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Optic Neuropathy (optic + neuropathy)
Kinds of Optic Neuropathy Selected AbstractsBrain barrier dysfunction in Cuban Epidemic Optic NeuropathyEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2008A. González-Quevedo Monteagudo Background and purpose:, There are practically no references to cerebrospinal fluid(CSF) studies in tropical or nutritional neuropathies. In the present paper we present the results of CSF studies in patients with Cuban Epidemic Optic Neuropathy (CEON) during epidemic and endemic periods, with an appraisal as to the contribution of brain barriers, function in the pathophysiology of this disease. Methods:, Two hundred and five patients with CEON were studied during the epidemic period (1992,1993) and 12 patients outside the outbreak (1995,1997). CSF protein determination and electrophoresis were carried out, as well as serum and CSF albumin and immunoglobulin G (IgG) quantitation for calculating IgG and Qalb indexes, in order to evaluate intrathecal IgG synthesis and the permeability of the blood,CSF barrier (B-CSF B). Results:, One fourth of the patients had increased permeability of the B-CSF B, but damage was more frequent between 16 and 60 days from onset of disease, disappearing after 120 days. B-CSF B dysfunction was more prevalent in patients with severe neurological impairment, although it was not related to the severity of ophthalmological damage. The group of patients studied outside of the outbreak (endemic period) showed similar results. Discussion:, The possible association of increased permeability of the B-CSF B with oxidative stress, which lies on the basis of this epidemic outbreak, is discussed. [source] Posterior Ischemic Optic Neuropathy Associated With MigraineHEADACHE, Issue 7 2008Rod Foroozan MD Posterior ischemic optic neuropathy (PION) is an uncommon form of optic nerve ischemia that results from damage to the intraorbital, intracanalicular, or intracranial optic nerve. It has been reported perioperatively, in association with systemic vasculitis, and in the nonsurgical setting with no identifiable cause. Review of the literature reveals only 2 patients with PION associated with migraine in a single report. We report a patient who developed PION in the setting of a migraine headache without any other identifiable risk factors. [source] Surgical Management of Compressive Optic Neuropathy due to Orbital Osseous LesionsTHE LARYNGOSCOPE, Issue S3 2010Gregg H. Goldstein M.D. No abstract is available for this article. [source] 4121: Combined OCT retinal nerve fibre layer analysis and VEP in neuro-ophthalmic diseaseACTA OPHTHALMOLOGICA, Issue 2010P GOOD Purpose Ocular Coherence Tomography (OCT) has become a valuable tool in assessing retinal nerve fibre layer thickness (RNFL) in Patients with optic nerve disease. This study is designed to compare RNFL thickness n with Visual Evoked Cortical Potentials (VECP)in patients with known optic nerve disease and comparing these to a group of patients with primary open angle glaucoma (POAG). Methods Twenty Patients (37 eyes) with clinically determined optic nerve disease underwent pattern reversal VECP and also OCT using a Spectralis OCT system. Assessment of global and segmental RNFL was made. Six Patients were diagnosed as Dominant Optic atrophy, 3 with Lebers Optic Neuropathy (LHON), 6 with Nutritional amblyopia, 3 with Anterior Ischaemic Optic Neuropathy (AION), and 2 with Demyelinating disease. These Patients were also compared to a group of 10 patients (20 eyes) with Primary Open Angle Glaucoma POAG. Results Pattern reversal VECP were abnormal in 32/37 eyes (86%): 26/32 (81%) of these being of reduced amplitude, and 20/32 (62%) being delayed. Amongst the patients with POAG only 4/20 eyes (20%) had abnormal VECP, and none were delayed. Thinning of the RNFL occurred in 36/37 eyes (97%) with optic nerve disease; 24 (65%) had global thinning, and the remainder segmental thinning only. All of the eyes with POAG had RNFL thinning but only 6/20 eyes (30%) had global thinning. Bipolar cell thinning of the central retina was noted in 6 eyes with optic nerve disease. Conclusion OCT is a valuable tool in the assessment of patients with optic nerve disease. Thinning of the RNFL was a more consistent finding than delay of the VECP in optic nerve disease, and a combination of VECP and OCT is helpful in the differential diagnosis of low tension glaucoma and optic nerve disease. [source] Ocular complications of neurological therapyEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2005S. Hadjikoutis Treatments used for several neurological conditions may adversely affect the eye. Vigabatrin-related retinal toxicity leads to a visual field defect. Optic neuropathy may result from ethambutol and isoniazid, and from radiation therapy. Posterior subcapsular cataract is associated with systemic corticosteroids. Transient refractive error changes may follow treatment with acetazolamide or