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

Arteritic anterior ischaemic optic neuropathy and nonarteritic anterior ischaemic optic neuropathy are acute optic neuropathies, which have to be differentiated from each other. It was the purpose of this study to assess whether ophthalmodynamometry with an assessment of the collapse pressure of the central retinal artery (CRA) and vein (CRV) is helpful for that. Using a Goldmann contact lens-associated ophthalmodynamometer, the diastolic collapse pressure of the CRA and CRV were measured in six patients (eight eyes) with giant cell arteritis-induced anterior ischaemic optic neuropathy (GC-AION) and in 10 patients (12 eyes) with acute non-arteritic anterior ischaemic optic neuropathy (NAION). CRA collapse pressure was significantly (P=0.001; 95% confidence interval (CI): -68.7, -20.0) lower in the GC-AION group (52.7+/-24.6 arbitrary units) than in the NAION group (97.0+/-25.8 arbitrary units). CRV collapse pressure did not vary significantly (P=0.47). As measured by ophthalmodynamometry, CRA pressure is significantly lower in GC-AION than in NAION. CRV pressure does not vary markedly. These finding may be helpful for the clinical differentiation between GC-AION and NAION, and may give hints for the pathogenesis.
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PMID:Central retinal artery and vein collapse pressure in giant cell arteritis versus nonarteritic anterior ischaemic optic neuropathy. 1855 Nov 38

Ischemic optic neuropathies (IONs) are the most frequent acute optic neuropathy in patients older than 50 years. They are classified according to the location of the ischemic damage into anterior ION and posterior ION. Ischemic optic neuropathies may also be categorized based on the presence or absence of temporal arteritis as an underlying etiology. Anterior ION presents with sudden, painless visual loss developing over hours to days. Examination findings usually include decreased visual acuity, a visual field defect, color vision loss, a relative afferent pupillary defect, and a swollen optic nerve head. Posterior ION occurs in arteritic, nonarteritic, and surgical settings. It is characterized by acute vision loss without initial disc edema but with subsequent optic disc atrophy.
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PMID:Ischemic optic neuropathy. 1757 64

The need of blood flow to different organs varies rapidly over time which is why there is sophisticated local regulation of blood flow. The term dysregulation simply means that blood flow is not properly adapted to this need. Dysregulative mechanisms can lead to an over- or underperfusion. A steady overperfusion may be less critical for long-term damage. A constant underperfusion, however, can lead to some tissue atrophy or in extreme situations to infarction. Unstable perfusion (underperfusion followed by reperfusion) leads to oxidative stress. There are a number of causes that lead to local or systemic vascular dysregulation. Systemic dysregulation can be primary or secondary of nature. A secondary dysregulation is due to other autoimmune diseases such as rheumatoid arthritis, giant cell arteritis, systemic lupus erythematodes, multiple sclerosis, colitis ulcerosa, or Crohns disease. Patients with a secondary vascular dysregulation normally have a high level of circulating endothelin-1 (ET-1). This increased level of ET-1 leads to a reduction of blood flow both in the choroid and the optic nerve head but has little influence on autoregulation. In contrast, primary vascular dysregulation has little influence on baseline ocular blood flow but interferes with autoregulation. This, in turn, leads to unstable oxygen supply, which seems to be a relevant component in the pathogenesis of glaucomatous optic neuropathy.
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PMID:What is the link between vascular dysregulation and glaucoma? 1799 40

Anterior ischemic optic neuropathy (AION) is the most common cause of acute optic neuropathy after age 50, but may also occur in younger patients. The diagnosis is clinical and includes painless visual loss associated with a relative afferent pupillary defect and disc edema. In almost all cases, there is an underlying crowded optic nerve with a small cup-to-disc ratio. The visual prognosis is usually poor, although up to 43% of patients may improve over time. The fellow eye is involved in up to 15% of patients within 5 years, but the risk of recurrence in the same eye is less than 5%. There is no treatment for acute nonarteritic AION but it is essential to evaluate these patients for underlying treatable atheromatous vascular risk factors. A coagulation workup should also be considered in younger patients. It is essential to rule out giant cell arteritis in all patients over the age of 50 with ischemic optic neuropathies. Posterior ischemic neuropathy (in which the optic nerve is normal acutely) is rare and should be considered a diagnosis of exclusion.
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PMID:Ischemic optic neuropathies. 1900 40

Vasculitis affecting the peripheral nerves predominantly manifests as subacute, progressive, asymmetric sensorimotor polyneuropathy or mononeuritis multiplex, and more rarely as painful mononeuropathy, pure sensory neuropathy, neuropathy of the cranial nerves, plexopathy, or as autonomic neuropathy. Vasculitic neuropathy may occur isolated or non-isolated (systemic) together with involvement of other organs. Systemic vasculitis with involvement of the peripheral nerves is further subdivided into primary (Takayasu syndrome, giant cell arteritis, classical panarteritis nodosa, thrombangitis obliterans, Kawasaki disease, Churg-Strauss syndrome, Wegener granulomatosis, cryoglobulinemic vasculitis, Behcet disease, microscopic polyangitis, Schoenlein Henoch purpura) or secondary systemic vasculitis (autoimmune connective tissue diseases, vasculitis from infection, sarcoidosis, malignancy, drugs, radiation, or diabetes). In addition to routine laboratory investigations and nerve conduction studies, nerve biopsy is essential for diagnosing the condition and to delineate it from differentials, although its sensitivity is only approximately 60%. Therapy of non-viral vasculitic neuropathy is based on corticosteroids and cyclophosphamide alone or in combination. Additional options include azathioprine, methotrexate, mycophenolate mofetil, or rituximab. In single cases immunoglobulins, immunoadsorbtion, or plasma exchange have been successfully applied. In case of virus-associated vasculitis interferon-alpha plus lamivudine or ribaverin may be beneficial.
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PMID:Systemic and non-systemic vasculitis affecting the peripheral nerves. 1968 41

