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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "papilledema" describes optic disc swelling resulting from increased intracranial pressure. A complete history and direct funduscopic examination of the optic nerve head and adjacent vessels are necessary to differentiate papilledema from optic disc swelling due to other conditions. Signs of optic disc swelling include elevation and blurring of the disc and its margins, venous congestion, and retinal hard exudates, splinter hemorrhages and infarcts. Patients with papilledema usually present with signs or symptoms of elevated intracranial pressure, such as headache, nausea, vomiting, diplopia, ataxia or altered consciousness. Causes of papilledema include intracranial tumors, idiopathic intracranial hypertension (pseudotumor cerebri), subarachnoid hemorrhage, subdural hematoma and intracranial inflammation. Optic disc edema may also occur from many conditions other than papilledema, including central retinal artery or vein occlusion, congenital structural anomalies and optic neuritis.
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PMID:Papilledema: clinical clues and differential diagnosis. 154 98

This discussion reviews drugs that affect the eye, including antihyperglycemic agents; corticosteroids; antirheumatic drugs (quinolines, indomethacin, and allopurinol); psychiatric drugs (phenothiazine, thioridazine, and chlorpromazine); drugs used in cardiology (practolol, amiodarone, and digitalis gylcosides); drugs implicated in optic neuritis and atrophy, drugs with an anticholinergic action; oral contraceptives (OCs); and topical drugs and systemic effects. Refractive changes, either myopic or hypermetropic, can occur as a result of hyperglycemia, and variation in vision is sometimes a presenting symptom in diabetes mellitus. If it causes a change in the refraction, treatment of hyperglycemia almost always produces a temporary hypermetropia. A return to the original refractive state often takes weeks, sometimes months. There is some evidence that patients adequately treated with insulin improve more rapidly than those taking oral medication. Such patients always should be referred for opthalmological evaluation as other factors might be responsible, but it might not be possible to order the appropriate spectacle correction for some time. The most important ocular side effect of the systemic adiministration of corticosteroids is the formation of a posterior subcapsular cataract. Glaucoma also can result from corticosteroids, most often when they are applied topically. Corticosteroids have been implicated in the production of benign intracranial hypertension, which is paradoxical because they also are used in its treatment. The most important side effect of drugs such as chloroquine and hydroxychloroquine is an almost always irreversible maculopathy with resultant loss of central vision. Corneal and retinal changes similar to those caused by the quinolines have been reported with indomethacin, but there is some question about a cause and effect relationship. The National Registry of Drug Induced Ocular Side Effects in the US published 30 case histories of cataract suspected to be induced by allopurinol; numerous additional cases have been reported to the registry since. Phenothiazine, with an estimated 3% incidence of side effects, appears to be safer than other antipsychotic drugs, but the rate of ocular effects increases with the duration of therapy. Thioridazine and chlorpromazine are known to cause lens deposits and pigmentary retinopathy. There is a significantly high prevalence of thrombophlebitis and pseudotumor cerebri among women who use OCs and thrombotic retinal vascular disease, such as retinal vein occulsion, might be linked with them. It also is probable that, because of altered hydration of the cornea, there is a decreased tolerance to contact lenses.
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PMID:Drugs affecting the eye. 286 12

Optic neuritis is often the first manifestation of multiple sclerosis (MS). Sixteen patients with acute optic neuritis and one patient with benign intracranial hypertension (BIH) were investigated by magnetic resonance imaging, using a chemical shift selective double spin echo sequence. In 3 of the 16 patients, abnormalities were seen. In one patient with bilateral symptoms, signal hyperintensity and swelling of the right side of the chiasm were found. In another patient the optic nerve was found diffusely enlarged with only a marginally increased signal in the second echo. In the third patient an area of signal hyperintensity and swelling was seen in the left optic nerve. In the patient with BIH the subarachnoid space which surrounds the optic nerves was enlarged. Even using this refined pulse sequence, avoiding the major artefact in imaging the optic nerve, the chemical shift artefact, lesions were only shown in 3/16 (19%) of the patients with optic neuritis. Nevertheless, the presented chemical shift selective double spin echo sequence may be of great value for detection of retrobulbar lesions.
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PMID:Chemical shift selective magnetic resonance imaging of the optic nerve in patients with acute optic neuritis. 319 Sep 39

This review summarizes 169 cerebral vascular accidents in women taking oral contraceptives: 94 arterial (including 13 of the authors' cases), 20 venous, 37 neuroophthalmologic (5 of the authors'), and 18 undetermined diagnoses. The arterial accidents involved the carotid in 56, the vertebrobasilar in 27. Few were fatal; most were considered thromboses; none were due to hemorrhage; few could have been due to emboli or dissecting aneurisms. Aggravation or appearance of migraine was noted in 34 and transient focal cerebral ischemia in 28 cases before arterial accident. No definite time span was obvious, but many occurred 1-6 months or over 2 years after starting pills. Venous accidents were usually fatal, often extended thromboses of the superior longitudinal sinus. Clinically there was severe headache (85%), vomiting, fever without rapid pulse, alteration of consciousness, papillary edema, focal cerebral signs. Ophthalmologic accidents included retinal, arterial, and venous occlusion; paralysis of oculomotor nerve; optic neuritis; and pseudo-tumor-cerebri. The authors recommended caution with oral contraceptives in case of cerebral vascular episodes, migraine, visual disturbances, chorea, hyperlipidemia, and hypertension.
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PMID:[Cerebrovacular accidents and oral contraceptives]. 443 14

