Optic disc metastasis presenting as an initial sign of recurrence of adenoid cystic carcinoma of the larynx.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Mizota.
Explore the source record for details and available documents.
Purpose: To investigate the optimal pulse energy to do sclerostomy with an erbium YAG laser.Materials and Methods: The experiments were performed in enucleated porcine eyes. We changed pulse energy and examined the effects on surrounding tissue.Results: With the increase of pulse energy, the effects of the laser extended to the area surrounding the laser probe. At the threshold energy for doing full-thickness sclerostomy, the total energy was significantly higher than with higher pulse energy. And with pulse energy higher than 2 mJ, the total energy did not show any significant change. Histopathologically, the damaged area around sclerostomy became larger with the increase of pulse energy.Conclusion: The optimal energy to do full-thickness sclerostomy with this system seemed to be 2 mJ.
Purpose: The morphological observation of the human retinal changes caused by severely elevated intraocular pressure (IOP) in congenital glaucoma.Method: Light and electron microscopy.Subjects: One eye of a 15-year-old boy diagnosed as having congenital glaucoma was obtained after he had suffered from severe visual disturbance and ocular pain because of extensive elevated IOP, corneal leucoma, and exophthalmos.Results: Ganglion cells and nerve fibers in the inner layer were lost and replaced by Müller cell processes. The cellular elements in the outer layer were regularly arranged, but these cytoplasmic organelles were not very well developed. Most of the cellular elements of the whole retina contained many dense bodies. The retinal capillaries in the nerve fiber layer were lost or severly damaged, but some of these in the inner plexiform layer were intact. In the retinal arteries and veins marked thickening of the adventitial tissues was observed. These tissues consisted of remarkably increased and irregularly arranged collagen fibers, and a few elastic fibers scattered in some parts.Conclusion: It appeared that the pathological changes in the inner layer of the retina were caused by ischemia. The retinal vascular abnormality was thought to be the result of protective reaction against the severly elevated IOP.
Explore the source record for details and available documents.
A 38-year-old woman presented with diabetes insipidus. The T1-weighted images showed a loss of the hyperintense signal of the posterior pituitary and thickening of the pituitary stalk. DDAVP was started with the diagnosis of lymphocytic infundibulo-neurohypophysitis (LINH). Three months later, she complained of right visual acuity loss. MRI revealed right optic nerve swelling, compatible with the diagnosis of the retrobulbar optic neuritis. She had two other such episodes in the next 3 months. She developed a transient oculomotor and abducens nerve palsies as well. Each time the symptoms disappeared with corticosteroid therapy. The pituitary stalk became normal in size 6 months later. LINH and recurrent optic neuritis occurred in a short duration. Accordingly, a common causative background is suspected. Since the auto-immune process has been hypothesized as a cause of optic neuritis, our case may present further clinical evidence to support the hypothesis of an auto-immune mechanism for LINH.
PURPOSE: To investigate the role played by docosahexaenoic acid (DHA) in the retina, and more specifically, its ability to protect the retina from kainic acid (KA)-induced retinal damage. METHODS: Three-week-old female Wistar rats were used. DHA (1000 mg/kg per day) was fed to the rats for 7, 14, and 28 days, and the concentrations of DHA and arachidonic acid (AA) in the retina and serum were measured. In another group of rats, the right eyes were injected intravitreally with 3.12 nanomoles KA after DHA supplementation for 14 days. Electroretinograms (ERGs) elicited by different stimulus intensities were recorded before and on days 1, 7, and 14 after the KA injection. The amplitudes and implicit times of the a- and b-waves were compared. The number of cells in the ganglion cell layer (GCL) and inner nuclear layer (INL) were compared by histopathologic examination. RESULTS: The concentration of DHA in the serum and retina increased after DHA supplementation. The concentration of AA in serum decreased with DHA supplementation, but the concentration of AA in retina did not show any significant change. The b-waves of the ERGs recorded after KA injection were significantly attenuated in both groups of rats. However, the attenuation was significantly less in the DHA-supplemented rats than in gum arabic-supplemented control rats. The numbers of cells in the INL and GCL were significantly higher in DHA-supplemented rats. CONCLUSIONS: These results indicate that DHA supplementation can partially counteract KA neurotoxicity in the rat retina. DHA may play a role in modulating neuronal excitability by reducing KA-induced responses in the retina.