topiramate, and corneal deposits and keratitis with amandatine. Intraocular pressure can be elevated in susceptible individuals by anticholinergic drugs, including oxybutynin, tolterodine, benzhexol, propantheline, atropine and amitriptyline, and also by systemic corticosteroids and by topiramate. Nystagmus, diplopia and extraocular muscle palsies can occur with antiepileptic drugs, particularly phenytoin and carbamazepine. Ocular neuromyotonia can follow parasellar radiation. Congenital ocular malformations can result from in utero exposure to maternally prescribed sodium valproate, phenytoin and carbamazepine. Neurologists must be aware of potential ocular toxicity of these drugs, and appropriately monitor for potential adverse events. [source] A case of Adamantiades-Behçet disease with ischemic optic neuritis (posterior optic neuropathy)JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, Issue 11 2007Satoko Shima Summary Adamantiades-Behçet disease (ABD) may present with cutaneous and ophthalmologic finings. A 29-year old woman complained of fever and general fatigue, along with erythema nodosum and vesiculo-pustular lesions on the legs, acneiform lesions, genital ulcerations and painful oral ulcers. She also complained of reduced visual acuity, visual disturbance and blurred vision in the left eye. Her left visual acuity was 6/20. Light reflex in the left eye was reduced. The relative afferent pupillary defect (RAPD) was positive in the left eye where a central scotoma was present. The vitreous was clear; the optic disc, macula, retina and iris were all normal. Uveitis was not observed. The patient was diagnosed with ischemic optic neuritis (posterior optic neuropathy) with ABD. Histopathological findings taken from a blister on the leg showed subepidermal bulla, dense dermal neutrophil infiltration, and extravasation of erythrocytes, suggesting leukocytoclastic vas-culitis. She was treated orally with high-dose corticosteroids (methylprednisolone 500 mg/d) for three days. Her general condition and ophthalmic symptoms resolved completely. Optic neuropathy with ABD is very rare; we know of two previous cases [1, 2] of ABD with ischemic posterior optic neuritis. [source] 18 years experience of the use of proton beam in ophthalmic tumoursACTA OPHTHALMOLOGICA, Issue 2009L DESJARDINS Purpose Since 1991, more than 3000 patients were treated at Curie Institute by proton beam for uveal melanoma. All datas concerning tumor characteristics, treatment planning and follow up are registered in the data base Methods We have performed a retrospective review of patients treated before 2005. Patients were sent to Curie by their local ophtalmologist. Clip positioning and proton beam therapy with a dose of 60 grays in 4 fractions was scheduled; All patients were seen once a year in our clinic after treatment with liver ultrasounds twice a year. Results 2214 patients were treated, median age 61 years, median diameter 13,6 mm, median Thickness 4,7 mm. 20% of patients develloped metastasis,25% of patients died, 4% had local recurrences, 6,7% had secondary enucleations; With multivariate analysis Significant risk factors for metastasis were age (>60 ), tumor location, tumor diameter and tumor thickness( p<0,0001); Significant risk factor for local recurrence was tumor diameter (p<0,001) significant risk factor for secondary enucleation were tumor diameter (p<0,0001) and tumor thickness (p= 0,003) Neovascular glaucoma was 10% at 2years , 30% at 5 years and 34% at 10 years. Maculopathy was 40% at 2 years, 62% at 5 years and 66% at 10 years Optic neuropathy was 14% at 2 years, 29% at 5 years and 38% at 10 years At last follow up 36,2% of patients have more than 20/40 vision Conclusion Tumor control obtained by proton beam is excellent with a long follow up For big tumors news additional techniques like endoresections, additional TTT or antiVEGF could enhance globe preservation [source] Optic neuropathy secondary to radiotherapy for nasal melanomaCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2004Helen Garrott MB BS Abstract Optic neuropathy is a rare but important complication of radiotherapy used in the treatment of cancers of the head and neck, usually resulting in rapidly progressive blindness in one or both eyes. The case is presented of a 77-year-old woman with bilateral optic neuropathy resulting in blindness, secondary to radiotherapy for a melanoma of the nasal cavity. The onset of optic neuropathy occurred 9 months post-radiotherapy, at a cumulative dose of 6000 rad. The left eye was first involved, with the right eye becoming involved within 2 weeks. Despite treatment with oral anticoagulation and high dose intravenous methylprednisolone, there was progressive deterioration resulting in bilateral optic atrophy, with final visual acuities of perception of light in the right eye and no perception of light in the left eye. This case demonstrates that oral anticoagulation was ineffective in the treatment of progressive radiation-induced