Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. Headache is observed in 65-68%, facial pain in 34-53%, and neck pain in 9-26%. Horner syndrome consisting essentially of miosis and ptosis is detected in 28-41%. Cranial nerve palsy is reported in 8-16%; the lower cranial nerves IX-XII are most commonly affected, in particular the hypoglossal nerve. The facial nerve may also be involved; dysgeusia results mainly from involvement of the chorda tympani (0.5-7.0%) or the glossopharyngeal nerve. Transient pareses of the ocular motor (III, IV and VI) and trigeminal nerves have been observed. Pulsatile tinnitus is reported in 16-27%. About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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PMID:Clinical manifestations of carotid dissection. 1729 Jan 13

Nephrogenic systemic fibrosis is a severe disabling disease that can follow gadolinium-based contrast exposure. In this study we analyzed the clinical and laboratory records of patients with nephrogenic systemic fibrosis who had a history of exposure to gadolinium-based contrast media and identified their cardiac and vascular events. At autopsy, we found that the heart, blood vessels, and skin of three patients who died of cardiac and/or vascular complications had appreciable amounts of gadolinium, iron, and aluminum as measured by inductively coupled plasma-mass spectrometry and confirmed by x-ray fluorescence. Of the 32 patients with nephrogenic systemic fibrosis studied, 10 died at a median of 112 days after diagnosis. Cardiovascular events contributed to the mortality of 9 patients and included congestive heart failure, recurrent arrhythmias, hypotension, stroke, limb ischemia, posterior ischemic optic neuropathy and sudden death. Our results show that increased cardiac and vascular complications along with short survival in nephrogenic systemic fibrosis are associated with metal accumulation in the heart, blood vessels, and skin of these patients.
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PMID:Cardiac and vascular metal deposition with high mortality in nephrogenic systemic fibrosis. 1903 10

Phosphodiesterase type-5 (PDE-5) inhibitors are well tolerated and efficacious treatments for male erectile dysfunction that currently rank among the best-selling drugs worldwide. Since their introduction 10 years ago, there have been a number of reports of patients developing, within hours of PDE-5 inhibitor use, permanent visual loss due to nonarteritic anterior ischemic optic neuropathy (NAION), a common optic neuropathy that results from ischemia of the optic nerve head. In some of the cases, visual loss recurred upon rechallenge with the drug. However, as the bulk of the evidence suggesting a relationship between PDE-5 inhibitor use and NAION comes from case reports and small series, it is difficult to ascertain if a cause-effect relationship truly exists. In this paper, following a review of the transient visual side effects of PDE-5 inhibitors and NAION, we discuss the evidence for and against NAION occurring as a complication of PDE-5 inhibitor use.
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PMID:Nonarteritic anterior ischemic optic neuropathy with PDE-5 inhibitors for erectile dysfunction. 1852 98

Ischemic optic neuropathy is caused by ischemia of the optic nerve head in the region of the lamina cribrosa. Differentiation is made between arteritic (AION) and nonarteritic (NAION) forms. AION is the most common ophthalmological manifestation of giant cell arteritis and is usually well controlled with systemic steroid therapy. Temporal artery biopsy for confirmation of the diagnosis is mandatory. NAION is not a disease entity but rather the common pathogenetic pathway of a large variety of diseases and conditions and is often the result of several interacting factors. For this reason, there is no "standard therapy" for NAION. Careful interdisciplinary work up in NAION frequently reveals previously unrecognized diseases requiring treatment according to internal medicine standards. Adequate treatment frequently results in improvement of the affected eye and reduced risk of NAION in the other eye or of brain infarction.
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PMID:[Anterior ischemic optic neuropathy: Etiology, pathogenetic mechanisms and therapy]. 1881 Apr 58

Hyperbaric oxygen therapy (HBOT) is a primary or adjunctive therapy for a variety of medical disorders including some involving the eye. This paper is the first comprehensive review of HBOT for ocular indications. The authors recommend the following as ocular indications for HBOT: decompression sickness or arterial gas embolism with visual signs or symptoms, central retinal artery occlusion, ocular and periocular gas gangrene, cerebro-rhino-orbital mucormycosis, periocular necrotizing fasciitis, carbon monoxide poisoning with visual sequelae, radiation optic neuropathy, radiation or mitomycin C-induced scleral necrosis, and periorbital reconstructive surgery. Other ocular disorders that may benefit from HBOT include selected cases of ischemic optic neuropathy, ischemic central retinal vein occlusion, branch retinal artery occlusion with central vision loss, ischemic branch retinal vein occlusion, cystoid macular edema associated with retinal venous occlusion, post-surgical inflammation, or intrinsic inflammatory disorders, periocular brown recluse spider envenomation, ocular quinine toxicity, Purtscher's retinopathy, radiation retinopathy, anterior segment ischemia, retinal detachment in sickle cell disease, refractory actinomycotiC lacrimal canaliculitis, pyoderma gangrenosum of the orbit and refractory pseudomonas keratitis. Visual function should be monitored as clinically indicated before, during, and after therapy when HBOT is undertaken to treat vision loss. Visual acuity alone is not an adequate measure of visual function to monitor the efficacy of HBOT in this setting. Ocular examinations should also include automated perimetry to evaluate the central 30 degrees of visual field at appropriate intervals. Interpretation of the literature on the efficacy of HBOT in treating ocular disorders is complicated by several factors: frequent failure to include visual field examination as an outcome measure, failure to adequately address the interval from symptom onset to initiation of HBOT, and lack of evidence for optimal treatment regimens for essentially all ocular indications. Because some ocular disorders require rapid administration of HBOT to restore vision, patients with acute vision loss should be considered emergent when they present. Visual acuity should be checked immediately, including vision with pinhole correction. If the patient meets the criteria for emergent HBOT outlined in the paper, normobaric oxygen should be started at the highest inspired oxygen fraction possible until arrangements can be made for HBOT.
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PMID:Hyperbaric oxygen therapy and the eye. 1902 63

