Fixation point after successful macular hole surgery with internal limiting membrane peeling.

BACKGROUND AND OBJECTIVE: This study evaluated the fixation points of macular holes using scanning laser ophthalmoscope microperimetry before and after surgery with internal limiting membrane peeling. PATIENTS AND METHODS: This prospective non-comparative study examined 21 eyes (21 patients) with macular holes. Hole size and distance between preoperative and postoperative fixation points were measured. RESULTS: The fixation points were located on the superior edge of the macular hole in 18 (86%) cases preoperatively and shifted centrally in 15 (71.4%) cases postoperatively. Macular hole size correlated well with the distance moved by the fixation points (r = .83, P < .0001). CONCLUSION: Scanning laser ophthalmoscope microperimetry facilitated pinpointing of fixation points before and after surgery. The correlation between macular hole size and fixation point shift suggests that the retina around the hole moves centripetally after surgery.

Involvement of retinal neurons and pigment epithelial cells in a murine model of sandhoff disease.

BACKGROUND/AIMS: To investigate the effects of deficient degradation of glycolipids on the morphological appearance of all retinal cells in a murine model of G(M2) gangliosidosis (Sandhoff disease). METHODS: The morphological appearance of the retina in Sandhoff mice at symptomatic stages (3 and 4 months of age) was examined by immunohistochemistry, lectin histochemistry and electron microscopy. RESULTS: Under a light microscope, intense immunoreactivity for G(M2) ganglioside was observed in the ganglion cell, inner plexiform, and inner nuclear layers in the Sandhoff mice. The ganglion cell layers and retinal pigment epithelium in the Sandhoff mice were stained intensely with concanavalin A agglutinin and succinylated wheat germ agglutinin. Ultrastructural studies revealed numerous inclusions in the cytoplasm of retinal ganglion cells and other neuronal cells (particularly amacrine cells), whereas we failed to detect apparent involvement of photoreceptor cells. In addition to the cytoplasmic inclusions in the retinal neurons, vacuolation was evident in the retinal pigment epithelium. CONCLUSION: These findings suggest that neuronal cells and pigment epithelial cells are more vulnerable to the deficient ganglioside degradation than other retinal cells in Sandhoff mice.

[Case of unilateral alteration due to hypertensive encephalopathy].

We report a patient of a 20-year-old woman of Takayasu's arteritis and hypertensive encephalopathy. The symptoms started with headache and vomiting following status epilepticus. On arrival at the emergency room in our hospital, fever was apparent and cerebrospinal fluid examination revealed pleocytosis. After the admission, the patient presented with hypertension, decreased right brachial pulse and the difference between bilateral brachial arterial blood pressures on examination. There had been no history of arterial hypertension. The MR angiography revealed stenoses of the bilateral cervical, especially right cervical, right middle cerebral and left renal arteries. Brain MRI showed transient hyperintense lesions of the left fronto-parieto-occipital cortices and subcortical white matter in FLAIR and diffusion weighted images. These alterations suggested the presence of reversible vasogenic edema induced by hypertensive encephalopathy. We need to be aware of young patients with convulsion, especially young women, who has arterial hypertension as well as the difference with blood pressures between extremities.

Impaired neurite outgrowth in the retina of a murine model of Sandhoff disease.

PURPOSE: To investigate the effects of lysosomal storage on the morphologic appearance and the neurite outgrowth capability of the retina in a mouse model of G(M2) gangliosidosis (Sandhoff disease). METHODS: Histopathologic appearances of retinas in Sandhoff (SD) mice at 3 and 4 months of age were examined by light and electron microscopy. Retinas of SD mice and wild-type (WT) mice at 1, 2, and 4 months of age were cultured in collagen gel in the presence or absence of brain-derived neurotrophic factor (BDNF), and neurite outgrowth was examined. RESULTS: Morphologic studies revealed accumulation of G(M2) ganglioside in the retinal ganglion cells of SD mice in a time-dependent manner. The number of neurites from the retinal explants after 7 and 10 days in culture were significantly lower in 2- and 4-month-old SD mice than in the age-matched WT mice. The application of BDNF significantly improved neurite outgrowth from the retina in both SD and WT mice at 2 months of age. At 4 months of age, BDNF was much less effective at stimulating neurite outgrowth in the retina of SD mice than in retina of WT mice. CONCLUSIONS: These results indicate that lysosomal storage of G(M2) ganglioside impairs the capability of neurite outgrowth in retinal ganglion cells in culture and that BDNF is effective at diminishing this impairment during the early stage of the disease.

The role of c-fos in cell death and regeneration of retinal ganglion cells.

PURPOSE: To investigate the effect of c-fos on apoptotic cell death and regeneration of damaged retinal ganglion cells (RGCs) in tissue culture of retinal explants. METHODS: Retinas from transgenic mice carrying the exogenous c-fos gene under the control of the interferon (IFN)-alpha/beta inducible Mx-promoter (Mx-c-fos), c-fos-deficient mice, and littermate control mice were dissected and cultured in a three-dimensional collagen gel culture system, followed by an analysis of TdT-dUTP terminal nick-end labeling (TUNEL) staining and measurement of neurites that emerged from explants. RESULTS: Compared with littermate control mice, Mx-c-fos transgenic animals showed a higher ratio of TUNEL positivity in the RGC layer from early in the culture period that correlated with the small number of regenerating neurites. In contrast, the c-fos-null mutated mice showed a still-lower ratio of TUNEL-positive cells. Nevertheless, the number of regenerating neurites was significantly lower in the initial phase, although the drastic increase in density of neurite regeneration was observed in the late period of culture. CONCLUSIONS: These findings suggest that c-fos is involved in both apoptotic cell death and regeneration of damaged RGCs. Elucidation of the precise c-fos-mediated cascade involved in RGC apoptosis and regeneration is significant in realizing neuronal survival and regeneration.

