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T Fukuchi

Publications and source records attributed to T Fukuchi.

86 records · Page 5Linked to original sources

[A case of alternating Tolosa-Hunt syndrome].

A 50-year-old woman developed third, fourth, and fifth cranial nerve palsies in the right associated with frontal pain in the ipsilateral side. Oral administration of prednisolone (30 mg/day) was initiated. The painful ophthalmoplegia improved dramatically following this treatment. Three months later, the patient developed the third, fourth, and fifth cranial palsies in the left which was contralateral to the previous episode. The patient had pain in the left frontal region. The corticosteroid therapy was again effective. Cavernous sinus and orbital venographies demonstrated a constriction of the right superior ophthalmic vein in the first and third parts, with a partial filling of the cavernous sinus. The left superior vein and cavernous sinus were normal. A left carotid arteriogram showed a slight deformity of the carotid siphon in the left. The glucose tolerance test demonstrated a mild diabetic pattern. Diabetic ophthalmoplegia can also be suspected in this case, however, the finding of a partial filling of the right cavernous sinus was indicative of Tolosa-Hunt syndrome. Therefore this case was diagnosed as Tolosa-Hunt syndrome. Alternating relapsing Tolosa-Hunt syndrome involving the third, fourth and fifth cranial nerve as seen in this case is very rare. There are many diseases which may demonstrate similar symptoms; i.e. parasellar tumor, aneurysm, diabetic ophthalmoplegia, multiple cranial neuropathy, etc. The pathologic process involved in Tolosa-Hunt syndrome is poorly understood and it appears that the clinical entity of this syndrome should be questioned. We believe that it is necessary to clarify the precise pathologic process involved in this syndrome and its relation with other similar syndromes exhibiting similar symptoms.

Female↗

Comparative study of experimental choroidal neovascularization by optical coherence tomography and histopathology.

PURPOSE: To study the development, progression, and regression of experimental choroidal neovascularization (CNV) by correlating the cross-sectional images from sequential optical coherence tomography (OCT) with histopathologic sections of the same retinal regions. METHODS: Laser photocoagulation was performed in the posterior pole of the eye of 4 rhesus monkeys to induce CNV. Funduscopy, fluorescein angiography (FAG), and OCT were performed on day 1 and weekly for 13 weeks. Histological serial sections of CNV tissue were compared to corresponding OCT images. RESULTS: In the developmental stage of CNV, the CNV was observed by OCT as a nodular high reflex area continuing from the highly reflective retinal pigment epithelium (RPE). Histopathological studies showed that the CNV was composed of tightly packed proliferated RPE and immature vascular endothelial cells. In the active stage, OCT revealed a thick multi-layered high reflex area under the sensory retina. This high reflex area corresponded with the CNV membrane that consisted of newly formed blood vessels with wide vascular lumens and proliferated spindle-shaped RPE cells. In the regressive stage, OCT revealed a dome-like, white-colored highly reflective layer continuing from the RPE layer with moderate reflection beneath the layer. Histopathologically, the neovascular tissue was enveloped by mono-layered, cuboidal-shaped RPE cells with melanin granules. CONCLUSION: Optical coherence tomography images clearly demonstrated the positional relationship between the CNV and the RPE. Optical coherence tomography imaging provides information on the CNV which complements conventional examinations by funduscopy and FAG.

Animals↗

Cell adhesion glycoproteins in the human lamina cribrosa.

PURPOSE: The distribution of the cell adhesion glycoproteins, laminin, fibronectin, tenascin, vitronectin, thrombospondin, and entactin/nidogen, was examined in the human lamina cribrosa. METHODS: Frozen sections of the optic nerve head from 7 normal human elderly donors were stained by immunohistochemistry. RESULTS: All six glycoproteins were detected in this tissue. While laminin and entactin/nidogen were observed linearly, reflecting the localization of basement membranes, fibronectin was identified diffusely. Marked tenascin immunoreactivity was apparent in the lamina cribrosa, but little or no tenascin staining was detected in the sclera. Vitronectin showed a fine fibrillar staining pattern in the lamina cribrosa, and, to a lesser extent, in the sclera and pial septa. Thrombospondin staining was apparent only in the sclera and the lamina cribrosa, which traversed the optic nerve. CONCLUSIONS: These results indicate that extracellular matrix components in the lamina cribrosa differ from those in the sclera or pial septa. This study is the first report that the human lamina cribrosa includes vitronectin and thrombospondin.

