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

In this paper the painful syndromes of temporal arteritis, polymyalgla rheumatica, glaucoma, trigeminal neuralgia, post-herpetic neuralgia, and temporomandibular joint dysfunction have been described. These conditions occur commonly in the elderly. The dangers of blindness occurring in temporal arteritis or polymyalgia rheumatica, the importance of early diagnosis in glaucomatous headache, the value of Tegretol in trigeminal neuralgia, the paucity of therapeutic agents in post-herpetic neuralgia and the value of dental treatment in tempor-mandibular joint dysfunction have been stressed.
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PMID:Chronic pain syndromes in the elderly. 88 Jan 67

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

Pain around the eye can be caused by local ophthalmic disorders or by disease of other structures sharing trigeminal nerve sensory innervation. In general, most ocular causes for pain also cause the eye to be red, thus alerting the examiner to the focality of the problem. However, conditions like eyestrain, intermittent angleclosure glaucoma or neovascular glaucoma, and low-grade intraocular inflammation can be painful and not be associated with obvious redness. Ocular signs and symptoms also occur with numerous other causes of headache. Double vision in association with periocular pain can result from orbital lesions, isolated cranial neuropathies, and cavernous sinus lesions. Pupillary abnormalities like Horner's syndrome may result from a variety of painful conditions, including cluster headache, parasellar neoplasms or aneurysms, internal carotid dissection or occlusion, and Tolosa-Hunt syndrome. Pain with a dilated and unreactive pupil may reflect a benign condition like Adie's syndrome or ophthalmoplegic migraine, or it may herald the presence of a life-threatening posterior communicating artery aneurysm. Headache and transient visual loss can be manifestations of classic migraine, or be symptoms of ocular hypoperfusion from ipsilateral internal carotid occlusion or increased intracranial pressure from pseudotumor cerebri. In a young patient, head pain with a fixed visual deficit may result from optic neuritis, in an older adult, temporal arteritis may be the culprit. Ophthalmologic aspects of headache thus encompass problems that range from simple and benign to complex and formidable.
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PMID:Ophthalmologic aspects of headache. 202 Feb 23

A number of ocular and nonocular conditions may produce an acutely painful eye or orbit. A careful history and physical examination with special attention to the cornea, sclera, fundus, and cranial nerves will usually delineate the etiology of the pain. In particular, certain life- or vision-threatening conditions such as leaking internal carotid aneurysm, cavernous sinus thrombosis, orbital cellulitis, acute narrow-angle glaucoma, and temporal arteritis must be kept in mind.
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PMID:The acute painful eye. 327 85

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

From this and the previous article, the following points may be offered in summary: When comparing the elderly age group with the general population, the incidence of migraine headaches decreases with age, whereas other etiologies such as glaucoma, temporal arteritis, and cerebrovascular disease may assume a more prominent role in the differential diagnosis. Patients in the geriatric population are frequently taking a multitude of medications, and it is extremely important to carefully evaluate these for possible precipitants of headache. Furthermore, in elderly patients with other potential medical problems, particular attention should be paid to the possibility of various systemic causes of headache. Therapy for specific headache disorders should be tailored to the individual patient. Consider the patient's overall general, psychological, medical, and neurologic background. The physician must be aware of possible interactions of medications with the therapeutic intervention, as well as possible poor tolerance to specific medications due to preexisting medical or neurologic disorders. A complete history, obtaining information on the temporal pattern of headache, the distribution of pain, and precipitating and alleviating factors, is extremely important in evaluating the elderly patient. A careful physical examination, paying particular attention to possible disorders of extracranial structures, is indicated. A neurologic exam, including basic tests of higher cortical function, should be obtained. Important additional laboratory investigations include a complete blood count, erythrocyte sedimentation rate, and basic blood chemistries. Arterial blood gases should be obtained in patients who have pulmonary disease, a history suggestive of sleep apnea, or other disorders that may produce hypoxia and hypercarbia, resulting in vascular headache.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Headaches in older patients: Ddx and Tx of common nonvascular causes. 405 33