The diagnosis of optic neuritis is based on clinical signs and symptoms. Ancillary testing has little medical value, but is helpful to evaluate the risk of developing multiple sclerosis and for counseling the patients. In contrast to the common belief, the usual therapy with oral prednisone may be harmful. Only megadose therapy with 1000 mg methylprednisolone/day accelerates the recovery of visual function. Similar therapy is suggested in idiopathic intracranial hypertension. In patients with non-arteritic anterior ischemic optic neuropathy only optic nerve decompression sheath surgery is helpful.
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PMID:[Neuro-ophthalmology--new challenges]. 765 Aug 79

High resolution MRI of the anterior visual pathways was evaluated using frequency selective fat suppressed fast spin echo (FSE) sequences in conjunction with phased array local coils in patients with optic neuropathies. Fifteen normal controls and 57 patients were examined. Coronal T2 weighted fat suppressed FSE images were obtained in 11 minutes with an in plane resolution of 0.39 x 0.39 mm. The optic nerve and its sheath containing CSF were clearly differentiated. Central retinal vessels were often visible. In demyelinating optic neuritis and in anterior ischaemic optic neuropathy high signal within the nerve was readily delineated. Meningiomas and gliomas involving the optic nerve were precisely visualised both in the orbit and intracranially. Extrinsic compression of the optic nerves was readily visualised in carotid artery ectasia and dysthyroid eye disease. Enlarged subarachnoid spaces around the optic nerves were demonstrated in benign intracranial hypertension. High resolution MRI of the anterior visual pathway represents an advance in the diagnosis and management of patients presenting with optic neuropathy.
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PMID:High resolution magnetic resonance imaging of the anterior visual pathway in patients with optic neuropathies using fast spin echo and phased array local coils. 774 3

This study was undertaken to understand better how damage to the anterior visual pathway may affect the relationship between the visual and pupillomotor systems. The relative afferent pupillary defect and the interocular difference in visual field mean deviation (determined by the Humphrey Field Analyzer Statpac program) were correlated in 137 patients. A moderate linear correlation (r = .66) was found. In 25 patients tested by both static and kinetic perimetry, the correlation could not be significantly improved by considering field loss outside of 30 degrees. The correlation was further studied in four subcategories of diagnosis: optic neuritis (n = 36), idiopathic intracranial hypertension (n = 26), compressive optic neuropathy (n = 14), and anterior ischemic optic neuropathy (n = 7). In compressive optic neuropathy and idiopathic intracranial hypertension, the difference in mean deviation between the two eyes was associated with a larger relative afferent pupillary defect than in optic neuritis and anterior ischemic optic neuropathy. In optic neuritis, the correlation was the poorest. These results indicate that diseases of the afferent visual system may not necessarily affect visual threshold (as tested by static perimetry) and the pupillary light reflex (a suprathreshold test) in the same way.
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PMID:The relationship between static perimetry and the relative afferent pupillary defect. 844 95

We tested the hypothesis that a subset of the Farnsworth-Munsell 100-hue test (FM-100) would be a sensitive, specific, and practical means of monitoring color vision in patients with chronic optic nerve disorders. We retrospectively analyzed the records of 1,113 patients affected with optic neuritis (ON), Graves' ophthalmopathy with suspected optic neuropathy, or idiopathic intracranial hypertension with suspected optic neuropathy (IIH). One hundred six records of patients showed that an FM-100 had been performed (23 ON, 46 Graves', 37 IIH). Forty additional patients were studied prospectively (11 ON, 17 Graves', 12 IIH). The sensitivity and specificity of all possible 21 chip subtests were compared against the same statistics for the entire test. We found that for these three optic nerve disorders, a test consisting of chips 22-42 had nearly the same sensitivity and specificity as the entire test when compared with the clinical diagnosis. At 90% specificity, the ratio of sensitivities of the short version to the original version of the test were IIH, 53%/45%; optic neuritis, 85%/79%; and Graves', 67%/70%. The majority of the clinical value of the test can be achieved in one fourth of the original examination time.
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PMID:Evaluation of a significantly shorter version of the Farnsworth-Munsell 100-hue test in patients with three different optic neuropathies. 909 53

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

Optic neuropathy in uremia is rare. Although the consequences of optic neuropathy-blindness or substantial loss of vision-are devastating, only a few cases have been reported by way of single case reports and case series studies. The reported patients are heterogeneous with regard to the cause of neuropathy. We report the case of a patient with uremic optic neuropathy and summarize the other cases reported in the literature so far. Based on the data available from these reports, we propose a classification system, which includes nonischemic neurotoxic uremic optic neuropathy; ischemic optic neuropathy, more specifically anterior ischemic optic neuropathy; and optic neuropathy as a result of drug side effects, benign intracranial hypertension, and optic neuritis. The immediate institution of dialysis and corticosteroid therapy and correction of anemia and relative hypotension can optimize the chances of visual recovery for these patients. Close collaboration among nephrologists, ophthalmologists, and neurologists is important in this interdisciplinary emergency.
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PMID:Optic neuropathy in uremia: an interdisciplinary emergency. 1122


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