optic neuropathy. [source] Molecular screening of 980 cases of suspected hereditary optic neuropathy with a report on 77 novel OPA1 mutations,HUMAN MUTATION, Issue 7 2009Marc Ferré Abstract We report the results of molecular screening in 980 patients carried out as part of their work-up for suspected hereditary optic neuropathies. All the patients were investigated for Leber's hereditary optic neuropathy (LHON) and autosomal dominant optic atrophy (ADOA), by searching for the ten primary LHON-causing mtDNA mutations and examining the entire coding sequences of the OPA1 and OPA3 genes, the two genes currently identified in ADOA. Molecular defects were identified in 440 patients (45% of screened patients). Among these, 295 patients (67%) had an OPA1 mutation, 131 patients (30%) had an mtDNA mutation, and 14 patients (3%), belonging to three unrelated families, had an OPA3 mutation. Interestingly, OPA1 mutations were found in 157 (40%) of the 392 apparently sporadic cases of optic atrophy. The eOPA1 locus-specific database now contains a total of 204 OPA1 mutations, including 77 novel OPA1 mutations reported here. The statistical analysis of this large set of mutations has led us to propose a diagnostic strategy that should help with the molecular work-up of optic neuropathies. Our results highlight the importance of investigating LHON-causing mtDNA mutations as well as OPA1 and OPA3 mutations in cases of suspected hereditary optic neuropathy, even in absence of a family history of the disease. © 2009 Wiley-Liss, Inc. [source] Support for the idea that light is a risk factor in optic neuropathies, like glaucomaACTA OPHTHALMOLOGICA, Issue 2007NN OSBORNE Purpose: Retinal ganglion cell (RGC) axons in the globe contain many mitochondria and it has been hypothesised that light can interact with these organelles to affect RGC survival in glaucoma. Studies on different cell-types were conducted to support such a proposition. Methods: Near confluent cultures of RGC-5 cells, primary rat retinal cultures, fibroblasts with normal (BJhTERT) or mitochondria depleted of mtDNA (rho0) were transferred to incubators containing light (400-760nm; 800-2000 lux; generally 2 days). Some of the cultures were covered with white paper to exclude the light. The cultures were then analysed for cell viability, generation of free radicals (ROS) and for death by apoptosis. Results: Oxidative status and mitochondrial dehydrogenase activity in retinal cultures (-40±5%), RGC-5 cells (-20±4%) and BJhTERT cells (-13±3%) was reduced significantly by light. Light reduced the number of GABA-positive neurones (-42±6%) in retinal cultures. Light caused a 3-5 fold increase in TUNEL-positive cells in primary retinal, RGC-5 and BJhTERT cultures, than in the dark. ROS staining was also clearly elevated by light. The light-induced toxic effect on the different cell types was significantly blunted by antioxidants like vitamin E and lipoic acid. Moreover, light-induced apoptosis was caspase independent but PARP dependent. In contrast, rho0 cells that lacked functional mitochondria were unaffected by light. Conclusions: The present study shows that light can directly affect mitochondrial function to induce apoptosis. This supports the view that light can interact with the many RGC axon mitochondria to affect the viability of GCs and that this may be of significance in the progression of glaucoma. [source] Anterior ischemic optic neuropathy in moyamoya disease: a first case reportEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2007C. S. Chen Neuro-ophthalmological manifestations in moyamoya disease are usually the result of cerebrovascular involvement of the visual pathways. We report a case of ischemic optic neuropathy due to ocular hypoperfusion as a result of moyamoya disease, despite a prior internal to external carotid artery bypass with normal hemisphere perfusion. The blood supply of the optic nerve, a proposed pathogenesis of an anterior ischemic optic neuropathy and complications of the ocular ischemic syndrome are discussed. [source] White matter changes in Leber's hereditary optic neuropathy: MRI findingsEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007W. Küker Leber's hereditary optic neuropathy is a mitochondrial disorder causing bilateral optic nerve degeneration. It is sometimes associated with clinical signs of multiple sclerosis. We report MRI findings in two patients with LHON-MS and comment on possible distinguishing features of this disease entity. [source] The synthetic cannabinoid WIN55212-2 decreases the intraocular pressure in human glaucoma resistant to conventional therapiesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2001Anna Porcella Abstract The search for new ocular hypotensive agents represents a frontier of current eye research because blindness due to optic neuropathy occurs insidiously in 10% of all patients affected by glaucoma. Cannabinoids have been proposed to lower intraocular pressure by either central