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

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

Transitory oedema of the left orbit and maxillary sinus was revealed radiographically in an active phase of temporal arteritis. This is possibly caused by inflammatory changes of the soft tissues in these regions. Early signs of compromised retinal flow and anterior ischemic optic neuropathy were demonstrated with fluorescein angiography. This finding promoted early, immediate therapy.
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PMID:Unusual ocular manifestation in temporal arteritis. A case report. 47 83

Stereophotographs of the optic disc were reviewed in 78 patients with ischemic optic neuropathy (ION). Only 10% (6) of 61 nonarteritic (idiopathic) ION eyes developed optic disc cupping similar to that seen in glaucomatous eyes. Five of ten eyes with ION due to giant cell arteritis had cupping simulating glaucoma; however, two had elevated intraocular pressure, and the other three had large physiologic cups in the opposite eye. Optic disc pallor was proportionately more severe in ION eyes than in glaucomatous eyes of similar cup size. While there are similarities in the type of visual field loss in ION and glaucoma, the two disorders differ in the usual appearance of the disc after field loss has occurred and in the portion of the field most frequently affected. These observations suggest that if both disorders have an ischemic mechanism, there is a difference in the nature or distribution of the ischemia. There should be little difficulty under most circumstances in making the clinical differentiation between a disc that has suffered ION and a disc that has suffered pressure-induced damage, although occasional instances of ION may be classified as low-tension glaucoma on the basis of field loss and cupping without elevated intraocular pressure.
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PMID:Cupping of the optic disc in ischemic optic neuropathy. 92 94

In 1970 a 62-year-old physician with hypertensive vascular disease suffered a small infarction in the left optic disc, which left him with a subtle paracentral temporal visual field defect in that eye. In 1973 he had another separate and distinct episode in the same eye, which produced a dense lower nasal field defect. Careful Hruby lens examination of the disc under high magnification revealed focal arteriolar disease in the optic nerve head corresponding to the field defects, and fluorescein angiography confirmed these findings. The importance of differentiating ischemic optic neuropathy, hypertensive optic neuropathy, and temporal arteritis with optic nerve involvement is emphasized, and the therapy of each is discussed.
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PMID:Hypertensive optic neuropathy. 108 Mar 8

A 62-year-old lady with hypertension and diabetes developed bilateral, sequential ischemic optic neuropathy, progressive in the right eye. Because of a reported association between amiodarone and optic neuropathy with disc edema, the patient discontinued taking this medication; however, her visual loss continued. The differential diagnoses of bilateral ischemic optic neuropathy--including infiltrative optic neuropathy and temporal arteritis--were exhaustively investigated in this patient.
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PMID:Getting to the heart of visual loss: when cardiac medication may be dangerous to the optic nerves. 156 39

The fundus fluorescein angiograms of 13 patients with visual disturbance due to biopsy-proven giant cell arteritis (11 with anterior ischemic optic neuropathy (AION); 2 with visual obscurations only) were compared with the fluorescein angiograms from 33 patients with acute nonarteritic AION and 23 age-matched normal eyes. In all 13 patients with giant cell arteritis, the fluorescein angiograms showed a significant delay of choroidal filling time (mean 69 seconds) in comparison with either normal subjects (mean 5.8 seconds) or patients with nonarteritic AION (mean 5.5 seconds). In patients presenting with acute AION, the finding of delayed choroidal filling on fluorescein angiography should raise the index of suspicion of giant cell arteritis and lead to prompt investigation and treatment.
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PMID:Delayed choroidal perfusion in giant cell arteritis. 183 38

Corticosteroid treatment of acute idiopathic optic neuritis is still highly controversial. Controlled studies have indicated that visual acuity has been restored more rapidly after corticoid treatment. Long-term results however do not differ with the untreated control group. Corticoids are essential in the treatment of ischemic optic neuropathy, especially when occurring with auto-immune diseases or giant cell arteritis. Some authors believe that corticoids can be helpful during the acute phase of an idiopathic anterior ischemic optic neuropathy.
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PMID:Corticosteroid therapy in optic neuritis (optic neuropathy). 209 6

Severe cases of temporal arteritis often have infarctions of the optic nervehead. Such cases frequently have a decrease in the amplitude of the ocular pulse. This is in contrast to cases of anterior ischemic optic neuropathy not due to temporal arteritis. In addition to aiding in the diagnosis of temporal arteritis, monitoring of the ocular pulse may help in following the course of this disease.
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PMID:Loss of the ocular pulse in the acute phase of temporal arteritis. 254 65

A study of the eyeball was carried out using a double frequency Doppler transducer in 31 patients suffering from histologically confirmed temporal arteritis. These patients were divided into 3 groups depending on the results of the ophthalmological examination: group A: 20 patients; normal ophthalmological exam, group B: 5 patients; non specific ocular anomalies, group C: 6 patients; ocular lesions specific to temporal arteritis (ischemic optic neuropathy with amaurosis, dysoric nodules). Doppler examination demonstrated normal curves in the patients in groups A and B. The mean amplitude of systolic peaks was 7.9 mm in group A and 10.3 mm in group B (P = NS). These data did not differ from those of a control population of 22 subjects not suffering from temporal arteritis. On the other hand, group C demonstrated important anomalies on Doppler examination: lack of ophthalmic signal in one case; marked dampening of curves in 4 cases; zones of turbulence in one patient. The mean amplitude of systolic peaks was drastically decreased (1.8 mm). After steroid treatment, a significant increase in blood velocity was seen leading to a normalization of tracings in the majority of cases, including the patients in group C. Doppler examination would appear capable of reliably assessing the risk of ophthalmic complications of temporal arteritis when blood flow anomalies exist. On the other hand, patients with normal Doppler curves may be considered to be at little risk. Subjects at high risk should be urgently treated with high doses of steroids and can be regularly monitored by repeated Doppler examination.
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PMID:[Role of Doppler in the diagnosis of ophthalmic complications of Horton's disease]. 269 67

The records of 293 patients admitted to Padua University Eye Clinic with diagnosis of optic neuropathy were reviewed. Age and sex distribution of different types of optic neuropathies were analyzed. 84 patients (28.7%) with a mean age of 61.9 years had anterior ischemic optic neuropathy (AION). The mean follow up of these patients was 3 years. In less than 30% of patients stabilized visual acuity of the first affected eye was better than 20/200; however, patients younger than 65 showed a significantly (p less than 0.01) better visual acuity than patients older than 64. Involvement of the second eye was found in 26 patients with AION (30.9%), of whom only five were considered idiopathic. The latency before controlateral eye involvement was significantly (p less than 0.05) shorter in patients over 64 years of age than in the younger group. Commonly known associated conditions such as giant cell arteritis (3.6%), arterial hypertension (34.5%), diabetes mellitus (10.7%), both arterial hypertension and diabetes (8.3%), migraine (7.2%) or intracapsular cataract extraction (1.2%) were considered. The frequency of a number of risk factors was found out in patients with arterial hypertension and/or diabetes and in patients with idiopathic AION. Symptoms or signs of ischemic cardiopathy and/or peripheral nonarteritic vascular disease, TIAs prior to AION onset, elevated plasma cholesterol or triglyceride levels, excessive smoking were considered. These risk factors were not found in 11.1% of diabetic patients with AION, in 37.9% of hypertensives, in 14.2% of both diabetic and hypertensive patients and in 31% of patients with idiopathic AION. Our data seem to indicate that the onset of AION may be influenced more strongly from these risk factors than aging.
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PMID:Anterior ischemic optic neuropathy and aging. 277 May 22


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