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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pseudophakic patient reported blurred vision and diplopia one year after the surgery. We suspected that the origin of both these problems was subluxation of the intraocular lens. His blurred vision was eliminated by a cylindrical spectacle lens at an oblique axis. Monocular diplopia could only be eliminated occasionally. The displacement of the IOL is shown photographically in this report.
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PMID:Optical management of posterior chamber lens tilt. 363 Dec 14

A 64-year-old male with an incomplete spinal cord injury had been taking baclofen 20 mg tid for 2 1/2 months without side effects. His blood urea nitrogen and serum creatinine rose from 13 and 0.9 mg%, respectively, to 59 and 2.8 mg% after ibuprofen 600 mg tid was begun. The patient displayed baclofen toxicity, developing confusion, disorientation, bradycardia, and hypothermia. His blood pressure dropped and he complained of blurred vision. Ibuprofen discontinuation and fluid repletion corrected the renal indices. Rapid tapering of baclofen was accompanied by reversal of baclofen toxicity. Patients taking baclofen must be monitored closely for toxicity when declining renal function is present. Clinicians should be alert to the possibility of renal insufficiency developing when ibuprofen is initiated. This case demonstrates the potential for ibuprofen-induced renal insufficiency to reduce baclofen clearance, thereby leading to baclofen toxicity. Published reports of ibuprofen-induced renal insufficiency are reviewed and pertinent pharmacokinetics of baclofen discussed.
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PMID:Baclofen toxicity associated with declining renal clearance after ibuprofen. 648 61

A 31-year-old man with spastic paraparesis (diagnosed when he was 10 years old) and hyperglycinemia (diagnosed when he was 19 years old) had an intermittently swollen right eye and blurred vision. His right upper eyelid was S-shaped and edematous, the lateral canthal tendon was flaccid, and the eyelid everted easily. After the floppy eyelid syndrome was diagnosed, the patient underwent a tarsal strip procedure to shorten and tighten the lax upper eyelid. This relieved his symptoms, which have not recurred in the year since surgery.
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PMID:Floppy eyelid with hyperglycinemia. 649 16

Bromocriptine therapy may cause regression of prolactinomas and GH producing adenomas, but there is only few reports about the effect of bromocriptine against nonfunctioning pituitary adenomas and there is no reports about its histopathological changes. We report a nonfunctioning pituitary adenoma, which remarkably regressed during and following bromocriptine therapy. A 47-year-old man developed blurred vision on January 20, 1981. He was pointed out of bitemporal hemianopsia and of his left palor optic fundus. His endocrinological condition was panhypopituitarism and no hypersecreting hormones were found. Cranial computerized axial tomography showed huge dumbbell shaped high density mass extending from the enlarged intrasellar area to the floor of the third ventricle. On treatment with bromocriptine, 5 mg daily for 3 days, his visual acuity and field was remarkably improved. Treatment was continued with gradually increased doses of bromocriptine to 15 mg and so, remarkable shrinkage of tumor size about 50% was seen by computerized axial tomography by a month. In addition, by eight months, the tumor reduced to 22%. Transsphenoidal surgery revealed centrally necrotic tumor mass surrounded by peripheral fibrous one. Because of fibrous and hemorrhagic tumour, we could not remove it totally. The pathological specimen was examined by light and transmission electron microscopy. The tumor was diffuse-type chromophobe adenoma partially intersected by hypertrophied fibrous interstitial materials. Some tumor cells were stained faintly eosinophilic. The cytoplasms were shrunken and the tumor cells were clumped. The immunostaining of tumor was negative to all anterior pituitary hormones. The intracytoplasmic organellae, for example, rough endoplasmic reticulum, Golgi apparatus, were scanty but prominant deformed mitochondria and small secretary granules (the size of about 90-150 nm) were found by transmission electron microscope. We think that the tumor cells had various responsiveness to this drug and the one extreme was destruction of the nucleus, the irreversible change, and the other extreme was some cytoplasmic reduction, the reversible change. The histopathological changes were almost the same as those of prolactinomas treated with bromocriptine. In conclusion, the mechanism of shrinkage of nonfunctioning pituitary adenomas treated with bromocriptine is unclear but it is worth while treating inoperable or recurrent large nonfunctioning pituitary adenomas with bromocriptine.
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PMID:[Size reduction of a nonfunctioning pituitary adenoma after bromocriptine therapy: case report]. 671 37

A 71-year-old male with a null cell pituitary macroadenoma was given peripituitary region radiotherapy (4,346 Gy units) over a 1-month-period and 6 weeks later developed the rapid onset of blurred vision, diplopia, ataxia, incoordination, cranial nerve palsy, somnolence, and respiratory distress. His fixed neurologic deficits required ventilatory support, feeding tube placement, and chronic hospitalization until his death 1 year later. At autopsy, necrotic foci with dystrophic axonal calcification were found throughout the brainstem, associated with mild focal vascular hyalinization but without fibrinoid necrosis, telangiectasias or large vessel abnormalities. This unusual case of fatal "early delayed" radiation injury is compared to previous literature cases.
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PMID:Necrotizing brainstem leukoencephalopathy six weeks following radiotherapy. 760 98

