RESUMO
Los quistes coloides son lesiones intracraniales con una incidencia calculada en tres individuos por millón de personas en un año. Son tumores benignos de la porción anterosuperior del tercer ventrículo. El flujo normal del líquido cefalorraquídeo puede ser interrumpido por un gran quiste que obstruya el foramen de Monro. Los signos y síntomas asociados engloban un espectro amplio de características, desde una cefalea o específica hasta datos de hipertensión intracraneal; algunos quistes coloides se dan en el comienzo agudo de una hidrocefalia y pueden llevar a una muerte súbita. Caso: presentamos el caso de un adolescente masculino de 13 años de edad, de raza negra, quien dos días antes de su fallecimiento había manifestado cefalea. Al examen de autopsia se evidenció un quiste coloide del tercer ventrículo que produjo una hidrocefalia aguda obstructiva, con edema cerebral severo y herniación de amígdalas cerebelosas. En este artículo comentamos las características principales del quiste coloide y realizamos una breve revisión bibliográfica...
Assuntos
Humanos , Masculino , Adolescente , Cistos , Hipertensão Intracraniana/etiologia , Terceiro Ventrículo/anormalidades , Terceiro Ventrículo/fisiopatologia , Costa RicaRESUMO
A heterogeneous population of ependymal cells lines the brain ventricles. The evidence about the origin and birth dates of these cell populations is scarce. Furthermore, the possibility that mature ependymal cells are born (ependymogenesis) or self-renewed (ependymal proliferation) postnatally is controversial. The present study was designed to investigate both phenomena in wild-type (wt) and hydrocephalic α-SNAP mutant (hyh) mice at different postnatal stages. In wt mice, proliferating cells in the ventricular zone (VZ) were only found in two distinct regions: the dorsal walls of the third ventricle and Sylvian aqueduct (SA). Most proliferating cells were monociliated and nestin+, likely corresponding to radial glial cells. Postnatal cumulative BrdU-labeling showed that most daughter cells remained in the VZ of both regions and they lost nestin-immunoreactivity. Furthermore, some labeled cells became multiciliated and GLUT-1+, indicating they were ependymal cells born postnatally. Postnatal pulse BrdU-labeling and Ki-67 immunostaining further demonstrated the presence of cycling multiciliated ependymal cells. In hydrocephalic mutants, the dorsal walls of the third ventricle and SA expanded enormously and showed neither ependymal disruption nor ventriculostomies. This phenomenon was sustained by an increased ependymogenesis. Consequently, in addition to the physical and geometrical mechanisms traditionally explaining ventricular enlargement in fetal-onset hydrocephalus, we propose that postnatal ependymogenesis could also play a role. Furthermore, as generation of new ependymal cells during postnatal stages was observed in distinct regions of the ventricular walls, such as the roof of the third ventricle, it may be a key mechanism involved in the development of human type 1 interhemispheric cysts.
Assuntos
Encéfalo/patologia , Epêndima/crescimento & desenvolvimento , Hidrocefalia/patologia , Terceiro Ventrículo/fisiopatologia , Fatores Etários , Animais , Animais Recém-Nascidos , Bromodesoxiuridina/metabolismo , Contagem de Células , Proliferação de Células , Modelos Animais de Doenças , Epêndima/ultraestrutura , Regulação da Expressão Gênica no Desenvolvimento/fisiologia , Proteína Glial Fibrilar Ácida/metabolismo , Transportador de Glucose Tipo 1/metabolismo , Camundongos , Camundongos Mutantes Neurológicos , Microscopia Eletrônica de Varredura , Antígeno Nuclear de Célula em Proliferação/metabolismo , Terceiro Ventrículo/citologia , Tubulina (Proteína)/metabolismoRESUMO
Commissural nucleus of the solitary tract (commNTS) lesions transitorily (first 5 days) reduce mean arterial pressure (MAP) in spontaneously hypertensive rats (SHR), and lesions of the tissue surrounding the anteroventral third ventricle (AV3V region) chronically reduce MAP in other models of hypertension. In the present study, we investigated the effects of combined AV3V+commNTS electrolytic lesions on MAP and heart rate (HR) in conscious SHR. Baseline MAP and HR were recorded in male SHR before and for the next 40 days after sham or AV3V lesions combined with sham or commNTS lesions. The AV3V lesions produced no change in MAP in SHR, while commNTS lesions reduced MAP acutely (121 +/- 2 to 127 +/- 3 mmHg in the 1st and 5th days, respectively, vs. prelesion: 192 +/- 4 mmHg) but not chronically (from 10 to 40 days). However, combined AV3V+commNTS lesions reduced MAP of SHR chronically (119 +/- 2 to 161 +/- 4 mmHg, in the 1st and 40th day, respectively, vs. prelesion levels: 186 +/- 4 mmHg) or sham-lesioned SHR (187 +/- 4 to 191 +/- 6 mmHg). Sympathetic and angiotensinergic blockade produced less reduction in MAP in SHR with AV3V+commNTS-lesions, and there was no relationship between changes on water and food intake, body weight, or urinary excretion produced by AV3V+commNTS lesions with the changes in MAP. The present findings suggest that in the absence of the commNTS, the AV3V region contributes to the hypertension observed in SHR by mechanisms that appear to involve enhanced angiotensinergic and sympathetic activity.