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)

The findings in nine patients are presented who suffered from acute bilateral visual loss occurring within less than one week, and all showed optic disc edema. CT scans revealed no abnormalities and the CSF-pressure measured in 6 patients was normal. Four of the patients (22 to 53 years old) recovered completely under orally given prednisolone (about 100 mg/day). The recent history of three patients suggested that the optic neuropathy was associated with an infection. This parainfectious process may be identical to the bilateral optic neuritis described in children. Four older patients (55 to 63 years) did not respond to steroid therapy. Their vision did not significantly improve. They showed attenuated retinal arteries; therefore it can be assumed that ischemia plays a role in the pathogenesis of this second type of optic neuropathy. In none of the cases a toxic optic neuropathy could be confirmed. One patient who experienced a visual loss down to finger counting after throat-surgery without marked blood loss recovered partially after steroid treatment.
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PMID:[Bilateral optic neuropathy with papilledema]. 158 43

The amplitude of the second harmonic of the focal electroretinogram (ERG) in response to either modulation of the luminance of the uniform-field or the spatial contrast of a patterned field (pattern-reversal ERG) was measured in a group of normal subjects as well as in patients with two different types of unilateral dysfunctions, namely optic atrophy or temporary retinal ischemia. Such patients had a reduced visual acuity in their affected eyes but normal full-field flicker (20 Hz) ERG. In normal eyes, for the same stimulation area and modulation depth, the second harmonic of the uniform-field response is smaller (mean value 62%) than that of the optimal pattern (around 1.5 cycles/degree). The results on patients show that the second harmonic of the pattern response, but not that of the uniform-field response, is reduced in cases of optic atrophy secondary to trauma or optic neuritis. This result suggests generators different, at least in part, for the second harmonic evoked by modulation of either luminance or spatial contrast. By contrast, both responses are reduced in cases of temporary retinal ischemia. These findings are discussed in light of the recent literature on the origin of the pattern ERG. The possible clinical applications of the technique are outlined.
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PMID:Non-linearities in the focal ERG evoked by pattern and uniform-field stimulation. Their variation in retinal and optic nerve dysfunction. 361 May 49

This case report deals with a 29 year-old female patient with a prior history of a vestibular syndrome and elapsing optic neuritis that presented paroxystic episodes of painful tonic contractions affecting the right hemibody, especially the upper limb. In the hand the clinical picture was similar to that of the carpal spasm of tetany. When inducing a crisis with ischemia the electromyogram showed diplets, triplets, and multiplets following the appearance of an interference pattern syncronous with contraction of the hand. Occasionally an interference pattern was observed that was associated only to a subjective sensation of paresthesia. During the crisis and in the intercritical periods the following measurements gave normal results: serum calcium, phosphorus, sodium, potassium, magnesium, pH, and pCO2. The administration of calcium had no effect on the frequency and intensity of the crisis. The response to carbemazepine was dramatic, with complete cessation of the crisis and disappearance of the spontaneous activity in the electromyogram. Interruption of treatment one year later was followed by relapse of the painful tonic crisis. The importance of certain electromyographic features and the therapeutic response to carbemazepine in the differential diagnosis of painful tonic crisis and tetany are emphasized. The existence of two clinical-electromyographic patterns in painful tonic crisis is pointed out.
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PMID:[Painful tonic seizures in multiple sclerosis. Clinical and electromyographic aspects (author's transl)]. 724 68

We present the rare case of a 62-year-old woman with Churg-Strauss syndrome associated with a left third nerve palsy and a mononeuritis multiplex. Cranial nerve palsies are unusual in patients with Churg-Strauss syndrome, and the most frequent cranial nerve lesion observed is an ischemic optic neuritis. Third nerve involvement secondary to vasculitis-induced ischemia is extremely rare in this disorder.
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PMID:Churg-Strauss syndrome associated with third nerve palsy and mononeuritis multiplex of the legs. 765 94

Loss of retinal ganglion cells (RGCs) is a hallmark of many ophthalmic diseases including glaucoma, retinal ischemia due to central artery occlusion, anterior ischemic optic neuropathy and may be significant in optic neuritis, optic nerve trauma, and AIDS. Recent research indicates that neurotoxicity is caused by excessive stimulation of receptors for excitatory amino acids (EAAs). In particular, the amino acid glutamate has been shown to act as a neurotoxin which exerts its toxic effect on RGCs predominantly through the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. NMDA-receptor-mediated toxicity in RGCs is dependent on the influx of extracellular Ca2+. The increase in [Ca2+]i acts as a second messenger that sets in motion the cascade leading to eventual cell death. Glutamate stimulates its own release in a positive feedback loop by its interaction with the non-NMDA receptor subtypes. Ca(2+)-induced Ca2+ release and further influx of Ca2+ through voltage-gated Ca2+ channels after glutamate-induced depolarization contribute to glutamate toxicity. In vitro and in vivo studies suggest that the use of selective NMDA receptor antagonists or Ca2+ channel blockers should be useful in preventing or at least abating neuronal loss in the retina. Of particular importance for future clinical use of NMDA receptor antagonists in the treatment of acute vascular insults is the finding that some drugs can prevent glutamate-induced neurotoxicity, even when administered a few hours after the onset of retinal ischemia.
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PMID:Molecular basis of glutamate toxicity in retinal ganglion cells. 942 25

