous causes of neuropathy were not included. We studied the motor distal latency of right peroneal and cubital nerve and the sensory distal latency of median nerve by the use of electromyogram. The neuropathy incidence was 34.3%. One of the results was that conduction in males was slower than in the female control group; this disappeared in diabetic patients.

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We have studied 44 patients diagnosed of idiopathic Parkinson disease included in our database of rigid-akinetic syndromes. We have compared their demographic, environmental and clinical features with the ones that presented a group on 22 patients diagnosed of idiopathic Parkinson disease and had some first degree relatives with the same disease. Patients with familial Parkinson disease are distinguished from the ones that suffer from sporadic Parkinson disease because of an early start, greater consanguinity rate and greater frequency of a similar disease in their parents. Moreover, we have seen that familial Parkinson disease patients have drunk more water from wells during their lives than the ones that suffer sporadic Parkinson disease, present greater frequency of wide motoricity disorders, dystonia, night hypokinesia, fluctuations in relation to L-DOPA and greater frequency of early going grey. We have not found either epidemiologic data which could explain the appearance of familial cases or environmental causes which could produce familial Parkinson disease. Clinical differences between the two groups are likely due to an early start of symptoms in familial Parkinson disease cases. According to our data we could not conclude that between familial and sporadic Parkinson disease are significant differences in to justify two well-defined diseases. Even, the familial presentation of idiopathic Parkinson disease could be the normal form of Parkinson disease if long survival was a favourable factor of disease onset in pre-symptomatic persons.

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In the normal individual, the anterior choroidal artery (ACA) has a rather fixed angiographic trajectory, but in patients with intracranial tumors it almost invariably has a modified course, the nature of the modification being dependent on the topography of the lesion. Authors employ the parameters used up through the present for objectivating the course of the anterior choroidal artery, and add others of theirs own, especially in regard to the relative location of various points on the vessel (rather than their isolated positions). A total of 28 measurements were taken for each of the 132 angiographic series studied: 31 normal individuals and 101 with diverse intracranial lesions. Every value was entered into a computer along with (by numerical coding) personal data, incidental factors and, in the pathological series, the topography of the preferrent (primary) lesion and secondary lesion (tumoral extension), as well as the possible coexistence of hydrocephaly and/or transtentorial herniation. This procedure allowed for an exhaustive analysis of each factor involved, which could be studied individually or in combination within each of the groups and subgroups established. In this way the extensive results could be readily interpreted.

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The usually observed modifications of the deep phlebogram in the entire pathological series are: transmedial displacement of the internal cerebral vein (more or less evident but always significant), straightening of the superior arch of the internal cerebral vein, an important ventricular dilatation in most cases. The most reliable parameters are: Fisher's bisecting line and two of the parameters proposed by the author's: Monro-Phleboaxial-Line and Monro-Glabella-Bregma-Angle.

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