Aged↗

Distribution and expression of transforming growth factor-beta and platelet-derived growth factor in the normal and glaucomatous monkey optic nerve heads.

PURPOSE: Remodeling of the extracellular matrix occurs in the lamina cribrosa in progressed glaucomatous optic nerve damage including disc cupping. We examined immunohistochemical changes in the transforming growth factor (TGF)-beta and platelet-derived growth factor (PDGF) in the optic nerve head in an experimentally induced glaucoma model. METHODS: We used 3 cynomolgus and 2 Japanese monkey eyes. Glaucoma was induced by repeated argon laser photocoagulation of the chamber angle. Eyes were enucleated after disc cupping had formed 3 to 5 months after photocoagulation. The optic nerve head was examined for expression of TGF-beta1, -beta2 and -beta3 and PDGF-A and -B in frozen sections and by the biotin ExtraAvidin-alkali phosphatase method. RESULTS: Normal monkey eyes showed TGF-beta1, -beta2 and -beta3, and PDGF-A and -B in the optic nerve head including the nerve fibers, glial cells, and vascular cells. Glaucomatous eyes showed stronger expression of TGF-beta1 and -beta2 in the glial cells around the lamina cribrosa. The staining intensities for TGF-beta3, PDGF-A and -B were the same as in normal eyes. CONCLUSIONS: Eyes with experimental glaucoma showed higher expression of TGF-beta1 and -beta2 around the lamina cribrosa. These findings may show upregulation of extracellular matrix production as related to remodeling of the lamina cribrosa in glaucoma.

Animals↗

Experimental glaucoma model in the rat induced by laser trabecular photocoagulation after an intracameral injection of India ink.

A simple and reproducible rodent glaucoma model is required to elucidate the pathophysiology of damage to the optic nerve. We developed chronically elevated intraocular pressure (IOP) unilaterally in rats by injecting india ink into the anterior chamber of one eye using a 30-gauge needle. One week later, trapped carbon particles in the chamber angle formed a black band along the corneal limbus in the injected eyes. We performed direct laser photocoagulation without a gonio lens, and selectively burned the trabecular meshwork. Intraocular pressure was measured every week and laser photocoagulation was repeated until mean IOP in the experimental eyes rose above 25 mmHg. Unilateral IOP elevation was attained in all rats within 4 weeks. Twelve weeks after ink injection, we sacrificed the rats and excised the eyes for histologic analysis. The anterior chamber angle showed peripheral anterior synechia caused by laser photocoagulation, and carbon particles were engulfed by macrophages that infiltrated the ciliary cleft. In the optic nerve head, a remarkable decrease in the nerve fiber layer and cavernous degeneration were observed, suggesting glaucomatous optic nerve damage. This experimental rodent model should facilitate the study of the complex mechanisms involved in glaucoma.

Animals↗

Occult retinal pigment epithelial detachment in hyperviscosity syndrome.

We document and evaluate a serous retinal detachment in a patient with hyperviscocity syndrome. Optical coherence tomographic images of the serous retinal detachment in a patient with hyperviscocity syndrome were correlated with slit-lamp biomicroscopic findings, fundus photographs, fluorescein angiograms, and indocyanine green angiograms. Fluorescein angiography demonstrated venous and capillary bed abnormalities but no leakage or pooling of fluorescein corresponding to the retinal pigment epithelial detachment (PED) beneath the serous retinal detachment. Indocyanine green angiogram disclosed a delay of intrachoroidal circulation. Optical coherence tomography (OCT) revealed a large retinal pigment epithelial detachment beneath the serous retinal detachment. The occult retinal PED beneath the neurosensory retinal detachment was detected only by OCT in a patient with hyperviscosity syndrome. We suggest that gamma globulin, which is the hyperviscosity material, accumulated in the subretinal pigment epithelial space and blocked the leakage or pooling of fluorescein corresponding to the retinal pigment epithelial detachment.

Diagnosis, Differential↗