or peripheral effects but a specific mechanism for this action has never been elucidated. We recently demonstrated the presence of the central cannabinoid receptor (CB1) mRNA and protein in the human ciliary body. In the present study we show that the synthetic CB1 receptor agonist, WIN 55212,2, applied topically at doses of 25 or 50 µg (n = 8), decreases the intraocular pressure of human glaucoma resistant to conventional therapies within the first 30 min (15 ± 0.5% and 23 ± 0.9%, respectively). A maximal reduction of 20 ± 0.7% and 31 ± 0.6%, respectively, is reached in the first 60 min. These data confirm that CB1 receptors have direct involvement in the regulation of human intraocular pressure, and suggest that, among various classes of promising antiglaucoma agents, synthetic CB1 receptor agonists should deserve further research and clinical development. [source] Malignant tumors of the nasal cavity and paranasal sinuses,HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 9 2002Teri S. Katz MD Abstract Purpose To evaluate the role of radiation therapy in patients with nasal cavity and paranasal sinus tumors. Materials and Methods Between October 1964 and July 1998, 78 patients with malignant tumors of the nasal cavity (48 patients), ethmoid sinus (24 patients), sphenoid sinus (5 patients), or frontal sinus (1 patient) were treated with curative intent by radiation therapy alone or in the adjuvant setting. There were 25 squamous cell carcinomas, 14 undifferentiated carcinomas, 31 minor salivary gland tumors (adenocarcinoma, adenoid cystic carcinoma, and mucoepidermoid carcinoma), 8 esthesioneuroblastomas, and 1 transitional cell carcinoma. Forty-seven patients were treated with irradiation alone, 25 with surgery and postoperative irradiation, 2 with preoperative irradiation and surgery, and 4 with chemotherapy in combination with irradiation with or without surgery. Results The 5-year actuarial local control rate for stage I (limited to the site of origin; 22 patients) was 86%; for stage II (extension to adjacent sites (eg, adjacent sinuses, orbit, pterygomaxillary fossa, nasopharynx; 21 patients) was 65%; and for stage III (destruction of skull base or pterygoid plates, or intracranial extension; 35 patients) was 34%. The 5-year actuarial local control rate for patients receiving postoperative irradiation was 79% and for patients receiving irradiation alone was 49% (p = .05). The 5-, 10-, 15-, and 20-year ultimate local control rates for all 78 patients were 60%, 56%, 48%, and 48%, respectively. The 5-, 10-, 15-, and 20-year cause-specific survival rates for all 78 patients were 56%, 45%, 39%, and 39%, respectively. The 5-, 10-, 15-, and 20-year absolute survival rates for all 78 patients were 50%, 31%, 21%, and 16%, respectively. Of the 67 (86%) patients who were initially seen with node-negative disease, 39 (58%) received no elective neck treatment, and 28 (42%) received elective neck irradiation. Of the 39 patients who received no elective neck treatment, 33 (85%) did not experience recurrence in the neck compared with 25 (89%) of 28 patients who received elective neck irradiation. Most patients who received elective neck irradiation (57%) had stage III disease. Twenty-one (27%) of 78 patients had unilateral blindness develop secondary to radiation retinopathy or optic neuropathy; the complication was anticipated in most of these patients, because the ipsilateral eye was irradiated to a high dose. Four patients (5%) unexpectedly had bilateral blindness develop because of optic neuropathy. All four of these patients received irradiation alone. Conclusion Surgery and postoperative radiation therapy may result in improved local control, absolute survival, and complications when compared with radiation therapy alone. Elective neck irradiation is probably unnecessary for patients with early-stage disease. © 2002 Wiley Periodicals, Inc. Head Neck 24: 821,829, 2002 [source] Posterior Ischemic Optic Neuropathy Associated With MigraineHEADACHE, Issue 7 2008Rod Foroozan MD Posterior ischemic optic neuropathy (PION) is an uncommon form of optic nerve ischemia that results from damage to the intraorbital, intracanalicular, or intracranial optic nerve. It has been reported perioperatively, in association with systemic vasculitis, and in the nonsurgical setting with no identifiable cause. Review of the literature reveals only 2 patients with PION associated with migraine in a single report. We report a patient who developed PION in the setting of a migraine headache without any other identifiable risk factors. [source] Molecular screening of 980 cases of suspected hereditary optic neuropathy with a report on 77 novel OPA1 mutations,HUMAN MUTATION, Issue 7 2009Marc Ferré Abstract We report the results of molecular screening in 980 patients carried out as part of their work-up for suspected hereditary optic neuropathies. All the patients were investigated for Leber's hereditary optic neuropathy (LHON) and autosomal