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

Headache is the most frequent symptom for which a patient with giant cell arteritis (GCA) presents to a neurologist. Amaurosis fugax and ischemic optic neuropathy are well-recognized complications. Less commonly recognized neurologic complications include transient ischemic attacks, cerebral infarctions, acute confusional states (due to multi-infarct dementia), ischemic cervical myelopathy, and ischemic mononeuropathies. Because patients with GCA generally respond well to corticosteroid therapy, prompt diagnosis can minimize neurologic damage.
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PMID:Neurologic aspects of giant cell (temporal) arteritis. 826 30

Three patients with visual loss and normal fundi were discovered to have choroidal ischemia on fluorescein angiography. Each patient had a markedly increased Westergren erythrocyte sedimentation rate, but only one described symptoms of polymyalgia rheumatica, neck pain, and jaw claudication. Biopsy of the temporal artery confirmed giant cell arteritis in the two patients without constitutional symptoms. In one patient, typical anterior ischemic optic neuropathy developed the following day, whereas in the other two, anterior ischemic optic neuropathy later occurred despite the prompt administration of intravenous high-dose corticosteroids. Choroidal ischemia may be the first sign of giant cell arteritis in elderly patients with visual loss. Early diagnosis and treatment are mandatory in an attempt to forestall the development of anterior or posterior ischemic optic neuropathy, or central retinal artery occlusion in the affected or fellow eye.
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PMID:Visual loss caused by choroidal ischemia preceding anterior ischemic optic neuropathy in giant cell arteritis. 829 97

A 68-year-old man had visual loss secondary to isolated choroidal nonperfusion as a clinical manifestation of giant cell arteritis. Ophthalmoscopy disclosed scattered yellow-white lesions at the level of the retinal pigment epithelium in the posterior pole of the right eye. Intravenous fluorescein angiography demonstrated marked delay in choroidal filling of the macula in the right eye. There was no ophthalmoscopic or angiographic evidence of anterior ischemic optic neuropathy or central retinal artery occlusion. After approximately 72 hours of intravenous corticosteroid therapy, the patient's visual acuity improved and repeat intravenous fluorescein angiography showed normal choroidal circulation. Isolated choroidal ischemia is a potential cause of reversible visual loss in patients with giant cell arteritis.
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PMID:Choroidal nonperfusion in giant cell arteritis. 835 1

Clinical data and fundus fluorescein angiograms were analyzed from 35 patients with acute (onset less than four weeks) anterior ischemic optic neuropathy. Nineteen of the 35 patients (54%) had nonarteritic disease, and 16 patients (46%) had giant cell arteritis confirmed by biopsy. Patients with arteritis had higher erythrocyte sedimentation rates, larger cup/disk ratios, and delayed fluorescein dye appearance and choroidal filling times. Three additional patients with cranial arteritis confirmed by biopsy, but without visual loss, had angiographic characteristics similar to patients with arteritic ischemic neuropathy. We consider fluorescein angiography a valuable diagnostic adjunct in identifying patients with giant cell arteritis.
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PMID:Fluorescein angiography in the diagnosis of giant cell arteritis. 842 Mar 79

Particularly in patients over 40 years of age, disturbances of perfusion at the optic nerve head and retina are a frequent cause of acute visual acuity loss. As the most important disease entities, we must distinguish between ischemic optic neuropathy and arterial and venous perfusion disturbances. The prognosis with regard to visual acuity is, at any rate, serious: a considerable, persistent loss of vision must be expected. Unfortunately, at present there is no therapy available which could normalize perfusion quickly enough. In individual cases of ocular venous thrombosis, isovolumetric hemodilution can be effective. Use of argon-laser coagulation may markedly reduce the occurrence of severe complications (hemorrhagic glaucoma, vitreous bleeding). As an emergency measure, brief massage of the globe as well as administration of 100 mg prednisone and 250 mg acetazolamide are recommended. Disturbances in ocular perfusion call investigation with regard to hematological and vascular risk factors. It is always important to rule out giant-cell arteritis (Horton's disease).
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PMID:[Acute loss of vision due to ocular perfusion disorders]. 848 82

