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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tonic pupil is usually an idiopathic condition. In some cases, the cause of the ciliary ganglion lesion leading to tonic pupils is obvious. Rarely ischemia causes a lesion of the ciliary ganglion or the short ciliary nerves due to the good blood supply of the ciliary ganglion. Only two cases of tonic pupils in the course of giant cell arteritis are mentioned in the literature, but tonic pupils are probably much more common with this disease. Five cases are demonstrated here. All had associated ischemic optic neuropathy, and stagnation of the blood flow in the supratrochlear artery could be demonstrated in two cases by Doppler sonography. Tonic pupils may also occur when an oclusion of the internal carotid artery resolves, probably because of transient stasis of the orbital blood flow. In another case, tonic pupils were associated with choroidal ischemia (proved by video fluorescent angiography) of unknown origin. The diagnosis of tonic pupils was made by pharmacological testing for cholinergic hypersensitivity with 0.1% pilocarpine.
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PMID:[Tonic pupil caused by ischemia]. 279 12

The range of neuro-ophthalmologic signs in temporal arteritis is broad and includes diverse presentations of ischemic optic neuropathy, retinal infarction, transient ischemic phenomena, ophthalmoparesis, pupillary autonomic and anterior ocular segment dysfunction, cortical blindness and associated post-chiasmal field defects, and complex visual hallucinations. Neurovascular compromise can follow arteritic lesions at multiple neuroanatomic sites, and reflects different pathogenetic mechanisms and displays distinctive clinical features. A variety of temporal clinical profiles and differential responses to corticosteroids occur. This article reviews the broad range of neuroanatomic pathways affected by diverse and potentially interactive etiologic factors in this systemic arteritis.
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PMID:The clinical neuro-ophthalmologic spectrum of temporal arteritis. 305 3

The neuro-ophthalmologic spectrum of temporal arteritis (TA) is broad and includes such diverse presentations as ischemic optic neuropathy, retinal infarction, anterior ocular segment dysfunction, ophthalmoparesis, and cortical blindness. A common clinical dictum suggests that third nerve palsies are associated with pupillary sparing in this systemic arteritis. We present a biopsy-proven case of TA with parasympathetic pupillary involvement and ophthalmoparesis. Relative light-near dissociation and differential clinical response to adrenocorticosteroids occurred. Previous pathologic studies have suggested that clinically apparent parasympathetic pupillary dysfunction could follow arteritic lesions at several neuroanatomic sites and may, therefore, reflect different pathogenetic mechanisms and display distinctive clinical features. Our case effectively broadens the clinicopathologic locus of neuro-ophthalmologic expression in TA.
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PMID:Parasympathetic pupillary involvement in biopsy-proven temporal arteritis. 320 15

Giant cell arteritis is a visually devastating disease that primarily affects the over 55 age group. This granulomatous inflammation affects large and medium-sized arteries anywhere in the body. Systemic manifestations of this disease include: jaw claudication, scalp tenderness, malaise and vertigo. Decreased appetite and/or anorexia may also be seen. Ocular manifestations may include ischemic optic neuropathy with sudden markedly reduced visual acuity. Steroid treatment is used to protect the uninvolved eye. In its classic form the disease is monitored by adjusting the steroid dosage with the erythrocyte sed rate (ESR). Prognosis for visual restoration in the involved eye is poor.
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PMID:Giant cell arteritis. 323 Feb 40

A prospective study was conducted in 438 patients with anterior ischemic optic neuropathy (AION). There were 388 patients with nonarteritic AION and 50 with arteritic AION. The risk of bilaterality in patients with arteritic AION was found to be 1.9 times the risk in patients with nonarteritic AION (P = 0.0118). The cumulative incidence curve, considering the time taken to develop bilateral AION for nonarteritic cases was significantly (P = 0.0103) different from that for arteritic cases. The estimated 25th-percentile time to development of bilateral AION was much shorter in patients with arteritic AION (0.4 month) than in those with nonarteritic AION (32.4 months). In arteritic AION, unilateral as well as bilateral AION had almost invariably developed before systemic steroid therapy was started and not after, indicating that this therapy is effective in preventing the development of AION in giant cell arteritis. In nonarteritic AION, the risk of bilaterality was significantly greater in men (P = 0.0113) and in young (less than 45 years old) patients with diabetes (P = 0.0245), with no significant difference attributable to the other age groups or other associated systemic diseases. In this study, it was found that young diabetic men have a risk of AION developing in the second eye that is 1.56 times the risk in young diabetic women, 2.56 times the risk in women who either are nondiabetic or are not young, and 1.64 times the risk in both older men and nondiabetic men.
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PMID:Anterior ischemic optic neuropathy. VII. Incidence of bilaterality and various influencing factors. 365 62

