J Miralles de Imperial

Retinal ganglion cell death after acute retinal ischemia is an ongoing process whose severity and duration depends on the duration of the insult.

In adult Sprague-Dawley rats we have investigated retinal ganglion cell survival after transient intervals of retinal ischemia of 30, 45, 60, 90 or 120 min duration, induced by ligature of the ophthalmic vessels. Animals were killed 5, 7, 14, 21, 30, 60, 90 or 180 days later and densities of surviving retinal ganglion cells were estimated in retinal whole mounts by counting cells labelled with diAsp. This dye was applied, 3 days prior to death, to the ocular stump of the intraorbitally transected optic nerve. We found that retinal ganglion cell loss after retinal ischemia proceeds for different lengths of time. All the ischemic intervals induced loss of retinal ganglion cells whose severity and duration was related to the length of the ischemic interval. Following 30 or 45 min of ischemia, cell loss lasted 14 days and caused the death of 46 or 50%, respectively, of the population of retinal ganglion cells. Sixty, 90 or 120 min of retinal ischemia were followed by a period of cell loss that lasted up to 90 days and caused the death of 75%, 87% or 99%, respectively, of the population of retinal ganglion cells. We conclude that retinal ganglion cell loss after retinal ischemia is an ongoing process that may last up to 3 months after the injury and that its severity and duration are determined by the ischemic interval.

Anatomical and functional damage in experimental glaucoma

Glaucoma is a progressive neurodegenerative disease caused by retinal ganglion cell (RGC) loss. One important risk factor for glaucoma is elevated intraocular pressure and thus many animal models are based on spontaneous or induced ocular hypertension (OHT). Using these models it has been shown that RGCs initially suffer an impairment of the active axonal transport that progresses to a lack of passive diffusion along the axon. This axonal damage eventually causes the death of the parent RGCs in pie-shaped sectors of the retina, but there is also diffuse RGC loss, without involving displaced amacrine cells. Recent data show that OHT results in a protracted insult to the inner and outer retina that causes functional alterations and ultimately, degeneration and death of cones.

Obstrucción de la vena central de la retina en portador de factor V de Leiden y variante G20210A de la protrombina

espanolCaso clinico: Varon de 55 anos con deficit de agudeza visual en ojo derecho y un episodio de trombosis venosa profunda en la pierna derecha cinco anos atras. Presentaba una obstruccion de la vena central de la retina. El estudio de trombofilia mostro mutaciones en el gen del factor V (factor Leiden) y de la protrombina (G20210A).El paciente fue anticoagulado, no precisando fotocoagulacion laser en su evolucion. Discusion: Diversos trastornos de la coagulacion originados por mutaciones geneticas se han relacionado con un riesgo elevado de oclusion venosa retiniana, aunque diversos estudios no han demostrado una asociacion estadisticamente significativa. EnglishCase report: A fifty-five year old man complained of diminished visual acuity in his right eye and reported a deep venous thrombosis in his right leg five years ago. Examination showed a central retinal vein occlusion in the right eye. Mutations in the factor V gene and prothrombin gene were found in a thrombophilia study. The patient was anticoagulated and no laser photocoagulation was required. Discussion: Various coagulation disorders induced by genetic mutations are often associated with an increased risk for retinal vein occlusion although there are no statistically significant associations reported in the literature.

Retinopatía proliferativa por radiación

espanolCaso Clinico: Mujer de treinta anos, tratada con radioterapia por un glioma frontal tres anos atras, que referia deficit de agudeza visual en el ojo izquierdo (OI). Presentaba una retinopatia isquemica proliferante en OI y no proliferante en el derecho, lo cual fue confirmado mediante angiografia fluoresceinica. La paciente fue panfotocoagulada, quedando estabilizada la agudeza visual Discusion: La retinopatia por radiacion puede aparecer muchos anos despues de aplicada esta, por lo que los pacientes que reciben radioterapia de cabeza y cuello deben ser controlados para detectarla precozmente ya que se pueden beneficiar del tratamiento con laser. EnglishCase report: A thirty year-old-woman that had received radiotherapy three years before for a frontal glyoma consulted because of diminished visual acuity in her left eye. Examination showed a proliferative radiation retinopathy in the left eye and non-proliferative radiation retinopathy in the right eye that was confirmed by fluorescein angiography. The patient was treated with panretinal photocoagulation, and her visual acuity remained stable. Discussion: Patients receiving cranial or neck radiotherapy should be followed for long periods of time because radiation retinopathy may appear many years after the treatment. Follow-up may permit early diagnosis of ischemic radiation retinopathy that can benefit from laser photocoagulation.

Esthesioneuroblastoma: an atypical form of manifestation.

Esthesioneuroblastoma is a rare tumor that originates in the olfactory epithelium and can invade the orbit. We report a case in which the first symptom was a post-traumatic paralysis of the IV cranial nerve. Whether the tumor itself or the trauma or a combination of the two factors caused the paralysis is discussed.