A 35-year-old man with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with acute bilateral optic neuritis is described. At age 33, he noticed a tingling sensation in his toes followed by weakness in the lower limbs. He was admitted to our hospital because he became unable to walk without support. His motor and sensory symptoms gradually resolved during 7 months admission only with physical rehabilitation. At age 35, in July 1988, he noticed a tingling sensation in his toes and fingers, which reached to the knees and elbows in October 1988, when he developed weakness in the lower limbs. Motor and sensory symptoms were almost stationary thereafter and in March 1989, he experienced bilateral blurred vision of acute onset without ocular pain. He was readmitted to our hospital in April 1989. The neurological examination revealed decreased visual acuity of both eyes without any abnormality of the optic disks, mild weakness on flexion and extension of toes, an absence of Achilles reflex, and distal impairment of pain and touch sensations in the upper limbs, and of pain, touch and vibration sensations in the lower limbs. After laboratory examinations, CSF protein was elevated (122 mg/dl), and sensory nerve conduction velocity of the right median nerve was decreased (37.1 m/sec). The sural nerve action potential was not elicited on electrical stimulation. Central scotoma was found in both eyes by the visual field examination. P100 latency was seen to be normal by repeated pattern-reversal visual evoked potential (VEP) studies. CT and MRI of the brain were unremarkable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with acute bilateral optic neuritis with normal findings on pattern-reversal visual evoked potential study]. 801 88

We report a 64-year-old man with recurrent bouts of blurred vision who died after developing an abdominal mass. He was well until June of 1985 when he was 59-years-old when he had an acute onset of loss of vision in his right eye. He was treated by prednisolone with a complete remission. In August of 1986, he had another bout of blurring of vision in his left eye. Once he lost his left vision completely, from which he showed slow recovery. In January of 1987, he developed blurring of his right eye and loss of pain and touch sensation in his right leg. Since then he repeated loss of vision in his right or left eye five times, and he was admitted to our hospital in May of 1990. On admission, he was alert and oriented. General physical examination was unremarkable. Neurologic examination revealed bilateral optic nerve atrophy. He could not discriminate light or dark by either eye. Other cranial nerves were unremarkable. He could walk in a wide-base only with support; spasticity was noted in his left leg. Muscle strength was preserved. Deep reflexes were exaggerated in both legs with extensor plantar reflex bilaterally. Pain and touch sensation was decreased in the left leg by 30%, and vibration was diminished in both feet. Position sense was preserved. Routine blood counts and chemistries were unremarkable. Cranial MRI scans revealed multiple high-signal intensity lesions in both pontine bases, basal ganglia, thalami, and in the deep cerebral white matters. He was treated with oral prednisolone, plasmapheresis, lymphocytapheresis, and then immuran. His vision showed only slight recovery to discriminate light and dark. In October of 1990, slight weakness appeared in his both legs. In December of that year, he developed nausea, and a fiber colonoscopic study revealed a stenosis in the transverse colon. In March of 1991, he developed anemia and liver dysfunction. In July of that year, jaundice appeared, and his serum bilirubin was increased. In October, his leg weakness became more prominent, and his cranial CT scans at that time revealed a low density change in the right cerebellum in the right superior cerebellar artery territory; in addition, multiple low density spots were scattered to be seen in both cerebral hemispheres including the basal ganglia and thalamic areas with ventricular dilatation and cortical atrophy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 64-year-old man with recurrent blurred vision and an abdominal mass]. 816 57

We examined cone and rod electroretinograms to ganzfeld stimuli in a patient with crystalline retinopathy. The 54-year-old man complained of night blindness, blurred vision, and metamorphopsia in both eyes. His visual acuity was 10/200 in the right eye and 10/20 in the left eye; his subjective dark-adaptation threshold was elevated 1 log unit, and he made one tritan error on the Farnsworth Panel D-15. Specular microscopic examinations revealed tiny crystalline deposits in the limbal cornea bilaterally. Ophthalmoscopically, crystalline deposits were found in the posterior fundi. His light-adapted cone electroretinograms to white stimuli were diminished (about 30% of those of normal controls), with normal implicit times. His dark-adapted rod electroretinogram amplitudes were 10% of those of normal controls. The S-cone electroretinogram was not detectable to different spectral stimuli with strong white background, while the L-M-cone responses appeared normal in waveforms with reduced amplitude. These ERG results indicated that the patient's S-cone system is more highly impaired than the L-M-cone system, supporting the psychophysical evidence that the S-cone system is more vulnerable than other cone systems in retinal diseases.
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PMID:Nondetectable S-cone electroretinogram in a patient with crystalline retinopathy. 884 31

The deposition of copper on Descemet's membrane and the anterior and posterior lens capsule with extreme hypercupremia and IgG hypergammaglobulinemia has been previously described with multiple myeloma and pulmonary carcinoma. A 66-year-old man presenting with blurred vision was found to have bilateral golden-brown metallic dust-like deposits on the central region of Descemet's membrane and the anterior and posterior lens capsule. Laboratory investigations revealed an elevated serum copper level 10 times the normal level associated with a monoclonal gammopathy and a normal ceruloplasmin level. Copper binding to the serum proteins was investigated by three biochemical methods. The results demonstrated that the major copper binding fraction in the serum was IgG. N-terminal amino acid analysis of the IgG did not find the sequence of Asp-Ala-His, which has been shown to be a copper binding site in albumin. This is the first report of benign monoclonal gammopathy being associated with the ocular deposition of copper.
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PMID:Ocular copper deposition associated with benign monoclonal gammopathy and hypercupremia. 890 88

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68


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