Giant cell arteritis (Horton's disease) is an inflammatory panarteritis occurring most frequently in the elderly. Its common ocular manifestations are anterior ischemic optic neuropathy, choroidal ischemia and central retinal artery occlusion. We describe a case of Horton's disease revealed by a retinal detachment, optic neuropathy and severe choroidal ischemia. Prompt treatment with corticosteroids led to preservation of vision and resolution of the retinal detachment. This observation of a retinal detachment revealing a giant cell arteritis had not been yet reported in the literature.
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PMID:[Exsudative retinal detachment indicative of a giant cell arteritis. A case report]. 2156 51

Hypertrophic pachymeningitis (HP) is a rare chronic inflammatory disease of the dura mater, described in association with various infections, systemic vasculitides such as Wegener's granulomatosis and giant cell arteritis. However, HP in association with Takayasu arteritis (TA) has not been described. We report a young woman who presented with headache, seizures, and right third and fourth cranial neuropathy. Magnetic resonance imaging of the brain showed HP in bifrontal and right temporal region extending to cavernous sinus. She was also found to have systemic hypertension, stenosis of left subclavian, and left renal artery with narrowing of abdominal aorta, satisfying the diagnostic criteria for TA. A detailed evaluation for secondary causes of HP failed to reveal an alternative etiology. This report describes an unusual association of HP in a patient with TA, also emphasizing that seizures and cranial neuropathy may further expand the spectrum of neurological manifestations in patients with TA.
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PMID:Hypertrophic pachymeningitis in a patient with Takayasu arteritis: One more association? 2241 77

Purpose. To present a unique case of Non-Hodgkin's-Lymphoma- (NHL) associated compressive optic neuropathy. Method. An 89-year-old male presenting with acute unilateral visual loss and headache. Results. Patient was initially diagnosed with occult giant cell arteritis; however after visual acuity deteriorated despite normal inflammatory markers, an urgent MRI scan revealed an extensive paranasal sinus mass compressing the optic nerve. Conclusion. Paranasal sinus malignancies occasionally present to the ophthalmologist with signs of optic nerve compression and must be included in the differential diagnosis of acute visual loss.
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PMID:Compressive Optic Neuropathy Caused by Orbital Non-Hodgkin's Lymphoma. 2260 5

Churg-Strauss syndrome (CSS) is a systemic vasculitis with frequent respiratory tract involvement. It can also affect the nervous system, notably the optic tract. The present work reports the case of a 65-year-old man diagnosed as having CSS in the context of several acute onset neurological symptoms including muscle weakness and signs of temporal arteritis, including bilateral anterior ischaemic optic neuropathy (ON). Electroretinograms (ERGs) and visual evoked potentials (VEPs) were performed. Flash ERGs were normal whereas VEPs were highly abnormal, showing a dramatic voltage reduction, thus confirming the ON. The vision outcome was poor. Ophthalmological presentations of CSS have rarely been reported, but no previous case of sudden blindness documented by combined ERG and VEP investigations were found in the literature. The present case strongly suggests that the occurrence of visual loss in the context of systemic inflammation with hypereosinophilia should lead to considering the diagnosis of CSS.
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PMID:Initial neuro-ophthalmological manifestations in Churg-Strauss syndrome. 2278 94

Hypereosinophilic syndrome is a rare disorder of the hematopoietic system. The disease is characterized by continuously high number of eosinophils (>1.5 x 10(9)/L) for more than six months. Other possible causes of hypereosinophilia, such as allergic and parasitic diseases, malignant disease, Churg-Strauss disease and infection should be eliminated. The most common manifestations of hypereosinophilic syndrome are pulmonary, skin, gastrointestinal, cardiac difficulties and neurologic lesions. Numerous neurologic lesions have been described, in particular of the central and peripheral nervous systems. Review of the literature revealed the following to have been recorded so far: mononeuritis multiplex, sensory polyneuropathy, radiculopathy, myalgia, myositis and perimyositis, neuropathy, ataxia, paraplegia, ophthalmologic abnormalities, optic neuritis, hemiplegia-hemiparesis, spasmodic quadriplegia, seizures, meningitis, cerebral infarction, organic psychosyndrome, other mental changes, stroke, temporal arteritis, leptomeningeal dissemination, memory deficits and dysarthria.
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PMID:Neurologic manifestations of hypereosinophilic syndrome--review of the literature. 2292 4


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