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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonarteritic anterior ischemic optic neuropathy is a common cause of sudden, painless loss of vision present commonly on awakening from sleep. It most commonly affects middle-aged and elderly Caucasian men and women. Involvement of the opposite eye occurs within 3 years in less than 43% of patients. Hypertension, diabetes, and nocturnal hypotension are risk factors. A congenital small cup-to-disk ratio also predisposes to the optic nerve ischemia. There is no effective therapy to treat patients acutely or to prevent recurrence. After 6 months of careful follow-up, 57.3% of patients will have no significant change or worsening of their vision in the involved eye.
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PMID:Nonarteritic anterior ischemic optic neuropathy. 1572 60

Ocular involvements of Biermer's anaemia are rarely reported in literature. We present a case of Biermer's anaemia associated with diabetes. Ocular examination showed important conjinctival paleness, diffuse retinal ischemia, Roth's tasks, macular oedema and ischemic optic neuropathy. The patient was treated with vitamin B12 intramusculary. A month later, on examination, we noted a regression of optic neuropathy, the aggravation of ischemic retinopathy and persistence of macular oedema. The patient was treated with laser photocoagulation. The majority of ocular manifestations are reversible if treatment is underlaken early. The combination of diabetes with Biermer's anemia deteriorates the ischemic retinopathy and aggavates its prognosis.
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PMID:[Ocular findings in megaloblastic anemia associated with diabetes. A case report]. 1604 7

The purpose of this case report is to show the diagnostic potential of diffusion-weighted MR imaging in establishing the presence of ischemic optic neuropathy (ION). We report the MR imaging findings in a patient presenting with acute ION in whom diffusion imaging showed decreased water mobility as seen in patients with acute brain ischemia.
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PMID:Diffusion MR imaging in a case of acute ischemic optic neuropathy. 1648 86

Non-arteritic anterior ischemic optic neuropathy is caused by a transient optic nerve ischemia and results in permanent vision loss. Currently, there is no effective treatment for this ischemic optic nerve injury. This study characterized the duration and extent of ischemia induced after a coagulopathy injury to the optic nerve of adult rats. Acute ischemia was induced in adult rats by intravenous injection of Rose Bengal dye, followed by argon green laser treatment of the vessels at the optic disc. Rats were assessed in the short-term for hypoxyprobe-1 binding and expression of hypoxia inducible factor-1alpha (HIF-1 alpha) and fractin, markers of neuronal injury. Five months after injury, optic axon number was quantified. The coagulopathy injury resulted in short-term hypoxia in the optic nerve and retina. Tissues were hypoxic within 15 min of the coagulopathy injury, but normoxic by 24 h as measured by hypoxyprobe-1 staining. Both HIF-1alpha and fractin were upregulated in ganglion cells variably across the retina. Five months after the ischemic injury, there was a 71% reduction in optic axon number compared to controls. It is critical to have a reproducible and relevant method for producing transient hypoxia in order to test therapeutic strategies for rescuing injured neurons. The coagulopathy induced in this study resulted in a reproducible and transient ischemic optic nerve injury and long-term axonal loss. This ischemia shows similar, although not identical, morphological and physiological changes to those seen in the human eye after optic nerve ischemia. We are currently testing therapeutic strategies to protect ganglion cells from degeneration after this ischemic injury.
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PMID:Histological and morphometric evaluation of transient retinal and optic nerve ischemia in rat. 1673 Mar 39

Nitric oxide (NO) is a gas with diverse biological activities produced from arginine by nitric oxide synthetase (NOS). The loss of retinal ganglion cells is a hallmark of many ophthalmic diseases including glaucoma, retinal ischemia due to central artery occlusion and anterior ischemic optic neuropathy. It may well be significant in optic neuritis, optic nerve, trauma and AIDS. NO appears to be involved in the regulation of intraocular pressure, in the modulation of ocular blood flow and in apoptosis. This article gives a short and simplified overview of the biochemistry of NO and its role in physiology and pathogenesis of ocular diseases.
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PMID:[The role of nitric oxide in physiology and pathogenesis of ocular diseases]. 1688 53

Giant cell arteritis is a systemic vasculitis that affects large- and medium sized arteries. The most common ophthalmic manifestation of this disease is anterior ischemic optic neuropathy, leading to acute, painless visual loss in one or both eyes. It is caused by ischemia of the optic nerve head, which is mainly supplied by the short posterior ciliary arteries. Early diagnosis is the key to correct management and prevention of visual loss in the second eye. The treatment of choice for arteritic ischemic optic neuropathy is high dose of systemic corticosteroids. Only such treatment may prevent blindness. The authors presented a case of a 62 years man with anterior ischemic neuropathy in one eye, which was diagnosed as arteritic form caused by giant cell arteritis. The correct diagnosis was based on typical clinical signs of ischemic changes in the optic nerve head and diagnostic criteria for giant cell arteritis, advocated by American College of Rheumatologists.
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PMID:[Anterior ischemic optic neuropathy associated with giant cell arteritis. Case report]. 1688 58

