[Reversible posterior leucoencephalopathy syndrome: a case report and review of its physiopathology based on neuroradiological findings]. / Leucoencefalopatia posterior reversible: descripcion de un caso y revision de la fisiopatologia basada en hallazgos neurorradiologicos.

INTRODUCTION: Reversible posterior leucoencephalopathy is a clinico radiological syndrome first described in the last decade. The physiopathological mechanism governing it is not very well known. The currently accepted hypotheses are the generation of a vasogenic edema caused by failure of the mechanism that allows self regulation of the cerebral blood flow, and the production of a cytotoxic edema due to ischemia. Both experimental studies carried out in rats and the use of magnetic resonance imaging (MRI) to evaluate the diffusion of cerebral water support the first hypothesis. We report the case of a patient with reversible posterior leucoencephalopathy syndrome that was complicated by areas of cerebral infarction and we review the physiopathological mechanisms involved, basing our analysis on the findings obtained with MRI. CASE REPORT: A female patient was admitted to our hospital because of bilateral transient amaurosis, headaches, vomiting and arterial hypertension. MRI brain scans showed bilateral cortico subcortical lesions in the occipital parietal regions, frontal and right cerebellar hemisphere convexity, with hyperintense signal in T2 and diffusion weighted imaging. Some occipital parietal regions present a diminished signal on the apparent diffusion coefficient map. The patient was treated with intravenous antihypertensive drugs and full recovery was accomplished within 10 days. A month later, according to MRI scans, there were still hyperintense areas in T2 on both occipital lobes, which were compatible with cerebral infarcts. DISCUSSION: The mechanism that is most frequently involved in this entity is probably vasogenic edema. In our case there were, at the same time, areas of cytotoxic edema that progressed to cerebral infarcts. MRI with sequences that evaluate the diffusion of cerebral water is useful in distinguishing between the two mechanisms.

Leucoencefalopatía posterior reversible: descripción de un caso y revisión de la fisiopatología basada en hallazgos neurorradiológicos / Reversible posterior leucoencephalopathy syndrome: a case report and review of its physiopathology based on neuroradiological findings

Introduction. Reversible posterior leucoencephalopathy is a clinico-radiological syndrome first described in the last decade. The physiopathological mechanism governing it is not very well known. The currently accepted hypotheses are the generation of a vasogenic edema caused by failure of the mechanism that allows self-regulation of the cerebral blood flow, and the production of a cytotoxic edema due to ischemia. Both experimental studies carried out in rats and the use of magnetic resonance imaging (MRI) to evaluate the diffusion of cerebral water support the first hypothesis. We report the case of a patient with reversible posterior leucoencephalopathy syndrome that was complicated by areas of cerebral infarction and we review the physiopathological mechanisms involved, basing our analysis on the findings obtained with MRI. Case report. A female patient was admitted to our hospital because of bilateral transient amaurosis, headaches, vomiting and arterial hypertension. MRI brain scans showed bilateral cortico-subcortical lesions in the occipital-parietal regions, frontal and right cerebellar hemisphere convexity, with hyperintense signal in T2 and diffusion-weighted imaging. Some occipital-parietal regions present a diminished signal on the apparent diffusion coefficient map. The patient was treated with intravenous antihypertensive drugs and full recovery was accomplished within 10 days. A month later, according to MRI scans, there were still hyperintense areas in T2 on both occipital lobes, which were compatible with cerebral infarcts. Conclusion. The mechanism that is most frequently involved in this entity is probably vasogenic edema. In our case there were, at the same time, areas of cytotoxic edema that progressed to cerebral infarcts. MRI with sequences that evaluate the diffusion of cerebral water is useful in distinguishing between the two mechanisms