BACKGROUND: We report a 38-year-old female suffering from bilateral optic neuritis with lymphocytic adenohypophysitis. CASE: The initial symptom of the 38-year-old-female was diabetes insipidus. Magnetic resonance imaging showed swollen pituitary stalk and disappearance of the T1 shortening of the neurohypophysis. Immunological tests showed that the serum anterior pituitary antibody was positive. These findings suggested lymphocystic adenohypophysitis. Bilateral optic neuritis also occurred and the pattern visual evoked cortical potential (VECP) demonstrated increased P100 peak latency and reduction of amplitude. After steroid pulse therapy, the visual acuity and field improved and the pattern VECP became normal. Temporal hemianopia was not noted. CONCLUSION: A direct infiltration of the inflammatory change in the pituitary gland or some autoimmune problem was considered as a cause of the optic neuritis. In contrast to the VECPs of multiple sclerosis patients, the prolonged peak latency of pattern VECPs of this case were shortened in accordance with the recovery of visual acuity.
PURPOSE: To determine whether the Hsp27 protein can rescue retinal ganglion cells (RGCs) of rats from ischemia-reperfusion injury. METHODS: Retinal ischemia was induced in rats by clamping the ophthalmic artery within the dural sheath of the optic nerve. Immediately after removing the clamp and beginning the reperfusion, Hsp27 protein solution was injected into the vitreous, and electroporation was applied. To determine whether Hsp27 entered the RGCs, anti-Hsp27 immunohistochemistry was performed. The retinal damage was evaluated by counting the number of RGCs retrogradely labeled by 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine percholorate (diI) injected into the superior colliculus, and also by comparing the ratio of TUNEL-positive to all RGCs in the RGC layer. RESULTS: Electroporation successfully delivered Hsp27 protein into RGCs. In the Hsp27 electroinjected group, the number of RGCs 7 days after ischemia-reperfusion was significantly higher than in the control groups. The ratio of TUNEL-positive cells to all RGCs was lower in the group electroinjected with Hsp27 protein. CONCLUSIONS: Electroporation of Hsp27 protein into RGCs increased the resistance of the RGCs to the apoptosis induced by ischemia-reperfusion injury.
PURPOSE: To evaluate whether and how VECPs are useful in differentiating ION from ON. METHODS: We retrospectively studied 27 patients with non-arteritic ION and 69 patients with ON using pattern visually evoked cortical potentials (PVECPs) to 3 rev/sec stimulation (transient) and 12 rev/sec stimulation (steady-state). RESULTS: In patients with ION, non-recordable responses were found in 25% of those with transient VECP and in 74% of those with steady-state VECP. In ON patients, non-recordable responses were found in 34% of those with transient VECP and in 64% of those with steady-state VECP. The average peak latency of P100 component in those with ION was significantly shorter than in those with ON. The amplitude ratio (affected eye/fellow eye) of steady-state VECP was significantly higher in those with ION than in those with ON. The amplitude ratio of P100 showed no significant differences between groups. CONCLUSION: The P100 peak latency of transient VECPs and the amplitude of steady-state VECPs have the potential to differentiate between ION and ON.
PURPOSE: To investigate the optimal pulse energy to do sclerostomy with an erbium YAG laser. MATERIALS AND METHODS: The experiments were performed in enucleated porcine eyes. We changed pulse energy and examined the effects on surrounding tissue. RESULTS: With the increase of pulse energy, the effects of the laser extended to the area surrounding the laser probe. At the threshold energy for doing full-thickness sclerostomy, the total energy was significantly higher than with higher pulse energy. And with pulse energy higher than 2 mJ, the total energy did not show any significant change. Histopathologically, the damaged area around sclerostomy became larger with the increase of pulse energy. CONCLUSION: The optimal energy to do full-thickness sclerostomy with this system seemed to be 2 mJ.
PURPOSE: The morphological observation of the human retinal changes caused by severely elevated intraocular pressure (IOP) in congenital glaucoma. METHOD: Light and electron microscopy. SUBJECTS: One eye of a 15-year-old boy diagnosed as having congenital glaucoma was obtained after he had suffered from severe visual disturbance and ocular pain because of extensive elevated IOP, corneal leukoma, and exophthalmos. RESULTS: Ganglion cells and nerve fibers in the inner layer were lost and replaced by Müller cell processes. The cellular elements in the outer layer were regularly arranged, but these cytoplasmic organelles were not very well developed. Most of the cellular elements of the whole retina contained many dense bodies. The retinal capillaries in the nerve fiber layer were lost or severely damaged, but some of these in the inner plexiform layer were intact. In the retinal arteries and veins marked thickening of the adventitial tissues was observed. These tissues consisted of remarkably increased and irregularly arranged collagen fibers, and a few elastic fibers scattered in some parts. CONCLUSION: It appeared that the pathological changes in the inner layer of the retina were caused by ischemia. The retinal vascular abnormality was thought to be the result of protective reaction against the severely elevated IOP.
