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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

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

The initial section deals with basic sciences; among the various topics briefly discussed are the anatomical features of ophthalmic, central retinal and cilioretinal arteries which may play a role in acute retinal arterial ischemic disorders. Crucial information required in the management of central retinal artery occlusion (CRAO) is the length of time the retina can survive following that. An experimental study shows that CRAO for 97min produces no detectable permanent retinal damage but there is a progressive ischemic damage thereafter, and by 4h the retina has suffered irreversible damage. In the clinical section, I discuss at length various controversies on acute retinal arterial ischemic disorders. Classification of acute retinal arterial ischemic disorders: These are of 4 types: CRAO, branch retinal artery occlusion (BRAO), cotton wool spots and amaurosis fugax. Both CRAO and BRAO further comprise multiple clinical entities. Contrary to the universal belief, pathogenetically, clinically and for management, CRAO is not one clinical entity but 4 distinct clinical entities - non-arteritic CRAO, non-arteritic CRAO with cilioretinal artery sparing, arteritic CRAO associated with giant cell arteritis (GCA) and transient non-arteritic CRAO. Similarly, BRAO comprises permanent BRAO, transient BRAO and cilioretinal artery occlusion (CLRAO), and the latter further consists of 3 distinct clinical entities - non-arteritic CLRAO alone, non-arteritic CLRAO associated with central retinal vein occlusion and arteritic CLRAO associated with GCA. Understanding these classifications is essential to comprehend fully various aspects of these disorders. Central retinal artery occlusion: The pathogeneses, clinical features and management of the various types of CRAO are discussed in detail. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly (p<0.001) among the 4 types of CRAO; among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable or deteriorated in non-arteritic CRAO in 22%, 66% and 12% respectively; in non-arteritic CRAO with cilioretinal artery sparing in 67%, 33% and none respectively; and in transient non-arteritic CRAO in 82%, 18% and none respectively. Arteritic CRAO shows no change. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. Prevalent multiple misconceptions on CRAO are discussed. Branch retinal artery occlusion: Pathogeneses, clinical features and management of various types of BRAO are discussed at length. The natural history of visual acuity outcome shows a final visual acuity of 20/40 or better in 89% of permanent BRAO cases, 100% of transient BRAO and 100% of non-arteritic CLRAO alone. Cotton wools spots: These are common, non-specific acute focal retinal ischemic lesions, seen in many retinopathies. Their pathogenesis and clinical features are discussed in detail. Amaurosis fugax: Its pathogenesis, clinical features and management are described.
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PMID:Acute retinal arterial occlusive disorders. 2162 Sep 94

Transient monocular blindness is an acute episode of ischemic origin in which one eye has profound visual loss, followed by full recovery within one hour. Transient monocular blindness most often occurs in the setting of retinal ischemia secondary to carotid embolism, but other mechanisms have been reported, including thrombosis (most often in the setting of giant cell arteritis), hemodynamic disorders (secondary to severe carotid stenosis), or vasospasm. Transient monocular blindness is considered a transient ischemic attack originating in the carotid arteries, and must be managed the same as transient ischemic attack involving the brain, in order to prevent a subsequent stroke.
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PMID:Transient monocular blindness: Vascular causes and differential diagnoses. 2967 27

Transient monocular blindness is an acute episode of ischemic origin in which one eye has profound visual loss, followed by full recovery within one hour. Transient monocular blindness most often occurs in the setting of retinal ischemia secondary to carotid embolism, but other mechanisms have been reported, including thrombosis (most often in the setting of giant cell arteritis), hemodynamic disorders (secondary to severe carotid stenosis) or vasospasm. Transient monocular blindness is considered a transient ischemic attack originating in the carotid arteries and must benefit from the same management as transient ischemic attack involving the brain, in order to prevent a subsequent stroke.
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PMID:[Transient monocular blindness: Vascular causes and differential diagnoses]. 2977 64