Scleral buckling and pars plana vitrectomy for rhegmatogenous retinal detachment: an analysis of 542 eyes.

PURPOSE: To investigate the anatomical success rates of scleral buckling (SB) and pars plana vitrectomy (PPV) performed for rhegmatogenous retinal detachment (RRD) in a large case series and to identify prognostic factors for the primary anatomical success rates of surgical techniques. METHODS: We reviewed 542 consecutive eyes for primary RRD in this retrospective study. Follow-ups were performed for at least six months. In each of the two groups, 271 eyes were examined. The main outcome measure was the primary anatomical success rate. Multivariate analysis was also performed to determine whether independent risk factors of the preoperative parameters for redetachment exist. RESULTS: The primary anatomical success rates were 93.7% and 96.3% in the SB and PPV groups; and the final anatomical success rates were 100% in both groups (each with 271 eyes). In the SB group, eyes with macula-off had significantly lower primary anatomical success rates than those with macula-on (p = 0.002). Preoperative break location or lens status had no significant effect on primary anatomical success rates in either group. Multivariate logistic regression analysis using four variables, namely, sex, posterior vitreous detachment, macular status and preoperative visual acuity, showed that the macular status was an independent risk factor for redetachment in the SB group (p = 0.039, odds ratio 3.7). The six-month follow-up visual acuity was significantly better than the preoperative visual acuity in both groups (p ≤ 0.001). CONCLUSIONS: Both SB and PPV gave excellent primary and final anatomical success rates. The macula-off status was associated with a lower success rate in the SB group, although break location and lens status had no significant effect on success rates in either group.

Silicone intraocular lens surface calcification in a patient with asteroid hyalosis.

PURPOSE: To confirm a substance presence on the posterior intraocular lens (IOL) surface in a patient with asteroid hyalosis. METHODS: An 80-year-old man had IOLs for approximately 12 years. Opacities and neodymium-doped yttrium aluminum garnet pits were observed on the posterior surface of the right IOL. Asteroid hyalosis and an epiretinal membrane were observed OD. An IOL exchange was performed on 24 March 2008, and the explanted IOL was analyzed using a light microscope and a transmission electron microscope with a scanning electron micrograph and an energy-dispersive X-ray spectrometer for elemental analysis. To confirm asteroid hyalosis, asteroid bodies were examined with the ionic liquid (EtMeIm+ BF4-) method using a field emission scanning electron microscope (FE-SEM) with digital beam control RGB mapping. RESULTS: X-ray spectrometry of the deposits revealed high calcium and phosphorus peaks. Spectrometry revealed that the posterior IOL surface opacity was due to a calcium-phosphorus compound. Examination of the asteroid bodies using FE-SEM with digital beam control RGB mapping confirmed calcium and phosphorus as the main components. CONCLUSIONS: Calcium hydrogen phosphate dihydrate deposits were probably responsible for the posterior IOL surface opacity. Furthermore, analysis of the asteroid bodies demonstrated that calcium and phosphorus were its main components.

Cultured adult animal neurons and schwann cells give us new insights into diabetic neuropathy.

Since we introduced cultured dorsal root ganglia (DRG) neurons from streptozotocin (STZ)-induced diabetic mice as "an in vitro model to study diabetic neuropathy" (Sotelo et al., 1991), more than 30 papers have been devoted to the study of diabetic neuropathy with culture systems of neurons and Schwann cells derived from adult animals. So far, methods for dissociated cell culture of peripheral neurons (mainly DRG neurons) and Schwann cells, and for explant culture of peripheral ganglia and retinas have been applied to diabetic animals or patients. In addition to these diabetic cells, adult animal neurons and Schwann cells cultured under high glucose conditions and adult animal neurons exposed to diabetic serum have been utilized. The findings from these culture models clearly show that the exposure of mature neurons and Schwann cells to hyperglycemic conditions in vivo or in vitro can alter their biophysical and biochemical properties (e.g., cell viability, neurite outgrowth activity, polyol metabolism and electrophysiological features). Therefore, the cultured neurons and Schwann cells can be useful tools for investigating the precise mechanisms leading to diabetic neuropathy and the efficacy of therapeutic agents for the prevention and treatment of that condition.

Brain-derived neurotrophic factor enhances neurite regeneration from retinal ganglion cells in aged human retina in vitro.

To investigate the capability of neurite regeneration from retinal ganglion cells (RGCs) in an adult human retina and to evaluate the effect of neurotrophin on the neurite regeneration, an in vitro model for retinal explants was developed. A human retina was obtained from a 70 year old patient with retrobulbar carcinoma. The retina was excised and the retinal explants were cultured in serum-free medium with or without brain-derived neurotrophic factor. The capability of neurite regeneration was evaluated by counting the numbers of outgrowing neurites outside the retinal explants. In culture without brain-derived neurotrophic factor (control), there was no neurite outgrowth from the retinal explants after 2 days. And at 3 days in culture, a small number of outgrowing neurites were first observed outside the retinal explants. In contrast, within 24 hr in culture with brain-derived neurotrophic factor, there were a considerable number of elongating neurites with spread growth cones from the retinal explants. Immunohistochemical analysis revealed that these neurites were derived from RGCs. The addition of brain-derived neurotrophic factor increased the number of outgrowing neurites approximately 10-fold compared to that of the control at 3 days in culture. The enhancement of neurite regeneration induced by brain-derived neurotrophic factor continued for longer than 1 week in culture. In conclusion, an aged human retina can regenerate neurites from RGCs in vitro and brain-derived neurotrophic factor significantly promotes the regeneration.