34 patients with indirect traumatic optic neuropathy were studied to identify factors affecting outcome and surgical indications. 12 cases (13 eyes = group A) underwent surgery and 24 patients (24 eyes = group B) were managed without surgery. Age, optic canal fracture, visual acuity before treatment (initial visual acuity) and days until surgery (only group A) were employed as variables. Visual acuity improved significantly more in patients with initial visual acuity, hand movement (HM) or better than in those with initial visual acuity for light perception (LP) only or worse. When initial visual acuity was HM or better, vision improved significantly more in patients with surgery than in those without surgery (p = 0.0003 by Mann-Whitney U test). Days until surgery were correlated with visual improvement in patients with visual acuity HM or better. Age and optic canal fracture did not affect visual improvement or influence the decision for or against surgery.
The retinal toxicity of botulinum toxin A (BTA) was electroretinographically studied in rats. Sixteen rats were injected intravitreally with 10 ng of BTA. A response-amplitude series was recorded before and 1, 6, 13 and 21 days after the injection of BTA. BTA did not alter the amplitude and the peak latency of the a-wave. The amplitude of the b-wave was not changed except for 2 rats, in which the b-wave was diminished. The peak latency of the b-wave was significantly prolonged after injection of 10 ng BTA (p < 0.05). Except for these latter 2 rats, the results indicated that the dosage used therapeutically appears to have no deleterious effect on retinal integrity or function at least in the short term, but multiple injections or higher doses of BTA could alter retinal function.
Explore the source record for details and available documents.
PURPOSE: To compare the diagnostic value for optic neuritis between transient pattern visual evoked potentials (PVECP) and steady-state PVECP. SUBJECTS & METHODS: We retrospectively studied 86 eyes of 69 patients with optic neuritis who visited our clinic. PVECPs to 3 rev/sec stimulation (transient) and 12 rev/sec stimulation (steady-state), were recorded in all patients. RESULTS: All of the cases with non-recordable transient PVECP showed non recordable steady-state PVECP Conversely, the cases with non-recordable steady-state PVECP often showed measurable transient PVECP where the latency of the P100 component was delayed. In 51 cases with unilateral optic neuritis, the amplitude ratio of the P100; affected eye/non-affected eye was significantly smaller in the steady-state PVECP than in the transient PVECP CONCLUSION: To detect visual dysfunction in optic neuritis, a steady-state PVECP was more sensitive than a transient PVECP.
A 2-year and 7-month-old boy had sudden visual loss in both eyes and showed bilateral optic neuritis without systemic symptoms. Steroid therapy improved his visual acuity from 0.077 and 0.053 to 1.0 at 7 months after onset. Magnetic resonance imaging (MRI) of the brain showed high density in both optic nerves and multiple lesions in the white matter that were enhanced by gadolinium. We considered the diagnosis of demyelinating disease. Follow-up MRI showed no abnormal lesion. Both transient and steady-state pattern visually evoked cortical potentials were nondetectable at the onset, and the P100 component of the transient pattern reversed visually evoked cortical potential appeared to be delayed thereafter. It has since become shorter in parallel with visual acuity improvement.
ERGs and the azide responses were recorded from mice before and periodically up to 6 weeks after retinal pigment epithelium (RPE) damage by iodate injection to follow the recovery of retinal pigment epithelium and retinal function. At 14 days postinjection, there was a partial recovery of the maximal b-wave amplitude and the azide response but no further recovery was found after 14 days. The retinal sensitivity showed a slow recovery, and at 6 weeks postinjection did not differ from the pre-iodate sensitivity. These findings correlated with histological observations. We concluded that the recovery in ERGs resulted from RPE recovery and the large patchy area of recovered retina functioned normally.
Dp260 is a C-terminal isoform of dystrophin and is expressed specifically in the retina. Abnormal electroretinograms (ERG) in some Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) patients are likely linked to a disruption of Dp260. To clarify the importance of Dp260 in the retina, we examined dystrophin exon 52 knock-out mice, whose expression of Dp260 is impaired. We also confirmed the localization of Dp260 in the outer plexiform layer (OPL) of the retina. Disruption of Dp260 causes a change in the localization of beta-dystroglycan, which is normally found in the OPL of the retina. This suggests a requirement for Dp260 for normal formation of the dystrophin-dystroglycan complex in the retina. Dp71, also expressed in the retina, was, however, not detected in the OPL. The difference in localization of Dp260 and Dp71 implies that the two isoforms have different functions. The dystrophin exon 52 knock-out mice had a prolonged implicit time of the b-wave in ERG, although no significant change was observed in amplitude. These ERG findings differed from those of DMD and BMD patients, especially with regard to amplitude of the b-wave, but make it clear that Dp260 is required for normal electrophysiology.