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

Giant cell arteritis is a relatively common form of systemic vasculitis, best known for its predisposition to affect the extracranial branches of the carotid artery and associated potential for visual loss. Additional vascular manifestations include stroke, aortic aneurysm or dissection, and even aortic rupture. Cardiac manifestations include coronary artery disease, aortic valve insufficiency, or left ventricular dysfunction, which may occur independently from the valvular disease or hypertension. Physicians need to be vigilant for this disorder, particularly because the tragic end-organ outcomes such as visual loss can be effectively prevented with early use of corticosteroids. We review the pathophysiology and clinical manifestations of giant cell arteritis and present a rationale for diagnosis and therapy for this disease.
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PMID:Giant cell arteritis: diagnosis, management, and cardiovascular implications. 1730 91

Headache in an elderly patient can be a sign of serious, potentially life-threatening disorders. All patients require a full assessment, including a complete neurologic examination. Particular emphasis should be placed on excluding subarachnoid hemorrhage, subdural hematoma, giant cell arteritis, intracranial neoplasm, cerebrovascular accident, acute-angle-closure glaucoma, and infectious etiologies such as meningitis and encephalitis. Once life-threatening disorders are excluded, the geriatrician can focus on more benign etiologies such as migraine, tension headache, and medication withdrawal. Treatment depends on the underlying etiology. This article discusses headaches that require emergent treatment and then describes more benign etiologies of headaches.
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PMID:Headache in the elderly. 1746 18

The diagnosis and management of third nerve dysfunction vary according to the age of the patient, the characteristics of the third nerve palsy, and the presence of associated symptoms and signs. Third nerve palsies can result from lesions located anywhere from the oculomotor nucleus to the termination of the third nerve in the extraocular muscles within the orbit, and may be the herald manifestation of underlying neurological emergencies such as intracranial aneurysm, pituitary apoplexy, and giant cell arteritis. Recent advances in noninvasive neuroimaging facilitate early diagnosis, but the management of a patient presenting with isolated third nerve palsy remains a challenge.
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PMID:Third nerve palsies. 1757 67

The aims of this study were to assess how frequently giant cell arteritis (GCA) was a cause of first-ever stroke in 4,086 patients in the Lausanne Stroke Registry and to determine the risk factors, patterns, latency and current therapy at onset in patients with GCA plus stroke. GCA was recognized using the criteria of the American College of Rheumatology. We report on 6 patients (0.15%) with a histologically proven diagnosis of temporal arteritis and clinical and neuroradiological evidence of cerebral ischemia. The CT and MRI scans showed lacunar infarction in 3 patients, territorial infarction in 2 and were normal in 1. Stroke latency ranged from 0 to 2 months. All patients suffered from headache. We conclude that stroke is a rare, but dangerous, complication of GCA and that a combination of antiplatelet drugs and corticosteroids may be advisable for preventing stroke occurrence.
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PMID:Giant cell arteritis as a cause of first-ever stroke. 1763 Apr 82

We report a patient with a posterior circulation stroke that presented insidiously, progressed rapidly and had an unusual aetiology of vertebral giant cell arteritis that was not recognised in a timely fashion. General awareness of this cause might alert clinicians to consider the diagnosis in similar cases, as prompt intervention may improve outcomes.
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PMID:Insidious posterior circulation stroke with rapid deterioration due to vertebral giant cell arteritis. 1796 41

Giant cell arteritis (GCA) is a common form of vasculitis that predominantly affects the elderly. Cranial symptoms and elevated inflammatory markers are suggestive of the condition and the diagnosis is usually established by temporal artery biopsy. Corticosteroids are the mainstay of treatment for GCA and prolonged therapy is often necessary. Disease relapses and steroid-related adverse effects, however, are common. Serious complications of the disease may include visual loss, stroke, and aortic involvement with aneurysm formation.
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PMID:Management guidelines and outcome measures in giant cell arteritis (GCA). 1802 19

In the UK, 4% of general practitioner consultations are for headache, yet the natural history of these presentations is unknown. The objective of this study was to describe the outcome of new headache presentations to the general practitioner. This was a prospective case-control study in adults over a period of 1 year using data from the General Practitioner Research Database, UK. Records of patients who presented with primary headache (migraine, tension-type headache, cluster headache) or undifferentiated headache (no further descriptor) were examined for the subsequent year for subarachnoid haemorrhage, primary brain tumour, benign space-occupying lesion, temporal arteritis, stroke and transient ischaemic attack. We identified 21,758 primary headaches and 63,921 undifferentiated headaches. The likelihood ratio was 29 (9.9, 92) for a subarachnoid haemorrhage after an undifferentiated headache and increased with age. The 1-year risk of a malignant brain tumour with new undifferentiated headache was 0.15%, rising to 0.28% above the age of 50 years. For primary headache the risk was 0.045%. The risk for a benign space-occupying lesion was 0.05% for an undifferentiated and 0.009% for a primary headache. The risk of temporal arteritis was the highest of the conditions studied, 0.66% in the undifferentiated and 0.18% in the primary headache group. Accepting the limitations of this approach, our data can inform management guidelines for new presentations of headache in primary care and confirm the need for follow-up, even if a primary headache diagnosis is made.
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PMID:What happens to new-onset headache presented to primary care? A case-cohort study using electronic primary care records. 2128 22

