[Ultrastructural features of the synaptic plasticity in peritumoral cerebral oedema in humans]. / Aspectos ultraestructurales de la plasticidad sináptica en el edema cerebral peritumoral en humanos.

AIM: To provide an ultrastructural characterisation of the synaptic plasticity phenomena in peritumoral brain tissue in humans. PATIENTS AND METHODS: Sixteen peritumoral tissue biopsy samples were processed using conventional transmission electron microscope techniques. Clinical data and post-surgical follow-up were reviewed and analysed. RESULTS: In the peritumoral brain tissue there was a predominance of cellular or oncotic cerebral oedema. A large number of synapses were seen to be perforated with both convex and, although less frequently, irregular curvatures. Generally, the presynaptic terminals had an oedematous appearance, with oedematous mitochondria with cristolysis and electron-dense deposits in the mitochondrial matrix. The presynaptic terminals showed numerous synaptic vesicles of different sizes and which were sometimes arranged in small accumulations. Observations also confirmed the presence of endocytosis vesicles, which suggest high neurotransmitter reuptake. Some presynaptic terminals displayed degenerative changes. The postsynaptic terminals were seen to be oedematous and the dendritic spines displayed different shapes and spiny processes that were degenerated to varying degrees. Perisynaptic astrocytic prolongations were seen to be oedematous, with a variable number of glycogen granules. We propose a possible sequence of structural changes in the process of forming perforated synapses in peritumoral brain tissue. CONCLUSIONS: The ultrastructural findings observed in the synapses and their microenvironment can be considered to be significant with respect to the clinical manifestations and the sequelae in the patients who were studied. Moreover, they are linked to functional alterations in injured tissue, degenerative changes and neuronal death.

Aspectos ultraestructurales de la plasticidad sináptica en el edema cerebral peritumoral en humanos / Ultrastructural features of the synaptic plasticity in peritumoral cerebral oedema in humans

Caracterizar ultraestructuralmente los fenómenos de plasticidad sináptica en el tejido cerebral peritumoralhumano. Pacientes y métodos. Se procesaron 16 biopsias de tejido peritumoral mediante las técnicas convencionales para microscopía electrónica de transmisión. Se revisaron y analizaron los datos clínicos y el seguimiento posquirúrgico. Resultados.En el tejido cerebral peritumoral predominó el edema cerebral del tipo celular u oncótico. Se observaron múltiples sinapsis perforadas con curvaturas convexas y, en menor frecuencia, con curvaturas irregulares. Generalmente, los terminales presinápticospresentaron aspecto edematoso, con mitocondrias edematosas con cristolisis y matriz mitocondrial electrón densa.Los terminales presinápticos mostraron numerosas vesículas sinápticas de diferentes tamaños y ocasionalmente dispuestas en pequeños acúmulos. Se evidenció la presencia de vesículas de endocitosis que sugieren una alta recaptación de neurotransmisores.Algunos terminales presinápticos mostraron cambios degenerativos. Los terminales postsinápticos se observaron edematosos y las espinas dendríticas mostraron diferentes formas y aparatos espinosos degenerados en grado variable. Las prolongacionesastrocitarias perisinápticas se observaron edematosas, con cantidad variable de gránulos de glucógeno. Se propone una posible secuencia de cambios estructurales en el proceso de formación de sinapsis perforadas en el tejido cerebral peritumoral.Conclusiones. Los hallazgos ultraestructurales observados en las sinapsis y su microambiente pueden considerarse relevantes en relación con las manifestaciones clínicas y las secuelas de los pacientes estudiados, y se vinculan con alteracionesfuncionales del tejido lesionado, cambios degenerativos y muerte neuronal

To provide an ultrastructural characterisation of the synaptic plasticity phenomena in peritumoral brain tissuein humans. Patients and methods. Sixteen peritumoral tissue biopsy samples were processed using conventional transmission electron microscope techniques. Clinical data and post-surgical follow-up were reviewed and analysed. Results. In the peritumoralbrain tissue there was a predominance of cellular or oncotic cerebral oedema. A large number of synapses were seen to be perforated with both convex and, although less frequently, irregular curvatures. Generally, the presynaptic terminals had an oedematous appearance, with oedematous mitochondria with cristolysis and electron-dense deposits in the mitochondrialmatrix. The presynaptic terminals showed numerous synaptic vesicles of different sizes and which were sometimes arranged in small accumulations. Observations also confirmed the presence of endocytosis vesicles, which suggest high neurotransmitterreuptake. Some presynaptic terminals displayed degenerative changes. The postsynaptic terminals were seen to be oedematous and the dendritic spines displayed different shapes and spiny processes that were degenerated to varying degrees. Perisynapticastrocytic prolongations were seen to be oedematous, with a variable number of glycogen granules. We propose a possible sequence of structural changes in the process of forming perforated synapses in peritumoral brain tissue. Conclusions. The ultrastructural findings observed in the synapses and their microenvironment can be considered to be significant with respectto the clinical manifestations and the sequelae in the patients who were studied. Moreover, they are linked to functional alterations in injured tissue, degenerative changes and neuronal death

[Idiopathic hypertrophic pachymeningitis: a diagnostic dilemma]. / Paquimeningitis hipertrófica idiopática: un dilema diagnóstico.