Five cases of anterior ischemic optic neuropathy secondary to biopsy-proven giant cell arteritis are presented. In each case, cupping of the optic disc, which closely resembled glaucomatous cupping, was observed in the affected eye. The presence of glaucoma was ruled out on the basis of normal intraocular pressures and normal tonographic measurements of facility of outflow. These cases indicate that arteritic ischemic optic neuropathy can result in optic disc cupping, which closely resembles glaucomatous cupping. The similarities in the appearance of cupping of these discs with that seen in eyes with glaucoma suggest that the pathogenesis of cupping in glaucoma and in arteritic ischemic optic neuropathy may share some common mechanisms.
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PMID:Optic disc cupping in arteritic anterior ischemic optic neuropathy resembles glaucomatous cupping. 370 3

A 60-year-old woman with inadequately treated giant cell arteritis developed an acute unilateral ischemic optic neuropathy associated with bilateral carotid artery and orbital bruits. Angiography demonstrated vascular changes compatible with arteritis localized to the cavernous and petrous segments of both internal carotid arteries. After treatment with high dose steroids, the bruits disappeared.
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PMID:Bilateral carotid siphon involvement in giant cell arteritis. 373 6

A 78-year-old white woman had catastrophic visual loss in one eye due to temporal arteritis. Despite treatment with doses of oral corticosteroids high enough to normalize the Westergren erythrocyte sedimentation rate, she experienced progressive retinal ischemia with visual loss in the second eye. The use of 1,000 mg of pulsed intravenous methylprednisolone every 12 hours restored her vision. Brief hospitalization of patients with arteritic ischemic optic neuropathy for treatment with intravenous methylprednisolone may offer a significant chance of visual recovery of the involved eye and provide optimal protection to the uninvolved eye.
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PMID:Treatment of temporal arteritis with ocular involvement. 394 48

Temporal arteritis is a systmic disease with a predilecation for the cranio-temporal vascular area. Histologically it is a panarteritis. Diagnosis is based on the presence of lymphocytes, histiocytes and foci of epitheloid cells in the media of the temporal artery. The presence of giant cells is, however not obligatory. The present study emphasizes the value of biopsy of the temporal artery in diagnosing this disease. It, furthermore, also points out the 10-percent possibility of false negative biopsy results based on patchy vascular lesions. Tenderness to touch of the temporal artery, characteristic of temporal arteriitis, can be explained by perineural inflammatory infiltration of nerves in the adventitia of this artery. Examination under the electron microscope reveals almost complete destruction of the smooth muscles of the media by epitheloid cell granulomas. Massive neogenesis of collagen ensues. Furthermore, numerous myofibroblasts, macrophages and histiocytes are observed. Several macrophages close to each other create the impression of giant cells in the light microscope. The electron microscope image allows for clear differentiation between temporal arteritis on one hand and of arteriosclerosis on the other. Using the immunoperoxidase method in temporal arteritis, immune globulines are found intracellularly in plasma cells. Extracellularly, however, neither immune golbulins nor complement deposits are found in the vascular wall. Thus, the assumption that temporal arteritis represents a immune complex disorder cannot be maintained. The most frequent ophthalmologic complication in temporal arteritis is ischemic optic neuropathy. Histologic examination of a bulbus presenting anterior ischemic optic neuropathy in a case of temporal arteritis revealed predominantly lymphocytic infiltrations of the short and long ciliary arteries. No inflammatory infiltration was found in the central retinal artery. The development of anterior ischemic optic neuropathy can be explained by impaired perfusion or by occlusion of the short posterior ciliary arteries. In 60% of patients suffering from temporal arteritis, we found anticollagen antibodies in the serum. Collagenization of the vascular wall as observed in our electron-microscopic examinations must, therefore, be considered the paradoxical consequence of an immune reaction caused by collagen auto-antibodies. Collagen auto-antibodies play a decisive role in the maintenance and chronicity of the inflammatory process in temporal arteritis. In therapy, corticosteroids should not be administered according to rule but rather in doses adjusted to individual requirements.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Electron microscopic and immunohistologic studies of patients with Horton's temporal arteritis]. 638 7

The etiology of anterior ischemic optic neuropathy (AION), when not associated with giant cell arteritis, is usually unknown. Clinical, pathologic, and experimental studies have not determined a cause. The optic disc appearance in both the involved and normal fellow eye was studied in 51 patients with acute nonarteritic AION. The number of discs (both involved and fellow) without a physiologic cup was significantly greater than would be expected from normal population studies. The etiology of nonarteritic AION may be related to the anatomic configuration of the optic nerve.
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PMID:Optic disc structure in anterior ischemic optic neuropathy. 651 98


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