dominant optic atrophy (ADOA), by searching for the ten primary LHON-causing mtDNA mutations and examining the entire coding sequences of the OPA1 and OPA3 genes, the two genes currently identified in ADOA. Molecular defects were identified in 440 patients (45% of screened patients). Among these, 295 patients (67%) had an OPA1 mutation, 131 patients (30%) had an mtDNA mutation, and 14 patients (3%), belonging to three unrelated families, had an OPA3 mutation. Interestingly, OPA1 mutations were found in 157 (40%) of the 392 apparently sporadic cases of optic atrophy. The eOPA1 locus-specific database now contains a total of 204 OPA1 mutations, including 77 novel OPA1 mutations reported here. The statistical analysis of this large set of mutations has led us to propose a diagnostic strategy that should help with the molecular work-up of optic neuropathies. Our results highlight the importance of investigating LHON-causing mtDNA mutations as well as OPA1 and OPA3 mutations in cases of suspected hereditary optic neuropathy, even in absence of a family history of the disease. © 2009 Wiley-Liss, Inc. [source] Current safety and tolerability issues in men with erectile dysfunction receiving PDE5 inhibitorsINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2007W. J. G. Hellstrom Summary Aims:, Treatment of erectile dysfunction (ED) has been greatly advanced by the advent of phosphodiesterase type-5 (PDE5) inhibitors. Upon the introduction of these agents, their cardiovascular (CV) safety was a major concern, mainly due to their vasodilatory effects. We conducted an electronic literature review of data concerning the safety and tolerability issues of men with ED receiving PDE5 inhibitors. Results:, Although safety concerns have been raised, evaluation of CV safety and related adverse events in clinical trials has not revealed any atypical safety issues. Discussion:, No causal association has been established to date between non-arteritic anterior ischaemic optic neuropathy (NAION) and PDE5 inhibitors. In addition, there are established guidelines which provide recommendations for the safe and effective use of these agents in treating men with ED and associated comorbidities. Conclusions:, Clinical trial and postmarketing surveillance data confirm the safety and tolerability profile of the PDE5 inhibitors, even in patients with endothelial dysfunction-associated comorbidities. [source] A case of Adamantiades-Behçet disease with ischemic optic neuritis (posterior optic neuropathy)JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, Issue 11 2007Satoko Shima Summary Adamantiades-Behçet disease (ABD) may present with cutaneous and ophthalmologic finings. A 29-year old woman complained of fever and general fatigue, along with erythema nodosum and vesiculo-pustular lesions on the legs, acneiform lesions, genital ulcerations and painful oral ulcers. She also complained of reduced visual acuity, visual disturbance and blurred vision in the left eye. Her left visual acuity was 6/20. Light reflex in the left eye was reduced. The relative afferent pupillary defect (RAPD) was positive in the left eye where a central scotoma was present. The vitreous was clear; the optic disc, macula, retina and iris were all normal. Uveitis was not observed. The patient was diagnosed with ischemic optic neuritis (posterior optic neuropathy) with ABD. Histopathological findings taken from a blister on the leg showed subepidermal bulla, dense dermal neutrophil infiltration, and extravasation of erythrocytes, suggesting leukocytoclastic vas-culitis. She was treated orally with high-dose corticosteroids (methylprednisolone 500 mg/d) for three days. Her general condition and ophthalmic symptoms resolved completely. Optic neuropathy with ABD is very rare; we know of two previous cases [1, 2] of ABD with ischemic posterior optic neuritis. [source] Wilson's disease presenting with rapidly progressive visual loss: Another neurologic manifestation of Wilson's disease?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2001Paul J Gow Abstract Wilson's disease (WD) is a rare autosomal recessive disorder of copper metabolism resulting in copper-induced tissue damage that primarily involves the liver and central nervous system. The neurologic manifestations of WD almost universally involve a derangement of basal ganglia function or psychiatric disturbance. We report the case of a 46-year-old man presenting with end-stage liver disease caused by WD who had associated rapidly progressive optic neuropathy. We also discuss the possible association between the two conditions. [source] In Vivo Labeling of Mitochondrial Complex I (NADH:UbiquinoneOxidoreductase) in Rat Brain Using [3H]DihydrorotenoneJOURNAL OF NEUROCHEMISTRY, Issue 6 2000Deepa J. Talpade Abstract: Defects in mitochondrial energy metabolism have beenimplicated in several neurodegenerative disorders. Defective complex I(NADH:ubiquinone oxidoreductase) activity plays a key role in Leber'shereditary optic