INTRODUCTION: Idiopathic hypertrophic pachymeningitis (IHP) is a rare fibrosing inflammatory process of unknown pathogenesis that causes diffuse thickening of the duramater. In spite of the fact that this pathological entity has been linked to specific etiological agents such as syphilis, tuberculosis, mycosis and sarcoidosis, In recent years there has been an increase in the number of patients with IHP of undetermined cause. CASE REPORT: 58 year-old female with a long date history of oppressive headaches, frontally located at first, and later generalized, accompanied by weakness and asthenia; urinary incontinence, dizziness, vomiting, and gait ataxia. Physical examination revealed bilateral cerebellar signs, and optic atrophy. Magnetic resonance displayed a diffuse thickening of the falx cerebrii, and cerebellar tentorium, hypointense in T1 and T2- weighted images, and markedly enhanced following administration of intravenous Gd-DTPA. A biopsy obtained from the falx revealed conspicuous fibrosis, and focal chronic inflammatory mononuclear infiltrate. Complementary exams carried out in order to reveal a specific etiologic agent were negative. CONCLUSION: Due to the variable clinical presentation, and the difficulty to establish the etiology of the pathological process, to make the diagnosis of IHP usually represents a true dilemma. This diagnosis is often made by exclusion.

[Cerebrovascular disease: its relationship with cardiovascular and renal pathology in 134 clinical autopsies]. / Enfermedad cerebrovascular: su relación con cardiovasculopatías y nefropatías en 134 necropsias clínicas.

OBJECTIVE: To establish the relationship between cardiopathy and chronic nephropathy, and cerebral vascular pathology in clinical necropsies performed in adult patients. MATERIAL AND METHODS: The protocols of 861 clinical autopsies done during the lapse 1990-2000 were reviewed, of these, 134 cases with diagnosis of cerebrovascular disease (CVD) were selected. Analyzed features included: neuropathological study of CVD, renal and cardiovascular pathology, and cause of death. RESULTS: CVD represented 15.5% of all autopsies done during the study period. Ischemic CVD constituted 56.7% of the cases, whereas cases of hemorrhagic CVD accounted for 43.3% of the total. Causes included arterial hypertension (33%), atherosclerosis (19%), emboli and vascular malformations (13% each, respectively), coagulopathies (8%), angeiitis (4%), tumors (1%), and unknown origin (11%). Ischemic CVD was caused by atherosclerosis in 34.2% of the cases, lacunar infarcts in 32.8%, of embolic cause in 14.4% of the cases, angeiitis in 1.3%, and of unknown origin in 17.1% of the cases. Hemorrhagic CVD presented as intraparenchymal hematoma in 50% of the cases, as sub-arachnoid hemorrhage in 28%, as disseminated petechial hemorrhages in 19%, and intraventricular in 3% of the cases. Ischemic CVD was associated with hypertensive cardiopathy in 86.5% of the cases, and with nephrosclerosis in 51.3%, whereas hemorrhagic CVD was seen associated with the same pathological entities in 86.2% and 29.3% of the cases, respectively. Cerebral herniation was the cause of death in 2.6% of the patients with ischemic CVD, and in 74.1% of the patients with hemorrhagic CVD. CONCLUSIONS: CVD was associated with a high frequency of intercurrent pathological processes, namely hypertensive cardiopathy, atherosclerosis, nephroscleroisis, and other chronic nephropathies, that eventually interact, and constitute well known predisposing and/or concomitant factors to the cerebrovascular event

[Non neoplastic space occupying lesions mimicking central nervous system tumors]. / Lesiones ocupantes de espacio no neoplasicas que simulan tumores del sistema nervioso central.

OBJECTIVE: To establish the frequency and nature of space occupying lesions of the central nervous system (CNS) that mimic neoplastic growths. PATIENTS AND METHODS: We reviewed the clinical records, imaging and neuropathological studies of patients operated in different hospitals of Maracaibo, Venezuela during the period January 1 1996 July 31 2002. These patients had a pre operative diagnosis of CNS tumor, and their definitive diagnosis was non neoplastic disease. RESULTS: The 33 cases of expansive, non neoplastic growths represented 8% of 408 CNS lesions diagnosed during the study period. Approximately two thirds of the cases (63,36%) consisted of either inflammatory or vascular lesions, whereas the rest of the cases grouped miscellaneous conditions. CONCLUSIONS: Even though it is not frequent that non neoplastic lesions of the CNS mimic expansive growths of neoplastic nature, on occasions the clinical and neuroimaging features of both groups of entities are remarkably similar.

[Clinical and tomographic aspects of hemorrhagic cerebrovascular disease associated with hypertensive crisis in adults under 50 years of age]. / Aspectos clínicos y tomográficos de la enfermedad cerebrovascular hemorrágica asociada con crisis hipertensiva en adultos menores de 50 años.

The purpose of this study was to analyze both the clinical and tomographic aspects of the hemorrhagic cerebrovascular disease (HCd), associated with hypertensive crisis in adults under 50 years of age. Forty six patients, who were not under anticoagulant therapy, were not using illegal drugs, who had not a cerebral tumor disease, and who had neither arteriovenous malformations nor past traumatic episodes, were studied. Seventy eight percent of the patients had preexisted arterial hypertension, 30% of them had at least a previous emergency for a hypertensive crisis. Mortality for intracerebral hematoma (ICH) and for subarachnoid hemorrhage (SAH) was 21% and 23% respectively. In 68% of the cases, ICH was located in the deep structures of the brain. Asymmetric ventricular system, compression or the absence of mesencephalic cisterna were significantly associated (p > 0.01; p > 0.001 respectively) with higher mortality. There was not a significant difference between the deceased and the survivors in relation with their systolic and diastolic arterial pressure on admission to the emergency unit. A significant positive relation was found between the severity of the injury (percentage of patients with an Scale Coma Glasgow < or = 8 points) and the mortality percentage for the type of HCd (r = 0.81 for ICH; p < 0.001, r = 0.98 for SAH; p < 0.001). Age and a low Scale Coma Glasgow score on the admission, represent unfavorable prognostic factors. Due to the different criteria used to evaluate the tomographic characteristics of intracerebral hematomas, comparisons of the present results with other findings can be difficult.