We present the case of a 32-year-old man suffering from multiple sclerosis who had developed bilateral peripheral neovascularization of the retina. The main disease had been diagnosed 10 years before, whereas in his ophthalmic history the patient reported an incident of retrobulbar optic neuritis in his left eye occurring 3 years before. The patient was referred to our clinic in order to investigate the cause of a sudden loss of vision in his left eye. Ophthalmic examination and fluorescein angiography revealed the presence of a bilateral peripheral retinal neovascularization with an intravitreous hemorrhage in the left eye. Systemic clinical and laboratory investigation were negative for other causes of retinal neovascularization except multiple sclerosis, which is associated with periphlebitis in 10% of cases. Chronic retinal ischemia may lead to retinal neovascularization.
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PMID:[Bilateral peripheral retinal neovascularization in a patient with multiple sclerosis]. 1247 48

We report a case of an 18-year-old female, who was diagnosed as having systemic Behcet's disease with chief complaints of vision loss in the right eye and redness and pain in both eyes. In addition to an anterior necrotizing scleritis, she had several attacks of retrobulbar neuritis and lateral rectus myositis. She responded well to i.v. and topical prednisolone and her subsequent attacks were treated with i.v. cyclophosphamide (500 mg on presentation and on Days 7, 10, 12, 15, and 20; the cycle was repeated every 20 days). She benefited on this treatment and her vision improved dramatically. Her final acuity of 20/50 was thought to be due to presumed previous attacks of optic neuritis and anterior segment inflammation. During the five-month follow-up period, she had no other attacks. Ischemia and inflammation are common in Behcet's disease and sometimes thrombosis and vasculitic changes may cause a decrease in vision. In this case, the immunosuppressive therapy helped attenuate the inflammatory vasculitic episodes during the disease course.
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PMID:Myositis and scleritis associated with Behcet's disease: an atypical presentation. 1562 73

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

There are a number of illnesses that can mimic multiple sclerosis (MS). This pretty much includes any pathological process that can reflect injury to the central nervous system either in a transient or progressive basis. Typically, MS presents itself in individuals in their teens up to their late 30s. On occasion, however, one can see MS present in patients in their 60s. However, in retrospect, many of these patients might have had subtle manifestations of MS in their younger years. Visual obscuration or visual loss can be a manifestation of retinal ischemia, retinal migraine, or optic neuritis which might or might not evolve into a clinical picture compatible with MS. Cranial neuropathy, long tract signs, sensory disturbance, and/or gait ataxia can be related to a number of different processes such as illicit drug use, neurosarcoidosis, neuro-Behcet's disease, neuroborreliosis, HIV-related disease, neurosyphilis, vascular occlusive disease including vasculitis, connective tissue disorders, acute disseminated encephalomyelitis (ADEM), idiopathic transverse myelitis, neuromyelitis optica (NMO), or tropical spastic paraparesis. In addition, a constellation of symptoms, with questionable objective findings, along with normal MRI imaging, normal CSF results, and normal evoked response testing, when indicated, might identify a conversion disorder or possibly malingering. There are now established criteria for the diagnosis of MS, but initial presentations can be less than "textbook" in nature. With the advent of immunomodulating therapy, it has become more important to diagnose MS more effectively earlier on in the course of the illness. Prior to specific therapy for MS, astute clinicians did not necessarily move with alacrity to establish the diagnosis in patients with subtle or transient manifestations. This was in recognition of the fact that little could be offered to alter the course of the illness and a number of patients might never experience further problems if they were lucky enough to have their illness go into permanent remission after one minor exacerbation.
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PMID:Differential diagnosis of multiple sclerosis. 1753 52

The optic nerve is often affected in patients with glaucoma and multiple sclerosis. Conventional MRI can detect nerve damage, but it does not accurately assess the underlying pathologies. Mean diffusivity and diffusion anisotropy indices derived from diffusion tensor imaging have been shown to be sensitive to a variety of central nervous system white matter pathologies. Despite being sensitive, the lack of specificity limits the ability of these measures to differentiate the underlying pathology. Directional (axial and radial) diffusivities, measuring water diffusion parallel and perpendicular to the axonal tracts, have been shown to be specific to axonal and myelin damage in mouse models of optic nerve injury, including retinal ischemia and experimental autoimmune encephalomyelitis. The progression of Wallerian degeneration has also been detected using directional diffusivities after retinal ischemia. However, translating these findings to human optic nerve is technically challenging. The current status of diffusion MRI of human optic nerve, including imaging sequences and protocols, is summarized herein. Despite the lack of a consensus among different groups on the optimal sequence or protocol, increased mean diffusivity and decreased diffusion anisotropy have been observed in injured optic nerve from patients with chronic optic neuritis. From different mouse models of optic nerve injuries to the emerging studies on patients with optic neuritis, directional diffusivities show great potential to be specific biomarkers for axonal and myelin injury.
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PMID:Assessing optic nerve pathology with diffusion MRI: from mouse to human. 1875 87


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