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1.
Rev. chil. neuro-psiquiatr ; Rev. chil. neuro-psiquiatr;47(1): 50-66, mar. 2009. ilus
Article in Spanish | LILACS | ID: lil-554889

ABSTRACT

Revision is made to 121 Chilean patients with progressive adult spastic paraparesis (PSPs) associated to HTLV-I. Epidemiologic, clinical, diagnosis and associated illnesses aspects are analyzed as well as the pathogenesis. The follow-up of patients during several years allowed defining the evolutional profile, establishing the causes of death and studying the virus' behavior. Pathogenesis hypothesis arose from the neuropathological search to define the mechanisms of damage supported on immunohystochemical studies. It was confirmed that the CNS illness is a degenerative process linked to a central axonopathy which expresses flaws in the axoplasmic transport, particularly affecting the corticospinal tracts, although there is a more extended myeloencephalic involvement. Furthermore, the virus is capable of producing a multisystemic illness that may simultaneously involve the nervous system; the hematological system; the exocrine glands; the hepatic, lung, muscular and bone parenchymas.


Se revisan las paraparesias espásticas progresivas del adulto (PEPAs) producidas por el HTLV-I, en 121 pacientes chilenos. Se analizan los aspectos epidemiológicos, clínicos, diagnósticos, las enfermedades asociadas, y la patogenia. El seguimiento de los pacientes durante varios años permitió definir el perfil evolutivo, establecer las causas de muerte y estudiar el comportamiento del virus. De los casos con anatomía patológica surgieron hipótesis, que han permitido definir mecanismos de daño, sustentados en estudios inmunohistoquímicos. Se pudo confirmar que la enfermedad del SNC es un proceso degenerativo, vinculado a una axonopatía central que expresa fallas del transporte axoplásmico, que afecta particularmente la vía corticoespinal, aunque existe un compromiso más extenso mielo-encefálico. Además, el virus es capaz de producir una enfermedad multisistémica, que puede comprometer simultáneamente el sistema nervioso, el sistema hematológico, las glándulas exocrinas, el parénquima hepático, pulmonar, muscular y óseo.


Subject(s)
Humans , Male , Adolescent , Adult , Female , Middle Aged , HTLV-I Infections/complications , Paraparesis, Tropical Spastic/etiology , Paraparesis, Tropical Spastic/mortality , Paraparesis, Tropical Spastic/pathology , Axons/pathology , Cause of Death , Clinical Evolution , Chile/epidemiology , Follow-Up Studies , Paraparesis, Tropical Spastic/physiopathology
2.
Article in Chinese | WPRIM | ID: wpr-412239

ABSTRACT

Purpose To explore the effects of cervical sympathetic nerve on the axoplasmic transport of the trigeminal nerve. Methods 48 Wistar rats were used with the right side as experimental side and the left side as control side.5 μl of 30% horseradish peroxidare(HRP) solution was injected into the symmetrical areas on both sides of the infraorbital regions.Then 0.4 ml of suspension made up of 0.2 ml 0.5% bupivacaine and 0.2 ml hydroprednisone-A was injected into C5 transverse process on the right side,and 0.4 ml of 0.9% normal saline on the control side.The animals survived for 4,6,8,10,12,14h,and were killed after perfusing through the ascending aorta.The superior cervical sympathetic ganglia and the trigeminal ganglia on both sides frozen sectioned,and treated with TMB method.The HRP labeled cells in the sections were observed under light microscope.The positive labeled cells were classified and counted.The sum of mean area and the mean optical density of HRP labeled cells in superior cervical sympathetic ganglia and the trigeminal ganglia on both sides were analysed by image pattern analysis system. Results The labeled cells were found in the trigeminal ganglia of the experimental sides after 6 h,the control side,8 h.The velocity of HRP axoplasmic transport of the experimental side was (5.50±0.95)mm/h,the control side (3.99±0.81)mm/h(P<0.01).The sum of mean area and the product of the sum of mean area and the mean optical density of HRP labeled cells in the trigeminal ganglia of the experimental side were larger than those of the control side (P<0.01).The labeled cells were found in the superior cervical sympathetic ganglia on both sides after 8 h.The sum of mean area and the mean optical density of HRP labeled cells in the superior cervical sympathetic ganglia on the control sides were larger than those of the experimental sides (P<0.01). Conclusions Cervical sympathetic nerve can affect the velocity of the axoplasmic transport of the trigeminal nerve.The cervical local block slows accelerates the axoplasmic transport of the cervical sympathetic nerve and the axoplasmic transport of the trigeminal nerve.

3.
Article in Chinese | WPRIM | ID: wpr-554798

ABSTRACT

Objective To observe the effects of ciliary neurotrophic factor (CNTF) on the recovery of axoplasmic transport following incomplete injury of the optic nerves (ON) of the adult rats. Methods Moderate injury of the optic nerves of 50 adult female rats was induced by crushing the optic nerves for 10 seconds using hemostatic forceps. Recombinant human CNTF (rhCNTF) was injected into the vitreous cavity of CNTF treated group at 0, 1, 2, 4, and 8 weeks after injury. However, the same volume of distilled water was injected into the vitreous cavity of the control rats. The changes of axoplasmic transport were assessed by anterograde labelling combined with horseradish peroxidase (HRP) at 1, 2, 4, 8, and 12 weeks after injury. Results The labelling density at ON distal to the site of injury by HRP obviously decreased at 1 and 2 weeks after injury, and gradually enhanced at 4 weeks and peaked at 8 weeks after injury. The recovery ratios of axoplasmic transport in CNTF treated group and control group at 8 weeks after injury were 31 86% and 12 87%, respectively. No HRP reaction product was observed in the superior colliculus at 1 and 2 weeks after injury. There was significant difference of the HRP anterograde labeling density in ON and the superior colliculus between the CNTF treated group and the control group during 4 to 12 weeks after injury ( P

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