neuropathy and, possibly, Parkinson's disease, but there isno way to assess this enzyme in the living brain. We previously described anin vitro quantitative autoradiographic assay using[3H]dihydrorotenone ([3H]DHR) binding to complex I. Wehave now developed an in vivo autoradiographic assay for complex I using[3H]DHR binding after intravenous administration. In vivo[3H]DHR binding was regionally heterogeneous, and brain uptake wasrapid. Binding was enriched in neurons compared with glia, and white matterhad the lowest levels of binding. In vivo [3H]DHR binding wasmarkedly reduced by local and systemic infusion of rotenone and was enhancedby local NADH administration. There was an excellent correlation betweenregional levels of in vivo [3H]DHR binding and the in vitroactivities of complex II (succinate dehydrogenase) and complex IV (cytochromeoxidase), suggesting that the stoichiometry of these components of theelectron transport chain is relatively constant across brain regions. Theability to assay complex I in vivo should provide a valuable tool toinvestigate the status of this mitochondrial enzyme in the living brain andsuggests potential imaging techniques for complex I in humans. [source] Methylprednisolone exacerbates axonal loss following optic nerve trauma in ratsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2002KD Steinsapir PURPOSE: This study investigates the clinical dogma that very high doses of methylprednisolone helpful in spinal cord injury are also helpful in optic nerve trauma. Methods: The right optic nerve of 29 male rats received a 5 second traumatic crush followed 30 minutes later by one of five intravenous treatments (methylprednisolone 30 mg/kg, 60 mg/kg, 90 mg/kg, 120 mg/kg, or saline). Treatment was continued for three additional administrations at 6 hour intervals. Untreated sham controls (n = 7) were also prepared. Six weeks after injury, animals were sacrificed, perfused and optic nerves systematically counted. RESULTS: Axon counts (means +/, s.e.m.) were as follows: Saline = 16,670 +/, 8,900 (n = 5); Methylprednisolone: 30 mg/kg = 8,098 +/, 4,741 (n = 5); 60 mg/kg = 6,925 +/, 6,517 (n = 4); 90 mg/kg = 2,663 +/, 2,653 (n = 4); 120 mg/kg = 6,149 +/, 3,487 (n = 6). Consequently, the data revealed that saline treated animals retained more axons than those that were administered methylprednisolone (p < 0.02). CONCLUSIONS: We conclude that methylprednisolone exacerbates axonal loss following crush injury in the rat optic nerve. Based on the results of this study, clinical studies of traumatic optic neuropathy in the future should also examine the possibility that corticosteroid treatment may have an adverse effect on visual outcome following optic nerve trauma. [source] Effects of optic nerve injury, glaucoma, and neuroprotection on the survival, structure, and function of ganglion cells in the mammalian retinaTHE JOURNAL OF PHYSIOLOGY, Issue 18 2008A. J. Weber Glaucoma is an optic neuropathy that originates with pressure-induced damage to the optic nerve. This results in the retrograde degeneration of ganglion cells in the retina, and a progressive loss of vision. Over the past several years, a number of studies have described the structural and functional changes that characterize ganglion cell degeneration in the glaucomatous eye, and following optic nerve injury. In addition, a variety of different strategies for providing neuroprotection to the injured retina have been proposed. Many of these are based on the use of brain-derived neurotrophic factor (BDNF), a particularly potent neuroprotectant in the mammalian eye and the basis of our research in this area. Of particular importance is the fact that BDNF not only promotes ganglion cell survival following damage to the optic nerve, but also helps to preserve the structural integrity of the surviving neurons, which in turn results in enhanced visual function. The studies presented here describe these attributes, and serve as the foundation for ongoing work that suggests a need to think beyond the eye in the development of future treatment strategies. [source] Men's Sexual Health: Evaluating the Effectiveness of Print- and PDA-based CMETHE JOURNAL OF SEXUAL MEDICINE, Issue 9 2009Gregory A. Broderick MD ABSTRACT Introduction., Personal digital assistant (PDA)-based continuing medical education (CME) activities have become widely available. Aims., To evaluate the effectiveness of print- and PDA-based CME materials in erectile dysfunction (ED). Methods., CME materials describing links between ED and comorbid medical conditions, effects of certain lifestyle modifications on ED, and treatment of ED with phosphodiesterase 5 (PDE5) inhibitors were distributed as a print supplement and as electronic modules, viewed with PDAs. We evaluated how effectively these materials improved evidence-based clinical choices, using survey questions about case vignettes and comparing responses of CME participants (N = 85) and matched nonparticipants (N = 94). Main