We report a series of 21 consecutive patients seen at the Ophthalmology Department of the University Hospital Zurich, Switzerland, with the arteritic form of anterior ischemic optic neuropathy (AION). 19 patients had giant cell arteritis, one had periarteritis nodosa and one had cP-arteritis. They comprised 11 men and 10 women, ranging in age between 66 and 88 years. The median age was 80. We analyzed the course of events in each case before and after involvement of the first eye, as well as the frequency and possible causes of involvement of the second eye. The diagnosis was regarded as delayed when, despite typical signs, symptoms amd laboratory abnormalities, systemic vasculitis was not considered in the differential diagnosis. Treatment was considered inadequate if, following visual loss in one eye and diagnosis of a systemic vasculitis, a dose of 1 mg/kg prednisone or less was given, and/or the initial dose was reduced by more than 50% during the first month. Of 21 patients, 10 suffered bilateral visual loss. 8 of these 10 patients became legally blind. In 13 out of 21 cases there was no delay in diagnosis and treatment was adequately given. All 11 patients with unilateral involvement, who did not suffer a substantial loss in quality of life, belong to this subgroup. In 8 cases diagnosis was either delayed or treatment was inadequate. All of these patients had bilateral ocular involvement. In one patient, visual loss in the second eye could not be avoided despite correct diagnosis and treatment (M.A., No. 1). In this patient the interval between involvement of the first and second eye was very short (3 days). One patient had a mature cataract in the first affected eye and sought medical help only after his good eye became involved (K. F., No. 15). In this report we would like to draw attention to the extremely poor visual prognosis due to frequent bilateral ocular involvement in giant cell arteritis. Corticosteroid treatment cannot restore vision in the already affected eye, but it is, in the majority of cases, highly effective in preventing visual loss in the second eye. Thus, it is crucial to begin treatment immediately, to start with a high dose (preferably 1 g methyl-prednisolone i.v.), and to continue high-dose oral treatment long enough to prevent delayed visual loss in the second eye. The most vulnerable period appears to be the first month following involvement of the first eye. Caring for patients with giant cell arteritis who have lost vision in one eye is a challenge to all involved physicians. It resembles a "high-wire act" with the threat of blindness on the one hand and the dangers of long term corticosteroid treatment on the other. An interdisciplinary approach with ongoing communication between the family physician and the ophthalmologist is required.
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PMID:[The bane of giant cell arteritis from an ophthalmological viewpoint]. 900 21

Two elderly women had catastrophic visual loss due to giant cell arteritis. The other eyes of both were attacked within two weeks. Bilateral central retinal artery occlusion, negative temporal artery biopsy and relentless nature course were noted despite treatment with a high dose of corticosteroid in one case. Unilateral central retinal artery and ischemic optic neuropathy were noted in the other case with typical pictures in temporal artery biopsy.
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PMID:[Ophthalmic manifestations of giant cell arteritis--two cases report]. 925 6

Headache is the most frequent symptom for which a patient with giant cell arteritis (GCA) presents to a neurologist. Amaurosis fugax and ischemic optic neuropathy are well recognized complications. Less commonly recognized neurologic complications include transient ischemic attacks, cerebral infarctions, acute confusional states, multi-infarct dementia, ischemic cervical myelopathy, and ischemic mononeuropathies. Because patients with GCA generally respond well to corticosteroid therapy, prompt diagnosis can minimize neurologic damage.
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PMID:Giant cell (temporal) arteritis. 936 71

A 70-year-old man underwent coronary artery bypass graft complicated postoperatively by visual loss. The diagnosis was nonarteritic anterior ischemic optic neuropathy. Possible predisposing factors in this patient were hypotension, anemia, a "disk at risk," and internal carotid artery stenosis. In the postoperative setting, the erythrocyte sedimentation rate may be elevated, as it was in this case and does not by itself suggest a diagnosis of giant cell arteritis.
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PMID:Visual loss after coronary artery bypass surgery. 954 74

Two patients with biopsy-proven giant cell arteritis experienced bilateral transient vision loss after bending over and after getting up from a supine position. One patient had no demonstrable signs of carotid, ophthalmic, or anterior ciliary vascular disease, suggesting that his episodes of transient vision loss were due to vertebrobasilar insufficiency. The other patient experienced bilateral postural vision loss in the context of impending bilateral anterior ischemic optic neuropathy. Bilateral transient postural vision loss is an uncommon manifestation of giant cell arteritis that could reflect either severe bilateral vascular compromise of the anterior circulation or severe vertebrobasilar insufficiency. In either situation, prompt evaluation and treatment is indicated to prevent the irreversible sequelae of the disease.
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PMID:Postural vision loss in giant cell arteritis. 962 Dec 70


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