Introducción. La leucoencefalopatía posterior reversible es un síndrome clinicorradiológico descrito en la última década. El mecanismo fisiopatológico responsable no se conoce muy bien. Las hipótesis aceptadas son: generación de edema vasogénico por pérdida del mecanismo autorregulatorio del flujo sanguíneo cerebral y producción de edema citotóxico por isquemia. Estudios experimentales en ratas y la utilización de imágenes de resonancia magnética (IRM) que evalúan la difusión del agua cerebral, sustentan la primer hipótesis. Describimos un caso de leucoencefalopatía posterior reversible complicada con áreas de infarto cerebral y realizamos una revisión sobre los mecanismos fisiopatológicos involucrados, sobre la base de los hallazgos obtenidos en IRM. Caso clí- nico. Una mujer se internó en nuestro hospital por amaurosis bilateral transitoria, cefaleas, vómitos e hipertensión arterial. Las IRM de cerebro presentaban lesiones corticosubcorticales bilaterales en las regiones parietooccipitales, convexidad frontal y hemisferio cerebeloso derecho, con señal hiperintensa en T2 e imágenes de difusión. Algunas regiones parietooccipitales presentaban señal disminuida en mapa del coeficiente aparente de difusión. La paciente se trató con antihipertensivos endovenosos y se recuperó ad integrum en los 10 días siguientes. Después de 1 mes, en IRM, persistían áreas hiperintensas en T2 sobre ambos lóbulos occipitales, compatibles con infarto cerebral. Conclusión. El mecanismo involucrado con mayor frecuencia en esta entidad es probablemente el edema vasogénico. En nuestro caso, coexisten áreas de edema citotóxico que evolucionan a infarto cerebral. Las IRM con secuencias que valoran la difusión del agua cerebral son útiles para diferenciar entre ambos mecanismos (AU)

Variable patterns of anti-GM(1) IgM-antibody populations defined by affinity and fine specificity in patients with motor syndromes: evidence for their random origin.

Elevated titers of serum antibodies against GM(1)-ganglioside are associated with a variety of autoimmune neuropathies. Although much evidence indicates that these autoantibodies play a primary role in the disease processes, the mechanism of their appearance is unclear. Low-affinity anti-GM(1) antibodies of the IgM isotype are part of the normal human immunological repertoire. In patients with motor syndromes, we found that in addition to the usual anti-GM(1) antibodies, the sera contain IgM-antibodies that recognize GM(1) with higher affinity and/or different specificity. This latter type of antibodies was not detected in other autoimmune diseases. We studied the fine specificity of both normal and motor disease-associated antibodies using HPTLC-immunostaining of GM(1) and structurally related glycolipids, soluble antigen binding inhibition, and GM(1) affinity columns. Normal low-affinity anti-GM(1) antibodies cross-react with GA(1) and/or GD(1b). In the motor syndrome patients, different populations of antibodies characterized by their affinity and cross-reactivity were detected. Although one population is relatively common (low affinity, not cross-reacting with GA(1) and GD(1b)), there are remarkably few sera having the same set of populations. These results suggest that the appearance of the new antibody populations is a random process. When the different antibody populations were analyzed in relation to the three-dimensional structure of GM(1), a restricted area of the GM(1) oligosaccharide (the terminal Galbeta1-3GalNAc) was found to be involved in binding of normal anti-GM(1) antibodies. Patient antibodies recognize slightly different areas, including additional regions of the GM(1) molecule such as the NeuNAc residue. We hypothesize that disease-associated antibodies may originate by spontaneous mutation of normal occurring antibodies.

[Staging of bronchogenic cancer. Determination of mediastinal lymphatic involvement using magnetic resonance]. / Staging del cancro broncogeno. Identificazione dell'interessamento linfonodale mediastinico mediante risonanza magnetica.

Twenty-five patients with bronchogenic carcinoma were prospectively studied by both CT and MR during 10 days preceding thoracotomy. MR scans included contiguous axial and coronal slices. Results of CT and MR studies were compared with the surgical and pathological findings. Although no significant difference was found between the two imaging methods for the evaluation of mediastinal nodes. MR appear to be superior to CT in the aortopulmonary and subcarinal node areas.

Preliminary observations on lung cancer therapy by interstitial irradiation with iodine 125.

Interstitial implantation of I125 by thoracotomy represents a further therapeutic procedure for lung cancer. Two cases recently treated by this procedure are reported. The first case concerns a right apical carcinoma of the lung where interstitial implantation of I125 seeds was carried out in the unresectable apical neoplastic residue, after superior lobectomy. The second case concerns a smaller tumor unresectable due to the severely impaired respiratory function. Main indications to the procedure are reported.

[Aneurysms of the renal artery (author's transl)]. / Gli aneurismi dell'arteria renale.

After a review of the literature concerning the frequency, aetiology, roentgenologic diagnosis and treatment of the aneurysm of the renal arteries, the author reports 2 cases of renal aneurysm with hypertension causing segmental reduction of renal blood flow. The value of selective renal arteriography and aortography is stressed.