Outcome Measures., Effect size, measuring the difference in evidence-based clinical scores between participants and nonparticipants. Results., CME certificates were awarded to 3,557 participants (459 print, 3,098 PDA). Among survey respondents, significantly more CME participants recognized that ED was associated with greater risk for myocardial infarction (61% participants; 34% nonparticipants; P , 0.001) and was a strong marker for diabetes mellitus (37% participants; 9% nonparticipants; P , 0.001). In contrast, participants and nonparticipants both displayed a good understanding of the relationships of smoking, obesity, and sedentary lifestyle with ED and of using PDE5 inhibitors to treat ED in patients with prostate cancer or benign prostatic hyperplasia; this likely reflects a good baseline understanding of these topics. Participants and nonparticipants each displayed a poor understanding of the recommendations regarding nonarteritic anterior ischemic optic neuropathy and PDE5 inhibitor use. Patient reluctance to discuss sexual concerns was perceived as the most significant barrier to optimal ED management. Conclusions., Given patient reluctance to discuss sexual concerns, future CME activities should focus on educating health-care providers and patients that ED is a risk factor for cardiovascular disease and diabetes. Both print- and PDA-based CME on ED were effective; the large number of lesson completers suggests a trend toward on-demand, self-selected CME is positive. Broderick GA, and Abdolrasulnia M. Men's sexual health: Evaluating the effectiveness of print- and PDA-based CME. J Sex Med 2009;6:2417,2424. [source] Nonarteritic ischaemic optic neuropathy (NAION) after 36 h of intake of sildenafil citrate: first Egyptian caseANDROLOGIA, Issue 5 2009M. M. El-Domyati Summary Sildenafil citrate is a selective phosphodiesterase 5 (PDE-5) inhibitor and partial phosphodiesterase 6 inhibitor prescribed for erectile dysfunction. Post-marketing case reports of nonarteritic anterior ischaemic optic neuropathy (NAION) over the past few years suggest a potential link with PDE-5 inhibitors. We report a case of a 48-year-old male patient who had acute vision loss 36 h after the intake of 50 mg sildenafil citrate. NAION occurred at a period of minimal blood level of sildenafil citrate. So, erectile dysfunction drugs must be strongly considered with NAION even though their users may have neither predisposing nor precipitating factors for NAION and even if occurring at a time of minimal blood level of these drugs. [source] Retinal and Optic Nerve DiseasesARTIFICIAL ORGANS, Issue 11 2003Eyal Margalit Abstract:, A variety of disease processes can affect the retina and/or the optic nerve, including vascular or ischemic disease, inflammatory or infectious disease, and degenerative disease. These disease processes may selectively damage certain parts of the retina or optic nerve, and the specific areas that are damaged may have implications for the design of potential therapeutic visual prosthetic devices. Outer retinal diseases include age-related macular degeneration, pathologic myopia, and retinitis pigmentosa. Although the retinal photoreceptors may be lost, the inner retina is relatively well-preserved in these diseases and may be a target for retinal prosthetic devices. Inner retinal diseases include retinal vascular diseases such as diabetic retinopathy, retinal venous occlusive disease, and retinopathy of prematurity. Other retinal diseases such as ocular infections (retinitis, endophthalmitis) may affect all retinal layers. Because the inner retinal cells, including the retinal ganglion cells, may be destroyed in these diseases (inner retinal or whole retinal), prosthetic devices that stimulate the inner retina may not be effective. Common optic nerve diseases include glaucoma, optic neuritis, and ischemic optic neuropathy. Because the ganglion cell nerve fibers themselves are damaged, visual prosthetics for these diseases will need to target more distal portions of the visual pathway, such as the visual cortex. Clearly, a sound understanding of retinal and optic nerve disease pathophysiology is critical for designing and choosing the optimal visual prosthetic device. [source] Prostanoids in the Therapy of GlaucomaCARDIOVASCULAR THERAPEUTICS, Issue 1 2006Naruhiro Ishida ABSTRACT Elevated intraocular pressure (IOP) is one of the most important risk factors for the development of glaucoma, which is a progressive optic neuropathy. Lowering IOP is currently the only therapeutic approach to the therapy of glaucoma. Since the use of pilocarpine eye drops for glaucoma treatment was reported in the late 1870s, academic researchers and pharmaceutical companies attempted to discover new drugs with more potent, prolonged, and safer IOP-reducing effects. These persistent efforts finally paid off, and prostanoids with FP-receptor agonist activity were found to be very potent IOP-lowering agents. To date, three prostanoids (latanoprost, travoprost and bimatoprost) have been launched in many countries, and now a new FP-receptor agonist, tafluprost, is entering clinical development. All of these prostanoids are superior to the ,-adrenoceptor antagonists in their IOP-lowering efficacy, and no severe side effects have been reported in their long-term clinical use. In addition, tafluprost may be expected to improve ocular blood flow. Hence, prostanoids currently occupy center stage among glaucoma medications. It cannot be denied that in terms of efficacy, safety, patient compliance, and medical economy prostanoids are currently the first-line medicines among ocular antihypertensive drugs. [source] Visual recovery in a man with the rare combination of mtDNA 11778 LHON mutation and a MS-like disease after mitoxantrone therapyACTA NEUROLOGICA SCANDINAVICA, Issue 4 2002C. Buhmann Buhmann C, Gbadamosi J, Heesen C. Visual recovery in a man with the rare combination of mtDNA 11778 LHON mutation and a MS-like disease after mitoxantrone therapy. Acta Neurol Scand 2002: 106: 236,239. © Blackwell Munksgaard 2002. We describe a young man with prognostic unfavourable homoplasmatic mitochondrial DNA(mt DNA) 11778 Leber's hereditary optic neuropathy (LHON) point mutation and confirmed multiple sclerosis (MS). This combination of LHON and MS-like disease is rare in both sexes, and in men has been described in only a few case reports. In a 4-year follow-up during immunosuppressive therapy with mitoxantrone, we found a remarkable time delayed visual recovery 12 months after acute onset of rapid sequential bilateral subtotal visual loss followed by episodes of isolated acute demyelinative optic neuropathy. Visual recovery to such extent after this latency is uncommon in both mtDNA 11778 LHON mutation and optic neuritis (ON) in MS. Relapses in visual deterioration must be considered as extremely rare in LHON. This case might support the hypothesis of an immunological pathogenetic factor in combined LHON and MS, and possibly in LHON alone. We suggest a search for the LHON mutation in MS patients with predominant visual impairment, independent of patients' gender. [source] 4343: What next when the biopsy is negative in suspected giant cell arteritis (GCA)?ACTA OPHTHALMOLOGICA, Issue 2010A BOSCHI Purpose To present and discuss the approach of GCA when temporal artery biopsy (TAB) is negative. Recommendations for reducing the rate of negative TAB Methods GCA is the commonest vasculitis. Visual loss occurs in up to one-fifth of patients, which may be preventable by prompt recognition and treatment. Features predictive of ischaemic neuro-ophthalmic complications are: jaw claudication, diplopia, and temporal artery abnormalities on physical examination. These manifestations and particularly blindness and jaw claudication seems to be more commonly associated with positive TAB. Results Despite visual symptoms TAB may result negative. Rate of negative TAB varies from 7% to 40% in pat suspected of GCA. TAB should be done 2 to 6 weeks after commencement of treatment, and at least 1 cm. Contralateral biopsy is controversies, usually it increases the rate of GCA diagnosis of only 5%. Conclusion If TAB is still however negative, but clinical suspicion high or Ultra-Sound suggests GCA or complications typical of GCA, like anterior ischemic optic neuropathy, patient should be treat as biopsy-positive GCA patient. If the clinical suspicion is low, features considered atypical or alternative explanations available, rapid glucocorticoid therapy should be tapered. [source] 2423: Compartment syndrome in glaucoma damage, a new hypothesis?ACTA OPHTHALMOLOGICA, Issue 2010S ORGUL Purpose To evaluate the potential similarities in pathophysiology between non-arteritic anterior ischemic optic neuropathy (AION) and primary open-angle glaucoma (POAG). Methods The currently accepted views of the pathophysiology of AION and general understanding of the clinical picture of this ischemic condition were reviewed. Based on the hypothesis of the group in Wisconsin, who postulated a compartment syndrome of the anterior optic nerve within the tight anatomical structures of the lamina cribrosa, parallels were drawn for glaucomatous optic neuropathy, and a new hypothesis for the pathogenesis of the latter condition was suggested. Results The tight structures around, but also within the "disk at risk" observed in a majority of patients with AION are well compatible with the hypothesis of a compartment syndrome. Similar conditions may result from the restructuring process within the lamina cribrosa in POAG and lead to locally limited, but repeated "AION-like" processes, explaining why some patients progress despite reduced intraocular pressure. Conclusion The pathophysiology of POAG, especially in advanced cases, and AION seem to present similarities, which need to be better understood. [source] 3161: Traumatic optic neuropathy: diagnosis and managementACTA OPHTHALMOLOGICA, Issue 2010A CARTA [source] | |||||||||||||