Temporal arteritis is an insidious disease which, if not recognized and treated with high-dosage oral prednisone or intravenous prednisolone, can result in unilateral or even total blindness due to anterior ischemic optic neuropathy (AION) or closure of the central artery of the retina. Unfortunately, the symptoms and clinical signs of temporal arteritis mimic those of a number of other conditions including angle-closure glaucoma, hypertension, migraine, trigeminal neuralgia, temporomandibular joint syndrome, carotid artery occlusive disease, Foster-Kennedy syndrome, and nonarteritic AION. When a patient complains of a severe pain in the temporal region, along with scalp tenderness and a feeling of malaise or depression--with or without episodes of transient loss of vision--he or she should be referred for a diagnostic work-up which includes an erythrocyte sedimentation rate and a temporal artery biopsy. We present here a review of the recent literature concerning temporal arteritis, followed by a report of an unusual case in which high-dosage prednisone therapy was effective in relieving the patient's symptoms and lowering the sedimentation rate in spite of a negative temporal artery biopsy.
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PMID:Diagnosis and management of temporal arteritis: a review and case report. 823 73

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

Changes in vision or loss of vision are common complaints for patients presenting to the emergency department. Such complaints may represent a simple problem related to recent trauma, early evidence of a systemic disease, or may be a vision-threatening lesion. A logical and organized approach to the history and the physical examination of the patient with eye complaints is key to the diagnosis and treatment of the more significant causes of these complaints. This article reviews an organized approach to the patient with complaint of visual loss and considers the wide differential diagnosis. It focuses specifically on the evaluation of the patient complaining of visual changes resulting from central retinal artery occlusion, central retinal vein occlusion, retinal detachment, acute angle-closure glaucoma, giant cell temporal arteritis, and retrobulbar hemorrhage.
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PMID:Acute visual change. 988 42

Diagnosis and management of giant cell (temporal) arteritis (GCA) should be performed by physicians who can accurately monitor the ophthalmologic, neurologic, and systemic sequelae of the disease as well as the numerous side effects of systemic corticosteroids, which are typically necessary for treatment. When the diagnosis of giant cell arteritis is seriously entertained, early treatment with adequate doses of oral or intravenous corticosteroids should not be delayed until laboratory confirmation has been obtained. Unilateral or bilateral temporal artery biopsy should be performed on all patients with suspected GCA. A positive biopsy result mandates that higher doses of corticosteroids be used during the first 2 months, which comprise the critical period for risk of new ocular ischemia. A definitive, biopsy-proven diagnosis requires at least 6 months, and typically 12 months, of corticosteroid therapy. Common pitfalls include increasing the dose and prolonging the use of corticosteroids in response to increases in the erythrocyte sedimentation rate (ESR) unrelated to GCA or visual blurring that may be related to benign tear film abnormalities, corticosteroid-induced lens changes, and other ophthalmic conditions. The muscle stiffness of polymyalgia rheumatica (PMR) must be distinguished from the osteoarthritis and other painful conditions common in the elderly. After corticosteroid therapy has begun, continuing ophthalmologic evaluation is necessary to evaluate the effectiveness of treatment and whether ocular complications, such as glaucoma or cataract, develop. Careful attention must be given to early detection and prevention of systemic side effects of corticosteroid treatment. Patients may be given gastrointestinal protective agents, such as histamine (H(2))-blocking agents; vitamin D and calcium; oral hypoglycemic agents; and, if necessary, insulin and antihypertensive drugs. If bone density measurements warrant, hormones/supplementation to prevent or reverse osteoporosis may be prescribed. After the initial diagnosis and first 4 weeks of treatment, elevation of the ESR or C-reactive protein alone should generally not be used as signs of disease activity nor as a reason to increase the daily dose of steroids. If symptoms or signs of disease activity occur, the dose should be raised regardless of test results. Even with vigorous physician-patient education, however, a patient is occasionally unable to provide adequate historical information about response to therapy, and the physician is forced to rely on laboratory values as a measure of disease activity. After initial high-dose corticosteroid therapy, patients without a classic history and with negative biopsy results will generally receive a rapid taper to low doses of corticosteroids. The role of repeated temporal artery biopsy in the clinical management of GCA is unclear. Despite persistence of PMR and, in some cases, histologic evidence of inflammation in temporal arteries, patients do not frequently have recurrence of symptomatic GCA after 6 months or more of corticosteroid therapy. Under these circumstances, late vision loss is rare.
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PMID:Giant Cell Arteritis. 1109 95


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