Bilateral anterior ischemic optic neuropathy and bilateral ocular ischemic syndrome have been rarely reported as initial manifestations of Takayasu's arteritis (TA). Appearance of ocular symptoms in TA is closely related to extension and severity of involvement of the aorta and its major branches. Here we reported a case of 'carotid steal syndrome' secondary to TA in a 45 year old Turkish man, who had severe ocular and brain ischemia, presented initially with symptoms of ocular ischemic syndrome.
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PMID:Bilateral ocular ischemic syndrome as an initial manifestation of Takayasu's arteritis associated with carotid steal syndrome. 1694 56

Giant cell arteritis is a rare systemic vasculitis affecting large- and medium-sized arteries. Focal arteries lesions, include mononuclear cells infiltration of the vessel wall with giant cell formation. It is a disease of elderly persons and can result in a wide variety of systemic, neurological and ophthalmic complications, due to ischemia. The incidence of visual loss and ocular involvement varies between 14-88%, but one of the most common and severe complications is anterior ischemic optic neuropathy. The other ocular ischemic lesions include: central retinal artery occlusion, choroidal ischemia, diplopia, ocular motor paresis, anterior uveitis, cataract, ocular hypotony, corneal oedema and ulcerations, episcleritis and anterior scleritis, orbital cellulitis and pseudotumor. Because giant cell arteritis is potentially blinding disease, early diagnosis and immediate treatment with high dose corticosteroids may prevent further damage to the affected eye and prevent visual loss in the opposite eye. The purpose of this review is to revise established knowledge and to highlight the recent developments in diagnosis and management of giant cell arteritis.
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PMID:[A new approach towards giant cell arteritis]. 1702 3

Ischemic optic neuropathy (ION) is a common disorder caused by disruption of the arterial blood supply to the optic nerve. It can result in significant loss of visual acuity and/or visual field. An ischemic optic nerve injury was produced in rats by intravenous injection of Rose Bengal dye followed by argon green laser application to the retinal arteries overlying the optic nerve, causing a coagulopathy within the blood vessels and disruption of optic nerve and retinal perfusion. The effect of brimonidine tartrate eye drops on survival of retinal ganglion cell axons in this experimental paradigm was studied. One eye was treated and the contralateral eye served as a control. Four groups of animals were used for this study. Group 1 received 7 days of treatment with 0.15% brimonidine tartrate eye drops twice a day prior to the ischemic injury. Group 2 animals received 0.15% brimonidine tartrate eye drops twice a day for 14 days after photocoagulation injury. Animal groups 3 and 4 received eye drops of 0.9% NaCl twice a day either daily for 7 days before injury or daily for 14 days, respectively. All rats were sacrificed 5 months after the injury to ascertain long-term optic axon survival. Coagulopathy-induced optic nerve ischemia resulted in a 71% loss of optic axons. Treatment with brimonidine daily for the 7 days prior to the injury resulted in a greater survival of optic axons, with only a 56.1% loss compared to control. Brimonidine treatment every day for 14 days after the ischemic injury did not result in a significant rescue of optic axons compared to injury alone. In summary, the application of brimonidine eye drops for one week prior to an ischemic injury resulted in a statistically significant increase in survival of optic axons within the injured optic nerves. Brimonidine treatment of the eye after the ischemic injury did not result in axon rescue, and axon loss was similar to the injured optic nerves treated with saline only. These results suggest that brimonidine may have potential use for prevention of ION in at-risk patients.
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PMID:Neuroprotective effects of brimonidine treatment in a rodent model of ischemic optic neuropathy. 1711 77

Cervicocranial arterial dissection (CCAD) occurs when there is a tear in the intimal layer of the carotid or vertebral arteries with subsequent extravasation of blood into the subintimal layers. The dissection may be extradural, intradural, or extend over both segments. The contents of the subintimal layers are highly thrombogenic, and thus, embolism, vessel stenosis, or occlusion may follow. Symptoms of dissection may be caused by local injury to the blood vessel or by ischemia to the retina or brain. Thus, dissection should always be considered in patients who present with Horner syndrome associated with ipsilateral headache, carotidynia, ocular pain, or amaurosis fugax. Rare neuro-ophthalmologic presentations of dissection include anterior and posterior ischemic optic neuropathy; central retinal artery occlusion; ophthalmic artery occlusion; transient ophthalmoparesis; and third, fourth, or sixth cranial nerve palsy. The most common serious complication of dissection is ischemic stroke. No randomized controlled trials have evaluated therapies for patients presenting with CCAD. Thus, treatment is essentially empiric and often varies by region. Medical management is first line in most patients. Given the propensity for thrombus formation and early embolization or occlusion, acute anticoagulation using intravenous heparin or low-molecular-weight heparinoids followed by short-term, dose-adjusted warfarin is the treatment of choice for most patients with extradural CCAD who present early after symptom onset. The risk of cerebral ischemia is greatest in the first few weeks after dissection; thus, it is reasonable to recommend antiplatelet agents for patients who present late and have not had evidence of ischemia. Intradural dissection is rare but is associated with a meaningful risk of subarachnoid hemorrhage (SAH). As a result, anticoagulants and antiplatelet agents should not be used if SAH is suspected or confirmed. Endovascular intervention may be necessary in a small minority of cases with recurrent events despite anticoagulation or SAH due to intradural dissection. Of special note, CCAD is not considered a contraindication for tissue plasminogen activator use in acute stroke patients who are otherwise eligible for treatment.
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PMID:Cervicocranial arterial dissection. 1728 90


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