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Query: UMLS:C0022116 (ischemia)
 91,303 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

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

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

Tonic pupil is usually an idiopathic condition. In some cases, the cause of the ciliary ganglion lesion leading to tonic pupils is obvious. Rarely ischemia causes a lesion of the ciliary ganglion or the short ciliary nerves due to the good blood supply of the ciliary ganglion. Only two cases of tonic pupils in the course of giant cell arteritis are mentioned in the literature, but tonic pupils are probably much more common with this disease. Five cases are demonstrated here. All had associated ischemic optic neuropathy, and stagnation of the blood flow in the supratrochlear artery could be demonstrated in two cases by Doppler sonography. Tonic pupils may also occur when an oclusion of the internal carotid artery resolves, probably because of transient stasis of the orbital blood flow. In another case, tonic pupils were associated with choroidal ischemia (proved by video fluorescent angiography) of unknown origin. The diagnosis of tonic pupils was made by pharmacological testing for cholinergic hypersensitivity with 0.1% pilocarpine.
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PMID:[Tonic pupil caused by ischemia]. 279 12

Two adult diabetic patients with chronic asymptomatic optic neuropathy attributed to an ischemic etiology are reported. In one case the typical syndrome of ischemic optic neuropathy occurred in one eye, while the fellow eye had asymptomatic hyperemic optic disc edema that persisted for 6 months without optic atrophy. A minor visual field defect initially detected in that eye resolved spontaneously in 1 month. In the second case, a recent onset, middle-aged diabetic developed bilateral optic neuropathy and optic disc edema that persisted for 12 months, with minimal signs of visual dysfunction. Axoplasmic transport blockage from low-grade ischemia to the optic nerve may cause acute or chronic optic disc edema with minimal or no visual symptoms.
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PMID:Chronic asymptomatic ischemic optic neuropathy. A report of two cases in adults with diabetes mellitus. 296 25

Visual disturbance after marked and/or recurrent blood loss has been known for at least 25 centuries, since Hippocrates; however, so far its clinical features have been controversial and its pathogenesis enigmatic. The author studied seven patients, four of whom were seen soon after the visual loss and followed prospectively. A detailed review of the extensive literature and analysis of the cases provide relevant information on the subject. The blood loss is usually from the gastrointestinal (GI) tract, less often from other sites. There is typically a time lag between the bleeding and the onset of visual loss--usually up to 10 days, less often even 2 to 3 weeks. The ocular findings are typically those of anterior ischemic optic neuropathy (AION) and are usually bilateral. Considerable evidence has accumulated that blood loss, with or without arterial hypotension, causes increase in release of renin and endogenous vasoconstrictor agents (e.g., angiotensin, epinephrine, and vasopressin) because of activation of the sympathoadrenergic system and vasomotor center. Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION. In view of all the evidence, it is postulated that in the production of AION after blood loss, release of endogenous vasoconstrictor agents is probably a very important factor, with arterial hypotension an additional factor; increased platelet aggregation may also play a role.
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PMID:Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. 350 Apr 45

The optic disc appearance in the normal fellow eye of 126 patients with nonarteritic anterior ischemic optic neuropathy (n-AION) was compared with the discs in 23 patients with arteritic AION (a-AION) and 122 normal subjects. The number of discs with no cup was significantly greater (P less than 0.001) and the number of discs with a large cup was significantly fewer (P less than 0.001) in the n-AION group compared to the other two groups. No significant differences were found in cup size between the a-AION and normal groups. The pathogenesis of n-AION appears to be multifactorial. There is overwhelming evidence that ischemia is the primary factor. The size of the optic disc also plays a role, probably through a compressive effect at the level of the lamina cribrosa on axons subjected to ischemia. In contrast, a-AION occurs from posterior ciliary artery occlusion and disc size is not a factor.
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PMID:Anterior ischemic optic neuropathy. IX. Cup-to-disc ratio and its role in pathogenesis. 368 23

A 78-year-old white woman had catastrophic visual loss in one eye due to temporal arteritis. Despite treatment with doses of oral corticosteroids high enough to normalize the Westergren erythrocyte sedimentation rate, she experienced progressive retinal ischemia with visual loss in the second eye. The use of 1,000 mg of pulsed intravenous methylprednisolone every 12 hours restored her vision. Brief hospitalization of patients with arteritic ischemic optic neuropathy for treatment with intravenous methylprednisolone may offer a significant chance of visual recovery of the involved eye and provide optimal protection to the uninvolved eye.
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PMID:Treatment of temporal arteritis with ocular involvement. 394 48

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.
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PMID:Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy. 402 51

Two monocular normotensive patients with nonarteritic ischemic optic neuropathy and retinal ischemia unresponsive to steroid therapy were treated with intravenous norepinephrine. In both patients, improvement in vision began within minutes after moderate hypertension was produced. A third patient showed no response to this therapy in one eye with established ischemic optic neuropathy, but had prompt recovery of vision in the second eye early in the course of ischemic optic neuropathy. This patient returned with recurrent ischemic optic neuropathy more than 1 year later. At that time she was found to have essential hypertension. One patient could not be weaned from the norepinephrine infusion without recurrent visual loss. In the second patient, controlled hypertensive therapy restored visual acuity to 20/30 during two separate recurrences of ischemic optic neuropathy. Therapy of a later episode of ischemic optic neuropathy was delayed for 2 days, and vision did not improve with norepinephrine infusion. This eye subsequently became painful and required enucleation. Histopathological evaluation showed combined arterial and venous occlusions within the optic nerve and evidence of previous peripapillary choroidal vascular occlusion. Selected normotensive patients with ischemic optic neuropathy and retinal ischemia may benefit from controlled hypertensive therapy induced by norepinephrine infusion.
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PMID:Norepinephrine therapy of ischemic optic neuropathy. 621 76


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