It is accepted that tobacco smoking impairs different functions of the organ of vision and can be the cause of different eye diseases. It is well-known that tobacco smoke contains more than 4,000 substances, some of them exerting toxic influence on the eye by producing the ischemia or/and oxidative stress. In previous years, the association between tobacco smoking and cataract, age-related macular degeneration (ARMD), thyroid eye disease, anterior ischemic optic neuropathy and primary open angle glaucoma (POAG) were observed. It was also suggested that smoking might have a negative impact on the treatment of scleritis, thyroid eye disease and surgery of POAG. In last two years many interesting studies have been conducted on the influence of smoking on morbidity and the character of AMD, cataract, vascular diseases of the retina, cystoid macular edema complicating intermediate uveitis, refractive errors, thyroid eye disease and the function of the optic nerve and retina measured by electrophysiological techniques. Concluding there is increasing evidence that tobacco smoking is a risk factor in case of many eye diseases. This suggests that by eliminating smoking, it might be possible to decrease the morbidity of eye diseases in the future.
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PMID:[Present knowledge on the effects of smoking tobacco on the eye diseases]. 1918 88

A visual impairment occurs in about 50% of patients with giant cell arteritis (GCA), an amaurosis fugax (AF) in about 30%, and diplopia in about 10%. An arteritic anterior ischemic optic neuropathy was found in about 80%-90% of patients with visual loss and an arteritic central retinal artery occlusion in about 10%-20%. Without therapy, involvement of the fellow eye may occur within hours or days in a patient with unilateral blindness. Involvement of the anterior segment of the eye (iris ischemia, episcleritis) is rare. Ocular ischemic syndrome is defined by visual loss with hypotony, ischemia of the iris, and cotton wool spots (CWS). CWS may already occur with AF episodes. In the case of strong suspicion of GCA, immediate therapy with steroids is indicated. Duplex sonography and a gadolinium MRI examination are of diagnostic importance. A biopsy of the temporal artery may be carried out after the initiation of therapy.
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PMID:[Ocular findings and differential diagnoses in giant cell arteritis (Arteriitis cranialis)]. 1922 26

Giant cell arteritis is a vasculitis of large and medium sized arteries with variable clinical presentations. Arteritic anterior ischemic optic neuropathy is the most common cause of visual loss from giant cell arteritis and the ischemia related to this process is presumed to be secondary to luminal stenosis from intimal hyperplasia. This process has been found to be initiated and promoted by various inflammatory and pro-angiogenic factors.
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PMID:Giant cell arteritis and angiogenesis: a review. 1943 57

Most ischemic optic neuropathies are attributed to interference of blood flow originating within the posterior ciliary circulation. In patients with the most common type of ischemic optic neuropathy, nonarteritic anterior ischemic optic neuropathy (NAION), the microvascular ischemia predominantly affects the intraocular portion of the optic nerve. NAION most commonly occurs in eyes with small, "crowded" optic disks and usually does not result in optic disk excavation. We report a patient who presented with NAION and subsequently developed optic disc excavation typical of glaucomatous optic neuropathy.
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PMID:Optic disk excavation in nonarteritic anterior ischemic optic neuropathy. 2043 58

Giant cell arteritis (GCA) is a chronic granulomatous vasculitis of large and medium size vessels in the elderly. A new-onset headache is the most frequent symptom. An anterior ischemic optic neuropathy (AION) is one of the most common causes of permanent visual loss. There are four cases with unusual presentation of giant cell arteritis, scalp abscess, prolonged transient monocular visual loss (TMVL), bilateral central retinal artery occlusion (CRAO), and chronic ear pain. All patients had pathologically proven giant cell arteritis, and three of them progressed to blindness in the end. Scalp abscess is a rare sign in GCA. Delay in diagnosis because confusion of the abscess after scalp ischemia with other cutaneous lesions may result in death. TMVL is the forewarning symptom of AION or CRAO in GCA. Early recognition of TMVL is important to make early diagnosis of GCA to prevent blindness. Spontaneous ear pain is extremely rare, and reports have documented delay in diagnosis of GCA resulting in irreversible blindness.
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PMID:A variety of atypical manifestations in giant cell arteritis. 2052 53


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