Cerebrovascular accidents (CVAs) and multi-infarct dementia have rarely been reported as presenting symptoms of giant cell arteritis (GCA), although 3%-4% of patients with GCA may present with CVAs during the course of the disease. We describe 7 patients with biopsy-proven GCA who presented with stroke or multi-infarct dementia. Most of them had other symptoms of GCA when the disease began that were misdiagnosed or not noticed. The internal carotid arteries were involved in 4 patients and the vertebrobasilar arteries in 3, with bilateral vertebral artery occlusion in 1. Small cerebral infarction foci on cranial computed tomography (CT) scan and magnetic resonance imaging (MRI) were found in 5 cases, and cerebellar infarction, in 2. MR angiography showed intracranial arteritis in 4 cases. Treatment with glucocorticoids and adjunctive antiplatelet or anticoagulant therapy was given in all cases, with neurologic improvement in 5. Two patients died. Necropsy demonstrated generalized GCA involving the medium and small cerebral vessels in 1 case. Central nervous system involvement is a rare complication in GCA but is important to recognize, as it can be reversible if diagnosed and treated promptly. Suspicion should arise in elderly patients suffering from strokes with a quickly progressing stepwise course and associated headache, fever, or inflammatory syndrome. In these cases, temporal artery biopsy should be performed without delay. Early diagnosis of GCA and immediate initiation of corticosteroid treatment may prevent progressive deterioration and death. Additional antiplatelet or anticoagulant therapy should be evaluated according to the individual risk and benefit to the patient under care.
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PMID:Stroke and multi-infarct dementia as presenting symptoms of giant cell arteritis: report of 7 cases and review of the literature. 1901 5

Anti Phospholipid Syndrome (APS) is a relatively new conception of syndrome complex first noticed in 1983. It may be primary or secondary to other diseases like SLE, RA, Systemic sclerosis, behchet's syndrome, temporal arteritis, sjogren's syndrome psoriatic arthropathy etc. Clinical manifestations are consequences of vascular thrombosis and embolism like DVT, pulmonary embolism, stroke, TIA, complication of pregnancy with pregnancy loss. We report a 34 years married female housewife who presented with sudden onset of nausea, vomiting, vertigo, dysphagia, dysarthria and ataxia. She had a chronic leg ulcer. Neurological findings were consistent with lateral medullary syndrome due to stroke though she was normotensive, nondiabetic with normal lipid profile. She had history of two abortions in last three years. Investigations were done accordingly and she fulfilled the diagnostic criteria of APS. No secondary cause was detected after thorough clinical examination and laboratory investigations. She was treated symptomatically along with oral anticoagulation. She improved slowly but steadily.
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PMID:Anti phospholipid syndrome. 1918 54

Giant cell arteritis (GCA), is a systemic vasculitis which preferentially targets large and medium branches of the upper-body aorta. Typical clinical manifestations result from arterial stenosis/occlusion causing blindness, stroke and aortic arch syndrome. Aortic involvement leads to dissection and aneurysm. On the cellular and molecular level, GCA is a sequel of abnormal innate and adaptive immune responses that occur in the specialized tissue niche of the arterial wall. Based on recent pathogenic studies, a novel disease model for GCA is emerging. It is now understood that the series of pathogenic events begins with dendritic cells (DC) indigenous to the artery's outer wall, leading to inflammatory vasculopathy. Placed close to the vasa vasorum, vascular DC are highly sensitive in recognizing pathogen-associated motifs assigning immune monitoring functions to blood vessels. Thus the large vessels are actively involved in immune monitoring. Each vascular territory expresses a unique profile of pathogen-sensing receptors, emphasizing functional diversity amongst structurally similar arteries. Innate immune stimulators can transform vascular DC into efficient antigen-presenting cells, attracting, activating, and instructing T lymphocytes to acquire tissue-invasive features. Macrophages provide critical tissue-damaging effector functions, directly injuring wall-residing cells and promoting a remodeling process that leads to intimal hyperplasia and luminal occlusion. Novel diagnostic and therapeutic approaches to GCA need to focus on the key position of vascular DC and the signals that break the immunoprivileged state of the vessel wall.
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PMID:[Pathogenesis of medium- and large-vessel vasculitis]. 1922 27


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